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iRfcOT T36I 

Columbia Umbers^ 
in tfje Citj> of Jieto fiorfe 

g>ti)ool of Bental anb <2£ral gmrgerp 

Reference Hibrarp 




Kurt H. Thoma, d.m.d. 









.,' ' 


The right of reproduction of the original illustrations is 
strictly reserved. 

Copyrighted at the Registry of Copyrights, Washington, 
D. C, 1916. 

All Rights Reserved 







Digitized by the Internet Archive 

in 2010 with funding from 

Open Knowledge Commons 


The important discovery that septic lesions in the month 
may be foci or primary causes of many acute or chronic 
diseases of systemic nature has brought about great 
changes in the relationship between dentistry and medi- 
cine. The teeth, which formerly were regarded as organs 
totally apart from the rest of the body, are now considered 
as one of the most important gateways through which dis- 
ease may enter. The dentist who originally held it his 
duty mechanically to repair diseased or lost dental tissue 
is now confronted with a problem the vitality of which, 
if he has a sincere interest in the health of his patients 
and in the development of his prof ession, demands a new 
study of the septic conditions of the mouth. 

This book is intended for the practicing dentist as well 
as for the student. It aims to give a clear understanding 
of the pathology, treatment, and prevention of oral le- 
sions, and to familiarize the student with the recognition 
and nature of certain infectious diseases which may be 
caused by them. 

The practicing physician will also find this book of in- 
terest. In the search for the primary or secondary foci 
of systemic diseases he often has occasion to look into 
the condition of the oral cavity, as it stands out as an im- 
portant entrance for disease, although it has been until 
recently neglected as such. 

This volume has been written with a view to establish- 
ing a correct relationship between the condition of the 


oral cavity and the health of the patient, and also in the 
hope that a clear presentation may lead to a more general 
understanding of this new field. 

The author wishes to express his sincere thanks to those 
of his friends who have aided him in bringing his book 
before the profession. He wishes especially to express 
his indebtedness to Dr. T. B. Hartzel for his kind assis- 
tance in furnishing colored microphotographs of lesions 
produced experimentally in the rabbit ; to Dr. L. B. Mor- 
rison, of the Robert B. Brigham Hospital, for his compe- 
tent assistance in radiography of hospital cases; to Dr. 
William P. Cooke, for furnishing radiographs; to Dr. 
W. H. Potter, for his examination chart; and to Dean 
Eugene H. Smith, of the Harvard Dental School, for 
photographs of models of two cases showing the results 
of judicious extraction of decayed teeth in children. In 
connection with the more detailed compilation of the 
various parts of this volume, the author wishes to thank 
Miss Herf ord, for her efficient work in delineation, and 
Mr. John W. Cooke, for his aid in the preparation of the 

Kurt H. Thoma, d.m.d. 

43 Bay State Road, 

Boston, Massachusetts. 
July 3, 1916. 




The Infective Virus 1 

Bacterial Ferments 2 

Extracellular Ferments ; Intracellular Ferments .... 2 

Toxins (extracellular toxin) 3 

The Body Cell 3 

Ferments of the Body Cell 3 

Phagocytes 4 

Two Biological Laws • 4 

Protective Defences of the Body 4 

Resistance 4 

Decrease of Resistance ; Increase of Resistance 4, 5 

Bacterial Immunity 5 

Natural Immunity ; Acquired Immunity 5 

Toxin Immunity 6 

The Process of Infection 6 

Incubation 6 

Sensitization 7 

Protein Poison (Intracellular Toxin) Caused by 

Bacterial Destruction 7 

Protein Poison Caused by Bacterial Metabolism from 

the Body Cell 8 

The Action of the Bacterial Ferments 8 

The Influence of the Medium 8 

By-products of Bacterial Metabolism 8 

Toxin 9 

Clinical Picture of the Infection 9 

Influence of Quantity in Infection 9 

Influence of Bacterial Growth in Infection 9 

Influence of Virulence in Infection 9 

Acute and Chronic Infection 10 



Local Infection 10 

Local Effects 10 

General Effects 10 

Fever ; Changes in the Blood 10 

Geneeal Infection 11 

Toxemia 11 

Bacteremia 11 

Metastasis 11 

Secondary or Transported Infections 11 

The Focus 12 

Channels of Absorption 12 

Oral Foci 13 

Secondary Manifestation 13 


History 15 

Classification 15 



Acute Periodontitis and its Sequels 18 

Proliferating Periodontitis and its Sequels 19 

1. Acute Periodontitis and its Sequels. 



Acute Apical Periodontitis 19 

Acute Lateral Periodontitis 19 

Acute Interradial Periodontitis 19 




Traumatic Injury of the Tooth 20 

Infection from Adjacent Teeth .' 20 

Infection from Pus Pockets 20 

Thermal Shocks 21 

Chemical Action of Fillings 21 

Crowned Teeth 21 

Decay of Deciduous Teeth 21 

Decay of Permanent Teeth 22 

Filling Teeth with Infected Pulps 23 

Instrumentation 23 

Change in Oxygen Tension 23 

Course of the Disease. 

Acute Periodontitis 24 

Acute Alveolar Parulis 24 

Subperiosteal Parulis 24 

Subgingival Parulis 25 

Sinus into Mouth 25 

Sinus to the Face 25 

Sinus to the Antrum of Highmore 26 

Sinus to the Nasal Cavity 26 


Osteomyelitis 26 

Ostitis 26 

Necrosis 26 


Resolution 27 

Scar Bone 27 

Chronic Alveolar Abscess 27 

With Active Sinus 27 

With Closed Sinus 27 

Subacute Alveolar Abscess 28 

Exostosis of the Root 28 

Necrosis of the Root 29 



Diagnosis. (Local Symptoms, General Symptoms, 
Clinical Signs, Radiographic Examination.) 

Acute Periodontitis 29 

Acute Alveolar Abscess 30 

Dento Alveolar Parulis 31 

Chronic Alveolar Abscess 33 

2. Proliferating Periodontitis and its Sequels. 


Apical Granuloma 35 

Lateral Granuloma 35 

Interradial Granuloma 35 


Decay of the Tooth 36 

Incomplete Pulp Extirpation 36 

Inefficient Root-canal Treatment 37 

Inefficient Root-canal Filling 38 

Invasion of Bacteria 38 

Death of Pulp Without Access of Air 38 

Haematogenous Infection 39 

Course of the Disease. 

Proliferating Periodontitis 39 

Granuloma 39 

Subacute Attacks 40 

Exostosis of the Root 40 

Necrosis of the Root 40 


Resolution 41 

Osteomyelitis 41 

Cysts 41 

Diagnosis. (Local Symptoms, General Symptoms, 
Clinical Signs, Radiographic Examination.) 

Proliferating Periodontitis 42 

Granuloma 42 

Subacute Attacks 43 




PULP 45 

I. Alveolar Abscesses Due to Diseases of the Gum 45 

Etiology 45 

Course of the Disease 46 

Diagnosis (Local and General Symptoms, Clinical 

Signs, Radiographic Examination) 47 

II. Alveolar Abscess due to Difficult Eruption, 

Impaction, and Unerupted Teeth 47 

Etiology 47 

Course of the Disease 49 

Diagnosis (Local Symptoms, General Symptoms, 

Clinical Signs, Radiographic Examination). . .49, 50 


I. Abscesses of the Tongue 51 

1. The Simple Abscess of the Tongue 51 

Etiology 51 

Clinical Course of the Disease 52 

Diagnosis (Local Symptoms, Clinical Signs) 52 

2. The Phlegmonous Abscess of the Tongue 52 

Etiology 52 

Clinical Course of the Disease 52 

Diagnosis (Local Symptoms, General Symptoms, 

Clinical Signs) 53 

3. The Tubercular Abscess of the Tongue 53 

Etiology 53 

Clinical Course of the Disease 54 

Diagnosis (Local Symptoms, General Symptoms, 

Clinical Signs) 54 




II. Abscesses of the Salivary Glands and Ducts . . 54 

Etiology 55 

Primary Infections 55 

Secondary Infection 55 

Salivary Calculi 55 

Clinical Course of the Disease 56 

Diagnosis (Local Symptoms, Clinical Signs, Rad- 
iographic Examination) 56, 57 


Importance of Bacteriological Study 58 

Methods of Collecting Bacterial Specimens 59 

From Acute Abscesses 59 

From Chronic Abscesses and Granulomata of Teeth 

which are extracted 59 

From Chronic Abscesses and Granulomata in Apiec- 

tomy 60 

Methods of Bacterial Study 60 

Immediate Microscopic Study 60 

Inoculation of Artificial Culture Media 60 

Inoculation of Animals 61 

Review of the Bacteriological Study of Oral 

Abscesses 61 

Schreier, 1893, on Parulis 61 

Miller, 1894, on Acute Alveolar Abscess. . . 62 

Arkovy, 1898, on Chronic Alveolar Abscess . . 62 

Goadby, 1903, on Acute Abscess 62 

Partsch, 1904, on Zahne als Eingangspforte 

fur Tuberculose 63 

Monier, 1904, on Osteo Periostite (Alveolar 

Parulis) 63 

Vincent, 1905, on Suppuration Dentaire sous 

Periostique 65 

Mayerhofer, 1909, on Periostitis Dentalis 65 

Idman, 1913, on Acute A lveolar Abscess. . .66-70 
Gilmer, 1914, on Acute and Chronic Ab- 
scesses 70 

Thoma, 1915, on Actinomycosis of Dental 

Hartzel and Granulomata 70 

Henrici, 1913-14-15, on Streptococci of Chron- 
ic Oral Infections 71-75 



Author's Remark, 1916 75 

Steinharter, 1916, on Staphylococci causing Sec- 
ondary Infection 75 


Acute Periodontitis 77 

Acute Alveolar Abscess 77 

Dento- Alveolar Parulis 78 

Chronic Alveolar Abscess 78 

Proliferating Periodontitis 79 

Dental Granulomata 79 

Simple Granuloma 79 

Epitheliated Granuloma 81 

Granuloma with Lumen 82 

Cysts 82 


1. Involvement op Neighboring Parts 86 

1. Maxillary sinusitis 86 

Acute maxillary sinusitis 86-88 

Chronic maxillary sinusitis 88-92 

2. Pharyngitis 92 

3. Trismus 93 

2. Ophthalmic Disturbances 94 

1. Infectious conjunctivitis 95 

2. Suppurating Keratitis 95 

3. Scleritis 95 

4. Iritis 96 

5. Cyclitis 97 

6. Choroiditis 97 

7. Retinitis 97 

8. Intraocular optic neuritis 98 

9. Retrobulbar optic neuritis 98 

10. Glaucoma 99 

3. Aural Disturbances 100 

1. Otitis media 100 

2. Otalgia 101 

3. Reflex otalgia 101 



4. Infections op the Lymph System 102 

1. Lymphangitis 103 

2. Lymphadenitis 104-106 

3. Tubercular lymphadenitis 106 

5. Diseases of the Alimentary Canal 109 

1. Septic gastritis 110 

2. Septic enteritis 112 

3. Colitis 113 

4. Appendicitis 113 

5. Proctitis 113 

6. Gastric and duodenal ulcers 113 

6. Infectious Diseases op the Blood 115 

1. Septicemia 116 

2. Pyemia 117 

3. Toxemia 118 

Malaise 119 

4. Anaemia 121 

Pernicious anaemia 121 

Septic anaemia 122 

7. Infectious Diseases of the Heart 123 

1. Pericarditis 124 

2. Myocarditis 125 

3. Endocarditis (valvular and mural) 125 

8. Affections of the Nervous System . . . . 128 

1. Neuritis 128 

2. Neuralgia, trifacial 130 

3. Chorea 132 

4. Mental depression and melancholia 133 

9. Diseases of the Joints 135 

1. Acute arthritis 135 

2. Hypertrophic arthritis 137 

3. Gouty arthritis 137 

4. Infectious and atrophic arthritis 137-143 


Method op Oral Examination for the Physiclvn .... 145 

1. Examination of the Soft Tissues of the Mouth 145 

2. Examination of the Teeth. 145 

3. Enlarged Lymph Glands 146 



Method op Oral Examination for the Dentist 146 

Physical Examination 146 

1. General Health, of the Patient 146 

2. Diseases of the Soft Tissues of the Mouth 147 

3. Diseases of the Teeth 147 

Radiograph Examination 148 

1. Obscure Pain 148 

2. Diagnosis of Condition of Devitalized Teeth .... 148 

3. Prognosis before Root-canal Treatment 149 

Potter Case Charts 149 

Report Charts for Radiologists 149 


1. Treatment op Acute and Subacute Conditions . . . 150 

Removal of the Cause 151 

Rest of the Diseased Tooth 152 

Application of Counter-irritants 152 

Alveolatomy 152 

Incision 152 

Extraction 154 

Systemic Treatment (Palliative, Relief of Pain, 

Diet) 155 

Treatment of Sinus to the Face 157 

2. Treatment op Chronic Conditions 157 

Removal of Cause 160 

Treatment with Antiseptics placed into Root Canal 160 

Ionic Medication 161 

Apiectomy 162 

Extraction and Curettage 167 

Extirpation of Teeth 168 

3. Treatment op Abscesses Due to Diseases of the 

Gum 169 

Abscesses Due to Injury of the Gum 169 

Abscesses Due to Pus Pockets 169 

4. Treatment of Abscesses Due to Difficult Erup- 

tion, Impaction, and Unerupted Teeth 169 

Extirpation of Impacted and Unerupted Teeth. . . . 170 



5. Treatment op Abscesses of the Tongue 171 

Incision in Non-Tubercular Lesions 171 

Excision of Small Tubercular Lesions 172 

"Wedge Excision of the Tongue 172 

Treatment of Large Tubercular Abscesses on the 
Side of the Tongue 173 

6. Treatment of Abscesses of the Salivary Glands 

and Ducts 173 

Operation from the Floor of the Mouth 174 

Excision of the Glands 175 

7. Treatment of Systemic Complications 175 

Surgical Autoinoculation 176 

Restoration of Masticating Efficienev 177 


Prevention of Secondary Disease from Oral Ab- 
scesses 179 

Prevention of Periapical Infection 180 

Radiographic Diagnosis Before Root-canal Treatment 180 

Anaesthesia for Pulp Extirpation 181 

Complete Pulp Extirpation 181 

Cleaning and Enlarging the Canal 181 

Antiseptic Medication 182 

Ionic Medication 184 

Root-canal Filling 184 

Sterilization and Asepsis 185 

Summary of Important Factors to Prevent Periapical 

Infection 186 

Prevention of Devitalized Teeth 186 

Devitalization for Sensitive Dentine and Prostheses 

Not Justifiable 186 

Treatment of Hyperemia and Exposures to Prevent 

Devitalization 187 

Early Treatment of Caries and Prophylaxis 188 




To understand intelligently and fully appreciate the 
pathology, bacteriology, and treatment of oral abscesses 
and their secondary manifestations it is well to study 
first the phenomena of infection generally. The investi- 
gations made by Vaughan and Ehrlich and others throw 
new light on many of these questions. They solved prob- 
lems of greatest interest which formerly were only 
vaguely understood. For investigations on focal infec- 
tion we are indebted especially to Rosenow and Billings. 
It is my privilege to use freely in this chapter the state- 
ments of these authorities. 

In all infectious processes there are two principal fac- 
tors : the infective virus and the body cell. Besides these 
there is to be considered the environment in which the 
infection takes place, the unorganized fluids of the body. 


The infective virus may be a particular protein and 
physically different from the medium in which it exists, 
so that its substance and form can be recognized with the 
aid of the microscope. This we call a microorganism. 
It may, on the other hand, be a semi or wholly fluid pro- 
tein, not sufficiently differentiated from the medium to 
render it recognizable even with the most delicate micro- 
scope. Many such proteins pass through the finest 
porcelain filters and cannot be deposited even by the cen- 
trifuge from the fluids in which they exist. 

According to Vaughan, a living protein can be solid, 
semi-solid, gelatinous, or liquid, but need not be of a form 


which our limited senses are capable of recognizing, even 

when aided by the most perfect lens. It is capable of 
growth and reproduction, and in order to do this it must 
assimilate and eliminate. It can only procure this nour- 
ishment from material which is within its reach. 

A bacteria or another infective virus is, therefore, only 
able to live if it can split its surrounding media into 
groups which fit into the molecular structure of its cell. 
Therefore organisms which can make use of the proteins 
of the body in which they live are pathogenic for their 
host. If they cannot make use of the substances they 
live in they cannot cause an infection. 

The agents in an organism which prepare 

MENTS the f °° d fOT aSslmilati0n are Called fer_ 

ferments me nts. They are of analytic and synthetic 
natures. We also speak of intracellular and extracellular 


Extracellular Ferments. Extracellular ferments pass 
out of the cell and diffuse more or less widely through the 
medium which surrounds it. They are of analytic nature, 
rendering soluble the proteins of the medium, and the 
complex molecules are broken down into simpler struc- 
tures, some of which can be assimilated, while others 
remain as protein poison. The activity of the extra- 
cellular ferments is easily affected by modifications in the 
mediiun through which they diffuse. Species of a nim als, 
peculiarities of individuals, slight changes of tempera- 
ture, or changes in the tissue cause variations in the 
growth and multiplication of the bacteria. Hence it is 
that one kind of organism grows slowly under unfavorable 
conditions, causing chronic disease, while the same bac- 
teria under favorable conditions may cause violent acute 

Intracellular Ferments. The intracellular ferments 
remain in the cell in which they are elaborated and are 
in general nondiffusible. They bear a wider variation 
in temperature and are not so easily influenced by varia- 
tions of the composition of the medium in which they 
exist. While the extracellular ferments prepare the pro- 


teins so that they can be absorbed by the cell, it is left to 
the intracellular ferments to construct the molecules 
into the specific proteins which can be assimilated or 
built into the structure of the cells. 

toy ins Extracellular Toxin. Besides these fer- 

ments which are necessary to maintain 
life certain bacteria elaborate another excretion. 
This is a soluble extracellular substance known as 
toxin. It is also probably a ferment or a closely allied 
body. A remarkable characteristic of the toxins is that 
they are highly specific in their properties and have the 
power to stimulate the production of antibodies in the 
infected body. These antibodies are called antitoxins 
and are also specific. Antitoxin of diphtheria protects 
only against diphtheria toxin and not against that of any 
other organism. The number of bacteria-producing 
toxins, in large quantities at any rate, is small ; the diph- 
theria and tetanus bacilli are good examples of toxin- 
producing bacteria. 


The cells of the body also have ferments, as just de- 
scribed. There is no living organism which does not 
produce its ferment, and all ferments are produced by 
living organisms. The preparation of food for assimi- 
lation is due to ferment action. 

The ferments of the body cell also work 
op the analytically and synthetically. They are 

BODY CELL of extracellular and intracellular natures. 

Their primary function is to supply 
the cells which elaborate them with food. In 
doing this they also protect the cells to which 
they belong by destroying the harmful bodies both 
particulate and formless. They are, however, of 
a specific nature. While the ferments of the body cells 
of one animal may digest one or more bacterial proteins, 
they may be unable to break down the proteins of certain 
other infectious organisms. Another animal, under the 
same general conditions, may resist the latter organism, 


but prove incapable of combating the former. If they 
are able to break down the bacterial proteins these are 
destroyed and the animal will resist disease. 

Some cells not only destroy invading or- 
^J ganisms by their extracellular ferments, 

as just described, but even engulf entire 
bodies of bacteria and dispose of protein poisons, digest- 
ing them by the action of their intracellular ferments. 
Cells with such functions are the wandering leucocytes, 
lymphocytes, plasma cells, as well as fixed endothelial 
and connective tissue cells. 

Vaughan* formulated the following bio- 
TWO biologi- logical laws which well describe the 
CAL LAWS phenomena of infection. 

1. If the body cells are permeated or 
come in contact with a foreign protein (bacteria), the 
former elaborates a specific ferment by which the latter 
are destroyed. 

2. If the body cells are attacked by destructive fer- 
ments (toxins), the former form anti-ferments (anti- 
toxins) which have the office of neutralizing the ferments 
to protect the body cells. 


The body cells of the host attempt in the manner de- 
scribed to resist the growth and multiplication of the 
foreign proteins : this growth constitutes infection. The 
resistance in an animal or a person has 
resistance ^ een f ounc [ to be greater at one time and 
diminished at another. In youth the resistance is smaller 
than in old age. 

Decrease of Resistance. The proteolytic action of the 
body cells, which checks the progress of infection, can be 
greatly decreased or removed by any cause which lowers 
the general or local vitality of the tissue. Among these 
belong hunger and starvation, bad ventilation, overexer- 
tion, exposure to cold, acute or chronic diseases, and focal 
infection. Local affections such as injury, tissue changes 

* See Bibliography. 


from disease, the presence of foreign bodies, and the in- 
terference with the circulation of the blood also tend to 
lessen the vitality. 

Increase of Resistance. All conditions which are 
favorable to the health of the body increase its resistance 
and render the tissue cells more able to overcome the in- 
fection. Healthy food, beneficial exercise, and good 
circulation, fresh air and all prophylactic means further 
an increase in the resisting power of the body. The treat- 
ment of disease and the careful search for and surgical 
removal of chronic foci, from which protein poison or 
toxins are absorbed, will also remove causes which sap 
the vitality of the individual and lower the resistance 
against new infections. 

RArTF-Riai Natural Immunity. Natural immunity 
immunity * s ^ ue e ^ ner ^° ^ ne ^ ac ^ ^ na ^ bacteria are 

unable to feed upon the proteins of the 
body and therefore cannot live, or because they are de- 
stroyed by the specific ferment, formed as a protective 
measure by the body cells. There are germicidal agents 
found dissolved in the plasma as well as in the serum. 
These are probably extracellular ferments, while similar 
agents are found in these cells themselves, which are 
probably intracellular ferments. The first act directly 
on protein organisms if they are contained in the plasma 
or blood serum ; the latter act only after these organisms 
have permeated into the body cells which produce them. 
Cells which have such functions in a marked degree are 
called phagocytes. 

Acquired Immunity. Immunity is acquired either by 
disease or by therapeutic measures. 

Immunity which is due to recovery from an infection 
is the result of the development in the body, during the 
course of infection, of a specific ferment which on renewed 
exposures immediately destroys the infection. 

Immunity established by vaccination is similar to that 
induced by an attack of the disease. A vaccine is the 
same protein that causes the disease. It is, however, 


modified by passage through animals, by growth at high 
temperature, or by killing the bacteria by heat, so that 
it does not induce the disease but yet it must be so little 
altered that it will stimulate the body cells to form a 
specific ferment which will promptly on exposure destroy 
the infecting agent. This process also is called ''protein 
sensitization. ' ' 

toxin '^' understand toxin immunity it is neces- 

m m n ity sar 7 ^° nrs ^ understand toxin activity. The 
toxin, which is produced only by a small 
number of bacteria, is a soluble and diffusible ferment. 
It splits up the proteins of the body, setting free the 
protein poison. The body cells of animals are stimulated 
by this to produce an antitoxin which neutralizes the 
toxin and prevents its cleavage action. The antitoxin 
does not destroy the foreign proteins, as do the proteolytic 
ferments of the body cells, but only prevents the action 
of the elaborated toxin. 

Antitoxin for therapeutic purposes can be produced by 
injecting the toxin, gained by injecting a very virulent 
culture in broth, into an animal, usually a young horse. 
The serum of the horse then contains the antitoxin. Anti- 
toxin is rather a preventive than a cure. It is much 
more active if given before or in the very beginning of 
the infection. The inununity procured with serum con- 
taining antitoxin is but temporary. 


Pathogenic proteins entering the body feed upon man's 
proteins, and they convert the body proteins into bac- 
n cub ati on Serial proteins by their digestive ferments. 
They grow and multiply rapidly. This 
is essentially a process of building up, as no poisonous 
protein is liberated and the process goes on without any 
recognizable disturbance in the health of the body. We 
call this stage of infection the period of incubation. Dur- 
ing this period the body cells do not resist the growth 
and multiplication of the foreign protein. 


During the period of incubation the body cells are being 
prepared for their combat with the foreign proteins. 

From the action of the foreign protein 
TiON on the body cell we note the development 

in the latter of a specific proteolytic fer- 
ment, a new function. This process we call protein sen- 
sitization. It is a process of distinction of the invading 
organisms. The new ferment digests the invading pro- 
teins, setting free the protein poison. 
PROTEIN {Intracellular Toxin) caused by bacterial 

poison destruction. After the body cells have 

been sensitized the specific ferment which 
is formed starts at once to break down the bacterial cells. 
This, however, does not mean that the analytic process 
of the bacteria is stopped at this moment ; on the contrary 
the constructive action of the bacterial ferments con- 
tinues, the invading organisms still grow and multiply 
but the process of destruction is going on at the same time. 
A fight for supremacy ensues between the invading organ- 
isms by their f ermentive action of bacterial construction 
and the defending body cells by their destructive action 
of their newly-formed proteolytic ferments. All bacteria 
contain an intracellular poison which is a group in the 
protein molecule and is neutralized in most organisms by 
combination with nonpoisonous groups. Therefore such 
proteins have no action until they undergo molecular dis- 
ruption. It is the action of the proteolytic ferments 
which splits the molecules of the invading proteins, set- 
ting free the protein poison (intracellular toxin) which 
makes the symptoms of the disease appear. Protein 
poison is not a true toxin, although the term toxin is 
loosely applied to all poisons of infectious origin. It is 
formed during all processes of infection, while true toxin, 
as we have already seen, is a special ferment character- 
istic of certain bacteria. Protein poison is produced by 
destruction of the bacterial proteins, is not affected by 
heat and does not excite the formation of an antibody and 
differs probably in quality with the variety of the 


Protein Poison Caused by Bacterial Metabolism from 
the Body Cells. It has already been described bow bac- 
teria split by their extracellular ferments the surround- 
ing media of their host. From the newly-formed struc- 
tures some are absorbed and others remain as protein 
poison. The intracellular ferments split again into mole- 
cules which are ass imil ated and built into the structure 
of the cell, and substances which are excreted. These 
by-products of extracellular and intracellular bacterial 
metabolism may be harmless or may be important protein 
poisons. Their nature depends upon the special action 
of the ferment as well as the quality of the media of the 
host in which the bacteria grow. 

The action of the bacterial ferments. The action of 
the bacterial ferments is of greatly varied nature. There 
are proteolytic ferments, hemolysin, nuclease, lab- 
ferment, lipase, diastatic ferments, invertase, pectase, 
gelase, oxydase and katalase. 

The Influence of the Medium. There is usually a sub- 
stance which the bacteria are able to digest particularly 
easily, but if this is not present they will attack harder 
and less accessible material. The chemical make-up of 
the medium naturally has a great deal to do with the 
result and with the by-products of bacterial metabolism. 

By-products of Bacterial Metabolism. The by-prod- 
ucts of the extra- and intracellular ferment action of the 
bacteria are almost always relatively strong poisons to 
the host. Various colored pigments are formed which 
have not been studied very much. From nitrogenized 
bodies, or proteid substances which constitute the greater 
proportion of animal tissue, there are formed complicated 
protein poisons, ammonia, ptomaines, alkalies, hydrogen 
sulphid, aromatics (Indol, Skatol, Phenol, Tyrosin) and 
gases such as Nitrogen. From carbohydrates and animal 
fats there are formed acids (lactic acid, Formic acid, 
acetic acid, butyric acid) and gases (carbon dioxide, Ni- 
trogen, methane, Hydrogen). 

This process of bacterial action is a decomposition, re- 
sulting in various combinations of the by-products of the 


metabolism. These by-products can almost always be 
recognized by the sense of smell and it is small wonder 
that such substances if absorbed into the system cause 
diseases of all kinds. 

Toxin. Toxin is a term which is clinically applied in a 
loose manner to any poisonous substances formed during 
the process of infection. It includes in this sense fer- 
ments, extra- and intracellular toxin, and any protein 
poison produced by the process of bacterial metabolism. 

In its strict sense the term toxin is, as we have already 
seen, applied only to the specific extracellular bacterial 
poisons, as these alone cause the body cells to produce 


The clinical picture and course of the infection depend 
upon several factors. 

Influence of Quantity in Infection. The number of 
pathogenic organisms introduced into the body plays a 
great role. A small number of bacteria may die, while 
from a large number a certain amount is sure to survive 
and cause disease. 

Influence of Bacterial Growth on Infection. Bacteria 
differ as to the rapidity with which they grow. This de- 
pends mostly upon the conditions they find; if the body 
proteins are easily digested they grow rapidly but if 
they can make use of the proteins of their host only with 
difficulty and if the circumstances under which they have 
to grow are unfavorable, as exclusion of oxygen for 
aerobic bacteria, the growth and multiplication is slow. 
This also has its reaction upon the body cells. If the 
infective virus multiplies rapidly, sensitization of the 
body cells is general and starts early. If the infecting 
organism finds less favorable conditions for its growth it 
multiplies slowly and the body cells are sensitized locally. 

Influence of Virulence in Infection. With bacteria 
whose virulence is great, disease will be produced quickly 
by a small number of bacteria, while a very large number 
is necessary if the bacteria is of the low virulent type. 


Acute and Chronic Infection. If the pathogenic or- 
ganisms enter the body in large number, increase rapidly, 
or are highly virulent, and sensitization of the body cells 
therefore is marked, starts early and is general, the 
developing disease is acute. If only few organisms in- 
vade the body, or if the infecting organisms multiply 
slowly and find unfavorable conditions, if sensitization 
of the body cells is mild and only local, the disease takes a 
chronic course. 


If the infecting virus and the sensitization of the body 
cells is limited to a certain part of the body, we call the 
infection local. 

The effect of the toxins (protein poisons) 
effects upon the body cells gives rise to various 
kinds of inflammation such as serous, fibri- 
nous, purulent, necrotic, gangrenous or proliferative. 
Serous exudations into the subcutaneous tissue follow 
certain bacterial infections in certain tissues, while the 
same or other bacteria cause purulent inflammation in 
other tissues or under other conditions. 
general Fever. Heat is produced during the 

EFFECTS processes of infection from the following 

sources: (1) from the unaccustomed 
stimulation and consequent increased activity of the 
cells which supply the ferments; (2) from the cleavage 
of the foreign protein; and (3) from the reaction between 
the proteolytic ferment of the body cells and the foreign 
proteins, especially if active and virulent poison is lib- 
erated. Fever must therefore be regarded as a benefi- 
cent process although it often leads to disaster, especially 
if the reaction takes place with great rapidity. The tem- 
perature is the most delicate test of the severity of the 

Changes in the Blood. The microbian proteins almost 
always produce an increase in the number of leucocytes 
and a decrease in the amount of protein. The red blood 
cells are sometimes directly injured by some of the bac- 
terial substances. 



If the infective virus is distributed widely through the 
whole body and if sensitization of the tissue cells is gen- 
eral, we speak of general infection. Today we know 
that infections are never entirely localized and that there 
is always absorption of bacteria or of the toxins formed 
by the infectious process. 

toxemia ^ e resm ^ f rom absorption of bacterial 

toxins (either true toxins or toxins of 
bacterial metabolism) varies according to the quality and 
amount absorbed. If the system is flooded by large 
amounts, so that there are marked symptoms of intoxi- 
cation, we have the picture of acute toxemia. The 
process, however, may go on for years without causing 
gross symptoms, and we have a chronic toxemia which 
often causes physical discomfort and mental depression. 
bacteremia ^ e Dac "teria are absorbed in quantity 

into the blood and multiply, we have an 
acute general infection called septicemia, which is of 
most severe character, resulting often in death. 

Frequently, however, we find conditions when bacteria 
are not potent enough to cause gross symptoms of infec- 
tion, although they actually wear out the cells, whose duty 
it is to combat and kill them, thus lowering the resistance 
of the body. 

metastasis ^e P resence °^ bacteria or toxins in the 
blood and tissue fluid may cause new in- 
fections or diseased conditions in other parts of the body, 
which are either predisposed by lowered resistance or 
which have a special affinity for the injurious agent. 


Billings says: "The knowledge of the principle of sec- 
ondary infection is of importance for preventive as well 
as therapeutic treatment. The recognition and the re- 
moval of the focus is imperative to prevent secondary 
disease and is demanded as a fundamental principle to 
stop the progression of ill-health/' 


It has just been shown that bacteria and toxins are 
absorbed from local infections into the blood and that 
new infections occur at remote parts of the body. This 
is called secondary or transported infection, a process 
which has been discovered only recently but which is of 
frequent occurrence. 
the focus The focus may be found in any part of the 

body and may be an acute or chronic local 
infection. Foci are sometimes apparent, but often only 
recognized after careful examination by the specialist. 
They may be in the nose and adjacent sinuses, the oral 
cavity, the throat, the alimentary canal, or the genito- 
urinary system. 

channels of ^ ac ^ er ^ a an( ^ their products are absorbed 
absorption tn r011 g]i two channels, the blood and the 

lymph system. They are carried into the 
blood by passive entrance through the stomata of the 
capillary walls, by growth of the bacteria through walls 
of the vessels, and by carriage into the blood by leu- 
cocytes. They also may reach the blood by the way of 
the lymph vessels after their transmission through the 
lymph glands. The deeper the infection is seated in the 
tissue, and the greater the pressure of the accumulated 
bacterial products, the larger is the amount of absorption. 
Also the tissue in which the infection occurs is of im- 
portance. Mucous membrane absorbs easily. An ab- 
scess enclosed by bone gives no chance for infiltration or 
extension; therefore the pressure is great and the bac- 
terial products are absorbed readily. If there is a sinus 
the pressure is decreased and the amount of absorption is 
diminished. When abscesses or other lesions discharge 
their exudates into the mouth, they reach different parts 
of the alimentary canal where a new focus may be formed, 
especially if the pus supply is long continued. But sec- 
ondary lesions may in turn also become foci for further 
and more general infection. Such conditions must not be 
mistaken for the primary cause of the focal disease, but 
they should be removed so that they will not serve to 
further prolong and intensify the disease. (Billings.) 


oral foci Oral foci may cause secondary infections 
via the capillary or lymph system. Ab- 
sorption is most likely to be caused by blind, acute, or 
chronic abscesses, but occurs also from pyorrhoea pockets, 
diseased gums, and other lesions of the mucous membrane. 
But infection may also occur by pus discharging into the 
oral cavity, as in pyorrhoea, and suppurative gingivitis 
caused by poorly fitted crowns and bridges, and in alve- 
olar abscesses with sinus ; the result then is mostly a local 
infection such as stomatitis, pharyngitis, or an infection 
of the alimentary canal, as septic gastritis, enteritis, or 
appendicitis. But if the surface immimity of the diges- 
tive tract is overcome, the alimentary canal will become 
a new focus, bacteria being absorbed, causing further sec- 
ondary infection. 

Oral abscesses, especially of the unsuspected chronic 
type, are in these days of overdentistried teeth a common 
infection and are of greatest importance in the diagnosis 
and treatment of secondary disease. The unsuspecting 
and deceived individual is usually not aware of the men- 
ace which has undermined his health or is ready to cause 
the most terrible chronic diseases if the conditions for 
secondary infections are right. 

The part of the body affected and the dis- 
SECON D ARY ease produced by absorbed toxins and bac- 
T!ONS ESTA " teria depends upon several factors. The 
different toxins have special affinities for 
a certain tissue. The varieties of bacteria have prefer- 
ences to grow in certain tissues and even strains of a cer- 
tain class of bacteria have a predilection of the place in 
which they may accumulate. Some forms of streptococci 
grow only in conditions with abundant oxygen supply (en- 
docarditis), while others prefer places of decreased oxy- 
gen tension (arthritis). The part of the body in which 
they start a secondary infection is often predisposed 
by traumatic injury or lowered resistance from other 

A place which is liable to become affected by secondary 
disease may at other times be the seat of the focus, while 


lesions which usually are primary infections can be 
caused by transported or secondary infection. Alveolar 
abscesses are almost always primary lesions whether they 
are the cause of secondary disease or not, but occasionally 
abscess formation starts on devitalized teeth, with perfect 
root-canal fillings from haematogenous infection, due to 
diseased tonsils or some other focus. 


Fig. 1. — Predynastic Egyptian Skull from Upper Egypt, shows loss 

of bone due to abscess condition on the buccal roots of the upper 

first molar. The pulp in this tooth was exposed from abrasion. 

Fig. 2. — Oeclusial view of upper jaw of same skull showing abra- 
sion of the teeth and the exposed pulp chamber of the first molar. 


Fig. 3. — Prehistoric Peruvian skull from the cave Huaricauc. There 

is a great deal of bone lost in the upper incisor region from acute 

abscess condition. 



...~~^»» Abscesses of the teeth are known to have 
occurred centuries ago. We find their bone 
destructive processes both about the jaws of ancient civi- 
lized people such as the Egyptians, as well as in ancient 
native tribes. 

The older literature knows only the alveolar abscess 
with acute symptoms of calor, dolor, rudor, and tumor, 
while the discharge of pus from sinuses on the gum which 
gave the patient no discomfort was an obscure quantity 
neglected by the dentist who then considered it his duty 
only to relieve pain and plug cavities. Later this con- 
dition was considered the termination of the acute alve- 
olar abscess which did not yield to treatment. It was 
called chronic alveolar abscess. 

Abscess sacks found adhering to extracted roots or 
teeth furthered the knowledge of the pathology of the 
dental abscesses, and in cases where neither the gum nor 
the tooth showed any sign of suppurating condition, the 
term " blind abscess" was applied. The blind abscess 
usually gave no apparent discomfort and therefore was 
classified with the chonic abscess. At that time, teeth 
with diseased pulps were either neglected by the patient, 
or if treatment and relief of pain was sought, extracted. 
But when the value of the teeth for mastication became 
better understood, men set out to preach the saving of 
teeth, and methods were invented to treat the pulpless 
teeth. I do not believe that the fathers of conservative 
dentistry meant to convey the meaning of the doctrine 
which became popular. It is not reasonable to try to 


save every tooth, no matter how diseased it is and how 
inaccessible the root-canals may be. But it was expected 
of every dentist that his greatest aim should be to save 
all teeth and that it showed lack of ability to be obliged 
to sacrifice a tooth. On account of the difficulty of root- 
canal operations and the obscurity of the achievement, 
the results frequently were poor, even if careful technique 
were employed, and miserable if carelessly incompetent. 
Because recommendation of extraction was looked upon 
with disfavor, the many overdentistried teeth with incom- 
plete root-canal work were left in the mouth. The result- 
ing condition was apparently normal. There was no 
discomfort or perhaps only slight grumbling sensations, 
overlooked by dentist and patient. 

Not until the X-rays were applied for diagnosis in 
dentistry have we discovered the true condition of such 
teeth, and since the progressive dentist secures the ser- 
vices of the dental radiologist, or has an X-ray machine of 
his own, we stand before the grave fact that most pulpless 
teeth are the cause of chronic inflammatory processes in 
the alveolar process of the maxillary and mandibular 
bone, which give no trouble or only the slightest local 
symptoms, but are the cause of much ill-health and dis- 
^, a «-.«-»■*-. ^« Oral abscesses are best divided into three 

CLASSIFICA- -, -,. i ,-1 ,. t , 

_.«.. classes according to their etiological 

factors : 

1. Alveolar abscesses caused by diseases of the dental 

2. Alveolar abscesses due to other causes than diseases 
of the dental pulp. 

3. Abscesses of the tongue, salivary glands, and ducts. 

The first class is by far the most important one ; it in- 
cludes acute alveolar abscesses caused usually by acute 
diseases of the pulp and the chronic alveolar abscesses 
which are so commonly found on pulpless teeth. It has 
been estimated that these are found in the mouth of a 
large percentage of the population of the United States. 
In the Eobert B. Brigham Hospital, where the only 


patients are those who suffer from chronic diseases, I 
found such abscesses in eighty-eight per cent, of the pa- 
tients examined. The second class includes abscesses 
caused by pyorrhoea, infection of the gums, and impacted 
and unerupted teeth. These are by far less frequent 
than the previous group. 

In the third class we have conditions which are of 
rather rare occurrence and are frequently secondary to 
diseases of the teeth. However, abscesses may occur on 
the tongue and in the salivary glands and in ducts, which 
are due to various other causes. 



varieties Generally alveolar abscesses due to dis- 
eases of the pulp have been divided into 
two classes: the acute and the chronic condition. This 
division is selected, according to the large or small amount 
of discomfort the patient experiences, that is, according 
to the symptoms, without considering either the etiology, 
the histopathological picture, or the termination of the 
disease. We know that the acute alveolar abscess if not 
cured will terminate in the chronic form, but some of the 
so-called " chronic" forms occur without passing through 
the acute stage. As a matter of fact, since only a very 
small percentage of chronic abscesses have ever started 
with symptoms of discomfort, the classification of 
" acute" and " chronic" is therefore not scientifically 
correct. A closer study of the pathological stages shows 
that the acute abscess involves a process of destruction 
while the so-called chronic abscess is a process of inflam- 
matory new growth. This proliferating new growth is of 
a more or less circumscribed character, while the acute 
condition of destruction is of a diffuse nature, spreading 
into the adjacent parts. 

I shall therefore distinguish two varieties of alveolar 
abscesses due to diseases of the dental pulp. Both repre- 
sent a progressive chain of pathological changes, the first 
of a destructive, the second of a constructive, nature. 

1. Acute Periodontitis and its sequels — or changes of 
destructive nature beginning with acute periodontitis, 


Fig. 4. — Bicuspid with apical abscess. Incisor with lateral abscess. 
Molar with inter-radial abscess. 


culminating in acute alveolar abscess or alveolar parulis, 
and ending in chronic alveolar abscess and its sequels. 
2. Proliferating Periodontitis and its sequels — or 
changes stimulating inflammatory new growth beginning 
with proliferating periodontitis and resulting in a 


definition Acute periodontitis and its sequels are 
changes which involve suppurative de- 
struction of the surrounding tissues of the tooth, culmi- 
nating in a collection of pus in or about the alveolar 
processes, called alveolar abscess or alveolar parulis. 

Acute Apical Periodontitis. The natural outlet from 
the pulp chamber is the apical foramen, or the apical 
foramina, and therefore we find these openings the most 
common mouths of the infection, since they are the natu- 
ral passages through which infected matter may pass 
from the dental pulp chamber into the surrounding 
tissues of the apex of the tooth. . The sequel of the acute 
apical periodontitis is the " apical alveolar abscess." 

Acute Inter radial Periodontitis. This is inflammation 
which occurs between the roots of multirooted teeth from 
decay extending from the diseased dental pulp through 
the floor of the pulp chamber. Infection by perforation 
of the floor of the pulp chamber or inner sides of the roots 
with burr or root canal instruments also gives rise to this 
condition. Its sequel is the acute interradial alveolar 

Acute Lateral Periodontitis. Perforation of and in- 
fection through the lateral wall of a tooth by the burr or 
root-canal instrument gives rise to inflammation of the 
periodontal membrane, resulting in a lateral alveolar 

etiology ^ e diseases °f the dental pulp or pulp 

chamber are responsible for the formation 
of acute periodontitis, which later develops into the 
acute alveolar abscess. This condition is always due to a 


large invasion of virulent pyogenic bacteria. The causes 
of the infection are the following : 

Traumatic Injury of a Tooth. Injuries received by 
falling or from a blow result in inflammation of the pulp. 
The tooth may be fractured in the crown, exposing the 
pulp to outside influences, or fractured in the root, ex- 
posing it to the irritation caused by the fractured seg- 
ments. The hard substances of the tooth are almost 
always fractured if traumatic injury occurs, but occa- 
sionally this does not take place and pulpitis is then 
caused by injury to the tissue in the periapical regions. 
The same condition occurs occasionally from the action 
of orthodontia appliances, if force has been applied too 
abruptly or if the teeth are moved too rapidly. The in- 
terference with the circulation of the pulp and the lowered 
resistance of the tissue invite hematogenous infection, 
which results in suppuration of the tissues involved. In 
this way acute periodontitis may result from primary in- 
fection of the periapical region or by means of the pulp 
if the injury occurred in the crown or side of the root. If 
no therapeutic measures interfere, this will develop into 
an acute alveolar abscess. 

Infection from Adjacent Teeth. Suppuration often 
spreads in the cancellous part of the alveolar process 
causing acute infection of the periodontal membrane of 
adjacent teeth. If the infection occurs in this manner 
there is, however, less danger of involvement of the pulp 
if it is in good condition. Neighboring teeth are fre- 
quently involved to an extent which makes them so loose 
that their condition seems hopeless, but the pulp resists 
disease in these cases for a long period, and if the cause 
is removed in time, the periodontal membrane, the fibres 
of which have a wonderful resisting power to destruction, 
returns to normal and the tooth regains its firmness in 
the jaw. Occasionally, however, especially if drainage 
of the abscess is delayed, the pulp becomes infected, re- 
sulting in violent suppurating pulpitis. 

Infections from Pus Pockets. Pus pockets between 
the gum and the tooth are the result of the destruction 


Fig. 5 

Fig. 6 

Fig. 7 

Fig. 8 

Fig. 9 

Fig. 10 

Fig. 11 

Figs. 5 and 6. — Abscess caused by trauma. The tip of the teeth having been 


Figs. 7 and 8. — Show the treatment of the case Fig. 5. The tooth was extracted 

and replaced by a porcelain tooth, the root having been carved according to the 

X-ray picture and attached to the next tooth. 

Figs. 9, 10 and 11. — Show teeth with abscesses which have involved neighboring 



Fig. 12 

Fig. 13 

Fig. 14 

Fig. 15 


Fig. 16 

Fig. 17 

Fig. 18 

Fig. 19 

Figs. 12 and 13.— Apical abscesses due to pyorrhea pockets. 

Figs. 14 and 15. — Abscesses from temporary teeth. 

Figs. 16, 17, 18, and 19. — Abscesses due to decay of permanent teeth. In Figures 

17 and 18 the decay has started under the filling. 


of the alveolar process surrounding the tooth by pyor- 
rhoea alveolaris or of septic descending periodontitis 
caused by unclean, unsanitary, ill-fitting, eyiLcrowns and 
bridges as well as irritating fillings. The infection pro- 
gresses towards the apex, and when it reaches this part, 
it destroys the blood supply of the pulp, producing septic 
pulpitis and apical alveolar abscess, which usually dis- 
charges through the pocket. 

Thermal Shocks Conducted to the Pulp by Large 
Metal Fillings cause hyperemia of the pulp, and if the 
irritation is strong enough and continued, it will result 
in pulpitis, death of the pulp, and alveolar abscess. 

Crowned Teeth. Teeth, fitted with entire porcelain or 
gold crowns, either for purposes of restoration of lost tis- 
sue or for bridge work, are often believed to become 
devitalized because contact with air and with the fluids 
of the mouth is prevented. It is the author's opinion 
that this is not the real cause. The latest discovery in 
dental histology teaches us that the dentin metabolism 
comes from the dental pulp, while only the metabolism 
of the adult enamel is dependent on the fluids of the 
mouth. The metabolism of the dentin of a tooth, which 
is covered entirely by a crown, is therefore not interfered 
with. From practical experience we know that a great 
number of teeth with well-fitted, entire crowns, stay in 
perfectly healthy condition, while the pulps of others 
die. Two reasons can be attributed to the death of the 
pulp in these cases. It may be due to thermal shock, 
and from the grinding which is necessary to reduce the 
contour of the tooth. The second reason is decay, which 
has not been entirely removed, or, which is caused by ill- 
fitting crowns. 

Decay of Deciduous Teeth. Deciduous teeth are very 
frequently neglected and their office is very vaguely 
understood by most of the patients. The need of teeth 
for the purpose of mastication is most important in chil- 
dren because they require more nourishment than the 
adult to build up their bodies and to resist childhood 
illnesses. These should perform the function of masti- 


cation until the permanent teeth erupt. Their other duty is 
to hold the space open and prevent other teeth from mov- 
ing forward until the permanent teeth take their place, 
in order to prevent malocclusion. This function which 
concerns normal occlusion of the permanent teeth is of 
greatest importance and should stimulate us to keep these 
temporary teeth in good condition so as to prevent their 
pulps from becoming diseased. Acute abscesses form 
easily on deciduous teeth if the pulp has been infected on 
account of the physiological process of bone absorption 
caused by the eruption of their successors — and this in- 
fection is easily carried into deeper areas ; indeed, fistulas 
to the face, cervical and submaxillary adenitis caused by 
temporary teeth are very frequently found in children. 
If the disease has progressed to the stage of an acute 
abscess, the question arises whether these teeth should 
be extracted with malocclusion as a consequence, or 
whether they should be retained with the risk of infection 
and its serious possibilities involving the development, 
health, and even the life of the patient. 

Decay of the Permanent Teeth. Caries of the dentin 
if not stopped will progress in the dentinal tubules and 
cause suppurative pulpitis before the cavity has reached 
the pulp ; frequently, however, the cavity extends directly 
into the pulp chamber. The same process of infection 
develops from decay which has not been entirely re- 
moved, before restoring the shape of the tooth by crown 
or filling. The pulp may also be infected during the 
therapeutic act of excavating a cavity. Even a pulp 
exposure of minute size, almost always has suppurative 
pulpitis as a consequence, unless it receives the careful 
treatment which is called pulp-capping. This treatment 
is advisable only in children's teeth, when the root canal 
is wide open, which prevents strangulation during the 
usually resulting period of hyperemia and mild inflam- 
mation. In the cases where the decay forms an opening 
into the pulp chamber, the disease very seldom affects 
the periapical tissue. The exudates escape through this 
outlet, and after the stage of inflammation, the pulp tis- 


sue degenerates and frequently becomes hypertrophied, 
which is a measure of protection. But if suppuration 
occurs in a tooth with a filling, or where the natural open- 
ing becomes stopped up by food or other substances, the 
infectious matter is forced through the apical foramen 
and forms an acute alveolar abscess. 

Filling of Teeth with Infected Pulps. A tooth with an 
open root canal and a pulp or part of a pulp in acute in- 
flammatory condition should not be sealed up after the 
first treatment has been applied, because in doing so we 
would close the natural outlet through which the products 
of fermentation and suppuration make their escape ; these 
products would be forced through the apical foramen 
and infect the periapical tissue. Such treatment is often 
the result of acute periodontitis and acute alveolar 

Instrumentation. Instruments inserted into septic 
root canals and root-canal instruments used for cleaning 
of septic root canals act often as plungers forcing septic 
material through the apical foramen into the periapical 
tissue, inoculating directly the periodontal membrane and 
the bone. Such instruments should therefore not be used 
until the bacteria have been destroyed by antiseptic drugs. 
Perforation of the floor of the pulp chamber in multi- 
rooted teeth or piercing of the sides of a root with a root- 
canal instrument may also be the cause of acute periodon- 
titis and acute abscess. 

Change in Oxygen Tension. Very often a tooth with a 
diseased pulp is in a quiescent condition until the pulp 
chamber is opened in order to gain access for treatment. 
The patient will return the next day with all symptoms 
of an acute periodontitis, having suffered a great deal of 
pain during the night. This is due to a change in oxy- 
gen tension, and the bacteria which developed only slowly 
because of lack of oxygen now become extremely active 
on account of the access of air, causing suppuration 
which will progress through the apical foramen if the 
tooth is sealed hermetically after the operation. 


Acute Periodontitis. If bacteria or 


products of suppuration escape through 
the apical foramen, the periodontal 
membrane is first attacked, causing acute apical 
periodontitis. The swelling of the blood vessels 
and the serous infiltration enlarges the perio- 
dontal membrane and pushes the tooth for a short 
distance out of the socket. This stage of hyperemia 
is of short duration. Small particles of pus collect 
near the apical foramen and soon spread between the 
fibres of the periodontal membrane, which finally becomes 
dissolved. A tooth extracted at this stage shows, if the 
periodontal membrane adheres to the cementum, a red 
appearance in the apical region. The apical periodon- 
titis may spread over the whole surface of the root and is 
then called acute total periodontitis. 

Acute Alveolar Abscess. The inflammation now in- 
volves the linea dura, the compact layer of bone lining the 
alveolar socket. The bone is destroyed as suppuration 
progresses and the cavity formed fills with pus. This 
condition is called acute alveolar abscess. 

Alveolar Parulis. The pus which stands more or less 
under pressure proceeds in the cancellous part of the bone 
and finds its way through some Haversian canals, pene- 
trating the plate or dense cortical layer surrounding the 
bone. This stage is sometimes reached in a short time, as 
quickly as overnight, but at other times, especially in the 
mandible, it takes four to five days for the pus to burrow 
to the surface. 

Subperiosteal Parulis. The Haversian canals are en- 
larged and show in dissected skulls as small perforations 
through which the pus escapes between the bone and 
periosteum. The periosteum, like the periodontal mem- 
brane, is tough and has a considerable resisting quality 
to destruction. The pus therefore spreads under the 
periosteum and often accumulates in large quantity, 
sometimes causing a widely distributed oedematic swel- 
ling of the face. 


Fig. 20 

Fig. 21 

Fig. 22 

Fig. 23 

Fig. 20. — Acute periodontitis. 

Fig. 21. — Acute abscess. 

Fig. 22. — Subperiostial parulis. 

Fig. 23. — Sub-gingival parulis. 


fcV Mi! 


Pig. 24 

Pig. 25 

Fig. 26 

Fig. 27 

Fig. 28 

Fig. 29 

Fig. 30 

Fig. 31 

Fig. 24. — Sinus to the gum. 

Fig. 25. — Sinus to the palate. 

Fig. 26. — Sinus into the antrum. 

Fig. 27. — Sinus into the nasal cavity. 

Fig. 28. — Sinus to the cheek. 

Fig. 29. — Sinus to the gum of the lower jaw. 

Fig. 30. — Sinus to the skin of the lower jaw progressing along the outside of 

the bone.. 
Fig. 31. — Sinus to the chin. 


Subgingival Parulis. If the pus penetrates the perios- 
teum and collects under the gum we speak of a subgingival 
parulis. This stage is usually reached quickly, but, in 
other cases, only after the subperiosteal parulis has lasted 
for a long time. The rate depends on the resistance of 
the periosteum. The swelling caused by the subgingival 
parulis is more rounded, while the tumor of the subperios- 
teal parulis is flat. 

Sinus from Acute Alveolar Abscess into the Mouth. 
If the pressure of the pus at this stage is not relieved by 
surgical interference, the parulis will come to a point and 
break through the gum, usually opposite the apex of the 
root. This passage is called a sinus. The course of the 
pus, however, is not always so direct. If the periosteum 
is very resistant and if the pus accumulates in large quan- 
tity, it may follow the laws of gravity and least resistance 
and pierce the periosteum at a place quite remote from its 
source. Sinuses occur almost always at the buccal or 
labial part of the gum ; palatal sinuses are more rare and 
usually are derived from the superior incisor teeth and 
often lead some distance back into the mouth. Sinuses 
are still more rare at the lingual gum of the lower teeth, 
from which point the pus usually sinks downwards, in- 
volving the tissues of the floor of the mouth. 

Sinus from Acute Alveolar Abscess to the Face. If the 
pus does not readily find an outlet through the gum, it 
passes along fascias and muscles through submucous and 
subcutaneous tissue until it reaches the skin of the face. 
Here it collects in a similar way, as under the gum. It 
causes a swelling and extends the skin to its limit before 
it penetrates to the surface. (Fig. 30.) The course of the 
sinus is often a long and tortuous one. Sinuses to the skin 
occur especially from severe subperiosteal parulis and 
are often caused by ignorant application of heat or poul- 
tices to the outside of the face to relieve the pain. Sinus 
to the face from the upper jaw is not very common. If 
it occurs, the outlet usually is near the malar process, as 
seen in Pig. 28. In the lower jaw the pus settles more fre- 
quently into the tissue, breaking below the lower border 


of the mandible. The pus has been found to follow the 
course of muscles, finally finding an outlet on the neck or 
chest. From the inside of the mouth and from the front 
teeth the sinus, if it does not find any outlet to the gum, 
leads almost always to the chin. 

Sinus for Acute Alveolar Abscess to the Antrum of 
Highmore. The roots of the superior bicuspids and mo- 
lars sometimes extend into the antrum and are covered 
only by the linea dura of the alveolar socket. Acute 
abscesses of such teeth easily form a sinus into the antrum 
following the course of least resistance. This condition, 
of course, has acute inflammation of the antrum as its 

Sinus for Acute Alveolar Abscess to the Nasal Cavity. 
If an abscess on a superior incisor does not find relief by 
piercing the periosteum and gum, a sinus may be formed 
to the inferior meatus of the nose. 

Acute Osteomyelitis, or destruction of 

tions ^ e cance H° us P ar t of the bone, occurs 

always during the formation of an acute 
apical alveolar abscess. The disease spreads easily in the 
spongiosa of the bone and the neighboring teeth are usu- 
ally affected and are considerably loosened. If radical 
treatment is not undertaken at an early time, it may ter- 
minate in pyemia or septicemia, with fatal result. 

Ostitis, or death of the bone, cell by cell, may be caused 
by prolonged subperiosteal parulis where the pus finds 
no escape and destroys the outer plate of the bone. After 
reaching the cancellous part of the bone it continues as 
osteomyelitis, which is not different from the osteomye- 
litis which starts from within. 

Necrosis, or the death of bone en masse, is also fre- 
quently the result of the acute alveolar abscess. Necrosis 
may start from without by subperiosteal parulis where 
the blood supply from the periosteum is cut off by the 
pus which separates it from the bone. It may also start 
from within the bone by osteomyelitis, as a result of alveo- 
lar abscesses. It most always attacks the facial wall of 
the bone and is not often very extensive. The necrosed 


Fig. 32. — Skull showing large bone destruction due to abscesses. 


Fig. 33 

Fig. 34 

Fig. 33. — Ostitis of the hard palate caused by a tooth. 

Fig. 34. — Osteomyelitis of the mandible caused by an 
abscess on the lower first molar. The molar was ex- 
tracted before the patient came under the author 's 


part detaches from the healthy bone by absorption, the 
dead part being called a sequestrum. Pus discharges 
from a sequestrum in great amount until it is removed. 

Resolution. Return to the normal will 
TERMINATION not occur without early therapeutic 

Scar Bone. Frequently we find conditions which have 
become chronic and in which a certain amount of repair 
has taken place, usually leaving but a comparatively small 
area of lessened density immediately around the apices of 
the roots. This new bone which fills in the area de- 
stroyed during the stage of active suppuration, is very 
much more dense than normal bone and appears in radio- 
graphs as a lighter area of denser structure. This is 
called scar bone. (Figure 37.) 

Chronic Alveolar Abscess. After the pus has forced a 
sinus through the soft tissue, the swelling slowly subsides, 
and the flow of pus diminishes, the condition then passing 
into the chronic stage. Inflammatory granulation tissue 
is formed as an attempt of healing, which becomes en- 
closed by fibrous tissue to prevent the involving of larger 

Active Sinus. The suppuration, however, continues 
and the discharge flows through the original sinus or finds 
a new and shorter way, through the tissue which has been 
rendered more or less immune during the stage of acute 
inflammation. The walls of the sinus become fibrous 
forming an adhesion between the abscess cavity and the 
gum, or if the sinus leads to the face, between the abscess 
cavity and the skin. The skin on these places appears, 
therefore, fixed to the bone ; it is drawn towards the dis- 
eased root apex in funnel fashion. This depression har- 
bors the mouth of the sinus at its deepest point. Chronic 
abscesses discharge products of suppuration in large or 
small amount for months and years. 

Closed Sinus. The mouth of the sinus of a chronic al- 
veolar abscess sometimes becomes closed during a period 
of inhibition of pus formation. This is especially apt to 
occur if the discharge starts to drain through another 


passage, such as is the case if an opening occurs into the 
root canal when the process of decay breaks down the 
tooth. This not only gives relief to the discharge from 
the chronic abscess, but also relieves the primary source 
of infection due to the death of the dental pulp. The 
clinical picture of this condition is similar to the one of 
the blind abscess, with the exception of a scar on the gum 
or upon the face, formed by the closing of the mouth of 
the sinus. This sort of chronic abscess without sinus is, 
however, always a sequel to the acute abscess, while the 
true blind abscess is formed in an entirely different way, 
as we will see later. 

Subacute Alveolar Abscesses. The closing of the sinus 
by the process of granulation, during a period when sup- 
puration is subdued or drained through a cavity via the 
root canal, is usually not a stationary condition. The 
cavity may become closed up by food debris, or the in- 
fection may become active again. This happens par- 
ticularly during a period of lowered resistance, as during 
pregnancy, when all the effort of the system is directed 
to other parts. In recurring cases, this secondary proc- 
ess of suppuration is similar to the primary one. The 
pus accumulates in the cancellous part of the bone, the 
granulation tissue is destroyed, the sinus is reopened, or 
a new outlet is formed to drain the discharge. The symp- 
toms of the inflammation are, however, much less acute ; 
oedematic infiltration seldom occurs because the tissue 
has been rendered more or less immune by previous at- 
tacks. A subacute attack usually quiets down after 
a while and the condition continues as a chronic abscess 
with sinus, or the sinus may even become closed again. 
Such changes are liable to be repeated innumerable times 
with irregular intervals of quietude. 

Exostosis of the Root. The fibres of the periodontal 
membrane have a great power of resistance and usually 
they escape destruction if there is early and sufficient 
drainage of the acute alveolar abscess. But if a chronic 
periodontitis persists the cementoblasts are stimulated 
by irritation from the chronic inflammation to deposit 


Fig. 35 

Fig. 36 

Fig. 37 

Figs. 35 and 36. — Photographs of teeth showing 
exostosis of the z'oot. 

Fig. 37. — Molar with scar bone. 


Fig. 38 

Fig. 39 

Fig. 38. — Central incisor with acute abscess showing large bone destruction. 
Fig. 39. — Photograph of sub-gingival parulis caused by first bicuspid. 


new cementum causing hypercementosis, which is usually 
restricted to the place of disease, namely, the apex of the 
root. This thickening or bulging of the root is called 
exostosis and histologically shows an accumulation of 
lamellae of cementum containing an abundance of cement 
corpuscles and Haversian canals. 

Necrosis of the Root. In cases where the parulis has 
been severe, and the formation of a sinus retarded, as is 
almost always the case in prolonged subperiosteal parulis, 
we usually get destruction of the apical part of the perio- 
dontal membrane. The cement of the tooth is then ex- 
posed and the denuded area shows a rough surface from 
contact with pus, and if the chronic alveolar abscess lasts 
a long time the root becomes discolored, having first a 
greenish, and later an almost black appearance. Absorp- 
tion of tooth substance takes place at the apex which 
shows a ragged appearance if the tooth is extracted. The 
hard substances of the tooth have not the power to divide 
and expel diseased fragments, as in bone, but we will have 
to consider this absorption as a process of necrosis. The 
whole tooth represents the sequestrum, dead bone, cut off 
entirely from the blood supply which nourished it, from 
the inside through the pulp and from the outside through 
the periodontal membrane. In long standing chronic 
conditions, where the whole periodontal membrane has 
been destroyed, the tooth has the true appearance of dead 
tissue, the cementum of the whole root having a greenish 
black appearance. 

diagnosis Acute Periodontitis. Local Symptoms: 
If the periodontal membrane becomes in- 
fected from a septic pulp, the tooth becomes very tender, 
the beating of the pulse can be felt by the patient, and 
the tooth protrudes out of the socket. The pain is felt 
principally at night. Cold and hot food have no influ- 
ence, but mastication causes great pain because the tooth 
is, as the patient expresses it, too long. 

Clinical signs: The tooth which causes the trouble is 
sensitive or even extremely painful on percussion ; often 
it is also more or less loose. 


Radiographic examination: The radiograph at this 
stage of the disease shows a dark shadow of the thickened 
periodontal membrane. 

Acute Alveolar Abscess. Local symptoms: The stage 
of acute periodontitis is usually of very short duration. 
If relief does not come at once the pus will collect and 
form an acute abscess. The symptoms seem similar to 
the ones of acute periodontitis. Pain is very persistent 
and increases in severity ; it is constant, deep and throb- 
bing, sometimes excruciating. Hyperemia of the adja- 
cent tissue sometimes is so marked as to loosen the neigh- 
boring teeth. Oedematic swelling of the neighboring 
parts occurs. 

General symptoms: There is usually a marked rise in 
temperature ; fever up to 104° F. is not uncommon. Chills 
may precede the fever and general malaise accompanies 
the disease. 

Clinical signs: If an alveolar abscess has formed, the 
neighboring teeth usually become tender and it is difficult 
sometimes to find out which tooth has started the trouble. 
As the abscess starts from a diseased pulp, we can diag- 
nose the case by testing the vitality of the pulp. A 
discolored tooth or a tooth with a large filling should be 
suspected. But to find out definitely we can apply the ice 
test ; vital teeth give a reaction. The galvanic or the high 
frequency current can also be used. The teeth are dried 
and rendered isolated by putting a piece of cellu- 
loid or rubber-dam between their contact points ; the gal- 
vanic current is then applied. If the galvanic current is 
used, one electrode is held in the hand and the other, sur- 
rounded by cotton saturated with normal salt solution, is 
applied first to a healthy tooth. The patient notes the 
sensation the current produces in the healthy tooth. The 
teeth that are suspected are then examined in the same 
manner and if a tooth gives no reaction it can be con- 
cluded that its pulp is diseased. If a high frequency 
apparatus is at hand, we let a small spark jump at the 
suspected tooth, dried and isolated in the manner just 


described. Pain caused signifies that the pulp is 
healthy, as a diseased pulp gives no such reaction. 

Radiographic examination : Radiographs usually show 
distinct areas of lessened density where the bone has been 
destroyed by the process of suppuration. However, in- 
filtration of the cancellous part of the bone is sometimes 
visible on account of the fluoroscopic properties of the 
pus. The apex of the diseased tooth usually occupies the 
centre of the area. In the upper jaw where the apices are 
close to the surface, so that the pus may easily find an out- 
let and accumulate under the periosteum and gum without 
destroying a large amount of bone, sometimes, even de- 
stroying no bone at all, we may find no area of lessened 
density at all, the bone appearing perfectly normal. 

Alveolar Parulis. Local symptoms : After the pus has 
penetrated the bone, it accumulates under the periosteum, 
causing a flat swelling. In appearance the gum is highly 
inflamed and red, and the pain becomes very intense. 
Great relief usually occurs as soon as the pus penetrates 
the periosteum, when the high pressure is relieved and 
the pus collects under the gum, producing a ball-like 
swelling. If the abscess is on the palatal side, this part 
usually presents an enormous swelling, while parulis oc- 
curring on the buccal and labial sides, which usually is the 
case, is accompanied by an extensive infiltration of the 
surrounding tissue. The oedema sometimes partly or 
even entirely closes the eye if the trouble is in the upper 
jaw, while in the lower jaw, the floor of the mouth, lower 
part of the cheek and neck are principally infiltrated. 
The localization of this oedema is characteristic of the 
location of the diseased tooth. From a molar or bicuspid 
in the upper jaw where the upper part of the cheek is 
involved the corner of the mouth is drawn upwards, while 
the swelling from the lower parts draws the mouth down- 
ward. If an abscess occurs at the front teeth the re- 
spective lip is swollen and protruding. The submaxillary 
and submental glands for the front teeth are almost al- 
ways enlarged. When the pus is about to come to the 
surface we note that a yellowish spot appears. This is 


called pointing of the abscess. The abscess, however, 
does not always point near the tooth that is the principal 
cause. The pus sometimes travels under the periosteum 
for quite a distance and may penetrate at a convenient 
point quite remote from the place where it leaves the bone. 
A sinus discharging from the mucous membrane of the 
mouth or skin is not always connected with and caused by 
an abscessed tooth. Impacted teeth, sequestra, diseased 
salivary or lacrimal glands sometimes cause sinuses, but 
it is not difficult to ascertain the cause. 

Differential diagnosis : The lesions which may be mis- 
taken for parulis are those of epulis, g umm a and cyst. 
A true parulis resulting from a diseased pulp may also be 
mistaken for a parulis caused by an impacted, partially 
or entirely unerupted tooth, or by an abscess caused by 
pyorrhoea without involvement of the pulp. There is 
usually little difficulty in making the right diagnosis. 
Benign epulis is of slow development without any pain- 
ful symptoms; sarcoma in the mouth is very modified, 
and the only malignant epulis we have to consider is car- 
cinoma. Patients with carcinoma usually have a 
neglected mouth, and the bad condition of the teeth and 
the swelling of the glands, frequently gives the clinical 
picture of parulis. The generalizing character of the 
carcinoma and the anamnesis of the disease helps in diag- 
nosis, and in a questionable case the histopathological 
picture of a piece excised for examination will decisively 
answer the question. Gummata are slow in growth ; the 
history and manifestations at other parts as well as the 
Wasserman test will give the desired information. Cysts 
are of slow growth and show no symptoms of inflamma- 
tion; an exploratory puncture gives escape to a clear, 
yellowish, odorless fluid. The diagnosis of parulis by 
impacted, unerupted teeth and pyorrhoea will be de- 
scribed in another place. That sinuses may also derive 
from glands, necrosed bone and impacted or unerupted 
teeth has already been mentioned, while oedema of the 
face also occurs from the salivary glands, if their ducts 
are obstructed or if infection involves them. 


General symptoms : Parulis formation is almost always 
accompanied by general malaise ; fever reaches its highest 
mark during the stage of subperiosteal parulis, and leu- 
cocytosis is very marked. The patient gets worn out 
from pain and loss of sleep, but as soon as the pus finds 
an outlet, the health improves rapidly. 

Clinical signs: The same that has been said for acute 
alveolar abscess and acute periodontitis is true for 
parulis. In addition we feel by digital examination a fluc- 
tuation which is especially marked in subgingival parulis. 
Pressing upon the swelling increases the pain consider- 
ably. If the abscess points or if a sinus has already been 
formed, there is little difficulty in making a diagnosis. 

Radiographic Examination: The radiograph, usually 
shows the amount of bony destruction and is employed to 
find which tooth is the causative factor, but in certain 
cases no areas of decreased density are visible. This is 
especially the case when the apices of the teeth are close 
to the outer surface, as in the upper central incisors. In 
extreme cases where films canot be put into the mouth and 
in cases with sinuses leading to the face, large extraoral 
pictures should be taken, as the cause is often far removed 
from the mouth of the sinus. 

Chronic Alveolar Abscess. Local symptoms: The pa- 
tient who always remembers and presents a history of the 
acute process almost always complains of subacute 
attacks, where the gum swells up slightly and pus empties 
into the mouth, and there is usually a sense of pressure 
and soreness of touch and lameness of the tooth. 

General symptoms: The submaxillary and submental 
lymph glands are usually slightly enlarged. Complica- 
tions such as tonsilitis, pharyngitis, and gastric and intes- 
tinal infections may occur due to pus which is discharged 
into the mouth, but infectious arthritis, endocarditis, 
toxemia, and other diseases may also set in, and these can 
be considered as general symptoms calling our attention 
to the causative factor. These complications will be con- 
sidered in a special chapter. 


Clinical signs: A sinus is almost always found on the 
gum, or face; if it has closed, there is a visible scar. 
Whether or not we have a healed condition, the extent 
of the lesion can only be ascertained, if the sinus is closed, 
by radiographic examination. 

Kadiographic diagnosis: The radiograph reveals the 
chronic abscess by an area of lessened density, it also 
discloses if there is exostosis or necrosis of the root apex, 
which is an important factor in the determination of the 
method of treatment. 


In the last decades, teeth have been devitalized for 
several reasons without realizing the danger of such pro- 
ceedings. Dentists knew only of the mechanical diffi- 
culties encountered in extirpating pulps and filling of 
root canals. The result of imperfect root-canal work 
was, however, not known until radiography was developed 
for dental use. When the so-called areas of lessened 
density were shown in radiographs at the apices of devi- 
talized teeth, little attention was paid to them ; they were 
considered a neglible quantity because the patient had 
no alarming symptoms of disturbance and often not even 
the slightest discomfort, and it was considered good den- 
tistry to retain such teeth rather than lose an important 
organ of mastication. But since the pathology and bac- 
teriology of these symptomless lesions has been studied 
more carefully and since the important discovery of focal 
infection, we have come to realize the grave fact that such 
septic conditions about the teeth may be more dangerous 
than the violent acute conditions, principally on account 
of the fact that their deceiving nature undermines the 
patient's general health and causes, if conditions are 
right, secondary infections in other parts of the body, the 
nature of which we shall study in a special chapter. 
definition Proliferating periodontitis and its sequel, 
the granuloma, are changes in which new 
formation of tissue from the periodontal membrane is the 
important feature; suppuration plays a secondary role 


Fig. 40 

Fig. 41 

Fig. 42 

Fig. 40. — Lateral granuloma. 

Fig. 41. — Apical granuloma. 

Fig. 42. — Interradial granuloma. 


Fig. 43 

Fig. 44 

Fig. 45 

Fig. 46 

Fig. 41 

Fig. 48 

Fig. 49 

Fig. 50 

Figs. 43, 44 and 45. — Granulomata caused by decay of the tooth. There is free eonimuxii- 

eation from the root canal into the mouth. 

Figs. 46, 47 and 48. — Granulomata caused by incomplete pulp extirpation. 

Figs. 49 and 50. — Granulomata due to broken instruments left in root canal. 


and does not involve the surrounding tissues. It is 
characteristic that the condition starts without the pa- 
tient's knowledge and without symptoms of inflammation. 
varieties Apical Granuloma. The most common 
seat of chronic periodontitis and its sequel 
and is the periapical region, at the outlet of the root 
canal from which the disease starts. 

Lateral Granuloma. Sometimes teeth have accessory 
foramina as high as the middle of the root. These may 
become a source of trouble if the root canal has to be 
treated. Perforations by root canal instruments at the 
side of a root are, however, more frequently the cause of 
lateral abscesses. 

Interradial Granuloma. The floor of the pulp cham- 
ber is sometimes penetrated in multirooted teeth by burrs 
or root-canal instruments, seldom by decay, causing 
granulomata or chronic abscesses between the roots. It 
it almost impossible to treat these interradial abscesses on 
account of anatomical difficulties. 

etiology Proliferating periodontitis is primarily 

caused as a protective reaction of the tis- 
sue against irritating excretions from the root canal, such 
as pus bacteria and toxins, or against injudicious appli- 
cation of irritating drugs, such as formaldehyde, sul- 
phuric acid and other medicaments used during root canal 
treatment. Ulrich believes that haematogenous infection 
is the explanation for all apical abscesses with the prob- 
able exception of teeth which have been capped following 
caries. I fully believe that haematogenous infection is 
the cause in certain cases, especially those of infection or 
reinfection after medicinal treatment, leaving an area of 
lowered resistance in the periapical region, such as a peri- 
odontal membrane or a denuded or necrosed apex ; but it 
seems to me very improbable that all or even a large 
amount of the cases should be due to this cause. The histo- 
pathological picture speaks so plainly for an irritating 
and infective source from the root canal, the fact that I 
discovered blind abscesses in persons in whom no other 
foci could be found after careful search, and the fact that 
the streptococcus, which is almost always found in the 


dentinal tubules, is also the bacteria which most fre- 
quently inhabits the granuloma, seem to me simpler and 
more probable reasons, especially where we have such an 
obvious source as the root canal from which infection may 
be continued. 

The microorganisms which sooner or later invade the 
granuloma are never very large in number. Their viru- 
lence has usually been decreased by unfavorable 
conditions, such as lack of oxygen and lack of nutrition 
where most of the organic matter has been removed, and 
the blood supply is cut off. The result is a symptomless 
or chronic inflammation walled off by the fibrous sack 
enclosing the granuloma, containing lymphocytes and 

Proliferating periodontitis can be caused whether the 
pulp chamber is open or closed and results from the fol- 
lowing conditions : 

Decay of the Tooth. If caries has destroyed the enamel 
and dentin, so that there is an opening into the pulp 
chamber, the products of decomposition have a chance to 
escape into the mouth. This prevents them from pene- 
trating through the apical foramen thereby infecting the 
deeper tissues surrounding the root of the tooth. While 
the disease of the pulp progresses slowly towards the 
apex, protective measures are taken by the surrounding 
tissue against the poisonous substances of fermentation 
and decomposition. The periodontal membrane prolif- 
erates and forms a granuloma, and harbors in its center 
fluids of decomposition and absorption. 

Incomplete Pulp Extirpation. The extirpation of the 
dental pulp is an operation which should not be under- 
taken except after serious consideration of its necessity 
and most careful prognostic study of the case. Our 
present knowledge of the alveolar abscess should warn 
us of the possible consequences of such an operation and 
teach us to make the greatest effort to save the pulp by 
prophylactic as well as by therapeutic means. A tooth 
should be radiographed to diagnose if a root is straight 


or bent and to ascertain the size, length, direction, and 
branching of the root canals. Some teeth are bent to 
such an extent, or their root canals are so obstructed by 
secondary deposits of dentin or pulp stones, that we are 
not able to remove the pulp entirely, no matter how 
skilled the operator and how much time is spent. We 
stand therefore before an impossible task. Among these 
cases belong many teeth which have moved forward dur- 
ing childhood on account of loss of an anterior tooth and 
these teeth have been moved for large distances for ortho- 
dontic purposes. This may result in bent roots. Most 
of the permanent teeth erupt long before the calcification 
of their roots is finished, and if force is applied at the 
stage of root formation, it will move the calcified part and 
bend the uncalcified apical region. 

If parts of diseased pulp are left to remain in the roots, 
in branches of the root canal, apical part or accessory 
foramina, this organic matter will, after the tooth has 
been filled, stimulate proliferation of the periodontal 
membrane and cause a granuloma. If a healthy tooth has 
to be devitalized to give attachment to bridge work or to 
remove pulp stones which cause neuralgia, the remaining 
pulp particles are often infected by careless treatment, 
or by bacteria supplied by the blood stream. The con- 
dition then is the same as if the pulp had been infected 
in the first place. 

Inefficient Root-canal Treatment. Root canals which 
have not been sufficiently treated previous to the insertion 
of the root filling, are liable to cause the same result as 
just described. After all the organic matter has been 
removed by mechanical and chemical means, we must still 
consider the bacteria which are growing in the micro- 
scopic dentinal tubules and the accessory apical foramina. 
These should be destroyed by antiseptics [ionic treatment 
with iodine was found specially helpful by the writer] or 
they will become the source of infection, which is espe- 
cially favored by incomplete or poorly condensed root 
canal fillings. The same condition occurs if root canal 


instruments are broken and left in the canals. They ob- 
struct the way to the apical part which is left in a septic 
and unfilled condition. 

Inefficient Root-canal Fillings. A root-canal filling 
which is perfect should seal the apical foramen hermet- 
ically so that no infection can pass from the tooth into the 
surrounding tissues. Scrupulous asepsis is also of great- 
est importance, not only during root-canal treatment, but 
also during root-canal filling. If the filling leaves a space 
at the apex containing organic matter, moisture, or air, 
or if the filling material is of such a nature that it shrinks, 
irritates or relies on antiseptic properties, which wear 
out with time, it gives chance for bacterial growth. 

Invasion of Bacteria. It may also be caused by inva- 
sion of bacteria, reaching the pulp by way of the dentinal 
tubules, which can be easily entered if the enamel has 
been removed. If this is the case several factors must 
be reckoned with. Danger of infection is certain if the 
tooth is young and if it must be greatly reduced to fit a 
crown, because the dentinal tubules in this case are larger, 
less calcified, and nearer the pulp. If these little wounds 
(sections through the dentinal tubules) are not carefully 
protected during the preparation of the tooth and during 
the time which elapses until the crown is set, bacteria 
which abound in the mouth will invade these dentinal 
tubules, multiply, and progress even after the crown has 
been set, until they reach the pulp and cause suppurative 

Death of Pulp without Access of Air. It is a well- 
known fact that the pulp of a tooth may become diseased 
because the irritating action of certain fillings forms 
progressive decay under a filling or a gold or porcelain 
jacket crown. It is usually due to lack of oxygen that 
such cases proceed in a chronic manner and often large 
apical granulomata are formed without symptoms of 
disease. If the pulp of such teeth is opened, it often 
results in a violent subacute attack due to the change in 
the oxygen tension. 


Fig. 51 

Fig. 52 

Fig. 53 

Fig. 54 

Fig. 55 

Fig. 56 

Fig. 57 

Fig. 58 

Fig. 59 

Fig. 60 

Fig. 61 

Fig. 62 

Figs. 51, 52, 53, 54, 55 and 56. — Granulomata caused by inefficient root canal fillings. 
Figs. 57, 58 and 59. — Granulomata from decay under fillings without access of air. 
Figs. 60, 61 and 62. — Granulomata occurring on crowned teeth. 

Fig. 63. — Skull of Italian showing bony destruction caused by an apical granu- 
loma on the left upper second bicuspid. 


Haematogenous Infection. Granulomata usually are 
due to direct entrance of the disease through the root 
canal but may also be caused as a secondary manifestation 
due to bacteremia, that is, the presence of the microorgan- 
isms in the blood. Any devitalized tooth has around its 
apex a place of lowered resistance with lowered oxygen 
tension due to the destruction of nerve and blood supply 
of the apex and contiguous bone areas, a destruction 
which may have been caused by the use of caustic and 
irritating drugs for root canal medication or the destruc- 
tive process of suppuration. 

Proliferating Periodontitis. The poison- 
TH^Dis^ASE ous P r0( lucts °f bacterial decomposition 
and fermentation reach the peripheral 
tissues of the tooth and stimulate protective new growth. 
If the tooth is extracted at this stage we find a marked 
thickening of slightly reddish character at the apical 

Granuloma. The proliferation usually goes on until 
the new growth has reached the size of a pea. Larger 
granulomata are, however, not uncommon; they may 
reach the size of a robin's egg. A fibrous layer surrounds 
the lesion, which is very thick in the beginning and firmly 
attached to the healthy part of the periodontal membrane. 
The extracted tooth usually carries with it such a granu- 
loma, or so-called abscess sack. Later, when the 
granuloma reaches larger sizes, it becomes thinner and is 
often destroyed by fatty degeneration, which decreases 
its resisting power to suppuration. In the center we find 
the seat of chronic inflammation, harboring often a small 
amount of pus or other products of degeneration and 
absorption, which are usually taken up by the lymph or 
capillary system. Destruction of bone depends upon the 
progress of the chronic inflammation. In the upper jaw, 
where the apices of the roots are close to the facial sur- 
face of the bone, the alveolar plate is almost always de- 
stroyed; in the lower jaw it is a most infrequent occur- 
rence to find the thick cortical layers of the mandible 


involved. If the tooth is extracted at this stage the 
abscess will usually remain in the jaw and has to be re- 
moved by careful curettage. 

The microorganisms which inhabit the granuloma have 
to struggle for their existence in this tissue which is 
formed by lymphocytes, leucocytes, and fibroblasts ; pus, 
therefore, is formed only in very minute quantity. 

Subacute Attacks. At one time or another the suppu- 
ration may become more active and destroy the fibrous 
tissue of the granuloma. The causes of such acute bac- 
terial activity may be lowered resistance of the body and 
wearing out of the cells, whose function is to destroy for- 
eign bodies. It may come from a change in oxygen ten- 
sion, a thing with which almost every dentist is familiar, 
namely, an acute attack after opening into the pulp 
chamber of the tooth which gives the air a chance to enter. 
It also may be caused by haematogenous infection, the 
invasion of another kind of bacteria, causing a mixed 
infection. In these subacute attacks the pus usually bur- 
rows a sinus to the gum, the tissues react, not, however, 
very actively, as in the acute abscess, because partial im- 
munization has taken place in the tissues surrounding 
the chronic condition. After the pus has evacuated, the 
signs of inflammation usually disappear without treat- 
ment and the sinus closes up. This, however, does not in- 
dicate that the abscess has now completely healed, but 
only signifies that pus formation has decreased and granu- 
lation predominates, which may be reversed at any favor- 
able time. 

Exostosis of the Root. If the fibers of the granuloma 
persist for a long time, so that the metabolism of the 
cementum is not interfered with, the constant irritation 
from the chronic inflammation stimulates the activity of 
the cementoblasts which results in new formation of 
cementum, which we call exostosis of the root. This usu- 
ally results in a bulbous form at the apex which makes 
extraction extremely difficult. 

Necrosis of the Root. If the apical part of the peri- 
odontal membrane has been destroyed, the nutrient 


Fig. 64. — Skull showing bony destruction due to a granuloma caused by a 
left upper bicuspid, bearing a gold crown. 


1 • .1 N 

Fig. 65 

Fig. 66 

Fig. 67 

i v X 

Fig. 68 

Fig. 69 

Fig. 70 

Fig. 71 

Fig. 72 

Fig. 73 

Fig. 74 

Fig. 75 

Figs. 65, 66, 67, 68, 69 and 70. — Radiographs of teeth with granulomata showing marked 

exostosis of the roots. 

Figs. 71, 72 and 73. — Radiographs of teeth with necrosed apices due to granulomata. 

Figs. 74 and 75. — Radiographs of teeth showing large osteomyelitic area. 


supply of the tooth is doubly cut off. The cementum, 
which at this stage contains numerous accessory apical 
foramina and Haversian canals, soon becomes infected 
and necrosed. The condition then is that of bone with 
the periosteum raised and no blood supply from within. 
Here such areas become separated and are expelled as 
sequestra. In the tooth this cannot take place, and we 
must consider the whole organ as the sequestrum which 
is retained by the remaining periodontal membrane at 
the cervical part of the root. In some cases, chronic in- 
flammation of the remaining periodontal membrane sets 
in, causing necrosis of the entire root, which then has a 
greenish appearance, a condition which is often spoken 
of as " gangrene of the root." 

Resolution. The condition of chronic 
yfoivi " abscess may be considered the termination 

for the larger percentage of the cases ; it 
may continue for years. Resolution never occurs with- 
out treatment. 

Chronic Osteomyelitis. The bone destruction, occur- 
ring as a result of the inflammatory granulation, involves 
an osteomyelitis even at its early stages. Fortunately, 
nature in most cases prevents an extensive involvement 
by circumscribing the lesion with a protective layer of 
fibrous tissue enclosing the seat of inflammation, as will 
be shown later in microscopic pictures. Osteomyelitis 
produced by such conditions is much less severe than in 
other parts of the body and frequently symptomless. 

Cysts. There has been much writing by German scien- 
tists tracing root cysts of larger or smaller dimensions 
back to epitheliated granulomata. Dependorf * has devo- 
ted a large amount of time to the study of the development 
of such cysts. He says that not all epitheliated granulo- 
mata will become cysts, and that cyst formation depends 
on a partial and concentric degeneration of the inner part 
of the granuloma first of all ; secondly, dependent on epi- 
thelium which is able to develop and proliferate, and 
thirdly, due to the interference with the blood supply, due 

* See Bibliography. 


to the chronic inflammatory conditions. The growth of 
the cyst is dependent upon chronic inflammatory condi- 
tions, which are enclosed in the lumen and which cause 
degeneration of the larger or smaller parts of the central 
core. The inner surface becomes lined with epithelium 
and the cyst may develop to almost any dimension. It is 
the author's opinion that cysts may form from epitheliated 
granulomata, although judging from the number of 
granulomata which do not form cysts, we may draw the 
conclusion that such a formation is decidedly rare- 

Proliferating Periodontitis. Local symp- 
D I AG N OS IS toms: It is characteristic of the prolifer- 
ating periodontitis that it occurs and grows without caus- 
ing any local symptoms. The tooth is not elongated 
because the growth occurs at the expense of the bone. 
Sometimes, however, the patient has a sense of pressure 
over the tooth and often the pulsation of the blood is felt 
in the vascular granulation tissue around the apex, espe- 
cially after violent exercise. 

General symptoms: In the beginning stage there is 
rarely any systemic involvement, although the writer 
has procured streptococci cultures from many apices of 
teeth which in radiographs showed only the slightest in- 
dication of proliferating periodontitis. In a hospital 
case of endocarditis such a small area prevented entire 
recovery and the removal was followed by rapid improve- 

Clinical signs : There are no signs which would indicate 
proliferating periodontitis. 

Radiographic examination: With the intraoral radio- 
graph we can diagnose the early stages of periodontitis. 
The dark line around the contour of the root which repre- 
sents the periodontal membrane is thickened at the apex, 
and in later stages we find distinct areas of lessened den- 
sity which indicate loss of bone taken up by the prolifera- 
tion of the periodontal membrane. 

Granuloma. Local symptoms: The granuloma very 
frequently gives no symptoms; a sense of pressure and 
lameness of the tooth may be noticed occasionally. 


General symptoms: At this stage we frequently find 
complications due to the absorption of toxins and bac- 
teria. Malaise, a tired feeling, and inability to do a day's 
work is a frequent indication of an intoxication which 
may come from oral lesions besides all the other complica- 
tions mentioned in the previous chapter. These con- 
ditions should be recognized and inquired into and looked 
at as a reason for careful diagnosis of the mouth by means 
of radiographs. 

Clinical signs : As clinical signs are absent at this stage, 
it is of greatest importance to rely on radiographic 

Radiographic examination: The granuloma shows in 
the radiograph as a circumscribed area of decreased den- 
sity and is easily recognized when present at the apex of a 
devitalized tooth. While there is usually little doubt 
about the location of an abscess on a single-rooted tooth, 
it is often more difficult to make a correct diagnosis on 
multirooted teeth, especially the upper ones. The upper 
first bicuspids should be radiographed from a bucco- 
mesial direction, while two radiographs are necessary to 
show distinctly the condition of the two buccal roots and 
the palatal root. The first is taken about perpendicular 
to the buccal roots, the other perpendicular to the palatal 

Subacute Attacks. Local symptoms: If suppuration 
becomes more active in the granuloma, the patient often 
feels a grumbling and lameness of the tooth which may 
disappear after several days. In other instances, the 
wall of the granuloma is broken down, resulting in a regu- 
lar subacute attack. The patient then experiences the 
symptoms of the acute abscess, pain, redness, fever, and 
swelling. The tissue, however, has been rendered more 
or less immune, and the symptoms of inflammation are 
more modified, sometimes hardly noticeable, at other 
times extreme. The condition, however, will usually pass 
through the stages of parulis until a sinus occurs on the 
gum to give exit to the accumulating pus. 


General symptoms: The general symptoms depend 
upon how severe and acute the attack is. There may be 
none at all, or they may be equal to an acute process pass- 
ing through the stages of parulis. 

Clinical signs : When the gum over the abscess is found 
to be swollen and in subacute condition, the guilty tooth 
is usually easily located. When the pulp has been dead 
for a long time, electric tests will give negative results, 
while in acute conditions there is usually some doubt, 
especially if the nerve fibres of the pulp have not been 
entirely destroyed. The patient usually tells upon ques- 
tioning a history of previous attacks or treatment of the 

Radiographic examination : Radiographs will reveal an 
area of lessened density on a devitalized and partly filled 
root. This is the important feature of differentiation 
between an acute attack, where the pulp has been diseased 
only recently and where there is no evidence of previous 
root-canal work. 


Fig. 76 

Fig. 77 

Fig. 78 

Fig. 79 


Fig. 81 

Fig. 82 

Fig. 83 

Figs. 76 and 77. — Radiographs of teeth showing small areas of lessened density indicating 


Figs. 79, 80 and 81. — Radiographs of teeth showing large areas of lessened density 

indicating grannlomata. 

Figs. 82 and 83. — Radiographs of teeth with subacute abscesses. The root canals of the 
teeth have been partly filled, indicating chronic disease of long standing. 


Fig. 84 

Fig. 85 

Fig. 86 

Fig. 87 

Fig. 88 

Fig. 89 

Fig. 90 

Fig. 91 

Figs. 84, 85 and 86. — Badiographs of teeth showing dark areas about their necks representing pus 

pockets caused by mechanical injury. 

Figs. 87, 88, 89 and 90. — Badiographs of teeth showing dark areas indicating pus pockets at the 

alveolar border. 

Fig. 91. — Badiograph showing a lower incisor with an apical abscess caused by pus pockets, mesial 

as well as distal. The tooth is vital. 



We have noted in the preceding chapter that the largest 
percentage of the oral abscesses are due to diseases of the 
dental pulp. However, other forms of abscesses in and 
around the alveolar process occur which are due to dif- 
ferent causes. These sometimes give almost the same 
symptoms as some of the already described types and it is 
important to distinguish them because their treatment 
is so widely different. 

According to the etiological factor we can distinguish 
alveolar abscesses due to diseases of the gum and alveolar 
abscesses due to difficult eruption, impaction and un- 
erupted teeth. 

1. Alveolar Abscesses due to Diseases of the Gum. 

etiology Injury of the Gum. The gum is occasion- 

ally injured by the use of a toothpick or a 
bristle of a toothbrush which may become lodged between 
the gingival margin and the tooth. An inflammation may 
occur if the wound had been infected, involving not only 
the gum but frequently the cervical part of the periodon- 
tal membrane and the periosteum, resulting in a marginal 
periodonditis with subgingival parulis formation. Other 
causes are poor fillings, either projecting into the gum or 
lacking in contour, faulty bands and gold crowns, which 
project into the gum instead of being closely fitted around 
the neck of the tooth. After the cement by which they 
are fastened has washed away, these places will harbor 


contaminated food and be the seat of fermentation and 
later suppuration. A similar condition occurs under 
fixed bridges, which can be properly cleaned neither by 
patient nor dentist, the gum becomes inflamed, and after 
the removal of the bridge we often discover an extensive 
ulcerated area. The vile odor which is released after 
removing such appliances speaks for itself and makes 
superfluous further comment as to its unsanitary and 
disease breeding properties. 

Pus Pockets. Pus pockets such as are characteristic 
of pyorrhoea alveolaris sometimes become closed up. 
This, or any other reason which prevents the pus from 
escaping at the cervical margin, causes accumulation of 
pus or abscess formation. 

In abscesses caused by injury of the gum, 

the disease ^ e ^ n ^ ec ^ on i- s usually superficial. The 
pus is seldom formed under the perios- 
teum, but accumulates between the periosteum and gum 
in the submucosa of the mucous membrane. A red swel- 
ling is formed at the gingival margin, a small parulis, 
which heals spontaneously after it breaks or after an in- 
cision is made. In more deep-seated cases the ligamen- 
tum circulare and periodontal membrane may become 
infiltrated. The Haversian canals then become 
infected, causing destruction of the cervical part of the 
alveolar process. If pus pockets such as occur in py- 
orrhoea alveolaris or other forms of marginal periodon- 
titis are the cause of the abscess, the accumulation of pus 
is usually more deeply seated than in the case of injury 
of the gum. On account of the closure of the natural 
outlet at the cervical margin the pus will invade the alve- 
olar process and find its way to the surface of the gum. 
The process usually passes through the stages of subperi- 
osteal and subgingival parulis, which, however, gives no 
very severe symptoms as the tissues have been pretty 
well immunized by the long existing chronic inflamma- 
tion. This destructive process may, however, be halted 
any time if the outlet at the gum margin is reopened, when 
the disease continues in its former chronic form. 


diagnosis Local an d general symptoms: The pa- 
tient experiences about the same discom- 
fort as in the parulis formation already described, only 
perhaps in a modified way, because the tissue has almost 
always been more or less immunized by a preexisting and 
causative chronic condition, as in pyorrhoea, or because 
the abscess is very superficial and little destruction is 
necessary to form an outlet for the discharge. 

Clinical signs: Upon examination, a tumor-like swel- 
ling is seen nearer the gum margin than in true alveolar 
abscess and parulis. The surrounding tissues are less 
involved. There is usually no history of pulp disease; 
the tooth may be vital or devitalized. The patient often 
remembers that the gum had been injured or there may be 
indication of pyorrhoea from the general condition of the 
mouth. The differential diagnosis may be established by 
the radiograph. 

Radiographic examination: Very often we are left in 
doubt, whether we have to deal with a true alveolar ab- 
scess, caused by a diseased pulp, or whether the condition 
is wholly periodontal. Especially doubtful cases are those 
where the tooth has a gold crown or large fillings, as both 
are conditions which indicate the involvement of the pulp. 
The importance of knowing whether the pulp is involved 
or not is evident if we consider the first and most impor- 
tant therapeutic measure, the removal of the cause. A 
radiograph will help a great deal in diagnosis; if there 
is no area of lessened density at the apex of the tooth, we 
know that the abscess is not formed from a dead pulp, 
and often we see a large dark area at the neck of the tooth 
indicating marginal destruction of the alveolar process 
due to a gingival abscess or parulis. 

2. Alveolar Abscess Due to Difficult Eruption, Im- 
paction or Unerupted Teeth. 

etiology Difficult eruption and partial impaction: 

The lower third molar is the tooth which 

most frequently is impacted, but also the upper third 

molar is often in irregular position. The reason is that the 


third molars are the last teeth to take their places in the 
dental area, and as the jaw is often too short (a result of 
civilization) to accommodate all the teeth, the third molar 
becomes locked under the bulging of the crown of the 
second molar. In the lower jaw there is an additional 
obstacle, the ascending ramus, the terminal boundary of 
the part of the mandible that accommodates the teeth. 
The cuspid teeth are the next in the series which are most 
likely to be impacted, the reason being that the tooth in 
abnormal conditions does not appear until long after the 
lateral incisors and the first bicuspids are in place. While 
the lower third molars and cuspids are most likely to be 
impacted, any tooth in the lower as well as the upper jaw 
may become impacted if the space which they are to oc- 
cupy is taken up by other teeth, or if the malposition has 
been assumed at an early period during the development 
of the tooth germ. 

Inflammation may start before the tooth has pierced 
the gum, from the irritation caused by biting on the tissue 
overlying the occlusal surface of the tooth. In most 
cases, however, the infection occurs after the gum has 
been pierced by the erupting cusps and may be due to 
food and fluids of the mouth entering through this wound. 
The soft tissue does not adhere to the enamel of the crown, 
as it does to the cementum on the root by means of the 
periodontal membrane and ligamentum circulare, and 
therefore foreign material is free to pass deep into the 
tissue around, slowly erupting teeth both impacted and 
normal. In other cases the infection is due more to irri- 
tation of the gum, which is crowded over the occlusal sur- 
face during mastication and becomes bruised by the teeth 
of the opposite jaw. In such conditions inflammation 
again sets in and is maintained. 

Unerupted Impacted Teeth. In some cases teeth grow 
in an entirely horizontal or even downward direction 
and are so interlocked, that it is impossible for them to 
come to the surface. Such teeth may lie dormant for 
several years but at any time may suddenly become asso- 
ciated with active pathological conditions, when exert- 
ing pressure on the tissue towards which they grow. It 


Fig. 92 

Fig. 93 

Fig. 94 

Fig. 95 

Fig. 96 

Fig. 97 

Fig. 98 

Figs. 92, 93, 94 and 95. — Radiograph showing dark areas indicating abscesses caused by impacted 
but partly erupted wisdom teeth. In Fig. 93 the pulp has been involved and periodontitis caused at 

the apex. 

Fig. 96, 97 and 98. — Radiographs of unerupted molars showing dark areas indicating abscesses. 


Fig. 99 

Fig. 100 

Fig. 101 

Fig. 102 

Fig. 103 

Fig. 104 

Fig. 105 


Fig. 106 

Fig. 107 

Fig. 99. — Radiograph showing impacted second and third molar. 

Fig. 100. — Kadiograph shows impacted second molar which had been broken off. The third molar 

is partly erupted and prevents the second molar from coming up. 

Figs. 101 and 102.— Radiographs show impacted temporary molars. 
Figs. 103, 104, 105, 106, 107 and 108. — Radiographs show other impactions causing more or less troubh 


seems to be a physio-pathological law that any abnormal 
pressure in the body causes resorption of the part most 
easily dissolved. This in turn forms a place of lowered 
resistance and is liable to infection. Infection may occur 
from a blind abscess on a neighboring tooth or through 
the blood. 

After the infection has taken place the 

the: di<5e-a«sf P rocess °f inflammation may take on a 
chronic course. This is especially the 
case if there is an outlet for the pus through the gingival 
opening made by the erupting tooth. This outlet, how- 
ever, is rarely adequate, pus is accumulated and when 
under pressure is forced deeper into the bone as well as 
into the soft tissue. The inflammation then extends to 
the adjoining parts, involving the fauces, mucous mem- 
brane and muscles about the ramus. A pharyngitis often 
sets in, trismus of the muscles of mastication is of common 
occurrence, and deglutition becomes difficult. The abscess 
usually passes through the stages of alveolar parulis, and 
the trismus becomes so marked that the patient is unable 
to open his mouth. At this time usually there is a sinus 
formed, the pus evacuates and the movements of the jaw 
become less constrained. If no surgical procedure res- 
tores the condition to normal, the patient may have recur- 
rent attacks of the same character at frequent intervals. 
If the impacted tooth causes absorption of another tooth, 
this is sometimes carried so far as to involve its pulp. 
Such conditions cause severe neuralgic pains, and if the 
pulp becomes infected severe alveolar abscesses. 
diagnosis Local symptoms: The local symptoms 
are usually well marked but not character- 
istic or distinctive of the cause. There is intense pain, 
sometimes almost unbearable, referred to the ear, eye, 
forehead, or opposite jaw. If the condition is due to a 
third molar, the patient complains of a sore throat and 
inability to swallow ; often the mouth can be opened but 
very little. There may be extreme swelling of the face on 
the affected side ; at other times the external swelling is 
less marked, all the infiltration being on the inside of the 


General symptoms: There is usually fever up to 104° 
F., general malaise, and the patient often presents serious 
symptoms, especially if severe pain has caused continual 
loss of sleep. 

Clinical signs: If a third molar is the cause of the 
trouble, examination of the mouth is often very difficult. 
.Ankylosis should be excluded, which is a disease of the 
mandibular joints and is usually not accompanied by 
severe pain or temperature. Pus can frequently be 
pressed from the swelling and often a white cusp is seen 
sticking out from the inflamed gum. If we have to do 
with an unerupted tooth the radiograph will be the only 
means by which a positive diagnosis can be made. 

Radiographic diagnosis: The radiograph is a most 
valuable means of detecting the real cause of the trouble 
and is furthermore a valuable aid in determining the 
mode of operation. Partly erupted impacted teeth can 
be taken on small, intraoral films, but unerupted teeth 
should be taken on large extraoral films or plates, because 
there is a possibility of malposition. Third molars have 
been found in the ramus as far up as the mandibular notch 
and as low down as the angle of the ramus, places which 
cannot be reached with intraoral pictures. For impacted 
upper teeth in the anterior region of the mouth, a large 
film placed between the teeth with an exposure from well 
above the head will give in most cases good results. For 
impacted cuspids in the lower jaw the rays should be 
directed somewhat from underneath, as these teeth are 
often situated as low as the lower border of the mandible. 
Stereoscopic radiographs would be more desirable in 
many cases, as an ordinary radiograph is flat and does not 
give the exact location of the tooth. For example, you 
cannot tell whether the impacted cuspid in Figure 107 is 
external or internal to the other teeth ; however, the tak- 
ing of stereo-radiographs requires a great deal of skill and 
necessitates the use of special apparatus. The stereo- 
radiographic technique is still in the process of develop- 
ment ; good results, however, can be obtained, and in diffi- 
cult cases these pictures, which give a perspective view, 
are of great value. 


Fig. 109. — EadiograpMe plate showing an impacted upper third molar in the pos- 
terior wall of the antrum. Symptoms covering a period of one year prior to its 
discovery: Periodical unilateral headaches, with ent're absence of nu, but bad 
taste in the mouth every morning. There is a sinus opening just back of the 
second molar. The tooth discharges half a dram of pus in twenty-four hours. 

Reproduced by courtesy of Dr. Gibbons. Radiograph by Dr. A. TV. George. 


Fig. 110. — Radiographic plate by which an unerupted lower third molar was 
discovered at the angle of the jaw. Note the large cyst. 



Thus far abscesses occurring in and about the mandi- 
bular and maxillary bones have been described; these 
are by far the most common ones. The tongue and sali- 
vary glands are, however, occasionally the seat of abscess 


The tongue is comparatively rare as the seat of inflam- 
mation and infection, but if abscesses of the tongue occur, 
we have a condition which may bear grave results. 
Diffuse infiltration frequently occurs and often spreads 
to the posterior part of the tongue, and, on account of its 
increased size, causing difficulty in breathing which often 
can be relieved only by tracheotomy. 
. „-.„.-, Three varieties of tongue abscesses shall 

VAR5ET8ES u j .i j ° 

be described. 

1. The simple abscess of the tongue. 

2. The phlegmonous abscess of the tongue. 

3. The tubercular abscess of the tongue. 

1. Tide Simple Abscess of the Tongue. 
^^.«. ~~w Circumscribed abscess formation of the 

ETIOLOGY , », -, , 

tongue is very oiten due to injury or en- 
trance into the tongue of a foreign body, such as a fish 
bone, during mastication. More often, however, there 
are sharp, broken-down teeth which cause the primary 


injury, and if such teeth are abscessed, discharging pus 
from sinus or pocket, the wound at once becomes infected. 

~. .*.._.. The infection usually assumes a more or 

course chronic appearance, causing a tumor- 

like thickening at the infected part. If no 
therapeutic interference occurs, the abscess may break, 
but more frequently it will end in the phlegmonous type. 
„..„ MAeie Local symptoms: The simple abscess of the 
tongue causes more or less local discomfort. 
The place where the lesion occurs is extremely tender to 
touch, causing difficulty in eating and speaking. 

Clinical signs: If the tongue is palpitated, one can 
feel distinctly a hard swelling in the substance of the lin- 
gual muscle ; the tongue is usually slightly enlarged, which 
causes indentations on its sides because it is crowded 
into the interdental spaces. In the first stages it may be 
hard to differentiate this lesion from gummata and tu- 
mors, but later when the signs of inflammation are more 
marked and when there is discharge of pus, there is 
usually no doubt about the diagnosis. An exploratory 
incision or puncture may be made ; this should be deep 
enough to reach the seat of trouble and will, if pus is 
drawn, verify the diagnosis. 

2. The Phlegmonous Abscess of the Tongue. 

etiology Injuries due to infected foreign bodies, as 
already described, and injury from carious 
teeth surrounded by septic conditions very often take on a 
more acute form than the one just described. Progressive 
alveolar abscesses may also cause phlegmonous abscesses 
of the tongue, if their course involves the deeper, posterior 
lingual muscles. 

In the phlegmonous abscess of the tongue, a purulent 
or fibrino-purulent infiltration, causes a diffuse swelling. 
The size of the tongue increases rapidly, the anterior 
part is pushed forward and no longer has room between 
the teeth. The soft palate and the mould are pushed 


Fig. 11 L 

Fig. 112 

Fig. 111. — Simple abscess of the tongue. 
Fig. 112. — Tubercular abscess of the tongue. 


upward and the epiglottis downward into the larynx. In 
severe cases, swallowing is impossible, causing the saliva 
to flow out of the month, and even breathing is rendered 
difficult. If the epiglottis becomes enlarged by oedematic 
swelling, tracheotomy may be necessary, but more often 
the disease is less grave, pus discharge occurring sooner 
or being facilitated by early surgical interference, which 
is possible if the center of the infection can be located. 
diagnosis -k° ca l symptoms: The patient complains 
of the tongue being swollen and too large, of 
difficulties in swallowing and breathing. If the tongue 
comes in contact with hard food, it causes a great deal of 
pain and the saliva often flows from the mouth. 

General symptoms: The pulse is generally increased 
in rate, the temperature rises, and may reach the high 
marks of septic conditions. 

Clinical signs: Examination of the mouth is usually 
impossible on account of the muscular trismus and the 
sensitiveness of the tongue to touch. The cervical and 
submaxillary lymph glands are involved at an early stage 
of the disease and are extremely tender to touch. Later 
there is marked angina, causing the patient to bend the 
head forwards on the chest, which somewhat facilitates 
the breathing through the nose. 

3. Tubercular Abscesses of the Tongue. 

Tubercular abscesses of the tongue may be 
primary or secondary infections. Tubercu- 
lar bacilli are found in mouths of healthy persons and 
primary tubercular infections may therefore occasionally 
occur at an injured part of the tongue. This, however, 
is said to be a rare condition. Secondary infection is 
more common, slight wounds on the tongue caused by 
carious teeth or sharp artificial dental prostheses are 
easily infected by the bacilli of the saliva and expecto- 
rated material. 


Tubercular abscesses of the tongue occur 
course mostly on the tip, the sides, and the mucous 
membrane reflection between tongue and 
floor of the mouth. When first seen they are very small 
nodules of yellow. A clear infiltration develops, becom- 
ing gradually thick and increasingly visible. The lesion 
usually extends deep into the substance of the tongue, 
developing a fissure or an ulcer. Tuberculosis fissures are 
very short, often stellate or branching, and are generally 
single. The margin is indicated, causing an elevation of 
the edges which are liable to caseate, forming a foul and 
ragged surface. The tuberculosis ulcer is the more ag- 
gressive form of the fissures and presents edges which are 
a little thrown up, but not undermined, and are usually 
sharp in outline. The secretion is small in quantity and is 
of grayish yellow color. Pale red flesh warts, and here 
and there small gray knots may be visible. 
diagnosis -k° ca l symptoms: Tuberculosis of the 
tongue is seldom noticed early by the pa- 
tient, as the lesions first are very small and produce no 
symptoms; later they become tender and pain becomes 

General symptoms: The patient may suffer from 
pulmonary tuberculosis or lupus of the face. However, 
he may be perfectly well, the lesion of the tongue being a 
primary infection. 

Clinical signs: The appearance of the tubercular le- 
sions of the tongue has already been described. Bacteri- 
ological examination of the sputum and excretions is 
important for making a sure diagnosis. A negative 
Wasserman test excludes gummata, but carcinoma of the 
tongue is often difficult to differentiate from tuberculosis 
with certainty. 


Abscesses of the salivary glands and ducts may be 
divided into primary and secondary infections. The sub- 
lingual and submaxillary glands are most frequently 


involved by primary infection, the disease entering 
through the salivary ducts. The parotid gland is more 
often the seat of secondary infection, the bacteria entering 
the gland through the circulation. Salivary calculi are 
also to be considered. They may either cause or be 
caused by infection. 

etiology Primary Infection. The primary infection 
of the salivary glands may be due to a con- 
tinuous septic process, such as necrosis or ostitis of the 
mandible, or alveolar abscesses from lower teeth. The 
pus burrows through the tissue, following the path of 
least resistance, and often reaches the submaxillary gland, 
causing Ludwig's angina, a disease which, however, is not 
restricted to the submaxillary gland, but attacks the 
muscles of the floor of the mouth and neck. More com- 
monly, however, the infection enters by way of the ducts, 
originating from pus discharged by sinuses of abscessed 
teeth, pyorrhoea pockets, or other forms of oral sepsis. 

Secondary Infections. Haematogenous infection of 
the parotid gland is known to occur occasionally after 
infectious diseases, such as scarlet fever, typhoid fever, 
measles, meningitis, appendicitis, chalecystitis, and acute 
abscesses. Any focus causing secondary infection seems 
therefore to cause disease of the parotid gland and in very 
rare cases of the other salivary glands. 

Salivary calculi. Calculi are more commonly found 
in the sublingual and submaxillary ducts and glands and 
are of rather rare occurrence in the parotid gland. The 
question whether the calculus is primary or secondary to 
the infection has not yet been entirely settled. The be- 
lievers in the primary origin of the calculi think that the 
infection is due to its irritating presence. The men who 
believe in the infectious origin of the calculi founded 
their idea upon microscopic investigations. They think 
that calcium phosphate or carbonate is deposited in con- 
centric fashion around organic exudates as epithelial cells, 
leucocytes, bacterial emboli, or mucin, or that precipita- 
tion of the salts may be due to direct bacterial activity. 


Whether primary or secondary, the calculus plays an 
important role in the infections of the salivary glands, 
and cases which will not yield to treatment and which 
recur often harbor in their ducts or glandular substance 
calculi which are a source of irritation and reinfection. 

Stones may be found in Stenson's or Wharton's duct 
or in the body of the glands. They most frequently occur 
in Wharton's duct and the sublingual gland. 
clinical ^ ^ e disease starts from the mouth, the 
course infection often does not progress farther 
than a short distance through the duct. The 
duct walls become swollen, accumulation of products of 
infection occurs, and calculi may be formed. Either con- 
dition obstructs the flow of saliva. During the time of 
glandular activity, at meal times, and if tasty food is seen, 
a tumor like a swelling will occur at the site of the obstruc- 
tion, causing more or less pain until the duct is suffi- 
ciently dilated to allow excretion. Abscess formation 
usually occurs, discharging either through the duct or 
forming a new sinus to the mouth. 

In ascending duct infections, the process spreads 
through the accessory ducts, finally involving the glands 
and interlobular tissue. In the parotid gland the abscess 
may point towards the face, the mouth, the external 
auditory canal, or may extend upwards into zygomatic 
fossa. In the submaxillary and sublingual gland, the 
abscess will break either to the mouth or through the floor 
of the mouth to the skin of the submandibular region or 
the neck. The salivary fistula occuring in this fashion 
is extremely difficult to heal and often can be closed only 
by radical surgical procedures. 

In the secondary infections the bacteria are carried 
to the glands in the blood stream and the abscess starts 
in a blood vessel and progresses to the adjacent parts. 
diagnosis ^ oca ^ symptoms: The patient usually com- 
plains of marked swelling in the region of 
the gland which may frequently change its size. If the 
duct is affected, the swelling becomes especially marked 
during glandular activity. If the abscess and stone lie 


Fro. 113 

Fig. 114 

Fig. 113. — Swelling under the tongue on the left side. 

Fig. 114. — Eadiograph showing salivary calculus causing 

the condition indicated in the picture above. 


in the substance of the gland, the swelling is usually of a 
more inflammatory nature. At times, due to some un- 
known factor, probably renewed bacterial activity, there 
are sudden reactions and the patient complains of intense 
pain. Such attacks occur at irregular intervals and 
cause a large amount of suffering. 

Clinical signs: During the attacks, we usually find 
the characteristic symptoms of acute abscess formation 
with more or less swelling of the neighboring tissue, which 
is not alone due to the accumulation of saliva in the gland, 
but to oedematic infiltration, especially so in streptococcic 
infection. The corresponding lymph glands are en- 
larged, soft, and tender in acute conditions, hard and 
solid in cases of longer standing, which have passed more 
or less into a chronic stage. There may be discharge of 
sero-purulent material through the inflamed orifice of 
the duct or a fistular bidigital palpitation and careful 
exploration of the duct with a fine silver probe may reveal 
a stone, but if the trouble is harbored in the gland itself, 
this method of diagnosis will be found unsuccessful. 

Radiographic examination: Radiographic diagnosis 
is of greatest importance in glandular affections. Extra- 
oral, as well as intraoral films, are of greatest value ; they 
not only tell us whether there are calculous obstructions, 
but also give us their location, a helpful aid for the opera- 
ting procedure. For sublingual calculi and stones in 
Wharton's duct, a large film may be placed between the 
patient's teeth, the head being bent in an extreme back- 
ward position so that the rays can be directed from the 
submandibular region vertically on the film. Submaxil- 
lary calculi may be taken by the same method or by plac- 
ing a film or plate under the mandible, more towards the 
diseased side, reaching farther back than the angle of 
the jaw. The picture is taken from above with the mouth 
wide open. 

The treatment of the abscesses of the tongue and sali- 
vary glands will be found in the general chapter of treat- 
ment of abscesses. 



importance The careful scientific study of the bacteria 
OF the found in oral abscesses requires a great 

ogkJaiTstudy ^ ea * °^ ^ me an( ^" P a ti ence on account of 
the many varieties which normally in- 
habit the mouth. These may become the direct cause of 
abscesses or inhabit the lesions accidentally, living upon 
the products of decomposition. It is especially the culti- 
vation and isolation of the anaerobic bacteria which ren- 
ders the investigations difficult. No one has been able to 
demonstrate that one type of bacteria causes one typical 
form of dental abscess and it has generally been accepted 
that any one of the pyogenic bacteria may cause abscesses 
in the mouth. It has been observed and demonstrated 
that it is not so much the variety of the bacteria which 
determines the course of the disease but that it depends 
upon the number, vitality, and virulence of the invading 
organisms and, moreover, upon the abundance or scarcity, 
as quality of the media ; such as organic matter in the root 
canal, whether an abscess will develop as an acute or 
chronic condition. But also secondary invasions of bac- 
teria and the different combinations of mixed infections 
determine slight changes in the pathological picture, such 
as the production of gases, odor of the exudates, and color 
of the pus. The variations, however, are so manifold and 
the bacterial causation so accidental that a study of the 
bacteriology of the dental abscesses was found a fruitless 
task, and furthermore, an undertaking of small practical 
importance, until lately, when the process of focal infec- 
tion was discovered. The bacteriological question, then, 
becomes at once one of first importance, if we look at the 


Fig. 115 

Fig. 116 

Fig. 115. — Kadiograph, showing granuloma from which the smear 
below was made. 

Fig. 116. — Microphotograph of a smear taken from abscess seen in 

Fig. 115. Note the two chains of streptococci and groups of 


Specimen prepared by author; stained with methylen blue. 


unfilled root canal containing remnants of diseased pulp, 
or the acute and chronic dental abscess and the granuloma 
as a focus from which not only bacteria may become ab- 
sorbed and distributed to other parts of the body, but 
where protein poisons (see Chapter I) may be generated 
and taken up by the circulation, thus causing general 
toxemia or local disease of certain delicate tissues. We 
have already seen that the protein poisons which are 
formed during infection differ, among other things, 
according to the species of the invading bacteria and it 
is therefore desirable to know which of the bacteria en- 
countered in these lesions produce secondary disease, 
either by direct infection or by the formation of patho- 
genic poisons which become absorbed and may cause auto- 
intoxication similar to that of intestinal origin. 

The study of the bacteria of dental abscesses, which was 
first undertaken to find the etiological factor of the local 
lesion, has now become of new importance, but from a 
different reason, namely : that of investigating the effect 
of pathogenic or saprophytic bacterial life in a certain 
part of the body called a focus such as a root canal, ab- 
scesses, or granuloma upon other parts of the body. 

From Acute Abscesses. Wash the mucous 
methods OF membrane thoroughly with a mild anti- 
bacterial. se Ptic mouth wash (the spray may be 
specimen used). Apply iodine on the gum, and as 
soon as the incision is made, introduce a 
sterile pipette deeply into the abscess to collect the pus. 
The pipette is then sealed and sent to the laboratory. 
Instead of the pipette a sterile syringe may be used. 

From Chronic Abscesses and Granulomata of Teeth 
which are Extracted. First of all remove the tartar or 
other deposits from the tooth and spray the mouth and 
teeth with an antiseptic solution, then scrub the mucous 
membrane in the region of the offending tooth as care- 
fully as possible. Pack sterile gauze on either side of 
the tooth to exclude saliva, dry the mucous membrane 
with gauze and compressed air, and saturate tooth and 
gum with tincture of iodine. The ligamentum circulare 


is then cut free from the tooth, after which iodine is em- 
ployed a second time to destroy bacteria which always 
lodge immediately under the mucous membrane. Extract 
the tooth and place the forceps holding the tooth on a 
piece of sterile gauze, apex of the tooth uppermost. Cu- 
rette with a sterile instrument the alveolar socket from 
which the tooth was extracted to remove the granulations, 
and smear some of the removed tissue over the slant sur- 
face of a culture tube. Two plantings may be made, one 
for aerobic, the other for anaerobic cultures. Imme- 
diately after the operation clip off the apex of the removed 
tooth with sterile Rongeur forceps and drop it into an- 
other culture tube. It is advisable to let it drop into the 
water of condensation and smear it afterwards over the 
surface of the media. 

From Chronic Abscesses and Granulomata in Apiec- 
tomy. As this operation is performed under the princi- 
ples of asepsis no further precautions need to be taken. 
The amputated root is at once dropped into a culture 
tube held and opened by an assistant. Other cultures are 
made from the removed granulation tissue. 

Immediate Microscopic Examination. 
bacte > rial )F ^ us gained from acute abscesses may be 
STUDY examined directly under the microscope 

by making the usual cover glass prepara- 
tions. Also, from chronic condition may we secure cover 
glass preparations by smearing the end of the root or a 
piece of infectious granulation tissue over the cover glass. 

Inoculation of Artificial Culture Media. Specimens 
gained from acute or chronic abscesses by the methods 
already described may be inoculated on artificial media 
for special identification, and pure cultures may be made 
of the bacteria which perhaps have already been recog- 
nized in a general way in a cover glass preparation. 

The cultures should be grown on various media and 
both under aerobic and anaerobic conditions. Anaerobic 
bacteria are especially hard to cultivate and it is of great- 
est importance to inoculate the media without loss of time 
so as not to endanger the vitality of the anaerobes. 


Inoculation of Animals. The animals which are or- 
dinarily used for inoculation are rabbits, guinea pigs, and 
mice. Rabbits and guinea pigs are usually inoculated by 
the subcutaneous or intraperitoneal method. A very 
simple method in rabbits is the intravenous inoculation. 
The tip of the ear is held by thumb and fingers of the left 
hand, while the right manipulates the syringe. The 
needle is pushed through the skin on the external surface 
into the posterior vein which runs along the margin of 
the ear. By the exercise of care and gentleness the ani- 
mal may thus be inoculated without being anaesthetized 
or even held by an assistant, especially if the fur between 
its ears is stroked for a short time. 

Animal inoculation is used to find out whether the bac- 
teria in question are pyogenic or not. The animal usually 
dies of the same disease that was produced in man. If 
bacteria taken from a questionable focus produce in the 
animal the same disease the patient suffers from, we can 
conclude that we have found the organism which causes 
the systemic disease. 

Schreier* (1893) gives in his article the 
the bacter- reSTinL s °f n i ne examined cases. In five 
iological cases he took his material from the in- 
study OF flamed periosteum, involved by an 

^!^ A _ B " alveolar abscess, and in four cases from 

a subgingival parulis. In three cases he 
found only the diplococcus pneumoniae, in three cases 
only the staphylococcus pyogenes albus, in the remaining 
three cases he found both the diplococcus and the staphy- 
lococcus present. He concludes from this that periostitis 
(acute abscess) is due to infection by pus producing bac- 
teria and especially to the diplococcus pneumoniae, which, 
he adds, was also found in two abscesses due to caries 
examined by Nannotti* ; Miller and Sieberth contest that 
Schreier 's diplococcus is identical with the diplococcus 

* See Bibliography. 






Staphylococ. p. albus 

Case 1. 


Case 2. 


Case 3. 


Case 4. 


Case 5. 


Case 6. 


Case 7. 



Case 8. 



Case 9. 



Nannotti 1891 

Case 1. 


Case 2. 


Miller* (1894) examined two cases of alveolar abscesses 
and found in one two different varieties, in the other one 
variety of a coccus. 

Arkovy* (1898) examined four cases of periostitis 
alveolaris chronica diffusa (chronic alveolar abscess, as a 
sequel to the acute alveolar abscess) and found in one case 
the bacillus gangraenae pulpae alone, in two cases to- 
gether with the staphylococcus pyogenes aureus and 
albus, and in another case there was no growth on the 
culture plates. 

Aekovy 1898 

Bac. gangeenae pulpae 

Staphylococ. p. 


Staphylococ. p. 


Case 1. 


Case 2. 




Case 3. 




Case 4. 

Goadby* (1903) pronounces the cocci as the bacteria 
found in almost all the alveolar abscesses. He examined 
twenty cases and very often finds a staphylococcus de- 

* See Bibliography. 


scribed under the name of staphylococcus viscosus. The 
staphylococcus he finds in half of the cases, the staphy- 
lococcus aureus in three cases, and sometimes also the mi- 
crococcus tetragenus. In two cases with fetid pus he 
discovered the bacterium coli and in four cases of diffuse 
alveolar abscesses he grew besides the staphylococcus al- 
bus a constant anaerobic bacterium which formed long 
threads and produced much gas. When stained with 
methylen blue it took the color irregularly. He was not 
able to get a pure culture. This is the first mention of 
the discovery of an obligate anaerobic microorganism in a 
pathological process of dental origin. 

Partsch* (1904) reports a well observed case of 'tuber- 
culosis of the jaws near the apex of a root and for the 
first time described the microscopic picture of a tuber- 
cular periodontitis. 

Monier* (1904), a Frenchman, was the first to make 
a study of the anaerobic bacteria in connection with his 
bacteriological study of six alveolar abscesses. In Case 

VI, a boy of the age of nine, who was suffering with 
" osteo-periostite" (alveolar parulis) caused by a carious 
left lower first molar he found a micrococcus and a bacil- 
lus by microscopic examination and gram stain of the 
lightly fetid pus. On the surface of agar cultures fine 
gray colonies grew, which he identified as streptococci. 
In the depth of the agar cultures where there is exclusion 
of air he found longitudinal and round granular colonies 
which he identified as the bacillus Ramosus. In Case 

VII, a woman at the hopital * Saint- Antoine, the follow- 
ing diagnosis was made: Osteo-periostite, absces bien 
collects, overture (large alveolar parulis with sinus) on 
the left superior or lateral incisor. Microscopic exami- 
nation of the very liquid, fetid, grayish pus shows leuco- 
cytes in the stage of destruction scarcely stained. He 
found gram positive micrococci of small number and a 
gram positive bacillus; besides these a gram negative 
bacillus. Aerobic cultures yielded a scarce growth of 
streptococci and in anaerobic cultures he found the bacil- 

* See Bibliography. 


lus f ragilis in large quantity and the bacillus Ramosus in 
small numbers. Case VIII lie saw in consultation at the 
"hopital de VInstitut Pasteur" with " Osteo-periostite du 
maxillaire inferieur avec oedeme considerable (alve- 
olar parulis, with large oedematic swelling) caused by a 
right lower bicuspid. The abscess broke during the ex- 
amination ; he found streptococci, staphylococci albi, and 
numerous anaerobic bacteria, among them the bacillus 
Ramosus. As the material could not be collected with 
the necessary precautions, the study of this case was not 
further followed up. Case IX was a patient who suf- 
fered from an enormous swelling in the submaxillary 
region, extending over the whole cheek, suborbital region 
and subhyoid region caused by a tooth in the left lower 
jaw. There was intense trismus, the skin was covered 
with an erysipelitic reddish color. During the night 
there was delirium, the swelling became fluctuating in 
the submaxillary region and an opening was made with 
thermocautery. Examination of the horribly fetid 
pus showed partly destroyed leucocytes and a veritable 
mixture of microorganisms. He found bacilli of fine and 
short form often encapsulated, V-shaped bacilli, cocci in 
chains, and a rare bacillus occurring in filaments. Cul- 
tures yielded a streptococcus, bacillus Fragilis and Ramo- 
sus which were most abundant; the other unnamed bac- 
teria could also be obtained in pure culture. Case X, 
23atient with ll absces volumineux de la voute palatine" 
(palatal alveolar parulis) from a right upper incisor 
tooth. The pus which was mixed with black blood showed 
on microscopic examination only fragments of leucocytes 
which hardly stained. The enormous quantity of bac- 
teria consisted of diplococci, curved bacilli, often of the 
shape of a V, which were gram positive, a short and fine 
bacillus and a rare bacillus of very large form, both gram 
negative. Inoculation on the surface of agar yielded no 
growth whatever, but the anaerobic bacteria were very 
abundant. He isolated the bacillus Fragilis, the curved 
bacillus which was identified as bacillus Ramosus and the 

See Bibliography. 



diplococcus which was found to be the coccus foetidus. 
The large bacillus which was seen in small quantity grew 
in large white, coarse cultures and was found to be a 
bacteria that had not yet been described. This case is 
interesting because a large amount of pus was produced 
in this abscess without the presence of any aerobic bac- 
teria but was due to four anaerobes. Case XI, a young 
girl at the "hopital des Enfants-Malades," had suffered 
with a great deal of pain from a left inferior first molar 
for three months. The abscess broke first into the mouth 
and later formed a sinus to the outside of the face. Micro- 
scopic examination of the abundant pus showed well 
stained leucocytes, and gram positive curved bacilli some- 
times occurring in chains of two. Surface cultures 
stayed sterile but in the middle, deprived of air, he ob- 
tained cultures of the bacillus Ramosus, which was the 
only microorganism found. 







B. Bamosus 

B. Fragilis 


Case VI 



Case VII 




Case VIII 


Case IX 





Case X 






Case XI 


Vincent* (1905) writes in his article "La symoiose 
fusospirillaire ses di verses determinations pathologique" 
that he found seven times in seventeen cases of "suppu- 
ration dentaire sous periostique" (subperiosteal parulis) 
the association of fuso spirillae, once as a pure infection. 

Mayerhofer* (1909) thinks the streptococci are the pri- 
mary cause of " periostitis dentalis" (alveolar parulis). 
In examining twenty-two cases of pus gained from un- 
opened abscesses and twenty-eight cases of pus taken 

* See Bibliography. 



from sinuses on the gum, he found thirty times strepto- 
cocci in pure culture, fourteen times streptococci and 
bacilli, twice streptococci and staphylococci, once staphy- 
lococci and bacilli, twice stapylococci alone, and once ba- 
cilli alone. He thinks that staphylococci are perhaps 
present only on account of secondary infection of media 
prepared by streptococci and that the bacilli are etiolog- 
ically without importance. Apparently he made no 
attempts to grow anaerobes. 

Mayeehofee 1909 




30 cases 


14 cases 



2 cases 



1 ease 



2 cases 


1 case 



Idman* (1913), of the Pathological Institute of the 
Helsingfors University (Finland), has written the most 
complete and thorough bacteriological study of the acute 
alveolar abscess published in the "Arbeiten aus dem 
Pathologischen Institut der Universitat Helsingfors/' 
His publication is based upon most careful and painstak- 
ing research work, each analysis representing four weeks 
of steady, tedious work. 

He described his method of obtaining and inoculating 
the culture, the preparation of the fourteen different 
media used and the staining methods for coverslip exam- 

He examined eight cases of undoubted dental origin 
which had not undergone therapeutic treatment at any 
time, contamination from the fluids of the mouth was 
carefully excluded, and by careful technique, the pus was 
aspirated by a Pravaz syringe and emptied into a sterile 
test tube. The different media were inoculated as soon 
as possible, never later than an hour was allowed to elapse, 

* See Bibliography. 


so as not to endanger the vitality of the anaerobes. The 
oxygen tolerating bacteria were grown on agar (Titer 15- 
18), blood agar and glucose agar (Titer 15-18). The ob- 
ligate anaerobes were gained by shake cultures in series 
of 10-12 tubes of Agar (Titer 2-3), 10-12 tubes of glucose 
agar (Titer 15-18), 10-12 tubes of ascites glucose agar 
(Titer ca. 8) and 10-12 tubes of Indigo-glucose agar. 
Some of the isolated bacteria he tested as to their viru- 
lence by subcutaneous inoculation into rabbits or guinea 
pigs, using 5-10 c.c. of a young bouillon culture. To study 
the microorganisms gained in these cultures he used 
gram stain, the polychrom-methylen-blue-tannin method, 
and Ziehl's carbofuchsin stain. 

Case A. A woman thirty years of age, with subgingival 
parulis, caused by a suppurating pulpitis. The thick yel- 
low pus was of neutral reaction and odorless. Microscopic 
examination and cultivation showed an oxygen tolerant 
streptococcus and bacillus mesentericus and obligate 
anaerobes identified as a streptococcus, Bacillus Ramosus 
and Idman's bacillus No. 13. 

Case B. A nineteen year old peasant boy presented a 
subgingival parulis from a putrescent pulp. The pus 
which showed a slightly alkaline reaction, was odorless. 
The bacteria he isolated were the oxygen tolerant strep- 
tococcus, staphylococcus albus, micrococcus tetragenus 
and the elongated cocci Idman No. 6, the obligate ana- 
erobes, bacillus ramosus. Case C was a patient presenting 
a subperiostal parulis from a first molar. The yellowish 
white pus was of extremely fetid odor and slightly alka- 
line. Cultivation and isolation yielded the oxygen tole- 
rant corynebacterium pseudodiphtheriticum and the 
obligate anaerobic streptococcus anaerobicus, bacillus 
ramosus, bacillus thetoides, bacillus perfringens. Case 
D, a young man, age seventeen, with subperiosteal pa- 
rulis. Microscopic examination of the exudates showed 
an abundant bacterial flora which were cultivated and 
identified as follows: Oxygen tolerant; streptococcus, 
bacillus Idman* No. 3, obligate anaerobic ; streptococcus, 

See Bibliography. 



staphylococcus parvulus, bacillus ramosus, bacillus the- 
toides, bacillus perfringens, bacillus bifidus communis 
and bacillus Idman No. 14. Case E, also a case of subper- 
iosteal parulis with thick yellowish pus without odor nor 
reaction yielded the oxygen tolerant bacillus Idman No. 3 
and the obligate anaerobe bacillus ramosus. Case F, a 
case of subperiosteal abscess, contained thin pus of 
strongly alkaline reaction. The following bacteria were 
found : oxygen tolerant ; streptococcus, obligate anaerobe ; 
staphylococcus iungano, staphylococcus parvulus, bacil- 
lus thetoides, bacillus ramosus and bacillus fusiformis. 
Case G, a subgingival abscess with grayish white pus of 
neutral reaction, contained large oxygen tolerant cocci 
single, double and in packs, (staphylococci) also small 
oxygen tolerant streptococci. The obligate anaerobes 
were found to be streptococci and the bacillus ramosus. 
Case H, a subgingival abscess, was not fully completed. 
It contained oxygen tolerant staphylococci and the ba- 
cillus ramosus. 

Oxygen Tolerant 

Obligate Anaerobic. 























• r* 











• iH 

















1— 1 









































Case A 






Case B 






Case C 






Case D 










Case E 



Case F 







Case G 





Case H 




Fig. 117 

Fig. 118 

Fig. 117. — Eadiograph of a tooth with large granuloma which proved 
to contain colonies of actinomyces. 

Fig. 118. — Microphotograph of a section of the above granuloma. 

Specimen prepared by author; stained with methylen blue and Eosin. 


The animal experiments undertaken with these bacteria 
he reported under a special head, describing the isolated 

Bacillus pseudodiphtheriticum (aerobic) was injected 
into guinea pigs in the form of a 5 c.c. of a 22-hour old 
bouillon culture. There was an increased temperature 
on the second day, no other pathological conditions. 

Aerobic streptococci, two of which form no haemolysis, 
two others cause a very weak haemolytic phenomenon, 
were not all used for animal experiments. One strain of 
the latter was injected subcutaneously into a rabbit and 
caused only temporary decrease of weight, but no other 
pathologic conditions. 

Bacillus ramosus (anaerobic) was tested on rabbits. 
Five of the isolated strains were used, two immediately 
after the isolation. Ten c.c. of a three to seven days' cul- 
ture was injected subcutaneously. None produced an ab- 
scess at the place of inoculation. In each case he ob- 
served a slow decrease in weight lasting from two to three 
weeks. Only one case resulted in death of the animal 
after thirty-three days ; in all the other cases the animal 
slowly recovered. 

Bacillus perfringens (anaerobic) proved pathogenic 
for guinea pigs. After injection of 3 c.c. of a fresh 
bouillon culture an extensive local infiltration occurred 
which showed, when cut, a foamy oedematic secretion re- 
sembling saliva which contained the bacteria in pure 
culture. With one strain experiments were made to in- 
crease the virulence, which was successful after passage 
through two guinea pigs. The third animal died inside 
of thirty-six hours after injection of 3 c.c. of a fresh 
bouillon culture. Culture from the heart blood gave a 
positive result. 

Bacillus bifidus communis (anaerobic) caused no path- 
ogenic effects in rabbits from injection of 10 c.c. of a 
bouillon culture. 

Bacillus thetoides (anaerobic) was used only in one 
strain for animal experiments. The weight of the rab- 


bits decreased slowly for one week, after which they 
recovered. Only on the second day there was an increase 
in temperature. 

Streptococci anaerobic, no animal experiments. 

Staphylococcus parvulus caused no pathologic con- 
ditions in rabbits. 

Staphylococcus iungano caused no pathologic con- 
ditions after injections of 10 c.c of a bouillon culture. 

In regard to these animal experiments, it must be 
remembered, when compared with the results of Hartzel- 
Henrici, that the organs of these inoculated animals had 
apparently not been examined pathologically, and that the 
pathogenicity of the bacteria was only judged from local 
effects and as to the life or death of the animal. Hartzel- 
Henrici observed the low virulence of streptococci infec- 
tions when injected into animals, producing death only 
after a long period if at all, although there were serious 
lesions developing in some of their important organs 
which can only be demonstrated in microscopic sections 
of the diseased parts. 

Gilmer* (1914) . Gilmer, who reports bacterial exami- 
nations of acute and chronic abscesses, in a general way, 
found streptococci in aerobic cultures, and occasionally 
the staphylococcus albus and aureus, and the micrococcus 
catarrhalis. In anaerobic cultures he found streptococci 
and the bacillus fusif ormis either alone or in mixtures, as 
well as a black pigment-forming organism which usually 
did not appear for about five days. 

Thoma* (1915). The author reported in a paper read 
before the American Academy of Dental Science his re- 
sults of cultures taken since November, 1914, of all 
abscessed teeth in the hospitals as well as in his private 
practice. He concludes that any microbes belonging to 
the flora of the oral cavity may be found in oral abscesses. 
Streptococci which grew aerobically and anaerobically 
were found in the majority of cases, sometimes as pure 

* See Bibliography. 


Fig. 119. 

Microphotograph of a section of a granuloma containing colonies of 

Specimen prepared by the author and stained by the Gram-Weigert Method. 


cultures, but frequently mixed with staphylococcus albus 
and aureus. Besides these he often found an admixture 
of many other pathogenic and saprophytic bacteria such 
as the bacillus fusiformis, bacillus coli, the influenza 
bacillus, and the bacillus proteus. 

In two cases he found the fungus of actinomycosis. 
This organism has been demonstrated several times in 
root canals by Partsch* and was found by the author in 
a large granuloma of an upper lateral incisor, and in the 
root canal as well as in a granuloma of a lower bicuspid 
of another patient. Both men were city people, there 
were no clinical symptoms of general actinomycosis of the 
jaws of soft tissue, which is due to the fibrous encapsula- 
tion of the lesion. The first granuloma was removed, by 
the regular method of thorough curettage used by the 
author, the character of the abscess was not discovered 
until later when the specimen, a part of the granuloma, 
was examined. There was no recurrence of the disease. 
The other granuloma was adhering to the tooth and the 
fungus of actinomycosis was found when the specimen 
was prepared. In order to verify the findings different 
stains were used, the colonies in the form of rosettes with 
club-shaped radiating filaments were clearly visible, as 
seen in Figure 118 and Figure 119. 

Hartzel and Henrici* (1913, 1914 and 1915) . The mouth 
infection research corps of the National Dental Associa- 
ciation, consisting of Thomas B. Hartzel, Henrici and 
Leonard, started in September, 1913, a closer study of 
1 'the relationship growing out of the transplantation of 
the chronic mouth infections to other parts of the body 
and a study of the areas of inflammation in the human 
and animal body which have been induced by these trans- 
planted organisms." They were the first who undertook 
to study systemically the bacteria found in the 
dental abscesses in regard to their systemic effects 
rather than as to their etiological local importance. Their 

* See Bibliography. 


bacteriological research work has sought to determine by 
animal inoculation the character of the damage wrought 
in the various organs of the body by the introduction of 
intravenous injections of living organisms cultivated 
from lesions in the mouths of the patients studied. The 
bacteriological study reported October, 1914, and 
November, 1915, in the Journal of the National Dental 
Association alone represents an enormous amount of 
work and the conclusions drawn from the pathological 
study of the animal experiments mark a classic epoch in 
the study of dentistry. 

The first report is based upon a study of eighty-two 
cases, the second report was published after about two 
hundred additional cases of chronic periodontal infections 
had been bacteriologically examined. Attention was 
from two reasons directed almost solely to the strepto- 
cocci, first because they were constantly present and fre- 
quently were the sole cultivable organisms obtained, and 
secondly, because the research workers made the relation- 
ship of dental infections to rheumatism their immediate 
problem. They however also obtained the staphylococ- 
cus albus, the bacillus coli, the bacillus proteus, the 
bacillus florescens non-liquefaciens and the pneumo- 
coccus. Aerobic as well as anaerobic cultures yielded 
the same results. Cultures made from healthy teeth have 
constantly been found sterile. The cultural features of 
the streptococci of these dental lesions then received the 
writer's attention. On blood agar two kinds of colonies 
were obtained: " green" colonies, which produced a green 
halo, and gray colonies without halo. With regard to 
sugar fermentation reactions for an indicator, for which 
a beef serum with one per cent, of the various sugars 
added had been used with acid fuchsin decolorized by 
potassium hydroxide, they found that the majority of 
cases ferment either ramnose (streptococcus salivarius) 
or salicin (streptococcus mitis). Only in one case had a 
manite fermenter been observed (streptococcus fecalis). 


_ 5 ■Zme^&t 


J^ •<». 


'^t^r l 

-^*«^ ' / ' <? 


^» ;i *£*j 

Figure 120. 
Chronic myocarditis. The section shows the heart muscle of a rabbit which died 16 
days after an injection of streptococci from case No. 55. The section shows an area of 
fibrosis with several giant cells. 

Figure 121 
Acute myocarditis. Section of heart muscle from a rabbit which died 48 hours after 
an injection of streptococci from case No. 60. The section shows an area of lympholdal 

Both illustrations reproduced by courtesy of Dr. Hartzel. 











a ■ 


















Acid, Coag. 






















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Acid, Coag. 






Acid, Coag. 





Acid, Coag. 







Acid, Coag. 





Acid, Coag. 






Acid, Coag. 







Acid, Coag. 






Acid, Coag. 







Acid, Coag. 





Acid, Coag. 



















Acid, Coag. 










Acid, Coag. 






Aeid, Coag. 


















Acid, Coag. 





Acid, Coag. 











Two facts stand out prominently from their work: 
members of the streptococcus viridans group are con- 
stantly present in chronic dental infections, especially the 
streptococcus salivarius and the streptococcus mitis, and 
the common pus-producing haemolytic streptococci are 
constantly absent. 

In their animal experiments they used rabbits exclu- 
sively, being more susceptible to streptococci than other 
laboratory animals. In their first article they describe 
seven animal experiments from cases which they selected 


for special research study out of one hundred examined 
patients. In the second article they mention that they 
had inoculated two hundred and twelve additional rabbits 
with twenty-two different strains of streptococci. From 
these inoculations they are impressed by the compara- 
tively low virulence of these streptococci, though in the 
end the damage wrought by them in the animal economy 
was serious and in some instances irreparable. Some of 
the animals did not die at all, and most died a relatively 
long time after the inoculation. Of the animals that died, 
the most striking features were a progressive emaciation 
and loss of strength. The lesions produced in the ani- 
mals were of diverse character occurring in the arteries, 
joints, kidneys and heart. The most common lesions 
produced were those frequently associated with rheu- 
matism, namely, myocarditis, consisting either of diffuse 
infiltration of lymphocytes in submaxillary nodules com- 
posed of aggregations of lymphocytes or in areas of 
fibrosis with occasional giant cells. The kidneys were 
frequently also the seat of disease, consisting of abscesses 
which contained either polymorphonuclear leucocytes 
alone or associated with lymphocytes, and which in some 
cases contained bacterial emboli, or small aggregations of 
lymphocytes along radial vessels of the medulla. The 
arterial lesions which occurred occasionally were destruc- 
tive lesions of the tunica media of the aorta in the ascend- 
ing portion of the arch with a hypertrophy of the under- 
lying intima. 

The hearts, kidneys and large vessels of sixteen healthy 
rabbits were also examined ; no lesions could be found. 

The added illustrations have been kindly sent to me by 
Dr. Hartzel to illustrate this splendid work of his re- 
search corps, and I here take one more especial occasion 
to express my appreciation of his courtesy, which I feel 
sure will also be greatly appreciated by the interested 
reader, and induce him to study in detail the important 
investigations published by Dr. Hartzel and his asso- 
ciates in the various dental and medical magazines. 


rs r 

Figure 122 
The section shows an area of wide spread infiltration with lymphocytes and poly- 
morphonuclear leukocytes in the kidney of a rabbit which died 48 hours after an injection 
of streptococci from case No. 59. This was the second passage of this streptococcus 
through rabbits. 

: *»-''fc. 

Figure 123 
This plate shows a localized polymorphonuclear abscess in the medulla of the kidnej 
of a rabbit which died 48 hours after an injection of streptococci from case No. 60. 

Both illustrations reproduced by courtesy of Dr. Hartzel. 


Author's Remark. — The investigations of Hartzel and 
other scientists give the reader the impression that the 
streptococcus is the only bacteria of the flora found in 
oral abscesses, which should be seriously considered, and 
that other bacteria may be looked at, either as contamina- 
tion or organisms whose activity is restricted to the local 
lesion. Medical writers also, Rosenow particularly, 
whose research work has almost revolutionized the etio- 
logical theories about certain systemic infectious diseases, 
considers the streptococcus-pneumococcus group as the 
causative factor of secondary lesions, caused by transpor- 
tation from the focus through the blood stream. Amongst 
the large number of bacteria which may be found in oral 
abscesses, there are without doubt others which may be- 
come absorbed and cause secondary disease or which 
produce toxins, which when taken into the circulation 
may affect certain tissues and lower the health of the 
patient. One of the most commonly found bacteria, 
besides the streptococci is the staphylococcus. It may be 
often found alone or together with others. Dr. Stein- 
harter has very recently undertaken bacteria experiments 
with this organism. While the organisms had not been 
taken from oral abscesses, I shall nevertheless add an 
abstract of his experiments, so as to show that other bac- 
teria than the streptococcus group should be considered 
dangerous to the rest of the body. 

Steinharter* 1916. The author published two articles, 
the first on gastric ulcers, the second on experimental pro- 
duction of acute arthritis by inoculating animals with 
staphylococcus cultures. Gastric ulcers were produced by 
injecting an emulsion from the agar growth (prepared 
by suspending a twenty-four-hour old culture on agar 
slant in 10 c.c. normal saline) or from the broth (by sus- 
pending in 15 c.c. of saline the centrifugal sediment of a 
twenty-four-hour old 150 c.c. broth growth). One quar- 
ter to 1 c.c. of the emulsion was injected with 1 c.c. of a 
weak acetic acid solution. Forty rabbits were used for 
the experiments, the hypodermic injections were preceded 

* See Bibliography. 


by a laparotomy, and the post-mortems revealed, if or- 
ganisms of special virulence were used (for instance, one 
freshly isolated from the appendix) invariably typical 
peptic ulcers from one quarter of an inch to one inch in 

Acute arthritis was experimentally produced by inject- 
ing intravenously an emulsion, prepared by suspending 
an agar slant culture in about 10 c.c. of normal saline. 
The dose used was usually 1 c.c. for a rabbit and 3 c.c. 
for a dog. It was found that the staphylococcus is apt to 
localize in the joints and produce typical lesions of arth- 
ritis, if the strain is of proper virulence, having a prede- 
liction for this region (staphylococci from joints for 
example have a decided tendency to again localize in 
joints) or if the tissue in which the organisms have lodged 
is suitably altered for their growth and action. 

The writer concludes that the staphylococcus may be 
caused very regularly to localize in the stomach after 
intravenous injection. It appears that the same organ- 
ism may be caused to localize in joints and produce typical 
arthritis. The published protocols show that in some 
cases arthritis was the only lesion found at autopsy but in 
other cases it was associated with one or more other 
lesions, namely duodenal ulcer, appendicitis, cholecystitis, 
myocarditis, pericarditis, endocarditis, nephritis, colitis 
and myositis. 


Fig. 124. — Microphotograph of the end of a tooth with an epitheliated granuloma. 

A — Lumen. B — Proliferating epithelium. C — Cholesterine spaces. 
D — Capsule of the granuloma. E — Blood vessel. F — Exostosed root end. 

G — Root canal. 
Stained with Mallory's connective tissue stain. Specimen prepared by the author. 



The microscopic study of abnormal conditions and dis- 
ease is not only of great interest to the pathologist, but 
of far-reaching importance for the understanding of the 
beginning, progress and termination of disease, as well 
as of greatest value for the development of the knowledge 
which furnishes the best foundation upon which intelli- 
gent treatment, be it of medicinal or surgical character, 
may be based. 

The infection of the periapical tissue of 
pfrio"- a tooth i s transmitted through the apical 

dontitis foramina from the diseased pulp and 

causes, if the amount and virulence of the 
injurious agent is right, what is clinically termed as acute 
inflammation of the periodontal membrane, or acute peri- 
odontitis. The reaction consists of circulatory disturb- 
ances and inflammatory exudation. The blood vessels, 
after an initial constriction, become dilated almost to 
twice their size and leucocytes accumulate along their 
walls. A serous infiltration with emigration of poly- 
morphonuclear leucocytes occurs which is seen in spaces 
formed between the fibres of the periodontal membrane. 
This causes an increase in size of the membrane, pushing 
the tooth out of its socket and gives the impression of an 
elongated tooth. If the condition continues, tissue de- 
struction sets in and we find small necrotic areas. This 
process is most marked near the apical foramina from 
where the suppuration spreads. 

acute After a comparatively short time the pus 

alveolar k as co ^ ec ^ e( i m larger quantity and the 
abscess bone forming the alveolar socket becomes 

involved. The fibres of the periodontal 
membrane still persist, become elongated, and parts of 
bone are absorbed. While the bone is destroyed the pus 


cavity enlarges and is called an acute alveolar abscess. If 
suppuration is very active and prolonged we find destruc- 
tion of the fibres of the periodontal membrane at the 
apical part as well as involvement of the cementum of 
the tooth which shows a necrotic appearance and has been 
observed to result in loss of more than half of the root 
of the tooth. 

After the destruction of the lamella of the 
alveolar alveolar socket the cancellous part of the 
parulis bone is freely infiltrated with pus. The 

Haversian canals are next involved by 
means of which the pus finds its way through the outer 
cortical layer of the bone. The periosteal tissue reacts 
at once causing a local infiltration of polymorphonuclear 
leucocytes and a widespread serous infiltration causing 
large oedematic swellings in the cheek and neck. The 
pus forms first under the periosteum (subperiosteal paru- 
lis) which presents a remarkable resistance to the destruc- 
tive processes of inflammation. After the periosteum has 
been penetrated, necrosis continues in the submucosa of 
the gum until it extends to its surface and forms a fistula 
which gives exit to the accumulated pus. 

After the process of destruction has 
alveol'ar reached its climax, nature makes an at- 
abscess tempt of healing by the formation of 

granulation tissue. The necrosed cells are 
dissolved by the leucocytes and either absorbed or expelled 
through the sinus. Fibroblasts and vascular endothelium 
are formed by proliferation to replace the necrosed tissue ; 
destroyed cells and serous or purulent exudation from 
remaining injurious agents may continue to pass through 
the newly-formed tissue to the surface. Endothelial leu- 
cocytes and lymphocytes may collect in large numbers in 
the deeper layers of the granulation tissue to counteract 
the irritating agents absorbed from the exudates. This 
condition clinically called chronic abscess may last for an 
unlimited period, the discharge from the fistula may in- 
crease at times, if the process of destruction becomes 
more marked, or may become less or even stop entirely 


Fig. 125 

Fig. 126 

Fig. 127 

Fig. 128 

FIG. 125. — Microphotograph of a simple granuloma. Part of the pulp lias been left in the 
root canal and the granulation tissue is seen to extend from the root canal through the 

apical foramen. The blue spot shows a necrosed area in the dentine. 
Fig. 126. — Microphotograph of a simple granuloma showing a distinct capsule. There is 

necrosis of the root and a lateral lumen. 
FIG. 127. — Microphotograph of a simple granuloma, showing capsule and three places where 

active pus formation is going on. 
FIG. 128. — Microphotograph of a granuloma with sinus in which pus formation has taken 

All four specimens were prepared by the author, and stained by Mallory's Phosphotungslic 

acid, Hematoxylin stain. 


for a certain period, a condition which is usually only tem- 
porary but frequently brings about the closure of the 
mouth of the fistula. This will reopen with more or less 
marked subacute symptoms as soon as the suppurating 
process has overcome the defense of the body, the process 
of repair. This picture should impress the importance 
of removing the cause, viz., a diseased dental pulp or the 
necrotic end of the root of the guilty tooth. Perfect 
repair is not possible as long as a necrotic root apex 

In contrast to the processes of suppura- 
proliferat- tion of the periodontal membrane stands 

dontitts ^ e mucn more common proliferating 

periodontitis and its sequels. This is a 
reaction to mild injurious agents such as bacteria in small 
numbers and of low virulence, of which the streptococcus 
mitis and salivarius are good examples and commonly 
found in these lesions. But also mild toxins or diluted 
stronger toxins as well as chemicals such as irritating 
drugs (formaldehyde) sealed in the root canal cause 
irritation of the periodontal membrane. The reaction 
occurs first near the apical foramina consisting in a focal 
accumulation of lymphocytes, an increase in cells and 
vessels and formation of plasma cells. Endothelial leu- 
cocytes and polymorphonuclear leucocytes may be more 
or less abundant according to the irritating agent causing 
the inflammation. 

The dental granuloma is the sequel of the 
granuloma proliferating periodontitis. Its histo- 
logical study is extremely interesting. 
The author has prepared microscopic specimens of about 
fifty of these lesions in the research laboratory of the 
Harvard Dental School and the following descriptions 
are principally based upon original investigations : 

Simple granuloma. The new formed tissue gains 
in size until it has the microscopic appearance of a red- 
dish sack which reaches generally the size of a large pea, 
but occasionally attains much larger dimensions. The 
pressure from the growing lesion causes resorption of the 


bone and on microscopic examination we find that the 
granuloma is surrounded by a fibrous capsule which ex- 
tends between the trabeculae of the bone. The fibres of 
the encapsulating layer originate from the periodontal 
membrane, which in some cases may become detached 
from the cementum of the apex, the tooth remaining in 
others in a more or less modified way. The communica- 
tions with the root canal usually persist, the granulation 
tissue seems to be continuous with remnants of pulp left 
in the apical part of the root canal, while at other times 
the granulation tissue grows into the root canal. The 
connection between the periodontal membrane and the 
peripheral fibrous capsule is often so strong that the 
granuloma is removed attached to the tooth in extraction. 
In the majority of cases, however, we find that the granu- 
loma remains in the jaws. The thickness of the capsule 
varies greatly and contains fibres, groups of which grow 
in various directions. This fibrous capsule is well illus- 
trated in the microphotographs, Figures 126 and 
127, and in the high-power drawing, Figure 129, stained 
by Mallory's Phosphotungstic-acid Hematoxylin 
method. Vessels and capillaries can be seen in all these 
illustrations of the fibrous capsule, they are usually sur- 
rounded by an increased number of plasma cells and a 
small number of leucocytes ; their lumen is often greatly 
increased, and the endothelial cells often show a prolifera- 
ting appearance. Red corpuscles are found in the ves- 
sels together with polymorphonuclear leucocytes and a 
granular substance. Such a vessel and capillaries as well 
as fibroblasts and infiltrated cells are especially well re- 
produced in Figure 130, an oil immersion drawing of a 
part of the capsule in a section stained with hematoxylin 
and eosin. These studies impress the great attempt 
which nature made to wall off the seat of inflammation to 
prevent spreading into the neighboring parts. It, how- 
ever, also demonstrates that this capsule does not prevent 
absorption as it contains a meshwork of capillaries and is 
penetrated abundantly by larger vessels and therefore 
its contents are in direct communication with the circu- 




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Fig. 129 


Fig. 130 

Fig. 129. — Lithograph of high-power drawing showing the construction of the capsule of the 

granuloma shown in Fig. 127. 

A — Blood vessels extending through the capsule. B — Inner part of the granuloma. 

C — Connective tissue fibres. 

Specimen prepared by the author and stained with Mallory's Phosphotungstic acid, Hematoxylin stain. 

Fig. 130. — Lithograph of high-power drawing showing the construction of the capsule of the 

granuloma shown in Fig. 124. 

A — Blood vessels. B — Erythrocytes in vessels. C — Erythrocytes in the tissue. 

D — Polymorphonuclear leucocytes. E — Endothelial cell of vessel. G — Plasma cell. H — Fibroblast. 

Specimen prepared by author, stained with Hematoxylin and eosin. 


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Fig. 132 

FIG 131 —Lithograph of high-power drawing of epitheliated granuloma as shown in Fig. 

124, showing the inner part. 

A-Fibroblast. B— Plasma cells. C— Hyalin bodies D— Eosinophils E— Lymphocytes. 

F— Leucocytes between epithelial cells. G— Island surrounded by epithelium. 

H — Epithelial cells. 

Specimen prepared by author and stained with Hematoxylin and Eosin. 

FIG 132 —Lithograph of high-power drawing of the inner part of the granuloma shown in 

Fig. 128, showing the upper branch of the sinus. 

A— Mouth of sinus. B— Plasma cells. C— Blood vessels. D— Leucocytes. 

E— Polymorphonuclear leucocytes. F— Pus cells. H— Epithelial cells. 

Specimen prepared by author and stained with Hematoxylin and Eosm. 


Fig 133 

Fig. 134 

Fig. 135 

Fig. 133. — Kadiograph showing lateral incisor just after the root canal had been 
treated and filled. A light circle marks the circumference of the granuloma. 

Fig. 134. — Photograph of the same granuloma shown in Fig. 133 after its excision. 

Fig. 135. — Microphotograph of granuloma shown in Fig. 133 showing a distinct 
capsule and numerous spaces which were occupied by cholesterin crystals. Note 
pink and blue appearance, the first represents fibrin, the second collagen formation. 

Specimen prepared by the author, stained by Mallory's connective tissue stain. 


lation. Bacteria and toxins may be absorbed by the capil- 
laries in the granuloma and transported to other parts of 
the body. The inner part of the granuloma is made up 
of granulation tissue (fibroblasts and vascular endoth- 
elium) infiltrated by one large mass of plasma cells. 
These are seen as cells with irregular cytoplasm which 
has marked basophilic properties containing from one to 
four nuclei in eccentric arrangement. If there are proc- 
esses of retrogression going on we find also numerous 
polymorphonuclear leucocytes, endothelial leucocytes, 
lymphocytes, eosinophiles and mast cells abundant more 
or less. Erythrocytes are found distributed sometimes 
throughout the granuloma, at other times only in the 
fibrous encapsulation; their presence is due to haemor- 
rhage of extended capillaries during extraction. 

Epitheliated granuloma. Remnants of the embryonic 
enamel organ are commonly found in the normal perio- 
dontal membrane of animals as well as man. They can 
easily be seen with the microscope and occur either in 
small groups, islands or in chains. But the presence of 
epithelium is not constant in the periodontal membrane, 
as has been demonstrated by Malassez, and therefore we 
do not find epithelium in all dental granulomata. This 
epithelium may be found only near the root of the tooth 
in small areas or it may be found throughout the granu- 
loma, having proliferated from the normal remnants, 
stimulated by the irritating influence of chronic inflam- 
mation. The cells of the proliferating epithelium differ 
in appearance from the cells of the epithelial islands; 
they become larger, the cytoplasm and nucleus become 
more distinct, and leucocytes invade the intercellular 
substance which loosely connects the various cells. The 
epithelial strands are of uneven thickened bands radiat- 
ing from the original island in various directions, and 
form when examined in a microscopic section a wide 
meshwork throughout the granulation tissue. The epith- 
elium has further the tendency to grow between live and 
necrosed tissue, and it has sometimes the appearance of 
encapsulating the seat of suppuration. 


Granuloma with Lumen. Suppuration of the simple 
or epitheliated granuloma frequently sets in either near 
the apical foramen from where the bacteria emigrate or 
farther in the center. If the destructive process becomes 
severe a subacute alveolar abscess results with subperios- 
teal or subgingival parulis and sinus formation. After 
the accumulated pus is discharged the symptoms will soon 
quiet down, but the pus formation may persist in a mild 
way and discharge through a chronic sinus, as seen in 
Figure 128. The granulation tissue first shows a large 
infiltration of polymorphonuclear leucocytes and later 
areas of necrosis in the center. After a while the pus 
may be resorbed and if the leucocytic infiltration stops, a 
lumen remains, containing necrosed tissue. (Figures 124 
to 127.) 

Besides suppuration we may also find fatty degenera- 
tion, especially at the periphery between the fibrous cap- 
sule and the granulation tissue. In old conditions there 
are also other retrograde processes such as the formation 
of cholesterin crystals, which are recognized by the rhom- 
boid shaped spaces left by the crystals, which dissolve 
during dehydration in alcohol. They can be demon- 
strated, however, in frozen section and appear as brown- 
ish crystals. Foreign body giant cells frequently 
surround one or more crystals, as seen in Figure 137. 
Compare also cholesterin spaces in Figure 124 and Figure 
135. Collagen is formed by the fibroblasts from the fibrin 
which stains blue with Mallory's aniline blue connective 
tissue stain in contrast to the fibrin and fibroglia fibres 
which are stained red, as seen in oil immersion drawing 
Figure 136. 

Another retrograde process is the hyalin formation 
which occurs in droplets of various sizes in the cytoplasm 
of the plasma cells (Russell's fuschsin bodies). This 
causes the cells to enlarge and often nothing remains of 
the cell but the acidophilic hyaline bodies. These are usu- 
ally diffusely scattered through the whole granuloma. 

Cysts. In the epitheliated granuloma with lumen we 
frequently find an attempt of the epithelium to line the 


Fig. 136 

Fig. 137 

Fig. 136. — Lithograph of high-power drawing showing the 

construction of the granuloma shown in Fig. 135. 

A, Fibroblasts, with fibroglia fibres. B, Fibrin. 

C, Collagen. 

Fig. 137. — Lithograph of high-power drawing showing 

the construction of another part of the granuloma shown 

in Fig. 135. 

A, Fibroblast, with fibroglia fibres. B, Fibrin. 

C, Erythrocyte. D, Connective tissue bundles. 

E, Space from cholesterin crystal. 

F, Giant cell enclosing cholesterin spaces. 


central space. This influenced the German writers to call 
Epitheliated gramilomata with lumen formation, "root 
cysts.'' Dependorf, in a lengthy article, describes with 
careful illustrations the formation of cysts from dental 
granulomata. The author agrees that cysts may be 
formed in both jaws from such conditions, but this must 
happen extremely seldom or we would meet with cysts 
more co mm only in these days where granulomata are 
found in almost everybody's mouth. 



The acute forms of oral abscesses have always been 
more or less feared, more because of their violent symp- 
toms than on account of the serious complications which 
may result if treatment is neglected or if the cause is 
not removed. The chronic forms, on the contrary, have 
mostly gone unnoticed, although they occur much more 
frequently. They were not properly recognized until 
the radiograph became essential as a means of diag- 
nosis and only recently we became aware of the fact that 
almost every devitalized tooth develops this condition. 
In my opinion, it is a fair estimate to say that seventy- 
five per cent, of the population of this country harbors 
this lesion in the mouth. In the Robert B. Brigham 
Hospital for chronic invalids I found that of eighty-two 
patients, seventy-three suffered from chronic abscesses; 
some of them also had pyorrhoea, and in the mouths 
of these seventy-three patients I found three hundred and 
thirty-four abscesses. 

The fact that these chronic abscesses give little or no 
local symptoms is the reason why the dental profession 
at large has not been aware of what is going on. But 
the last few years the deceiving character of these lesions 
has come to light. Radiographic diagnosis, keen obser- 
vation and research have revealed the knowledge of the 
grave consequences of such conditions. These septic foci 
not only are liable to spread disease to the adjoining 
parts, but also cause disturbances in organs and tissues 
quite remote from the teeth. 

Continuous Infection. The infection is liable to spread 
to adjoining parts and involve large areas of the mandib- 
ular or maxillary bones, the antrum of Highmore or the 


Referred Nervous Irritation. Reflex manifestations 
from one branch of the fifth nerve to another or to com- 
municating nerves is of quite frequent occurrence, but 
often such pains are due to the most obscure causes, found 
only after a most painstaking examination. 

Infections through the Alimentary Canal. Abscesses 
with sinuses or pyorrhoea pockets as well as septic sur- 
face lesions of the mouth discharge their pus into the oral 
cavity where it mingles with the fluids of the mouth and 
when swallowed reaches the stomach and intestine. The 
persisting infection through this channel gives rise to 
most serious diseases of the mucosa of the alimentary 
canal. From these secondary lesions bacteria may be 
absorbed into the circulation, in turn causing other dis- 
eases by haematogenous infection. 

Lymphatic Infection. The lymphatic system and espe- 
cially the lymph glands have the office of absorbing and 
disposing of harmful substances, such as liberated in all 
inflammatory conditions. A certain amount of pus may, 
however, reach the circulation via the lymph system, 
while not infrequently we find the lymphatics or the 
glands seriously affected. 

Haematogenous Infection. Abscesses especially of the 
proliferating type which have no outlet into the mouth, 
contain, as we have seen, numerous capillaries and blood 
vessels. Absorption of products of inflammation into the 
blood stream is usually small in quantity, but constantly 
wears out the protective cells and causes diseases of the 
blood and secondary infections in other parts due to 
transported bacteria, or toxin, or both. The bacteria and 
products of infection are not only absorbed from the 
original focus, but also from secondary diseases of the 
lymph system or the alimentary canal as already men- 

The complications which arise from septic foci in the 
mouth will not be classified in this book according to the 
mode of infection, but the various disturbances and dis- 
eases which have been found due to oral abscesses will be 


considered in turn. Case reports are here given so as to 
illustrate the connection of the oral abscesses with the 
various systemic diseases. 

1. Involvement of Neighboring Parts. 

The infla mm ation, whether from acute or chronic ab- 
scess, is liable to spread to adjacent parts. The spreading 
to and involvement of other teeth has been mentioned at 
another place. It has also been explained that necrosis, 
osteitis, or osteomyelitis is involved in every case of alve- 
olar abscess in a mild and localized way. These diseases 
may become continuous and involve large parts of the 
maxillary and mandibular bones if the conditions are 

Maxillary sinusitis or empyema of the 


antrum of Highmore is very frequently 

met with by the rhinologist as well as by 
the oral surgeon. About 75% of the cases are due to 
dental origin and most are a sequel to oral abscesses. 

Etiology: Acute maxillary sinuses occur 
maxTllary on ^ as ^^u^ °f nasa l or dental diseases. 
sinusitis ^he nasa l sources are coryza, influenza, 

tuberculosis and syphilis of the nasal mu- 
cous membrane, and any suppurative process in the nose 
or other accessory sinuses. Dental sources are acute al- 
veolar abscess on an upper bicuspid or molar discharging 
into the antrum, infection from a chronic abscess or osteo- 
myelitis in the maxillary bone. Infected dental pulps 
and root canal instrumentations have been mentioned as 
etiological factors in cases where the roots project into 
the antrum. Infection is liable to occur from the extrac- 
tion of a tooth or root, if a root is pushed into the antrum, 
or if infected tissue or pus is forced into it and by the 
introduction of unclean instruments. 

Symptoms: The cheek on the infected side becomes 
reddened and tender, and often there is a marked oede- 
matic swelling which may close the eye. The patient com- 
plains of a fullness in the affected side, with a dull throb- 
bing pain, and generally malaise, dizziness, and photo- 


phobia. There may be discharge of pus through the nos- 
tril, or if the patient lies in bed, into the pharynx. Often 
the osteum is closed up, when the pain and fullness be- 
comes more marked, and is relieved if part of the pus 
escapes into the nose. Headaches and neuralgic face- 
aches are principally found in less severe cases. 

Clinical signs: Fever is always present in acute cases 
and may reach 104 °F. An examination of the nares 
shows usually crusts of pus and congested mucous mem- 
brane. In doubtful cases the patient should be asked to 
sleep on the suspected side and notice in the morning 
whether there is any discharge upon turning the head to 
the other side. The patient may be asked to apply suc- 
tion to the nose while closing the nostrils. Transillumi- 
nation shows bright illumination under the orbit of the 
healthy face and darkness on the other. Radiographic 
examination is the surest means of diagnosis. The dis- 
eased antrum presents an opaque appearance on a frontal 
plate, and a lateral view shows the cause if it is of dental 
origin. Intraoral films are a great help to diagnose the 
etiological factor, but are of no value in the diagnosis of 
the condition of the antrum. 

Treatment of Acute Maxillary Sinusitis from the Nasal 
Cavity. In cases of nasal origin the treatment is under- 
taken through the nose, but also in certain dental cases 
this treatment is indicated, especially if the inflammation 
of the antrum occurs after an extraction, the socket hav- 
ing healed up before the complication sets in. 

1. Irrigation Through the Natural Orifice. In mild 
cases, which respond easily to treatment, daily irrigation 
and medication through the osteum is sufficient. 

2. Perforation of the Nasal Wall. If drainage and 
treatment through the natural orifice is not sufficient, per- 
foration of the naso-antral wall with a trocar and cannula 
is recommended. The opening should be made as near 
the floor of the antrum as possible. This closes up in a 
comparatively short time, and resection of a larger part 
of the wall is recommended if a more permanent opening 
is desired. 


Treatment of Acute Maxillary Sinusitis from the Oral 
Cavity. It has already been stated that in a large number 
of cases maxillary sinusitis is due to abscessed teeth. The 
radical removal of the cause is naturally the first step, 
but this also furnishes an opening into the antrum 
through which treatment can be undertaken. The open- 
ing is enlarged with the surgical burr and all granulations 
and diseased bone should also be carefully removed. The 
antrum is then washed out through the wound by inserting 
a sterile soft rubber catheter, to which the antrum syringe 
or fountain syringe is attached. Use lukewarm normal 
salt solution. If the osteum is closed, spray the antral 
side of the middle meatus with Sol. Adrenalin hydro- 
chlorid 1 :6000. This will contract the mucous membrane 
and reopen the natural passage way. After the washing 
has been completed, close the wound with sterile gauze. 
The washing can be repeated in the same maner until the 
antrum is healed, when the socket should be closed by a 
plastic operation. If the antrum is opened accidentally 
after extraction, and curetting for alveolar abscess, espe- 
cially if we desire to remove diseased bone, it is advisable 
to clean first the socket thoroughly and then insert a 
sterile soft rubber catheter, washing the antrum out as 
above. Carefully close the wound, and if no reinfection 
occurs the condition will heal without trouble. 

Etiology : The chronic form of maxillary 
max?llary sinusitis or chronic empyema of the an- 
sinusitis tram frequently follows the acute form. 

Often we find old chronic cases which 
never were preceded by any acute or painful condition. 
In these cases granulation is very pronounced and the 
cavity is filled with polypi. Abscessed teeth play a most 
important part in the etiology of chronic maxillary 

Symptoms : Pain in the cheek, which is often of neu- 
ralgic character, is almost always the symptom from 
which the patient seeks relief. The discharge of pus 
through the nostril of the affected side is at times very 
marked and, moreover, it is often of very offensive odor. 


The osteum becomes occasionally obstructed, which in- 
creases the severity of the symptoms. The patient almost 
always loses weight. General malaise, arthritis, gastric 
disturbances from swallowing pus, and mental depression 
frequently accompany the disease. 

Clinical signs: What has been said for the acute con- 
dition is also true for the chronic. The differentiation of 
acute and chronic empyema of the antrum cannot be 
easily made either by transillumination or by radio- 
graphic examination. The history of the case and con- 
sideration of the etiological factor will help in ascertain- 
ing the condition, but a sure diagnosis can only be made 
by actual examination. Holmes's naso-pharyngoscope is 
a great help for this purpose. A short incision in the 
canine fossa allows us to make an opening through 
the anterior wall with a surgical burr, through which 
the naso-pharyngoscope is inserted. The condition of the 
mucous membrane, the amount and quality of new growth 
can plainly be seen. This is the safest way of making a 
differentiating diagnosis. 

Treatment: The cause of the disease has to be ascer- 
tained and thoroughly removed. Frequently we find 
cases of maxillary sinusitis which have not improved, al- 
though a great amount of time has been spent for treat- 
ment. After careful examination we find that a tooth is 
continuing to reinfect the mucous membrane. To try to 
save one tooth if two are involved is poor judgment if we 
consider how difficult a task it is to cure chronic maxillary 

There are a large number of methods for treatment of 
chronic empyema. 

Treatment Through the Alveolar Border. The method 
of draining the antrum through the alveolar process has 
been in great favor with the dentists. Some have even 
gone so far as to treat the antrum through the root canal 
of a tooth. If we compare the small size of a root canal 
even when enlarged with the capacity of the antrum hold- 
ing 12 to 52 c.c. of fluid we must see the impossibility of 
such an undertaking, not to speak of the consideration of 


that tooth and the infected periapical tissue as a causa- 
tive factor which ought to be removed. The tooth socket 
sufficiently enlarged with a surgical burr is the most ideal 
place for drainage, as it is at the lowest level. The an- 
trum should be washed with the greatest aseptic precau- 
tions. A soft rubber catheter can be introduced and is 
connected either with the fountain or the antrum syringe. 
I use warm normal salt solution or mild antiseptics as 
washings, occasionally with application of fifteen per 
cent. Argyrol. After washing the antrum, care should be 
taken to remove all the moisture, as the antrum is an air 
sinus with dry mucous membrane. Frequently I use 
filtered compressed air for this purpose, administered 
through the catheter. The washings should be under- 
taken first daily and later at intervals until there is no 
discharge for two weeks. It is important to construct a 
rubber or gutta percha obturator to fit into the alveolar 
socket principally to prevent food and saliva from enter- 
ing the antrum, but also to keep the opening from closing 
up. After the antrum has healed the socket should be 
closed permanently by a plastic operation. 

Operation Through the Canine Fossa. In cases where 
examination of the antrum reveals granulations and new 
growth, the foredescribed method is not sufficient to re- 
sult in a cure. Surgical removal of all growth is indi- 
cated. In cases of malignant growth, the lining mem- 
brane should be removed radically, but in all cases of 
polypous and granulating character the tendency is to be 
contented to remove the growth and not the membrane. 
A great deal depends in this operation on being able to see 
all parts of the antrum, and the operation should there- 
fore be performed from the place which gives the best 
access to vision as well as instrumentation, and this is the 
canine fossa. 

The antrum is opened from the canine fossa by excising 
the anterior wall with chisel and surgical burrs. The 
opening should be made large, but care should be 
taken not to injure the nerves and vessels of the teeth. 
After the cavity has been freed from polypi, or other 



Fig. 138. — Antrum exposed so as to show the abscess formed at the 
floor by the upper first molar. 


Fig. 139 

Fig. 140 

Fig. 139. — Radiograph of Case No. 1, showing the condition of the upper first 
molar, causing the disease of the antrum. 

Fig. 140. — Radiographic plate of Case No. 1, showing healthy antrum (dark) on 
the left side of the picture, diseased antrum (cloudy) on the right side. 


growth, and from bone septa, the extraction of the in- 
volved teeth is undertaken. Chronic abscesses are to 
be extensively removed and osteomyelitic bone is curetted. 
After washing out all debris and diseased tissue the cavity 
is dried out, the alveolar wound closed by sutures, and the 
antrum packed with antiseptic gauze which should re- 
main in place for about forty-eight hours. Then the 
gauze is removed, the cavity again irrigated, dried and 
repacked. This treatment should be continued for about 
ten days, after which time an obturator, which has been 
constructed from gutta percha or rubber, is inserted to 
keep the antrum open for irrigation and observation 
until it is entirely healed. The plug then can be left out 
and the antrum is closed by a plastic operation. 

Operation Through .Canine Fossa and Treatment 
Through Nasal Wall. (Caldwell-Luc.) The operation is 
undertaken through the canine fossa which is closed up 
immediately afterwards. The after-treatment is then 
continued through the opening in the antro-nasal wall 
which is usually of permanent character. 

Operation Through Canine Fossa and Treatment 
Through Alveolar Socket. The canine fossa operation is 
performed as described, but the alveolar wound is kept 
open. The opening in the canine fossa is closed after the 
healing has progressed to a satisfactory stage. An ob- 
turator is constructed for the alveolar opening to close 
the communication of the antrum and mouth after each 
irrigation. When the condition is cured, the alveolar 
opening is also closed by plastic methods. 

<5TRATivE ^ ase !• (Chronic maxillary sinusitis 
CASES with, polypoid granulations.) The pa- 

tient, a man of 41 years of age, presented 
symptoms of chronic maxillary sinusitis. A frontal radio- 
graph is shown in Figure 140, and the cause was ascer- 
tained by an intraoral film, Figure 139. The upper first 
molar shows chronic abscesses on all roots, which appa- 
rently infected the antrum. Examination of the nose re- 
vealed no infectious condition. Surgical treatment was 
undertaken by opening through the canine fossa. A large 


amount of polypoid granulation was found, the antrum 
was almost entirely filled with it. I removed the granu- 
lations, extracted the tooth and removed all diseased bone 
with surgical burrs. The canine fossa was permitted to 
close after one week, and the treatment continued through 
the alveolar socket. After the treatment was completed 
so that no discharge collected during a period of three 
weeks, I closed the alveolar opening by a plastic opera- 

Case II. (Chronic maxillary sinusitis.) The patient, a 
man 36 years of age, suffered from obscure pain in the 
maxillary region. The two upper bicuspids on the af- 
fected side he said had been treated several times, when 
it was observed that a broach could be pushed up a sur- 
prisingly long distance. An intraoral film showed no 
extensive periapical condition; a frontal radiograph re- 
vealed a slight cloudiness of the antrum. I opened the 
antrum from the canine fossa. Inspection with the naso- 
pharyngoscope showed a condition similar to Figure 138, 
an antral abscess on the floor over each of the devitalized 
teeth. The roots extended into the antrum, and as there 
was no bone destruction, there was nothing to show in the 
film. Extraction of the teeth and curettage of the dis- 
eased part was the first step in the treatment, after which 
the slightly inflamed membrane yielded rapidly to treat- 

PHARYNGITIS P^^g^is ve3 T frequently occurs as a 
complication of abscesses on lower im- 
pacted wisdom teeth. The inflammation may spread over 
one side of the pharynx and cause the patient to consult 
the physician while the real cause is unnoticed on account 
of lack of symptoms. (Figure 95.) 

Symptoms : Examination of the mouth usually reveals 
the true character of. the condition. Sometimes the cusp 
of an unerupted wisdom tooth is visible, and upon pres- 
sure on the lingual part of the gum there is usually more 
or less discharge of pus through the gingival opening. A 
radiograph aids sure diagnosis. 

Treatment : The cause is to be removed at once. The 
pharyngitis should receive general and local attention. 


illustrative Case III. (Marked pharyngitis and 
CASE slight trismus.) The patient, a young 

man, went to his physician for treatment of the throat. 
He was referred to me and when he came to my office the 
next day he had a temperature of 101 °F., enlarged maxil- 
lary glands on the left side, and slight trismus of the 
muscles of mastication. On examination of the mouth 
and pharynx, I found the right side badly inflamed and 
a large amount of pus discharging from behind the lower 
second molar. The radiograph showed the cause of the 
trouble as an impacted unerupted wisdom tooth with ex- 
tensive abscess formation. 
__.,,,,..„ Trismus is a tonic spasm of the muscles 

TRISMUS p ,. ,. x 

oi mastication. 

Etiology: It is usually caused by an impacted wisdom 
tooth with abscess formation and periostitis. 

Symptoms: The patient complains of not being able 
to open the mouth except a small distance. Sometimes 
the teeth are locked in complete occlusion. Pain, inflam- 
mation of the pharynx, and swelling of the submaxillary 
glands are almost always found. 

Diagnosis: By means of an extraoral radiograph we 
are able to determine the cause in a very short time. 

Treatment : In mild cases we may use local anaesthesia. 
After the inferior alveolar nerve and tissues supplied 
have been anaesthetized in the pterygo-mandibular space 
by the intra- or extra-oral method, the patient is relieved 
of pain and usually is able to open the mouth sufficiently 
for the operation. It is advisable to insert a mouthprop 
for the patient to bite on. In very severe cases and diffi- 
cult impactions ether anaesthesia is advisable. The 
mouth then can be forced open by means of the mouth 
gag. A few days after the cause is removed the jaw 
regains its normal function. 

Case IV. (Mandibular trismus.) The 

CAS STRAT ' VE patient, aged 24, suffered from pain in 

the trigeminal region for several days ; he 

also complained of severe earache. He was scarcely able 

to open his mouth. An X-ray plate showed a right lower 


third molar which had been decayed and abscessed. The 
month was opened under ether anaesthesia and the tooth 
extracted. An iodoform wick was inserted for drainage, 
the patient improved rapidly and was entirely well after 
one week. 

2. Ophthalmic Disturbances. 

Ophthalmic disturbances due to oral conditions may be 
brought about in two ways: first, through nervous irri- 
tation, and, second, through haematogenous infection. 

The ophthalmic division of the fifth nerve, which is 
purely sensory, supplies the eyeball, the mucous mem- 
brane of the eye, the lacrimal gland, and the skin of the 
brow and forehead. A branch of the second division, the 
orbital nerve, communicates with the lacrimal nerve; 
therefore we have direct communication between the first 
and second divisions. However, the teeth are also con- 
nected with the eye through the second and third divi- 
sions via the Gasserian ganglion. The first division 
further communicates with the motor nerves of the eye, 
the third, fourth, and sixth cranial nerves. Reflex irri- 
tation from the oral cavity therefore may not only result 
in irritation of the parts of the eye supplied by the sensory 
nerves, but may also cause motor nerve disturbances in- 
terfering with the function of accommodation and con- 

Haematogenous infection, however, here plays an 
important role. To me it seems more probable that secon- 
dary ophthalmic disturbances should be of an infectious 
nature. They may also have been predisposed by reflex 
nerve irritation. In many cases there may be found a 
cause in the mouth for referred nervous irritation, but al- 
most always we can also discover a septic focus such as a 
chronic abscess, an abscess around and caused by an im- 
pacted tooth from which the secondary disease may have 
originated. There is no doubt that oral abscesses as well 
as oral nerve irritation cause ophthalmic disturbances in 
many instances, such as iritis, keratitis, scleritis, and 





Fig. 141. — Cross section through eye. 


other infectious diseases of the eye, as well as neurotic 
affections such as intraocular and retrobulbar optic 

infectious Conjunctivitis is an inflammation of the 
coimjuncti- conjunctiva, the thin mucous membrane 
vms lining the eyelids. We distinguish palpe- 

bral and bulbar types. It is also known as ophthalmia. 

Etiology : Infectious conjunctivitis is very often haem- 
atogenous in character, but may also be the result of 
direct contact, as by means of the fingers. It is fre- 
quently found in children and may easily be contracted 
from abscessed temporary molars if the child carries the 
finger from the aching tooth to the eye. 

Symptoms : The conjunctiva is of a brilliant red color 
and is swollen. The discharge is mucopurulent, some- 
times causing blurring of the sight. There are itching and 
smarting sensations referred to the lids, which feel hot 
and heavy. 

suppurative The inflammation of the cornea is called 
keratitis keratitis. 

Etiology : It is a process of infection caused by various 
organisms. It may come from conjunctival inflamma- 
tions or other direct and indirect infections. 

Symptoms: It begins with a dull, grayish or grayish- 
yellow infiltration of a circumscribed portion of the cor- 
nea. It may extend in area and in depth. There is pain, 
photobia (intolerance to light), lacrimation (excessive 
secretion of tears), and often blepharospasm (excessive 

scleritis ^ke inflammation of the sclera, which 
with the cornea forms the external tunic 
of the eyeball, is called scleritis. 

Etiology: Scleritis is often seen in connection with 
rheumatism, syphilis, and tuberculosis. Exposure to cold 
is sometimes an exciting cause. Reflex irritation and 
secondary infection from oral foci are not uncommon 

Symptoms: There is usually slight discomfort, lacri- 
mation and pain. 


illustrative Case ^ ' (Bulbar conjunctivitis.) The 
case " P a ^ en ^ a J owa S man, about twenty- 

two years old, had suffered for a long 
period from bulbar conjunctivitis of both eyes, for 
which he was treated by a competent ophthalmol- 
ogist, who, however, was not able to cure the 
condition permanently. The two upper central in- 
cisors had been devitalized and in the radiograph 
showed areas of lessened density around their apices. 
After each subacute attack of these abscesses he suffered 
from an attack of conjunctivitis. The root canals of both 
teeth had previously been treated, but the left tooth did 
not yield to treatment. I treated and filled the left in- 
cisor and immediately performed apiectomy. The pa- 
tient was normal for about four months, when he had a 
recurrence. The right eye, which formerly was the worst, 
showed only a slight conjunctivitis ; the left eye was mod- 
erately inflamed. The right central incisor again felt 
lame. I undertook at once to take radiographs of his 
whole mouth and found a devitalized right lower bicuspid, 
with slight periodontitis and poor root-canal filling. A 
right upper bicuspid showed an area of decreased density. 
Upon opening into this tooth the eye on the same side 
cleared up almost immediately. The tooth was treated 
twice with ionic medication and then filled with the chloro- 
form-resin-gutta-percha method. The left eye stayed in- 
flamed, the inflammation also extended into the conjunc- 
tiva and did not improve until the root of the right 
central incisor was amputated. A small granuloma was 
removed with the root end, which yielded a streptococcus 
and staphylococcus albus. Three days after the opera- 
tion, when the patient came to my office for the removal 
of the sutures, his eyes showed a clear and healthy ap- 
pearance. Before this case is dismissed apiectomy will be 
performed on the devitalized upper and lower bicuspids. 
iritis Iritis is the inflammation of the iris, and 

may be acute or chronic ; primary if devel- 
oping in the iris itself, secondary if the inflammation 
spreads from neighboring parts, such as the cornea. 


Etiology : Iritis is frequently dependent upon some con- 
stitutional disease and therefore may be caused by 
haematogenous infection. Frequently the focus is found 
in the nose or mouth. 

Symptoms: There is pain, photobia, lacrimation, and 
interference with vision. The iris appears swollen, dull, 
with indistinct markings. The color changes and becomes 
greenish to muddy according to the color of the eyes. 
cyclitis Iritis is frequently associated with cycli- 

tis which rarely occurs alone. (Iridocy- 
clitis.) It is an inflammation of the ciliary body and 
almost always involves the choroid. 

Etiology: The various causes of iritis are responsible 
for iridocyclitis. "The disease," writes May, "is often 
due to the influence of toxins of bacterial origin derived 
from the teeth (abscesses and pyorrhoea alveolaris) ton- 
sils, pharynx, nose, and sinuses." 

Symptoms : In iridiocyclitis we have the symptoms of 
iritis and in addition tenderness in the ciliary region and 
often swelling of the upper lid. 

choroiditis Choroiditis may be non-suppurative or 
suppurative. In the latter case there is 
usually an involvement of the ciliary body and the iris. 
It is then called iridochoroiditis. 

Etiology : The condition may be of ectogenous or endo- 
genous origin. The latter is due to septic infections from 
the oral (abscesses pyorrhoea) and nasal cavities, from 
intestinal autointoxication, syphilis and tuberculosis. 

Symptoms: In pure choroiditis there are no external 
signs; the symptoms are disturbances of sight. In iri- 
dochoroiditis there are symptoms of iridocyclitis which 
are acute and severe. 

retinitis ^ e i n A ainma tion of the retina is called 


Etiology : Retinitis occurs occasionally as a local lesion, 
but almost always is a manifestation of a constitutional 
disease, autointoxication or secondary infection. 

Symptoms: Diminution of acuteness of vision is usu- 
ally present. Pain is rare and there are no external 


intraocu- in this type of optic neuritis the head of 

NEumTis' ^ e °P^ C nerve is affected, causing marked 
visible changes in the disc. Intraocular 
neuritis is also called Papillitis. 

Etiology : Among the causes of this disease we have 
secondary infections from diseases of the nasal cavity, 
the sinuses and the mouth and teeth. 

Symptoms : Disturbance of vision varies and there may 
be complete blindness. There is no pain and no external 

retrobulbar Retrobulbar optic neuritis involves the 
optic orbital portion of the optic nerve, the 

neuritis process being an interstitial neuritis. 

It may be acute or chronic. 

Etiology: It may be due to direct extension from the 
orbit, general diseases or haematogenous infection. Oral 
sepsis plays an important part in the latter factor. 

Symptoms : In the acute form there is severe headache 
on the affected side, pain in the orbit aggravated by move- 
ment of the eye and rapid impairment of sight, beginning 
in the center of the field. In the chronic type there is 
diminution in acuteness of sight, foggy vision, especially 
in bright light, and blindness in the center. 

Case VI. (Retrobulbar optic neuritis.) 

case TRAT,VE: ^ e P a ti en ^' a voun g woman, was sent to 
me by an ophthalmologist of this city, with 

the following letter: "I treated Miss some three or 

four years ago for an acute retrobulbar optic neuritis of 
each eye. At that time we could trace no cause for the 

process. About ten days ago, Miss developed the 

same trouble again in her left eye. It is a coincidence 
that both at the time of this attack and at her previous 
attack she was having trouble with her teeth. I am send- 
ing her to you to get an opinion as to what sort of con- 
dition her teeth are in and as to whether there might pos- 
sibly be an infection there responsible for the ocular 
trouble. ' ' 

The patient complained of blurred vision ; she was al- 
most blind for near sight, but vision for distance was 


Fig. 145 

Fig. 146 

Fig. 147 

Fig. 148 

hn?w™;- 146 ' 14 v an ai\8.— Radiographs of Case No. 6, a patient suffering of a retro- 
bulbar optic neuritis. Both maxillary third molars are impacted. Areas indicating graim- 
lomata are found on devitalized teeth. 


Fig. 149 

Fig. 150 

Fig. 149. — Radiograph showing impacted un- 

erupted third molar causing otitis media in 

Case No. 7. 

Fig. 150. — Radiograph showing lower second bi- 
cuspid with decay under filling and granuloma 
causing otalgia in Case No. 8. 


not bad. Upon examination of the mouth several poorly- 
fitting gold crowns were visible. Kadiographic examina- 
tion revealed the following (Figures 145 to 148) : 

Lower jaw : All the molars of the left side showed areas 
which indicated chronic abscesses. A very large area on 
the right second bicuspid. 

Upper jaw: Third molar unerupted and impacted on 
both sides. Left upper first and second bicuspid and 
right upper first bicuspid, first and second molars also had 
apical infections to a greater or less extent. 

I extracted all these teeth, curetted thoroughly and 
treated the sockets with iodine. The patient reported 
improved ten days later, and since then has been steadily 
growing better. 

glaucoma Glaucoma is an important and co mm on 
disease of the eye which has for its charac- 
teristic an increase in intraocular tension. It may be 
primary or secondary. 

Primary glaucoma occurs without antecedent ocular 
disease, and is divided into inflammatory or congested 
acute and chronic stages and into non-inflammatory or 
simple varieties. 

Secondary glaucoma is the name given to cases of in- 
creased tension and other symptoms of glaucoma due to 
some other ocular diseases or injuries. 

Etiology : The exact cause of primary glaucoma is un- 
known. May thinks that arteriosclerosis, cardiac dis- 
eases, chronic constipation, the gouty and rheumatic 
diathesis are predisposing factors, all diseases which are 
more or less caused by toxic or bacterial absorption. 

Symptoms : There are different stages distinguished in 
acute inflammatory glaucoma. The prodromal stage: 
Sight appears to be obscured by a fog, with slight pain in 
eye and head. The active stage of glaucoma (glaucoma- 
tous attack) is characterized by rapid failure of sight, 
severe pain in the eye and violent headache, accompanied 
with nausea, vomiting, and general depression. After a 
few days or weeks, a decided improvement takes place, 
but the normal condition does not return. This condition 


is the glaucomatous stage. At any time there may be new 
attacks and with each succeeding attack the diminution 
in vision becomes greater until blindness ensues. This 
stage is called absolute glaucoma. Later the eyeball is 
apt to degenerate. 

Chronic inflammatory glaucoma is much more common, 
the symptoms resemble those just described, but are less 
intense and more gradual in onset. The termination is 
absolute glaucoma and finally degeneration. 

3. Aural Disturbances. 

Pain in the ear is a very frequent symptom of oral 
diseases, both the second division of the fifth nerve which 
supplies the upper teeth and the third division which 
supplies the lower teeth being in communication with the 
nerves of the ear. The maxillary division is connected 
with the tympanic plexus via spheno-palatine (Meckel's) 
ganglion, the vidian and greater superficial petrosal 
nerve. The mandibular division communicates with the 
tympanic plexus by way of the optic ganglion and the 
small superficial petrosal nerve. 

Such irritation of the middle ear referred 
media through nervous channels frequently pre- 

disposes the tissue for infection and 
through haematogenous transportation of bacteria may 
result in acute median otitis as well as chronic purulent 
infla mm ation of the middle ear and tympanum. Ab- 
scessed teeth may become foci for purulent otitis in two 
ways : first, by discharging a large amount of pus into the 
mouth, which may reach the tympanic cavity via the Eus- 
tachian tubes. It is well known that middle ear inflam- 
mations occur most frequently in children at the time 
when they are about to lose the temporary teeth, which 
very often are badly neglected and abscessed. The patho- 
genic connection between teeth and middle ear has, how- 
ever, not alone been demonstrable in children. Grayson 
reports that in adults he has failed a number of times to 


d e f g h 


Fig. 151. — Position of the lymph glands beneath the lower jaw 
(Preiswerk) . 

a, Submental lymph glands. ~b, Digastric muscle, c, Submax- 
illary gland, d, f, h, Submaxillary lymph glands, A, B, C. 
e, External maxillary artery, g, Masseter muscle, i, Parotid 



Pig. 152. — Schematic drawing showing which teeth are drained by the various 

lymph glands. 

A, B, C, the three submaxillary lymph glands, 
i S. M., S. M., the submental lymph glands. 


make much impression upon chronic purulent inflamma- 
tions of the tympanum until the dental cause had been 
otalgia Otalgia or pain referable to the ear may 

be from the Pinna, the external auditory 
meatus, the tympanic membrane, the tympanic cavity, 
and Eustachian tubes, from the mastoid process, or a re- 
flex manifestation. 

The jaws and teeth play a most important 
OTALGIA r ^ e * n re ^ ex otalgia. The pain may be 

continuous or periodical, with remissions 
and exacerbations. The cause may be found in the molar 
region, usually more in the lower than in the upper jaw. 
Impacted teeth, teeth with acute or chronic abscesses, 
periostitis, and wounds in that region play a great part as 
etiological factors. 

illustrative ^ ase VH- (Otitis media.) The patient 
CASE suffered from repeated attacks of otitis 

media of the right ear. There was a large 
amount of discharge from the ear. Treatment did not 
result in permanent relief, and pain persisted after the 
inflammation had subsided. The specialist she consulted 
during her last attack in San Francisco, before she left 
for the East, advised her to have her teeth examined. The 
patient was then referred to me, and I immediately took 
radiographs of her mouth. There was a large area over 
the right upper second bicuspid, shadows on each of the 
roots of the first molar and a badly impacted upper wis- 
dom tooth with pus discharge from an opening in the gum. 
I extracted the upper second bicuspid and first molar and 
extirpated the impacted third molar without disturbing 
the second molar. The granulomata were removed at 
once, after which the bone was thoroughly curetted. Local 
conductive anaesthesia was used for the operation, which 
also relieved the pain in the ear while it was in effect. 
During the after treatment the patient improved rapidly 
and was freed from the aural pain and inflammation. 
(Figure 149.) 

Case VIII. (Otalgia.) The patient, a young lady, 
referred to me by another patient, complained of earache 


on the right side; occasionally also had what she called 
faceache on the same side. She consulted two dentists, 
who failed to locate the cause of the trouble, and was about 
to go to an ear specialist when her friend, who had a simi- 
lar experience, the cause of which I was able to locate and 
remove, advised her to consult me first. I took radio- 
graphs of the teeth on the affected side, and found that 
the right lower second bicuspid had a large obscure cavity 
at the distal side, underneath the cervical margin of a 
gold filling. The pulp was involved and a granuloma had 
developed at the end of the root. There were no symp- 
toms that indicated this condition. The tooth was 
extracted and the bone curetted, which resulted in per- 
manent relief of the otalgia. (Figure 150.) 

4. Lymphatic Infections. 

There are two groups of lymph glands which drain 
the jaws and teeth and their mucous membrane. The sub- 
mental glands take care of the region of the lower incisor 
teeth. They are situated behind the chin, beneath the 
fascia, and between the two geniohyoid muscles. The 
other group are the submaxillary lymph glands. They 
are three in number. The anterior one lies internally to 
the lower border of the mandible and anterior to the 
external maxillary artery. It is connected with the re- 
gion of the superior incisors, cuspids, and bicuspids, also 
the lower cuspids, bicuspids and the lower first molars. 
The middle submaxillary lymph gland lies posterior to 
the external maxillary artery at the anterior part of the 
submaxillary salivary gland. It drains the parts contain- 
ing the maxillary first molar, but also partly the upper 
bicuspids and second molar. In the lower jaw it takes 
care of the three molars, but principally of the second 
molar. The posterior gland is situated at the posterior 
pole of the submaxillary salivary gland and is connected 
with the upper wisdom tooth exclusively, and also with 


the lower third molar, which is to small extent drained by 
the middle gland. 

These just described lymph glands are tributaries of 
the deep cervical lymph glands which accompany the ex- 
ternal and internal jugular veins. 

In a perfectly normal condition these glands are of 
very small size so that they are hardly noticeable ; they are 
seldom larger than the size of a pea, but in diseased con- 
dition they may become greatly enlarged. Lymphatic 
infections occur most frequently in children, but are not a 
rare occurrence in adults. 

Lymphangitis is an inflammation of the 
GUIS " lymphatic vessels, and also gives rise to 
inflammation of the tissue immediately 
surrounding them. It is rarely a primary condition and 
usually extends from the focus to the nearest lymphatic 
gland, but may continue from there to the next group of 
lymph glands. 

Etiology: The cause is always a septic condition. It 
occurs in the mouth occasionally from abscesses or other 
infections. The bacteria or their toxins are absorbed 
from the focus and cause inflammation while passing 
along the lymph channels. 

Symptoms : "We can easily recognize a lymphangitis by 
the pink or reddish colored streaks clearly visible on the 
skin. There is usually more or less pain along the lym- 
phatic vessels and a rise of the temperature. Lymphan- 
gitis from lesions in the mouth is only recognizable if the 
lymphatic channels beyond the submental or submaxillary 
lymph glands are affected, in which cases there is also 
swelling of these glands. The affection therefore does 
not point directly to the lesion and the cause has to be 
ascertained by radiographic examination. The affected 
gland, however, indicates the location of the focus. 

Treatment: The finding and removing of the cause is 
imperative and if this is done the inflammation will dis- 
appear in a short time. Hot applications can be applied 
as soon as the focus has been thoroughly opened and 
drainage established. 


ILLUSTRATIVE C ™\ /X (Lymphangitis.) The pa- 
c s tient, a woman 01 middle age, presented 

a lymphangitis extending from the left 
submandibular region to the left axilla and breast. The 
lymphatic channels were distinctly outlined in reddish 
color. The submaxillary and cervical glands were 
slightly enlarged and tender on pressure. "No pain in the 
mouth. Radiographic examination revealed a large area 
of lessened density around the left lower second bicuspid. 
(Figure 153. ) Examination showed slight swelling on the 
gum and pus discharge at the gingival margin if pressure 
was applied. The treatment consisted in extraction of 
the tooth, thorough curettage, and insertion of iodoform 
wick for drainage. This was changed until the discharge 
stopped and then left to heal up. Bacterial examination 
showed a streptococcus and staphylococcus aureus 
infection. The inflammation of the lymphatics grad- 
ually diminished and disappeared entirely after three 

lymph a- Lymphadenitis is the term applied to the 

denitis" inflammation of the lymph glands. We 

distinguish acute, chronic, and subacute 
lymphadenitis. Submaxillary, submental, and cervical 
adenitis are common complications of diseased teeth, es- 
pecially in children, and unfortunately it occurs fre- 
quently that the glands are removed without investigat- 
ing the unsuspected cause, which almost always is an 
acute or chronic abscess, from a temporary, permanent, 
or impacted and unerupted tooth. 

acute Acute lymphadenitis usually occurs in 

cervical LYM-connection with acute periodontitis and 
phadenitis acute abscesses. 

Etiology : Acute lymphadenitis is usually secondary to 
a septic infection. The focus for the submaxillary and 
submental lymph glands may be found in the orbit, zygo- 
matic and temporal fossae, the nose, the cheeks, palate, 
lips and especially the alveolar process and teeth of both 
jaws. Alveolar abscesses and stomatitis are the most 


Fig. 153 

Fig. 154 

Fig. 153. — Radiograph showing the tooth (second bicus- 
pid) causing lymphangitis of Case No. 9. 

Fig. 154. — Radiograph showing the lower second molar 
causing lymphadenitis in Case No. 10. 


Fig. 155 

Fig. 155a 

Figs. 155 and 155a. — Eadiographic plates of Case No. 11, showing the un- 
erupted third molars causing chronic lymphadenitis. There was a 

,„„^ ,T„,.„V.l, 


frequent causes. The toxins or bacteria themselves may 
be absorbed. 

Symptoms : The glands in acute lymphadenitis become 
only slightly enlarged, they feel elastic and soft, and are 
very sensitive on palpitation. But also the tissues sur- 
rounding the glands become affected by the process of in- 
flammation, the skin looks red and swollen, and in extreme 
cases the pus may burst through the capsule of the gland 
and force its way through the skin. 

Treatment: Find and remove the focus and use cold 
poultices and hot mouth wash until the abscess in the 
mouth has healed, then apply hot poultices to the glands. 
If suppuration has progressed beyond the stage where 
nature can take care of the condition, the glands should be 

illustrative @ ase ^. (Acute Lymphadenitis.) A 
case 7 oun g man, a medical student, con- 

sulted me for tenderness directly 
under his lower jaw. Upon examination, I found 
the middle lymph gland of the right submaxillary 
group slightly enlarged and very tender ; there was also 
enlargement of one or two of the cervical glands. The 
examination of the mouth revealed nothing except large 
amalgam fillings in the posterior teeth. I took a radio- 
graph of the right lower molars first, and was at once 
rewarded in finding a large area of lessened density ex- 
tending from the roots of the right lower second molar. 
A radiograph of the upper molars showed all teeth in 
normal condition. The pulp of the right lower molar had 
never been touched before, but apparently was infected. 
The reason why there were no other symptoms was prob- 
ably due to the thickness of the outer and inner plate of 
the mandible in this region, not allowing the pus to pene- 
trate quickly to the large cancellous inner portion, allow- 
ing the pus to accumulate without causing pressure or 
pain. When I opened into the pulp, I found what I ex- 
pected, namely, an extremely putrescent pulp. After the 
local condition was treated, the glands became normal in a 
very short time. (Figure 154.) 


CHRON8C If the lymph, glands are swollen and re- 

cervical main so on account of persistent infection 

nrUmc" ^ or a l° n g time, we have chronic lymph- 


Etiology: Chronic lymphadenitis is a secondary infec- 
tion. It is caused by continuous absorption, such as 
bacteria from chronic abscesses or pyorrhoea. 

Symptoms: The glands are usually much larger than 
in the acute condition. They are hard, are easily palpi- 
tated, and are not tender on touch. They are not adherent 
and seldom suppurate. 

Treatment : The focus should be removed because there 
is always danger of a secondary infection such as tuber- 
culosis, reaching the gland via the primary lesion. 
subacute Subacute lymph glands occur from sub- 
cervical acute attacks in the primary lesion. 

lymph A- Symptoms: Besides the symptoms caused 

denitis about the focus, we find the lymph glands 

very large and extremely tender. This is characteristic 
for subacute attacks. 

Treatment : The treatment is the same as for the acute 

illustrative Case XI ' ( Cnronic lymphadenitis.) A 
CASE yo un g lady of about 18 years, was sent 

to me with radiographs showing four im- 
pacted wisdom teeth. She complained of swellings in the 
submaxillary region, which from time to time became 
very tender and painful. On examination the gums 
around the wisdom teeth are found red and inflamed, dis- 
charging pus on pressure; the posterior submaxillary 
lymph gland on each side is much enlarged. I extracted 
all four impacted teeth under ether anaesthesia, and after 
the wounds had healed the glands diminished gradually 
to their normal size. (Figure 155.) 
tubercular Tubercular cervical lymphadenitis is more 
cervical frequent in children under six years, but 
lymph A- is not a rare occurrence in adults. That 
denitis y. occurs independent of general tubercu- 

losis due to septic infection from the mouth was 
shown by Professor Cantani in fifty clinical ob- 


servations at the Institute of Medical Clinic of the 
Royal University of Naples. 

Etiology : The cause is the tubercle bacillus, which may 
find its way to the glands via the lymph system or circu- 
lation from the tonsils or the teeth. Carious teeth with 
open pulp chambers are an ideal place for the entrance of 
such microorganisms. 

Symptoms : The glands first are enlarged and firm, and 
it is characteristic that in a short time other glands are 
involved and the structures in the vicinity of the glands 
become fused together. (Peri-adenitis.) It is also 
characteristic that the swelling of the glands does not go 
back after removal of the focus. In cases where the in- 
fection is secondary to tuberculosis of the lungs, bones, 
etc., the glands do not become excessively enlarged, but in 
primary infections we have large glands which tend to 
break down. 

Treatment : The treatment more or less depends on the 
question whether the patient suffers from general tuber- 
culosis or whether the cervical lymphadenitis is only a 
local infection. If the patient's general health is poor, it 
should be improved by outdoor life and plenty of good 
nourishment. In treating local conditions we should 
ascertain and radically remove the cause. Radiographic 
examination is necessary to ascertain abscesses resulting 
from teeth, because chronic abscesses give no symptoms 
or signs to indicate the condition. The removal of the 
cause, however, does not cure a cervical tubercular ade- 
nitis and many treatments have been advised for this 

Extirpation: Surgical removal according to many 
writers is not justified in cases of moderate size because 
they claim that tubercular adenitis is liable to recur. I 
think the reason for the recurrence may rather be found 
in the neglect or insufficient treatment of the cause than in 
the method. However, it may be advisable to try one or 
more of the other methods before resorting to radical 

Heliotherapy: This treatment consists in exposing the 
glands to direct sunlight. 


Radiotherapy: A series of X-ray treatments has been 
found to give good results. The X-rays are carefully 
filtered to prevent burning and the dosage is regulated 
according to the patient and the condition. About twenty 
treatments applied twice a week are said to be sufficient. 
This treatment is also advised in cases where suppuration 
occurs. The abscess may be punctured if a sinus does 
not already exist. X-ray treatment is also beneficial 
after extirpation to prevent recurrence. 

Injections of Antiseptics : Injections into the glands of 
iodine or carbolic acid have been advocated. De Vecchis, 
an Italian physician, has used the following method which 
had not failed him in a single case, and has the advantage 
of not causing a permanent scar or fibrous thickening, 
which fact is important from an aesthetic viewpoint, 
especially in women. After careful search for and 
removal or treatment of the focus or possible foci in the 
mouth and throat, he injects the following solution : 

Synthetic guaiacol Merck 6.0 

Metallic iodine 3.0 

Sodium iodid 6.0 

Glycerine 30.0 

Saccharin 0.5 

Aqua dest 10.0 

Mx et solve. 

Sig. for injections. 

With needles of special size he makes parenchymatous 
injections with this solution, turning the needle in all 
directions in the gland and liberating the drug drop by 
drop, using 1 to 2 c.c. in all. The injection is followed 
by slight massage and by application of tincture of 
iodine and warm cotton for twenty minutes. When 
suppuration has begun, he aspirates all pus-like liquid, 
and if the patient can be seen daily, he also uses gluteal 
injections of 1 c.c. each day. In regard to the paren- 
chymatous injections the operator should be particu- 
larly careful in regard to asepsis, so as not to cause 
mixed infection. After each injection the gland becomes 


more tumid, warmer and more reddish, but after one or 
two days it begins to diminish in size. The injection is 
repeated twice a week for three to four weeks ; the patient 
is directed to use an antiseptic mouth wash and gargle, to 
avoid smoking and drinking of intoxicating beverages, 
and is advised to live in the fresh air and sleep with the 
windows open, to eat as much as he can of the most 
nutritious food. 

illustrative ^ ase ^^' ( TuDercular lymphadenitis.) 
CASE (Case reported by Stark in Revue de la 

Tuberculose, July, 1896.) A youth who 
had always been healthy previous to his eighteenth year, 
developed at that age enlarged glands. Carious molars 
were present on both sides. The glands were removed and 
the teeth extracted. The glands proved to be tuberculosis 
and the cover slip preparations from the teeth revealed 
tubercle bacilli. 

5. Diseases of the Alimentary Canal. 

The mouth and teeth have a very close relation to the 
rest of the alimentary canal both in health and disease. 
There are three ways in which digestive disturbances 

1. Insufficient Mastication. The mouth is the place 
where the food should be properly prepared for digestion 
by crushing it into small pieces and mixing it with saliva. 
A full set of teeth, especially bicuspids and molars, is 
necessary to accomplish this. Lack of chewing surface, 
sore and carious teeth or malocclusion mean imperfect 
mastication, and consequently increased and unnecessary 
work for the stomach. "While such a condition leads to 
various ills connected with impaired digestion," says 
Hunter, "it is not the most important relation of dental 
diseases to general health." 

2. Swallowing of Bacteria and Pus. Most serious 
gastric and intestinal disturbances are liable to result 
from continuous swallowing of pus and bacteria, which 
are either mixed into the food during mastication or 


reach the stomach between meals. Oral diseases pro- 
ducing such conditions are numerous and common, oral 
abscesses discharging through sinuses into the mouth, 
stomatitis and pyorrhoea are of greatest importance. Ill- 
fitting crowns and fixed bridges, which often cause most 
contaminating unsanitary conditions, are also a source of 
gingival inflammation and ulceration. 

The discharge from these diseased conditions is con- 
tinuously taken into the stomach. For a long time the 
acids of the stomach have been looked at as destructive 
to such bacteria, but Smithies,* in a microscopic ex- 
amination of gastric extracts from 2,406 different 
individuals with "stomach complaint," showed that 
irrespective of the degree of acidity of such gastric 
extracts, bacteria were present in eighty-seven per cent. 
Hunter says there is a limit to the power of the stomach 
to destroy such organisms. Even in health it is never 
complete and is solely due to the presence of free HC1. 
But these powers become progressively weakened, when 
through any cause an increased and continuous supply of 
pus organisms is associated with a diminished and contin- 
ually lessening acidity of the gastric juice. During the 
intervals between digestion the acidity of the stomach 
reaches normally a low level which also gives bacteria a 
good chance to live and multiply in the stomach. 

These conditions lead eventually to deeper seated 
changes in the mucosa of the stomach, and also pass 
through into the intestinal tract. They pass through the 
small intestine, where they also may enter into the blood 
stream to the large intestine where they may exist in large 
numbers. In this fashion enteritis, colitis and appendi- 
citis may be caused. 

3. Haematogenous Infections of the Alimentary Canal 
Due to Oral Foci. Rosenowf writes that hemorrhages, 
superficial erosions and definite ulceration of the mucous 
membrane of the stomach and duodenum occur in man 
not infrequently during severe infections. He produced 

* Cited from Mayo : Mouth infection as a source of systemic disease. 

t Eosenow: The production of ulcer of the stomach by injection of streptococci. 


ulcers in the stomach or duodenum, or both, of eighteen 
rabbits, six dogs, and in one monkey by intravenous in- 
jections of certain streptococci, which have a certain 
grade of virulence. 

septic Many writers describe only acute and 

gastritis chronic catarrhal gastritis and mention 
bacterial infection invading the stomach 
from the nose and accessory sinuses, the throat and oral 
cavity as one of the causes. Hunter, however, distin- 
guishes a septic gastritis due to pyogenic infection of the 
stomach. The term acute and chronic is principally used 
to indicate a case which is temporary in its course or of 
a case which shows little tendency towards spontaneous 

Etiology : Professor Miller already recognized the fact 
that indigestion may be associated with foul mouth, and 
he brought a charge against the physicians that "their 
custom of disregarding dental diseases altogether as a 
factor in pathology is as unjust to their patients as it is 
discreditable to their profession." 

Septic gastritis is caused by continuous swallowing of 
pus organisms such as are discharged from oral abscesses 
with sinus and pyorrhoea pockets, infected tonsils or 
septic diseases of the nose. Not all these bacteria are de- 
stroyed, as has already been explained, and the mucosa 
becomes eventually infected, a septic catarrh is set up 
which is continuously sustained by influx of pyogenic 

Symptoms : Clamminess of the mouth, distaste of food, 
coated tongue and bad taste in the mouth are not so much 
manifestations of gastric catarrh as the direct result of 
oral sepsis. The real symptoms are indigestion, gastric 
discomfort, and nausea. 

Case XIII. (Subacute gastritis.) Re- 
case ported in Hunter's "Pernicious Ane- 

mia," page 231.) A lady, aged sixty-two 
years, suffered from subacute gastritis. The patient had 
severe intermittent sickness and gastric pain of eight 
months' duration, necessitating the use of morphia, with 


loss of weight and increasing weakness. Cancer was sus- 
pected, but on examination no sign of malignant disease 
was found in the stomach, the abdomen, the rectum or the 
uterus. Constant complaint was made of a bitter taste 
in the mouth, nausea, with loathing and distaste for all 
food. The tongue was coated with a dirty moist fur. 
The patient had false teeth both in the upper and lower 
jaws. The plates were scrupulously clean, and the gums 
beneath the plates were perfectly healthy. There were 
four remaining teeth, three of them decayed, suppurating 
around the roots, with pus welling up on pressure. There 
was no other sign of disease. A provisional diagnosis 
was made of gastritis caused by continual swallowing of 
pus. The roots were ordered to be extracted. A week 
later, the tongue was clean, the sense of taste returned 
for the first time for eight months, and there had been 
only one attack of pain. In another week, there was a 
return of the sickness, with vomiting on pain and slight 
fever. The vomit obtained two weeks later was watery, 
with rusty flakes consisting of mucous, fibrin, catarrhal 
cells, leucocytes and blood, the whole being loaded with 
streptococci, staphylococci and a few bacilli. A diagnosis 
was made of infective (septic) gastric catarrh. As a 
local antiseptic, three grains of salicylic acid were given 
thrice a day, with peptonized milk as food ; counter irri- 
tation was applied. There was complete cessation of all 
pain, and a steady recovery from that time onward. The 
patient gained weight rapidly and has since remained 
well (two years). 

Similar to septic gastritis Hunter distin- 
enteritis guishes a special form of the disease, 

namely, septic enteritis, which is in his 
experience a very common result of prolonged oral sepsis. 
Etiology: The bacteria which continuously enter the 
stomach and escape destruction naturally find their way 
into the intestine, where they finally infect the thin epithe- 
lial layer of the mucous membrane. 

Symptoms : There is more or less abdominal pain and 
diarrhea containing undigested food and mucous, whitish 
in color, and sometimes semi-solid. 


Case XIV. (Case of Enteritis.) Dr. 
case TRAT,VE Hunter's case reported in the British 
Medical Journal, November 19, 1904, page 
1361. The patient, aged thirty-seven. Foul oral sepsis ; 
most intense gastritis, enteritis and colitis, chronic renal 
disease, pericarditis, uraemia. Patient died, and micro- 
scopic examination of the stomach showed: intense gas- 
tritis with invasion of mucosa by masses of streptococci. 

The bacterial invasion descends along the 
coLms > ' CmS a l mien t ar y canal and may cause appen- 
proctitis dicitis, colitis and proctitis. The appen- 
dix is predisposed to infection on account 
of its poor blood supply (appendicitis is most commonly 
caused by the bacillus coli, the staphylococci and strepto- 
cocci). Haematogenous infection is also supposed to 
cause appendicitis, Poynton and Paine have caused it 
experimentally in rabbits with the organism isolated from 
rheumatic cases. If the colon is involved, the disease is 
called colitis, and if the mucous membrane of the rectum 
becomes infected, we speak of proctitis. 

Rosenow's work shows that in gastric and 
gastric intestinal ulcers the mucosa is attacked 

duodenal from behind through the blood stream. 
ulcers K is therefore a disease due to haemato- 

genous infection. 
Etiology: The bacteria causing these ulcerating con- 
ditions are supposed to have a selective affinity for these 
particular areas. Predisposing factors, however, may 
have a good deal to do with the localization of the disease. 
Clinicians have observed aggravations of symptoms in 
ulcer of the stomach following sore throat, and the asso- 
ciation of these conditions with septic foci in the mouth 
have been emphasized by various writers. Experimental 
evidence has been furnished by producing ulcers when 
injecting bacteria into the gastric artery by Rosenow's 
experiments on rabbits, dogs, and monkeys with the strep- 
tococcus. Steinharter* produced gastric ulcers experi- 
mentally in rabbits by injecting staphylococcus cultures 

* See Bibliography. 


of a special virulence and a weak acetic acid solution into 
the wall of the stomach. In the forty animals used for 
the experiments typical peptic ulcers were produced vary- 
ing from one quarter of an inch to one inch in diameter. 
He concludes: "In the light of the above results, it seems 
possible that the staphylococcus is responsible for certain 
cases of gastric ulcer in human beings. If by some means 
(through an erosion or trauma, etc.) a hyperacid gastric 
juice enters the tissues of a limited area of the stomach 
wall, and if the staphylococcus of proper virulence finds 
lodgment there, it does seem quite probable that the 
necessary conditions used in producing the experimental 
ulcer would be duplicated. 

Symptoms : About the first symptom of intestinal ulcer 
is the occurrence of pain lasting for an hour or two after 
the ingestion of a hurried meal, or after the taking of food 
that needs unusual activity of digestion. Hyperacidity 
and over-secretion, vomiting, and hemorrhages are other 
symptoms of this disease. The blood may be found in the 
vomitus or stool. 

Case XV. (Gastric ulcer.) (One of the 
cas1 TRAT,VE cases reported by Hartzel in the Journal 

of the National Dental Association, 
November, 1915, page 341.) The patient, a laborer, 
thirty-one years of age, of Irish descent, weighing on the 
average 160 pounds. Previous history, habits, and fam- 
ily history negative. His present illness began in October, 
1913, with heavy burning pains in the epigastrium after 
eating. In November he noticed blood in the stools and 
occasionally vomited blood clots. He went to the hospital 
for two weeks, where he was partly on a bread and milk 
diet, and then stayed at home for eight weeks before 
going back to work. After four weeks the pain reap- 
peared with the same symptoms. He was admitted to the 
University Hospital of Minnesota (Case No. 5356), on 
September 15, 1914. At this time the pain was absent, 
but an area of tenderness was noted over the stomach. 
He was thin, weak, unable to work, was constipated, with 
blood occasionally in the stools and blood clots occasion- 


ally in the vomitus. Physical examination showed him 
fairly well nourished, with marked anaemia, palpable 
cervical glands, submerged tonsils, had pyorrhoea and 
many old roots. The diagnosis was made as that of gas- 
tric ulcer, marked secondary anaemia, mitral insuffi- 
ciency, apical abscesses and pyorrhoea. Hemoglobin 
35%, red blood cells, 3,500,000, and leucocytes, 8,000. 

Between September 15 and October 1 oral infection was 
eradicated. All remaining upper teeth were extracted, 
also the abscessed lower molars. The remaining lower 
teeth were treated for pyorrhoea. 

On November 2 the physician in charge made the fol- 
lowing note: "Patient's condition has remarkably im- 
proved. His weight has increased twenty-three pounds. 
There is no abdominal pain. ' ' 

He was discharged on November 11, 1914, greatly im- 
proved, with no other treatment than a bread and milk 
diet and the elimination of the oral foci. 

He again presented for examination in March, 1915. 
He had been working and living as a lumber man, eating 
a full mixed diet and doing the heaviest kind of work, and 
has been perfectly well since leaving the hospital. He 
states that for one and a half years before admission here, 
he had been troubled almost continuously with stomach 
symptoms and has never had so long a period of freedom 
as this before. A blood count at this time showed the 
hemoglobin to be 77%. 

6. Diseases of the Blood. 

Today we know that infections are never entirely local- 
ized. Bacteria, their toxins and protein poison, produced 
during the process of infection and inflammation, or both, 
are always absorbed into the circulation, not only from 
the primary focus, but also from secondary lesions. 

The presence of bacteria and of protein poisons in the 
blood may cause diseases of violent and acute symptoms, 
or may be very latent in character, according to and de- 
pending on the number, virulence, and species of the 


bacteria, as well as the reaction and resisting quality of 
the defending blood cells. 

septicemia Septicemia is an acute general infection 
of the blood caused by bacteremia which 
occurs if living pyogenic bacteria exist and multiply in 
the blood. 

Etiology : Septicemia often results from cases of exten- 
sive acute suppuration or from absorption of bacteria in 
open wounds. It is predisposed by high virulence of the 
bacteria and lowered resistance of the patient. It occurs 
especially after surgical interference in septic conditions 
in patients with lowered resistance, and from persistent 
toxic and bacterial absorption, as from acute abscesses 
without outlet from the pus. In patients who are feeble 
from a long standing infection it is therefore advisable 
not to remove all foci at once, or the result may be 
fatal. The streptococcus which is found in almost all 
oral infections is the cause of septicemia, but also other 
pyogenic bacteria may produce the disease. 

Symptoms: After the inoculation the patient suffers 
from repeated chills, and the temperature rises to 105° F. 
The appetite is lost and the patient apathetic and de- 
lirious. The pulse becomes weaker and irregular and the 
temperature falls quickly before the exitus. Death usu- 
ally occurs in a few days, but sometimes the end is drawn 
out for several weeks. The diagnosis of septicemia is 
made by the severe and rapid constitutional symptoms 
and is differentiated from toxemia and sapremia by the 
blood test. A blood culture should be made at once, 
using great care to disinfect the patient's skin. Blood 
is withdrawn from the median basillic vein by means of 
a sterile aspirating syringe, and cultures are made in the 
ordinary manner. If bacterial growth is obtained, we can 
make a sure diagnosis of septicemia. 

Treatment : A great deal depends upon prompt, active 
and thorough treatment of the local lesion. A few hours 
make a great difference in the outcome. Free drainage 
should be established by a wide incision ; hot, moist, and 
large dressings should be applied and changed every few 


minutes. Saline infusions (1000 to 3000 c.c.) are ex- 
tremely useful; the diet should be regulated; and later, 
after the infection has subsided, tonics and stimulants 
should be given. 

pyaemia Pyaemia is an acute infection of the blood 

characterized by the presence of infected 
emboli in the blood, which in turn cause metastatic ab- 
scesses wherever they lodge. 

Etiology : The bacteria causing the infection in the pri- 
mary focus produce coagulation of the blood. This clot 
soon becomes infected, and portions of it are broken off 
and thrown into the circulation. It follows the venous 
system, where it may cause thrombosis or be carried to 
the heart and be distributed into any part of the circula- 
tion. The streptococcus is the commonest cause of this 
disease, but like septicemia it may also be caused by the 
bacillus coli, staphylococcus, pneumococcus, and bacillus 

Symptoms: The symptoms are the same as of septice- 
mia and usually start with a severe rigor followed by 
profuse sweating. The temperature is of intermittent 
character and rises up to 105 ° F. Abscesses usually make 
their appearance after a week and affect any part of the 
body. In chronic pyaemia the symptoms are less marked. 

Treatment : The radical treatment of the primary focus 
is to be undertaken at once. The lesion should be freely 
opened, the septic material removed without disturbing 
the leucocytic area, which would allow absorption and 
further contaminate the blood stream. Establish free 
drainage and irrigate often. Anti-streptococcic serum 
may be used and also autogenous vaccine as soon as it can 
be made. The outcome of the disease depends upon the 
resistance of the patient and virulence of the bacteria 
and is often fatal. 

Case XVI. (Pyemia.) (Reported by C. 
CASE TRAT,VE ^- Haman, Wisconsin Medical Jour- 
nal, March, 1903.) Patient, a man 
of forty years, seen in consultation with Dr. W. 
E. Bruner. An upper molar had been extracted a 


week preceding, the face was swollen from an alveolar 
abscess. The right eye was very prominent. He had a 
high evening temperature of 104 to 106° F., with morning 
intermissions. In a few days the other eye became promi- 
nent, which is quite characteristic of cavernous sinus 
thrombosis, and is accounted for by the venous connection 
between the teeth and periodontal structures and the cav- 
ernous sinus. The veins from the teeth empty into the 
pterygoid plexus. The pterygoid plexus communicates 
with the cavernous sinus directly by means of small veins 
passing through the foramen Vessalii, foramen or ale and 
foramen lacerum medium, and indirectly through the 
facial vein which empties into the sinus. The diagnosis 
of sinus thrombosis was confirmed. The patient lived 
about a week. 

Toxemia is a term which expresses a con- 
dition due to the absorption of toxins. 
Toxin in its strictest meaning is produced only by a small 
number of bacteria, as we have already seen, such as the 
diphtheria and tetanus bacilli. Generally, however, we 
speak of toxemia as a condition which may be caused by 
the absorption of any poisonous substances originated 
from bacteria or bacterial activity. If the poison is pro- 
duced by saprophytic bacteria which live on dead 
material, we speak of "sapremia." 

Etiology : Toxemia is due to the absorption of poisons 
created by bacterial activity and tissue reaction. In true 
toxemia toxins only are absorbed from the focus, but the 
term is also applied to all those conditions where bacteria 
also have entered the circulation as long as these produce 
no acute general infection (septicemia). 

Foci which cause toxemia are found in the intestinal 
tract, the genito-urinary system, and nose, and adjacent 
sinuses, the throat, and the oral cavity. Oral abscesses 
play the most important role in the mouth, but toxic 
absorption is also caused from unclean crown and bridge 
work, stomatitis, and pyorrhoea on account of the absorb- 
ing quality of the mucous membrane. All lesions in the 
mouth are caused or inhabited by the largest variety of 


pathogenic and saprophytic bacteria. They grow in com- 
binations, inhabiting the diseased tissue simultaneously 
or acting at different stages of the decomposition, which 
makes possible the production of a large variety of chemi- 
cal substances, as has already been described in the first 
part. These poisons may have special actions on certain 
tissues. It is well known that the diphtheria toxin, for 
example, is especially prone to attack the nervous system 
and to cause peripheral neuritis. 

Symptoms: Toxemia may be very severe, beginning 
with chills, a rapid rise of temperature reaching 104° F. ; 
there may be anorexia, headache and prostration, and 
later delirium, stupor or coma. In the less severe or 
chronic cases, which are of very frequent occurrence, the 
principal complaint is malaise. 

Malaise is a condition caused by a certain 
or 'chronic amoun ^ °f toxin or bacteria, or both, en- 
toxemia tering the circulation. The disease is not 

acute and violent as in acute septicemia 
and acute toxemia, probably on account of insufficient 
number and virility of the bacteria absorbed, and of the 
small amount of poison liberated to cause severe intoxi- 
cation. The blood pressure is lowered and the symptoms 
are best expressed by the complaint of the patient of the 
inability of doing mentally or physically the accustomed 
day's work. Slight exertions cause disproportionate 
fatigue. An abnormal amount of rest is required, the 
appetite is often poor, the skin has usually a grayish, 
sallow appearance, the lips lack the color of health, there 
is loss of weight, constipation, and benumbed mental 

Treatment : The foci may not be apparent, and it may 
require a thorough search to locate the lesion from which 
the absorption takes place. It should be remembered that 
a very small focus may, on account of its persistence and 
its chronic nature, cause a small but continuous infection 
of the blood. The radical removal of such foci is the first 
step in the treatment ; there is frequently more than one 
focus and it is important to remove all the septic con- 


ditions. If the tonsils are diseased, it does not mean that 
oral abscesses may not participate. The treatment of the 
cause is often sufficient to result in a cure ; in other cases, 
it is advisable to give tonics and stimulants. 

Case XVII. (Toxemia.) Patient, a 

CASES RAT,VE y ourL £ l a( ty? a college student, consulted 
me about a tooth which had been unsuc- 
cessfully treated. She had no symptoms of discomfort 
in her mouth, but upon questioning, complained of a tired 
feeling and frequent intermittent fever of about eight 
months standing. A radiograph showed a lower six-year 
molar with poor root-canal filling, but no pronounced 
periapical destruction. The second bicuspid, which is the 
tooth in question, presented a very large area of lessened 
density at the distal side of the apex. The tooth was at 
once extracted and the bone curetted. The patient im- 
proved rapidly ; the fever did not recur. (Figure 156.) 

Case XVIII. (Toxemia.) Patient, a man of middle 
age, asked two years ago for a careful examination of his 
teeth. He complained of an intoxicated feeling in his 
head, which manifested itself principally in the morning. 
His ability to think was greatly decreased, smoking made 
him ill, while before he was able to smoke a moderate 
amount. Radiographs of his teeth showed abscesses on 
the upper right incisor, upper left cuspid, first and second 
bicuspid. I opened these teeth; a vile odor came from 
the canals. Apiectomy was performed on the lateral in- 
cisor after the root canal was properly treated and filled. 
The cuspid and two bicuspids I cleaned thoroughly with 
the sulphuric acid method, and treated the canals with 
f ormocresol, and ionic medication. The root canals were 
filled, but the points projected through the apical fora- 
men. During the treatment the patient improved 
greatly and at the end his head felt perfectly clear so 
that he could again do his ordinary day's work. He also 
said that he was again able to smoke without discomfort. 
After eight months he came back saying that the old 
trouble recurred in a mild form. A new radiograph 
showed the areas of lessened density the same as before 


the treatment. I amputated the roots of the two bicus- 
pids at once, and later I performed the same operation 
on the cuspid. The patient reported an almost imme- 
diate change, and so far, permanent improvement. He 
later told me of another condition which apparently came 
from the teeth. He had the upper bicuspid tooth treated 
in Paris some time preceding and remembered distinctly 
that from this date he was afflicted with constipation. 
After the first treatment of the teeth he got rid of this 
condition entirely, and did not need any drugs until it 
returned with the toxemia. Again it was permanently 
relieved after the surgical removal of the abscesses. The 
interesting part about this case is the fact proven that 
root canal treatment neither with antiseptic nor ionic 
medication cured the abscess permanently, although the 
treatment was thorough and much longer continued than 
was necessary according to general rules. The bacterial 
growth and production of toxin was inhibited for a few 
months, but was only lying dormant until the infectious 
process slowly recovered. (Figures 157, 158.) 
anaemia Anaemia is a reduction in the amount of 

blood as a whole or of its corpuscles, or of 
certain of its constituents. There is primary or idio- 
pathic anaemia due to increased destruction due to some 
existing disease. Among the primary anaemias belong 
chlorosis, a disease of young girls, and pernicious anae- 
mia, the cause of which is not definitely understood. 
Among the secondary anaemias belong acute and chronic 
secondary anaemia. Hunter separates a special class 
which he calls septic anaemia. 

Pernicious anaemia, or Addison's anae- 
anaemia m ^ a ' Hunter says, is characterized by 

imperfect action of the blood-making or- 
gans, the absence of haemalytic and bone marrow changes, 
and characterized by pigment changes in the liver, kidney, 
and spleen. The disease is usually fatal. 

Hunter, who has done so much good work on this sub- 
ject, thinks that a large number of cases grouped as 
pernicious anaemia are really of an infectious nature with 


no bone marrow and pigment changes. The true per- 
nicious anaemia, however, he regards as a chronic infec- 
tive disease in which gastric disturbances, altered 
digestion, absorption and auto-intoxication, as well as 
oral abscesses and pyorrhoea alveolaris, may be a most 
important antecedent and concomitant, but not the only 
etiological factors. They precede the disease-creating 
conditions which permit the contraction of the specific 
(haemalytic) infection underlying the real characteristic 
features of the disease. 

Septic anaemia is a term used by Hunter 
anaemia ^ or a ^ cases °^ secondary anaemia which 

are of a septic infectious nature. Many 
of the cases diagnosed as pernicious anaemia, and espe- 
cially all anaemias comprised within Biermer's definition 
of progressive pernicious anaemia, show a predominant 
septic factor. These are distinguished from pernicious 
or Addison's anaemia by the absence of haemalytic and 
bone marrow changes and absence of pigment changes in 
kidneys, liver, and spleen. 

Etiology: Septic anaemia is caused by absorption of 
bacteria or the poisons of bacterial activity and may come 
from foci in the nose, sinuses of the oral cavity (abscesses, 
pyorrhoea) , and infections in the stomach and intestine, 
or chronic suppuration in any other part of the body. 
Prognosis is favorable if the cause is removed in time, 
but the disease may have a severe and fatal course. 

Symptoms : Dirty yellow, anaemic complexion, loss of 
bodily and mental vigor, with loss of weight. Not infre- 
quently there is slight fever. The red blood corpuscles 
are reduced, but seldom below two millions, and haemo- 
globin is about forty-five per cent, on the average. 

Case XIX. (Anaemia.) (Eeported by 

case TRATIVE T " B> Hartzel > Journal of the Allied Den- 
tal Societies, October, 1914, page 52.) 
This is one case out of four which came under the obser- 
vation of the writer. The patient, a Scandinavian of 
fifty-three years, presented himself with a history of his 
illness, having started seven years ago with slight at- 


Fig. 156 

Fig. 157 

Fig. 158 

Fig. 156. — Radiograph showing right lower second bicuspid 
causing toxemia in Case No. 17. 

Figs. 157 and 158.— Radiographs of Case No. 18, showing four 


Fig. 159 

Fig. 159a 

Figs. 159 and 159a. 

-Radiographic plates of Case No. 20. The arrows 
indicate the granulomata. 


tacks for a few minutes each day of chills and fever, 
followed by vomiting. These attacks had no relation to 
his meals. Since this time he had gradually, but inter- 
mittently, grown weaker. He had trouble for some time 
with swelling of the limbs and with dizziness. His color 
became pale and yellow, and he grew dull and listless. 
When admitted to the Eliott Hospital in Minneapolis, 
Minnesota, he was weak, yellow in color, with constant 
pain in his stomach, and seemed only dully conscious. 
The case was diagnosed by the medical staff as pernicious 
anaemia, with slight cardiac enlargement, mild pyorrhoea 
alveolaris and rarefaction about two root ends. He was 
put on iron and arsenites, and there seemed to be but 
little improvement, except a slight improvement in the 
blood count, until his mouth was put in good condition by 
the dental staff. Since that time he has been steadily 
improving. His consciousness had returned to normal 
and his other symptoms have been much improved. The 
most striking picture, however, is presented by his blood 
count, which has steadily risen from 900,000 red blood 
corpuscles and 15% haemoglobin to 2,630,000 red blood 
corpuscles and 61% haemoglobin. The only serious set- 
back occurred June 16, which was coincident with the 
occurrence of a dental abscess, at which time the haemo- 
globin dropped back from 61% to 55%, and the red blood 
cells from 2,630,000 to 1,800,000. After extraction of the 
abscessed tooth, the last blood count jumped from 
1,800,000 to 2,500,000, and the haemoglobin is the highest 
it has been since commencing his record, namely, 65%. 

7. Diseases of the Heart. 

The infective diseases of the heart are caused by haema- 
togenous infection due frequently to the streptococcus 
viridans, but may also occur in connection with typhoid 
fever, pneumonia, influenza, diphtheria, tuberculosis, 
and syphilis. Dr. Richard C. Cabot, in an analysis of 
six hundred successive and unselected cases of heart dis- 


ease, found that he could group 93% of these six hundred 
cases under four etiological headings : 1, Rheumatic, that 
is, presumably streptococci, 46% ; 2, Nephritic, 19% ; 3, 
Arteriosclerotic, 15%, and 4, Syphilitic, 12%. The 
streptococcic infections of the heart have their origin in 
a large majority of cases before the twenty-second year. 
It begins young, it is essentially a chronic disease, and if 
severe or progressive, handicaps those afflicted during 
the prime of life, and often causes death before maturity. 
On account of the severe prognosis, every effort should 
be made to eliminate all septic foci in the body as a pre- 
ventive measure, especially the ones which are liable to be 
caused and harbor the streptococcus. Streptococcic in- 
fections of the tonsils and teeth are of very frequent 
occurrence in children and form an ideal entrance for 
disease. At this place it is necessary again to call atten- 
tion to the importance of removing both tonsilar and 
dental foci, both on account of the intimate relation 
between these organs and the danger of the persistence 
from a see min gly unimportant lesion after the principal 
ones have been removed. The temporary teeth, especially 
the temporary molars, are very often pulpless and ab- 
scessed and suffered to remain in the mouth, partly 
because they cause no pain and partly for orthodontic 
reasons. It is, however, much better to sacrifice those 
temporary teeth and take a chance on the possibility of 
malocclusion rather than on the possibility of heart in- 
fection and life itself. 

The pericardium, myocardium, and the valves, have the 
same general blood supply and therefore they are all 
liable to haematogenous infection resulting in pericar- 
ditis, myocarditis, and endocarditis (valvular and mural). 
pericarditis P er i car ditis is an infection of the pericar- 
dium occurring in children at an early 
age. Its most frequent etiological factor is systemic in- 
fection from infections in other parts of the body, but it 
also may occur as a continuous infection from diseases of 
the pleura as well as the myocardium. 


myocarditis ^e car( ^ ac musculature very frequently 
becomes attacked by secondary infections ; 
it may be due to the streptococcus, the gonococcus, the 
pneumococcus, or other microorganisms. The microscope 
reveals lesions in the heart muscle which explain cardiac 
irritability and later indications of cardiac distress from 
infective diseases. 
-*.r*«^ „ nrMT.r- Endocarditis is the inflammation of the 

ENDOCARDITIS ,. . , « ., -, , ■, . 

lining membrane ot the heart, and is 
usually confined to the valves (valvular endocarditis) and 
rarely to the walls (mural endocarditis). It is princi- 
pally caused by the streptococcus and especially by the 
streptococcus viridans (rheumatism), which may be 
transported from a primary focus, such as the tonsils, 
abscesses on the teeth, etc. The streptococcus causing 
endocarditis grows best in high oxygen tension, and is 
usually extremely virulent. The circulating blood fur- 
nishes oxygen in abundance and furnishes an ideal con- 
dition for an abundant vegetative growth on the valves 
and walls of the endocardium. Syphilis, that is, the spiro- 
chaeta pallida, is another important etiological factor. 
Typhoid, scarlet fever, pneumonia, influenza, diphtheria, 
and tuberculosis occasionally involve the valves, but show 
a marked predilection for the myocardium. 

Endocarditis occurs in two forms: acute endocarditis, 
characterized by the presence of vegetation with loss of 
continuity (simple endocarditis), or of substance in the 
valve tissues (ulcerative endocarditis) ; chronic endo- 
carditis is a slow sclerotic change, resulting in thickening 
and deformity. 

Treatment : The infectious diseases of the heart are of 
a very grave and often fatal nature. Careful study leads 
specialists to believe that in a large number of instances 
heart disease in the adult originates in childhood, and all 
energies should be put into the recognition and treatment 
of these diseases in the early stages. Eustis* says that 
endocarditis in its earliest stages is not surely recogni- 

* Endocarditis in Children. Boston Medical and Surgical Journal, September 

Zy 19i0 


zable, but that it is important to begin treatment, in order 
to be effective, before a diagnosis can be made. This 
means that infections diseases as rheumatic (the term 
used in its broadest sense) attacks, and chorea in children 
should be treated as cases of acute endocarditis. In these 
cases of suspicious heart disease, we should remove septic 
foci, such as diseased tonsils or abscessed teeth. It should 
be remembered that absence of pain in the mouth or 
teeth is not a sign of healthy condition, but on the con- 
trary, that the most dangerous septic foci, chronic ab- 
scesses, are often entirely symptomless and unsuspected 
by the patient, and that sometimes, if the removal of 
diseased tonsils does not give the desired result, there 
may be an unknown focus on one or more teeth which 
can only be discovered by the radiograph. Such a focus, 
although small, may be the cause of persistent infection. 
In removing such foci it is of greatest importance not to 
go about it in a wholesale manner; this might result in 
absolute harm. Eustis reports a heart case where a 
severe relapse of chorea occurred immediately after the 
extraction of several teeth. The practice of removing 
tonsils, adenoids, and abscessed teeth, all at one time, is 
very frequently undertaken in order to save the patient 
repeated shocks of general anaesthesia, but is poor policy, 
as it is liable to cause exacerbations of the disease we try 
to cure. The foci should be removed gradually, the ton- 
sils separately, and the teeth one by one ; this can be done 
easily and without causing great shock if local anaesthesia 
is used, which is a most excellent method for operations 
in the mouth. It also gives the operator a much better 
chance to curette and inspect the abscess cavity, a most 
important part of the operation. 

The recovery from heart diseases is extremely slow; 
strict rest in bed for weeks or months is almost univer- 
sally advised in these cases even for several weeks after 
the temperature and pulse have reached normal. This is 
a most difficult thing I find for many dentists to under- 
stand ; they think the patient should recover immediately 
after the foci in the mouth have been removed. 


Case XX. (Subacute endocarditis.) 

case TRAT,VE ^^ e V&tieiat, a D °y> a S e( i thirteen, born in 
Russia. He had been in this country for 
two years. He had had the measles when very young and 
scarlet fever some five years before coming to this coun- 
try. He never had had any sore throat. 

Seven months ago he started to have pain in the joints, 
mostly in the shoulder region, associated with fever. 
Shortly afterwards he complained of pain over the pre- 
cardia and of dyspnea upon exertion. He was kept in 
bed except for meals. 

Physical examination showed lungs negative; heart, 
apex visible and palpable in fifth interspace, 11 cm. 
from the midst ernum. Over the apex was felt a distinct 
presystolic thrill. Sounds of a fair quality but rapid. 
At mitral area is heard a presystolic murmur. Over aorta 
is a diastolic murmur and over pulmonic area is a systolic 
murmur. Abdomen is full, soft, and tympanitic 
throughout. No masses or tenderness. Knee jerks pres- 
ent. No glands in neck, axilla, or groin. Pulse equal, 
regular, of waterhammer variety. Capillary pulse 

Patient was admitted to the Robert B. Brigham hos- 
pital on November 6. Temperature 100.6° F. ; pulse, 
140 ; respiration, 28 ; blood pressure, 125-80. He was put 
on a light diet and kept in bed. I ordered X-rays taken 
of his teeth, which showed shadows representing granu- 
lomata at the roots of the two lower first molars and one 
upper first molar. I extracted the upper first molar on 
December 11, and the right lower first molar on December 
14, both under local anaesthesia. Cultures from the 
upper molar revealed a streptococcus and staphylococcus 
infection. From the lower molar a pure streptococcus 
infection was demonstrated. On December 23 a slight 
downward tendency of temperature was reported, the 
pulse still being variable. He received vaccine treatment 
beginning January 10, 1915, which, however, did not 
improve his condition. On February 3, the third six-year 
molar was extracted, and yielded a streptococcus culture. 


The patient improved materially after this and was ad- 
vised to have his tonsils out, as they were enlarged, but 
left the hospital on February 28 at his father's request. 
He was again examined at the hospital in June, 1916. 
He was greatly improved : no temperature, better pulse, 
is able to go about and to attend school. Regurgitation 
and mitral stenosis are still present and will probably re- 
main as permanent defects. (Figure 159.) 

8. Affections of the Nervous System. 

Nerve affections due to oral conditions are either local, 
remote, or general. The local conditions arise from 
direct infection of the branches of the maxillary or man- 
dibular division of the fifth nerve by septic condition, or 
are caused by pressure, such as is frequently caused by 
impacted and unerupted teeth. The pain is usually 
referred to other branches of the fifth or to communi- 
cating nerves which may result in complaints in other 
organs such as the ear and eye, where not infrequently 
aural or ophthalmic disturbances are produced by the 
referred irritation. These conditions have already been 
described under their respective headings. If nerves in 
other parts of the body are infected, we speak of remote 
infection, and if a large number is involved, we speak of 
general nerve infection. The two latter conditions are 
caused by haematogenous infection or intoxication. The 
bacteria and poisons created by bacterial activity or the 
latter alone are absorbed from the primary focus and 
certain toxins are thought to have a special affinity for 
the nervous system. The poisoned blood irritates the 
nerves and causes certain disturbances such as neuritis, 
chorea, insomnia, and mental depression. 
neuritis Neuritis is an inflammation of the nerve 

trunks ; it may be in a single nerve local- 
ized, "or involving a large number of nerves,' ' called 
general or multiple neuritis. 

Etiology : Localized neuritis is usually caused by cold, 
traumatism, or extension of inflammation from neigh- 


boring parts. This condition is of frequent occurrence 
in the mouth. Alveolar abscesses, or impacted teeth, 
maxillary sinusitis, and osteomyelitis often involve in- 
flammation of parts of the second or third division of 
the fifth nerve. Postoperative pains after operations on 
the jaws are also well known and are due to traumatic 
injury of or continuous traumatic inflammation of the 

General neuritis has a very complex etiology : organic 
poisons, as alcohol, ether, lead, arsenic, mercury, etc., and 
poisons caused by infections, such as streptococcus, infec- 
tions, diphtheria, typhoid fever, smallpox, scarlet fever, 
syphilis, and others. 

Hunter and other authors think that oral sepsis plays 
a great role in the etiology of toxin neuritis. Hunter* 
gives three well-studied cases of typical general neuritis 
prevailing for many years (Case 3 for fourteen years), 
and in all cases there resulted immediate improvement 
from the removal of the septic oral conditions. 

Symptoms : In localizing neuritis there is pain of a bor- 
ing or stabbing character felt in the course of the nerve 
and in the parts supplied. In general neuritis there is 
no constant intense pain in the nerves, but there is numb- 
ness and tingling in the hands and arms or part supplied, 
a so-called paresthesia, which is often described as the 
"pins and needles" sensation. There may also be altera- 
tions in the muscular power and abolition of deep reflexes. 
illustrative Case XXI. (Local neuritis.) The pa- 
case tient, a woman of about thirty-seven 

years, complained of local neuritis in the 
lower jaw. An X-ray plate was taken and showed a large 
area of lessened density about a root in the lower jaw. 
The inflammatory process involved in this case the in- 
ferior alveolar nerve and was the direct cause of the 
neuritis. After removal of the root and curettage, fol- 
lowed by occasional treatment, the condition disappeared 
^completely. (Figure 160.) 

* Hunter: Pernicious anaemia, pp. 303-305. 


trifacial Neuralgia is a pain in a nerve or nerves 
neuralgia °^ radiating character. Trigeminal neu- 
ralgia attacks mostly only one branch of 
the nerve, but in rarer cases two or all divisions may be 
involved. It is characteristic for the disease that no 
inflammatory conditions occur in the part where the pain 
is located. 

Etiology: The cause of trigeminal neuralgia is fre- 
quently of obscure character and often cannot be located 
even after the most painstaking search. It is said to occur 
from general and local causes. The general causes are a 
result of toxemia such as produced by infectious diseases. 
The local causes are more important. They may be due 
to diseases of the eye, middle ear, nose and accessory 
sinuses, or especially the oral cavity and teeth. 

The diseases of the oral cavity most commonly cause 
trifacial neuralgia. Pulpstones or nodules often occur 
in the pulp chamber of a tooth, causing pressure upon the 
nerve fibres of the pulp. Impacted and unerupted teeth 
are also an important factor. The pressure exerted by a 
developing tooth which grows in a wrong direction may 
be extremely great and sometimes even causes absorption 
of parts of the permanent tooth which stands in its way, 
even exposing its nerve. Pieces of alveolar process are 
sometimes fractured after extraction and escape dis- 
covery, or such pieces or ends of roots may be forced into 
the cancellous part of the bone and cause, especially in the 
lower jaw on account of the mandibular canal, pressure 
upon the nerve. Abscesses on unerupted and impacted 
teeth and chronic abscesses in general may, besides being 
a focus from which toxic absorption takes place, be the 
cause of trigeminal neuralgia. They usually give no local 
discomfort, but may be causing irritation and inflamma- 
tion of branches of the fifth nerve, causing in turn a reflex 
neuralgic condition. 

Synrptonis : The pain many times is only a slight and 
bearable one, but in other cases it is of most excruciating 
character. Some patients have a continuous mild pain 
with severe attacks at irregular intervals. The interim, 


Pig. 160 

Fig. 160. — Eadiographic plate of Case No. 21, showing a large osteo- 

myelitic area caused by the root which remained under a bridge. The 

diseased area extends into the mandibular canal causing neuritis of the 

inferior alveolar nerve. 


Fig. 161 

Fig. 162 

Fig. 161. — Eadiograph of lower molar with cavity beneath the gum (dark area around 

the filling) of Case No. 22. 

Fig. 162. — Kadiographie plate showing impacted lower third molar which caused 

neuralgia in Case Xo. 23. 



during which the patient is either free of pain or where 
there is only a dull aching, may last minutes, hours, or 
days. The attacks sometimes are of such terrible charac- 
ter that the patient is tempted to commit suicide. 

The attacks occur either spontaneously or may be in- 
duced by movements of the mouth, washing of the face, 
or touching the lips or cheek with the fingers. 

Diagnosis : Diagnosis of trigeminal neuralgia requires 
the most painstaking search for general as well as local 
causes. It is principally a process of elimination of one 
possible cause after the other. The use of the radio- 
graph is imminent for examination of the oral cavity. 
Plates should be taken first to make sure that there are 
no impacted, unerupted, or supernumerary teeth or odon- 
tomas in remote parts of the maxillary or mandibular 
bones. The plates also give us a general idea about the 
teeth. Films from different angles should then be taken 
of all the teeth for a more detailed diagnosis, and only the 
very best negatives are good enough to ascertain the pres- 
ence or absence of abscesses and pulpstones. 

Dr. Henry Head believes that neuralgic pains resulting 
from teeth have definite areas of reference in relation to 
the tooth involved. These areas have been ascertained by 
gently pinching the loose skin, and if the right spot is 
touched, there is often a distinct exacerbation of pain 
from the tooth. The following table is from Behan's 
book on "Pain." 


Reference Area 



Fronto nasal region 



Naso labial region 


First Bicuspid 

Naso labial region 


Second Bicuspid 

Temp '1 or maxillary 


First Molar 

Maxillary region 


Second Molar 

Mandibular region 


Third Molar 

Mandibular region 



Mental region 



Mental region 


First Bicuspid 

Mental region 


Second Bicuspid 

Hyoid or mental 


First Molar 

Hyoid ) Also in ear and just behind 


Second Molar 

Hyoid > angle of jaw and tip of 


Third Molar 

Sup. Laryngeal ) tongue on same side. 


Treatment : Treatment of neuralgia consists of removal 
of the cause and treatment of the symptoms. In cases of 
obscure persistent nature, alcohol injection into the main 
trunks or the Gasserian ganglion are recommended. Neu- 
rectomy of the terminal branches or of the whole second 
or third division is advocated by the believers in the 
surgical methods, and as a last resort the removal of the 
Gasserian ganglion. 

Case XXII. (Trifacial neuralgia.) Pa- 
cases RAT,VE tien t> Mrs. S., was referred to me for 
radiographic examination to find the 
cause of an obscure neuralgia, which was referred to the 
right upper side of the jaws. A diseased condition of the 
bone in the upper jaw was suspected by her dentist. The 
radiograph, however, revealed an obscure pus condition 
about the root of the lower second molar concealed by the 
gum, causing necrosis of the root. The extraction of the 
lower molar stopped the neuralgia entirely. (Figure 161.) 

Case XXIII. (Trifacial neuralgia.) Patient, a young 
lady, complained of faceaches on the left side, which 
sometimes were very severe and interfered with her 
studies. X-ray showed an impacted lower wisdom tooth 
as well as abscesses on both ends of the first molar. I 
extirpated the impacted tooth, extracted the first molar, 
and curetted the abscess cavities. The patient made quick 
recovery and has been free of pain ever since. (Figure 162.) 
~..^_~. Chorea, or St. Vitus 's Dance, is a disease 
chiefly affecting children, characterized by 
irregular, involuntary contraction of the muscles, and a 
marked association with acute endocarditis and rheu- 

Etiology: The disease is most common in children be- 
tween the age of five and fifteen. Fright, injury, and 
mental worry are named as etiological factors ; the prin- 
cipal cause, however, seems to be of an infectious nature. 
It has already been said that chorea is closely related to 
endocarditis and rheumatism, which diseases we know to 
be due to streptococcemia, thanks to our modern under- 
standing enlightened by the splendid work of Rosenow. 


The foci which are looked for in the streptococcus infec- 
tions (arthritis, endocarditis) are therefore also possible 
foci for chorea, and practical experience confirms this 
supposition. Eustis* mentions two relapses, one of arth- 
ritis and one of chorea following tonsilectomy, and also 
reports another case where a severe relapse of chorea 
followed immediately after the extraction of several 
teeth. These relapses are due to an increased amount of 
bacteria absorbed from the unprotected wound and again 
teaches us to remove such foci one by one with an interval 
of several days between each extraction or operation. 

Case XXIV. (Chorea.) (Eenorted by 
case TRA M ' T ' Schamberg, Journal of the Allied 

Dental Societies, December, 1915.) A 
young girl, about fifteen years of age, was sent to the 
hospital with the following complications of diseases: 
chorea, muscular rheumatism, and a valvular lesion of the 
heart. She was observed in the medical ward and treated 
for some time without material improvement. When she 
was finally sent to Dr. Schamberg's clinic, the jactitation 
and convulsive movements of her body almost interfered 
with a thorough examination of her mouth. Yet, staring 
us in the face was a gold crown upon an upper front tooth. 
An X-ray was made of this part and an infection detected. 
The removal of the tooth and curettage of the bone was 
promptly followed by an improvement in the chorea, and 
at the end of several weeks the patient walked with 
scarcely any evidence of the disease. There was likewise 
such a pronouncd improvement in her other conditions 
that she was considered well enough to be dismissed from 
the hospital. 

Mental depression and melancholia are 
M ^b A i^£iJ-°h ,A diseases or perhaps symptoms of a more 

AND MENTAL , -, x \ -vm i i. 

DEPRESSION or l ess obscure nature. While it seems a 
far cry from oral infections to mental dis- 
eases, we have reliable reports from sincere men who 
have seen profound depression and melancholy disappear 

*Ettstis: Endocarditis in Children. Boston Medical and Surgical Journal, 
September 2, 1915. 


after the treatment or surgical removal of septic foci in 
the mouth. Such cures are convincing arguments that 
chronic intoxications from septic foci are some of the etio- 
logical factors in these conditions. 

Case XXV. (Mental depression with 
CASE oral sepsis as an important factor.) (Re- 

ported by C. Burns Graig.) The patient 
a woman aged fifty-nine, well preserved, and of more 
than average mentality. She came from a long-lived, 
non-nervous stock. The father died three years ago, the 
mother two years ago. During the week of the mother's 
death she had a nasal operation. Soon after this, finan- 
cial losses caused considerable worry. The patient con- 
tinued in reasonably good health for over a year. At 
this time she went to a fashionable sanitarium, more as a 
pleasure resort than for treatment. While there, she 
began to have attacks of dizziness. A physician told her 
she had mild heart disease and prescribed Nauhehn baths. 
After she had taken eleven baths a nervous breakdown 

When first seen, the patient was greatly depressed and 
nearly always in a state of agitation, at other times she 
spoke in a mournful tone without being able to give the 
exact cause of her depression. She said she was con- 
vinced she would not recover. 

Physical examination was entirely negative except 
pulse of 100 and condition of her teeth. Radiograms 
showed two abscesses on the roots of crowned teeth and 
a collection of pus beneath a faulty bridge. The stools 
when examined proved normal, except slight evidence of 
catarrhal colitis. Haemoglobin, 78%. Red blood cells, 
4,869,000. White blood cells, 6,500 ; differential showed 
mild increase in the lymphocytes. Urine normal. A test 
breakfast showed diminution in the hydrochloric acid con- 
tent. A serum Wasserman was negative and the spinal 
fluid was normal in every respect. 

A week of tonic measures was without noticeable im- 
provement. It was then decided to have the bridge work 
removed and the abscesses cured. During the following 


week the cloud began to lift and the patient began to have 
moments of better humor, and saw some possibility of 
looking at the brighter side of things. She was then sent 
to the country for two weeks from whence she returned 
in a comparatively happy state of mind. 

Case XXVI. (Melancholia.) (Reported by Van 
Doom, Dental Cosmos, June, 1909.) The patient, a young 
lady, was referred to Dr. Yan Doom as a case of melan- 
cholia. The patient had as little cause for mental depres- 
sion as one could possibly imagine, of which she was as 
well aware as the doctor. She had wealth, friends, a 
beautiful home, and the education and culture that should 
go with such a happy environment. Examination of 
the mouth revealed nothing serious. Radiographs taken 
by Dr. Lodge revealed a number of teeth with areas of 
absorption about their apices, of the existence of which 
she had not the slightest idea. Some of the teeth were 
extracted, others could be saved by treatment. Within 
a short time after the septic foci in the mouth had been 
removed, the patient was in normal condition. She had 
no recurrence of her melancholia up to the time of the 
essay (about one year). 

9. Diseases of the Joints. 

ACUTE Acute infectious arthritis, or rheumatic 

infectious f ever ? is an acute infection of the joints 
a dtuditic to focal disease. In children, carditis and 
chorea otten occur simultaneously; in 
adults, the systemic infection involves the heart less fre- 

The disease usually starts with irregular pains in the 
joints and slight malaise. There is slight chilliness, the 
fever rises quickly and within twenty-four hours the 
disease is fully manifest. Temperature between 102 and 
104° F. Pulse soft and usually above 100. The affected 
joints are painful to move, soon become swollen and hot 
and present a reddish flush. The disease is seldom limited 
to a single articulation and the joints are usually attacked 


successively. The course of the disease is extremely vari- 
able and depends whether there are also cardiac (endo- 
carditis, myocarditis, pericarditis), pulmonary (pneu- 
monia and pleurisy), and nervous (chorea, meningitis, 
polyneuritis, coma) affections. 

Etiology: The newer methods of bacterial culture 
(Eosenow) have proved the presence of infectious organ- 
isms in the joint fluid, in the synovial membrane and 
proximal lymphnodes where it may always be found dur- 
ing the height of the disease. The organisms belong to 
the diplococcus, streptococcus class. The focus is prin- 
cipally found in the throat (tonsils), nose, and accessory 
sinuses, and the oral cavity. 

Case XXVII. (Acute Infectious Arthritis.) Patient, 
a man, about thirty-four years of age, was sent to me for 
treatment. Had had measles followed by mumps, but no 
other childhood diseases. A month before consulting me 
he had rheumatic swellings and pain in the knees. The 
shoulders were next attacked, and after a short time all 
the large joints became involved. He took electric baths 
but did not improve. 

He was able to walk only with crutches. He showed 
me radiographs which had been taken of his teeth. There 
were areas of lessened density on the right upper central 
incisor and the left upper first molar. The broach which 
the dentist had inserted into the root canal extended 
directly into the antrum and a frontal plate of both an- 
tra showed an opaque area on the left side. I operated, 
opening through the canine fossa ; there was a large ab- 
scess at the floor of the antrum. I extracted the trouble- 
some molar and removed by curettage the diseased bone 
and abscessed areas. The antrum was washed daily. 
Apiectomy was then performed on the central incisor. 

The patient suffered an exacerbation in the knee joint 
and had to stay in bed for three days. After a week he 
started to improve gradually and after seven weeks, when 
the antrum had healed, he was entirely rid of arthritis. 
He walked into my office without difficulty ; his joints were 


Fig. 163 

Fig. 164 

Fig. 165 

Figs. 163, 164 and 165.— Radiographs of Case No. 27. There is 

an abscess on the upper central incisor and upper first molar, 

which infected the antrum causing acute arthritis of all the 



Fig. 166 

Fig. 167. 

Fig. 167 

Fig. 166.— Normal Land. 
-Hypertrophic Arthritis. Note the bo.iy overgrowth of many of the phalangeal joints, 
especially the terminal of the first and fifth phalanges. 


normal. He received no general treatment while I took 
care of him, and the improvement in the condition of 
the joints was wholly due to the removal of the infectious 
focus. (Figures 163 to 165.) 

Hypertrophic arthritis is the term used 
hypertro- by Goldthwaite, Painter, and Osgood for 
arthritis those cases in which the chief lesion is 
an outgrowth of bone in or very near the 
joint, but without destruction of joint tissue as a charac- 
teristic or important change. Most writers agree to 
classify these cases as hypertrophic, except Billings, who 
would deny this condition a class by itself, placing it in 
the group with atrophic arthritis as a result of joint 
infection. (Figure 167.) 

It is a disease of the latter half of life. There is usu- 
ally a history of trauma, or static disturbances. The 
disease does not show a tendency to steady progression. 
There is no true ankylosis, motion is limited only by 
interference of the exostoses. The X-ray shows the pres- 
ence of osteophytic outgrowths and marked marginal 
lipping of the joints. 

Etiology: Painter, who also recognizes the type of 
hypertrophic arthritis, believes it is not due to infection, 
but to a combination of trauma and faulty metabolism. 
gouty Glouty arthritis should not be confused 

arthritis with true gout, for many of the charac- 
teristics are lacking. It is a disease of the 
metabolism which may attack any damaged joint. It 
derives its name from the fact that the bones show the 
small pouched out spots called " Bruce 's nodes," which 
are also found in true gout. (Figure 168.) 

Painter divides the chronic infectious 
chronic IN- type of arthritis into infectious and atro- 
A ^.pQ l p H '^ AND phic. It has been established that the 
arthritis infectious group is found in earlier life, 
while the atrophic type is seen in 
persons of older age. In the Robert B. Brigham Hos- 
pital Painter classified twenty-five cases and showed that 
the average age of the infectious type is thirty-two years, 


of the atrophic type forty-nine years. "It seems, there- 
fore, logical to suppose," says Lawrence, "that atrophic 
and infectious arthritis are but different stages of the 
same process. ' ' The chronic infectious type, which occurs 
in early life, is called Still's disease in children. 

Etiology : Chronic infections and their sequel, atrophic 
arthritis, are much more common and more serious than 
the hypertrophic form. The two main causes of these 
two types are now generally held to be autointoxication 
and infection. (Figures 169 and 170.) 

Autointoxication is by some writers believed the etio- 
logical factor, because many investigators (Phillip, Cole, 
Beattie, and others) failed entirely to demonstrate bac- 
teria in the diseased joints. The toxin material may 
come from any part of the body and may be due either 
to continuous, persistent bacterial activity in some focus 
discharging toxins into the blood (toxemia), or to meta- 
bolic or digestive derangements. 

Bacterial infection of the joint tissue is believed to be 
the cause by other writers, S chillier, Poynton, Paine, and 
before all, Rosenow isolated three organisms belonging to 
the streptococcus pneumococcus group from the joints. 
Each of these organisms is convertible into the other types 
by cultural methods. These bacteria have a characteristic 
low grade virulence and grow best in a low oxygen tension 
and even grow anaerobically. Such a condition is found 
in the infected joints caused by the method by which the 
bacteria invade the tissue ; the vessels supplying the joints 
are closed by endothelial proliferation at the site and 
stimulated by the bacterial embolus. Injected into animals 
they produce arthritis, endocarditis, pericarditis, myosi- 
tis, and myocarditis. Steinharter* undertook such animal 
experiments, injecting staphylococcus cultures into rab- 
bits and dogs intravenously. The material used was pre- 
pared by suspending an agar slant culture in about 10 c.c. 
of normal salt solution. The usual dose of such an emul- 
sion was 1 c.c. for a rabbit and 3 c.c. for a dog. The re- 
sults as shown by the published protocols, indicate that 
the staphylococcus is apt to localize in the joints and pro- 

* See Bibliography. 


Fig. 168.— Gouty Arthritis. Note hypertrophic changes of the phalangeal joints and the 

small areas having a pouched out appearance just posterior to the distal end of the second 

portion of the phalanges, characteristic of gout. 


Fig. 169 

Fig. 170 

Fig. 169. — Infectious Arthritis. Note the periarticular swelling and irregular joint atrophy with 

thinning of the cartilage. 

Fig. 170. — Atrophic Arthritis. Note the general bony atrophic destruction of several joints with 

corresponding deformity. 


duce the typical lesions and symptoms (lameness) of 
arthritis. The organisms recovered from the arthritic le- 
sions have a decided tendency to again localize in joints. 
In some cases the arthritis was the only lesion found at 
autopsy, but in other cases it was associated with duodenal 
ulcer, appendicitis, cholecystitis, myocarditis, pericar- 
ditis, endocarditis, nephritis, colitis, and myositis. ' ' The 
results of localization obtained in connection with studies 
of staphylococci," says the writer, "are singularly sug- 
gestive of Rosenow's results with streptococci." 

The causative focus, is, according to Billings, usually 
found in the head, but may be found anywhere in the 
body. The most important places for infectious foci are 
found in the nose, throat (tonsils), oral cavity, the intes- 
tinal tract, and genito-urinary system. Septic foci may 
occur in different parts of the body simultaneously, as 
the tonsils and the teeth, or the teeth and the intestinal 
tract, and even may have a pathological connection. It 
is rather seldom to find a true condition where, for ex- 
ample, the only foci are found in the mouth, but it is 
evident that the sufferers from chronic arthritis have 
almost always an abundant number of septic lesions in 
the mouth, which without question may have been respon- 
sible for the disease. The lesions in the mouth from 
which haematogenous infection may take place are 
principally the different varieties of abscesses, pyorrhoea 
pockets, and septic bridgework. The streptococcus is 
most frequently found in oral abscesses, as has already 
been mentioned, and septic processes are found in the 
mouth of a very large percentage of people. At the 
Robert B. Brigham Hospital I examined eighty-seven 
patients, from which number seventy-two or eighty-nine 
per cent, had abscesses on from one to thirty-two teeth. 
The seventy-two patients had three hundred and forty 
abscesses and many suffered from pyorrhoea besides. 

Treatment : The treatment consists in general improve- 
ment of the metabolism by suitable diet and open-air 
existence. Then comes the search and removal of all 
possible foci of infection and absorption to eliminate 


radically any source which was originally responsible for 
the disease and may cause reinfection. The removal of 
the focus does not necessarily result in a cure, as the 
secondary joint lesions have developed to a certain extent, 
but it frees the system from the burden of continuously 
taking care of those conditions and gives the patient a 
chance for an effort towards recovery from other diseased 
conditions. Abscesses, as well as other pus conditions in 
the mouth, should therefore be radically removed, not 
only because the system absorbs from them bacteria and 
toxins, but also because many have sinuses into the mouth 
through which pus is discharged, which deteriorate the 
food and cause gastric and intestinal sepsis. It is also 
important to restore the masticatory apparatus to full 
efficiency. The teeth, which are missing, should be re- 
placed by plates or by removable bridge work, because 
it is not fair to expect that the stomach of a weakened 
patient will digest food which has not been properly pre- 
pared in the mouth. Local treatment of the diseased joints 
and consists of hydrotherapy and electric baking and 

illustrative Case XXVIII. (Infectious arthritis.) 
(From a report by Dr. Proctor.) The 
patient, a young girl, aged twenty-one, 
had always been in very good health. As a child she had 
mumps and measles. Has not had scarlet fever, diph- 
theria, or pneumonia. Eleven years ago the patient suf- 
fered considerably from nasal catarrh, with sore throat 
and swelling on the side of the neck. This was operated 
on and discharged for three or four months. Has not 
been subject to colds or sore throats since; the swelling 
on the neck did not recur. No tuberculosis or arthritis 
or carcinoma in the family history. 

On Sunday, August 16, 1914, the patient had an ul- 
cerated tooth (right upper central incisor) which was 
giving her some trouble. The following morning the 
pain had increased and the face was swollen. She went 
to the dentist to have it attended to. He lanced an 
abscess on the gum and gave her another appointment 


for the following Friday, August 21. During the interval 
between these visits the girl suffered very great pain and 
could not sleep nights. The dentist, however, filled the 
tooth with a gold filling and told the girl that she would 
have to expect more or less pain, but that the swelling 
would soon go away. When she went home from this 
visit her face was so swollen that her mother hardly knew 
her. After four or five days the face started to become 
normal and at the same time the left ankle began to get 
stiff, and shortly afterward the right ankle became 
affected, then the elbows and thumbs became stiff and 
swollen. The joints had not been particularly tender, 
but the condition showed a tendency to steady progres- 
sion until the patient could hardly walk on account of 
stiffness and pain. The first physician who took care of 
her thought that her trouble might be due to a run-down 
condition, and as she grew gradually worse under his 
treatment (she saw him two or three times for ten weeks), 
she was advised to consult another physician, who diag- 
nosed her case as infectious arthritis, with the abscessed 
tooth as the causative factor. He sent her to the Rhode 
Island Hospital, where she was admitted November 28, 
1914. Physical examination showed nose and throat 
negative, heart in good condition, lungs clear. Abdomen 
no masses, no tenderness. On December 22, the jaws 
started to get stiff, especially the right side, so that her 
eating was limited to well chopped or soft solid foods. On 
December 28, the terminal joints of the thumbs were 
swollen and a dull grating was produced on manipulating 
the joint. In March, 1915, the patient went home ; at this 
time the girl was perfectly helpless and unable to feed 
herself; she had to stay in bed. Dr. Painter, who saw 
the patient in December, 1915, found all the larger joints 
involved and the small joints of the hands. She was 
unable to sit up and could not move any of her joints 
without a great amount of pain. Figure 171 shows a 
radiograph of her fingers ; Figure 172 shows the condition 
of the devitalized tooth. Dr. Painter ordered massage, 
regulated the diet ; Dr. Proctor performed apiectomy on 


the upper central incisor on December 24, and removed 
the scar tissue, which yielded a streptococcus staphylo- 
coccus culture. The patient improved very much during 
the following three months, she was able to get up and 
go about, the mouth could be opened wider. In April she 
took cold and had a relapse. Dr. Proctor operated on 
her again on April 17, having better access to the mouth 
at this time. The root of the right lateral incisor, which 
was found devitalized, was amputated, and at the same 
time he removed the left lower third molar and second 
bicuspid, which showed abscessed condition. The pa- 
tient improved again and is now able to sit up in a chair. 

Case XXIX. Atrophic arthritis. Patient, a house- 
wife, of sixty-nine years, was admitted to the Robert B. 
Brigham Hospital on July 3, 1914. Had had measles, 
pertussis, scarlet fever and lung fever, when a child. Her 
present illness started two years previous. Both hands 
became swollen. This swelling was white and painless; 
later the feet became affected, and the eyes were inflamed. 
The process subsided slowly and she had not wholly re- 
covered when a second attack was suffered one year before 
entering the hospital. This time the hands, shoulders, 
neck and knees were affected and she has not recovered 
from this attack. Examination showed pupils equal and 
of normal reaction, tonsils not enlarged, throat negative. 
No glandular enlargement in neck, axillae or groin. 
Lungs negative, heart action irregular and systolic mur- 
murs heard at apex and transmitted to axilla. Spleen 
not palpable, kidneys not palpable, abdomen soft and full, 
no masses nor tenderness. 

Diagnosis: Infectious arthritis with atrophic changes. 
The patient received house diet and was kept in bed on 
account of the cardiac condition. X-rays of joints were 
taken. X-rays of intestine with bismuth meal were taken. 
The knees, elbows, and hands showed atrophic changes. 
These were contracted so as to make the patient appear 
as bent over. 

On October 2 the patient was ordered to the hydro- 
therapy room for electric treatment. On April 29, 1915,, 


Fig. 171 

Fig. 171. — Badiographic plates of one hand of Case No. 28, showing atrophic destruction of 
sev ral joints. Note the periarticular swelling. 

Fig. 173 

Pig. 172. — Radiograph showing the bone changes about the incisor which origin- 
ally had caused the infectious arthritis of Case No. 28, the radiograph had been 
taken about sixteen months after the patient had acute symptoms. 

!FiG. 173. — Radiographic plate of Case No. 29, showing areas of disease about the 
roots of the upper first molar and lower first and second molars. 


X-rays of her teeth were taken and showed areas of bone 
absorption on the upper left first molar and the upper 
right second bicuspid. There were also large areas on 
the left lower first and second molars, and the right lower 
second molar. (Figure 173.) 

I extracted the teeth and curetted the abscess cavities. 
After two weeks the patient had more motion in the 
fingers and wrists, although there were still areas of 
swelling and tenderness. Soon after, walking for a few 
steps was successfully attempted. Improvement con- 
tinued, and after three months she was able to walk up 
and down stairs, and made considerable gain in the use 
of her fingers on the piano. At the time of writing, May, 
1916, she is in good condition, up every day, eats and 
sleeps well, walks every day, and has considerable motion 
in her fingers. She will leave the hospital shortly. 



The mode of examination of the mouth is perhaps today 
the greatest shortcoming of the average dentist. The 
patient who trusts his family dentist entirely takes it 
for granted that the dentist's examination is complete 
and thorough, and believes that the mouth has been 
restored to a normal and healthy condition when being 
dismissed. The radiologist's exa min ation reveals many 
unsuspected abscesses in the mouths of patients, to whose 
mouths dentists have given conscientious if mis- 
taken attention. It often takes a good deal of explana- 
tion to righten the dentist's position in such cases and to 
sooth the patient's anger at having been deceived. While 
the dentist, of course, is not to blame for conditions which 
have been caused and have developed without his knowl- 
edge, the situation must be properly explained. The 
patient will be quick to realize that the dentist had only 
the best intentions in trying to save every tooth as an 
important organ of mastication and that he surely is not 
to blame for not having been able to accomplish the im- 
possible in correctly treating many abnormally devel- 
oped teeth and obstructed root canals, and for not know- 
ing that such dangerous septic conditions can exist in 
his patient's mouth without giving any symptoms. But 
today, with our modern means of examination, where 
X-ray machines are especially adapted for our purposes 
and where radiologists are to be found in almost every 
street, where there are professional men, there is no 
excuse for a dentist to neglect to ascertain the condition 
of all devitalized teeth in his patient's mouth. But he 
who only fills cavities, constructs bridges and makes 


♦ -w 

Fig. 174 

Fig. 175 

Fig. 176 

Fig. 177 

Fig. 178 

Fig. 179 

Fig. 174, 175, 176, 177, 178 and 179. — Radiographs of a mouth showing a large amount 
of crown and bridge work of recent date and a great many abscess areas. 


Fig. 180 

Fig. 181 

Fig. 182 

Fig. 183 

Fig. 184 

Fig. 185 

Figs. 180, 181, 182, 183, 184 and 185. — Radiographs of a neglected mouth showing 
broken-down teeth and abscess areas. 


plates and neglects other abnormal or diseased conditions 
which the patient does not particularly complain of, 
renders poor service to the public. The dentist is the 
man who has charge of the mouth and he has a great 
responsibility. It would put the dental profession back 
to the age of the mechanic should we undertake to con- 
cern ourselves only with mechanical restoration instead 
of investigating and treating every disease found in the 
region of our domain. What would we think of an 
ophthalmologist who would only correct abnormal condi- 
tions of the lens and would pay no attention to co-exist- 
ing iritis or other inflammatory diseases of the eye % But 
we find exactly parallel cases in the practice of many 

The physician often has occasion to in- 
method OF quire into the condition of his patient's 
P^fh.K. A-n.sN*. mouth, especially when in search of a 

EXAMINATION # i • A ' n t 

for the iocus or ioci oi the disease concerning 

physician which the patient is consulting him. Some 
medical men still have the idea that the 
mouth is a thing apart from the body which cannot have 
any influence upon the general health, others are too easily 
satisfied with the patient's statement that the dentist is 
visited regularly and that there is absolutely nothing 
wrong with the teeth, but the thorough physician will not 
be satisfied except with a report based upon a careful 
examination and radiographic diagnosis made by a den- 
tist or radiologist in whose judgment he can trust. 

A superficial examination of the mouth by the physician 
should include the following : 

1. Examination of the soft tissues of the mouth. The 
tongue, floor of the mouth, palate and gums should be in- 
spected. Stomatitis is easily detectable and in pyorrhoea 
the gums are inflamed and spongy, and pus can be 
squeezed out from underneath the gum. 

2. Examination of the teeth. Neglected teeth can be 
recognized at a glance ; there are many cavities and broken 
down teeth causing abscesses with or without visible 
sinuses on the gum. 


Overdentristried teeth are of a most deceiving nature. 
Teeth of dark appearance, gold and porcelain crowns and 
bridges always come under suspicion, because these are 
generally signs of devitalized teeth, and it makes no 
difference whether the gums are inflamed or normal, with 
no sinus, and no symptoms of inflammation whatever. 
Radiographs should be secured of such teeth as this is the 
only means of finding out their condition. 

Impacted and unerupted teeth should be investigated 
by the X-ray. If some teeth are missing and the patient 
does not remember that they were extracted it is possible 
that they are in malposition and cause disturbance. 

3. Enlarged Lymph Glands. If the submental or sub- 
maxillary lymph glands are enlarged, it is almost always 
a sign that some septic process is going on in the mouth. 
Abscesses, however, may occur without the involvement 
of the glands. 

The old method of dental examination has 
METHOD OF already been criticized in the first part of 
°v^h.*,A-n,Mu this chapter. But worse than the method 
for™ he of examination is the way the dentist 

dentist keeps his records. The card systems and 

books which are on the market are abso- 
lutely inefficient, for besides a place for bookkeeping they 
provide only for records of the fillings placed in the teeth 
and the crowns and bridges made for the patient. There 
is no arrangement that provides for the marking of root 
canal operations, for indicating abscess and pyorrhoea 
conditions, not to speak of other diseases which may be 
directly or indirectly connected with the conditions found 
in the oral cavity. 

The dentist should inquire into, examine and record the 
following conditions : 

..„_. 1. General Health of the Patient. The 

examination dentist should inquire into the general 

condition of the patient's health and if a 

history of systemic disease is found in connection with 

septic processes of the mouth, the patient should be en- 


Fig. 186 

Fig. 187 

Fig. 188 

Fig. 189 

Fig. 190 

Fig. 191 

Fig. 192 

Fig. 193 

Figs. 186 and 187, 

-Badiographs revealing deep cavities causing obscure pain, 
distal side of the first molar. 

Both on the 

Fig. 188. — Badiograph shows a large amount of unsuspected trouble. 
Figs. 189, 190, 191, 192 and 193. — Badiographs showing the value of X-rays before undertaking 
root canal work. In Fig. 189 note bent apex of second bicuspid with gold crown. In Fig. 191, 
cuspid with root bent at right angle. In Fig. 192, the foramina of some teeth are still widely 
open. In Fig. 193 there is a pulp stone in the pulp chamber of the first molar. 


Fig. 194 

mm i 

Fig. 195 

Figs. 194 and 195.— Radiographs of a mouth which was examined for foci and report chart 
indicating the granulomata and root canal fillings. 


couraged to consult a physician, whose cooperation should 
be secured to find out whether there is any connection 
between the two conditions and what further treatment 
besides the treatment of the oral condition could be of 
benefit to the patient. 

2. Diseases of the Soft Tissues. The tongue, palate, 
floor of the mouth and gums should be examined next. 
Abscesses, ulcers, cancers, gummata, palatal perforations 
and clefts, benign and malignant tumors, cysts, diseases 
of the salivary glands and ducts, inflammation of the 
throat, stomatitis and pyorrhoea may be noticed. 

3. Diseases of the Teeth. Malocclusion should be no- 
ticed in children, missing teeth and lack of masticating 
efficiency in adults. Cavities may be in plain view or may 
only be discovered after most careful exploration. If the 
patient complains of pain the teeth should be tested to 
find out diseased conditions of the pulp. Applications 
of ice or hot instruments to the various teeth, as well as 
the galvanic or high frequency current are useful aids 
to diagnosis. Acute periodontitis is recognized if a tooth 
is tender and pain is caused on percussion, acute abscesses 
and parulis are noticed in like manner, the latter causing 
noticeable swelling of the face and gum. Sinuses on the 
gum without complaint of pain and tenderness lead to 
chronic abscesses caused by devitalized teeth, and all de- 
vitalized teeth whether they cause apparent trouble or 
not should be recognized ; these are usually darker in ap- 
pearance, have large fillings or large cavities, porcelain 
crowns or gold crowns which may also serve as abutment 
of bridges. Such teeth should be radiographed to find 
out the periapical condition and the quality of the root 
canal fillings. Finally, the dentist should be on the look- 
out for impacted and unerupted teeth, which usually 
sooner or later become a source of serious trouble. In 
children they may cause malocclusion ; in adults, various 
abnormal and diseased conditions, as we have already 


It is impossible to make a thorough exam- 
graphic ination of the mouth without the use of 

examination radiographs in patients who have devi- 
talized teeth. If the dentist has not 
an X-ray machine of his own, he can easily secure 
radiographs of the suspected teeth from a dental 
radiologist, who will not only take the radiographs, 
but will also give valuable advice as to the in- 
terpretation of the pictures. It is indeed a great ad- 
vantage to be able to consult a man who as a specialist 
sees many cases and therefore has a much greater expe- 
rience in radiographic diagnosis than the general prac- 
titioner, and the fee for such services with the modern 
improvements has been reduced to a level which is in the 
realm of almost every person. 

Radiographs are principally taken to find obscure 
causes, to ascertain physical diagnosis, to diagnose ob- 
scure conditions, to prognose the outcome of therapeutic 
measures, the possibilities of treatment and the course of 
surgical technique. 

1. Obscure pain may be diagnosed by means of radio- 
graphs and found to come from decay under the gingival 
margin or under fillings, from impacted and unerupted 
teeth or cysts and acute abscesses. 

2. Diagnosis of Condition of Devitalised Teeth. The 
use of radiographs to find out the conditions of pulpless 
teeth has revolutionized the attitude towards devitaliza- 
tion of teeth. It made us realize the difficulty and value of 
good root canal fillings and the consequences of neglect 
and inability to perform perfect root canal work. Radio- 
graphs show whether the root fillings reach the apex or 
whether the canal is only filled part way. Broken root- 
canal instruments are detected as well as perforations at 
the side. The apex may show a ragged appearance, which 
is a sign of necrosis of the root ; or it may appear enlarged 
and bulging on account of exostosis of the cementum. 
There may be an area of lessened density around the apex 
showing loss of bone ; this indicates an abscessed condition 
or a granuloma. Similar areas occur sometimes on the 


f i I /i 

( ffl ( 

) h 



Fig. 196. — Eeeord chart as used by Dr. Potter and reproduced with his permission. 



side of a root or between the roots of multirooted teeth. 
There may also be absorption of bone at the cervical part 
of the alveolar process surrounding the bone, indicating 
pus pocket. 

3. Prognosis Before Boot Canal Treatment. It is of 
great importance to make sure of the probable outcome 
before involving the patient in lengthy and expensive 
root canal treatment. The radiograph may show normal 
canals, open apical foramina, accessory foramina, bent 
and curved roots, inacessible canals on account of sec- 
ondary dentine, pulp stones or broken root-canal instru- 
ments. Abscess formation and necrosis of the apex may 
be discovered which would indicate the necessity of sur- 
gical interference and generally gives an idea whether a 
tooth can be saved or not, whether the root canals can be 
treated with medicines, and the canal filled to the apex, 
whether apiectomy is practical and indicated to save the 
tooth or whether the tooth has to be extracted. 

All these findings should be recorded on a 
charts CASE chart. Professor William H. Potter, who 

realized the shortcomings of the ordinary 
dentist's examination charts, took much pains in arrang- 
ing a practical chart on which all dental conditions can 
be marked down. Figure 196 shows an examination re- 
corded on his chart. The plates also have historic 
interest: they are copies of originals from Carabelli*. 
The back of the chart is arranged for book-keeping. 

Similar but simpler charts have been made up by the 
author for reports of radiographic examination. This is 
sent with the radiographs and gives the dentist a better 
idea and clearer picture of the condition of the whole 
mouth, which can be verified by the radiographs. In this 
chart the radiologist can interpret the radiographic 
findings so that they are plainly visible. Such a chart 
is seen in Figure 195. 

* Carabelli : Die Anatomie des Mundes. 



The treatment of oral abscesses varies with the ana- 
tomical location and with the condition of the inflamma- 
tion. The treatments of the various conditions will be 
discussed under the following headings : 

1. Treatment of acute and subacute conditions. 

2. Treatment of chronic conditions. 

3. Treatment of abscesses due to diseases of the gums. 

4. Treatment of abscesses from impacted and un- 
erupted teeth. 

5. Treatment of abscesses of the tongue. 

6. Treatment of abscesses of the salivary glands and 

7. Treatment of systemic conditions. 

1. Treatment of Acute and Subacute Conditions. 

In treating acute conditions we should carefully differ- 
entiate between acute and subacute inflammation. In 
acute inflammation, especially in the beginning stage 
where there is little destruction of tissue, the tissue reacts 
easily to treatment and complete regeneration is possible. 
In subacute cases, however, a chronic condition has pre- 
viously existed, the root may be necrosed, and the reaction 
of the tissue is therefore not sufficient to produce com- 
plete recovery when the acute symptoms subside. The 
inflammation passes back into the quiescent and persis- 
tent chronic stage. It is therefore important to diagnose 
the cause correctly, and distinguish between the acute 
condition which occurred as a primary infection of the 
periapical tissue, from an infected pulp, and the subacute 


condition, which can be recognized by the history or by a 
radiograph showing that the root canal had been treated 
or filled previously. In the subacute cases, extraction is 
indicated unless the conditions are favorable for apiec- 
tomy, but before this operation can be performed, the 
same treatment is indicated as for the acute conditions 
until the symptoms quiet down, when the tooth can be 
filled and surgically treated. 

Acute periodontitis sometimes can be 
the cause topped and extensive alveolar abscess 

prevented by prompt removal of the 
cause. In the later stages of acute abscess it is of equal 
importance to eliminate the causative factor, which is a 
suppurating pulp. When opening into the tooth use a 
good sized round burr, holding the tooth firmly by making 
a plaster cast for each side, so as to decrease the jarring 
and to prevent further irritation. If there is much pain, 
conductive or general anaesthesia is indicated. Remove 
the largest part of the pulp in a gentle manner so as not 
to press infected material through the apical foramen. 
If the radiograph indicates that abscess formation 
has already begun, it may be advisable to enlarge 
the root canal and apical foramen so as to get reasonably 
free access to the abscess. All this is done under aseptic 
precautions. A mild antiseptic dressing is placed into 
the tooth, such as : 

Buckley's Modified phenol: 

Mentholis gr. xx 

Thymolis gr. xl 

Phenolis F3 iij MX 

Black recommends : 

01. cassiae 1 part 

Phenolis 2 parts 

01. gaultheriae 3 parts 

Mx oils and add melted crystals of phenol. 

Close the opening of the tooth with cotton dipped in liquid 
petroleum ; this prevents saliva from entering, but allows 


gases which may be formed in the canals to escape. 
Change the dressing daily until the tooth feels more com- 
fortable, when the dressing can be sealed into the tooth 
with base plate gutta percha. After the root canals have 
been cleaned and sterilized, they should be filled, so as to 
seal the apical foramina hermetically. Only by scru- 
pulous asepsis, careful treatment and technique can re- 
currence or chronic continuation be prevented. This tech- 
nique will be described in the chapter on prevention. 

To avoid further irritation the affected 
d Leased™ E e l° n g a ted tooth should be put at rest. 
tooth This is best done by building up the occlu- 

sial surface of all the teeth of one jaw 
with copper cement except in the position of the tender 

Counter-irritants are beneficial to help 
of counter^ a ^ sorD the abscess. Apply on both sides 
irritants °^ ^ ne g um > over the affected root, tincture 

of iodine, tincture of iodine and aconite, 
or chloroform; these are the most common counter-irri- 
tants. They should be applied to the dried mucous mem- 
brane. Suction cups containing counter-irritants are 
applied on the gum opposite the apex of the root. 

In some cases of acute abscess, we can 
latomy £ a ^ n sufficie^ drainage through the root 

canal to affect a cure. This is true for 
upper teeth if treatment is started before the destructive 
process has progressed too far. In lower teeth this is al- 
most impossible, because the process is not aided by gravi- 
tation. The abscess in the mandible is also of much more 
severe nature, more pain is produced, and a longer time is 
required, because of anatomical conditions, till the pus 
burrows an opening through the bone to the surface. 
Great relief and good drainage can be secured by an arti- 
ficial opening through the alveolar process. Under con- 
ductive or general anaesthesia we incise the gum, retract 
it to both sides, and with a large round burr drill through 
the process to the apex of the tooth. The opening should 
be made at the lowest level. The root canal can be opened 


at a future sitting, though I prefer to do it at once. If the 
apical foramen can be penetrated, irrigation through the 
tooth is indicated. Normal salt or mild antiseptic solu- 
tion should be used. Put a mild antiseptic dressing into 
the tooth, as already described, and a wick into the arti- 
ficial sinus to prevent premature closing of the wound. 
I prefer to use a cigarette wick made of rubber tissue; 
this does not disintegrate. The abscess should be irri- 
gated daily until no more pus is discharged, when the 
root canal can be filled. The wound should heal from the 
bottom ; this is accomplished by shortening the wick. If 
suppuration persists we must ascertain the cause. Usu- 
ally this comes from necrosis of the tooth and can only be 
cured by amputation of the diseased part. 

In cases presenting a subperiosteal or subgingival paru- 
lis, an early incision will quickly relieve the pain. The 
pus, which has already penetrated the outer plate of the 
bone and collected in large quantity under the periosteum 
or gum, cannot be expected to drain back through the 
bone and root canal of the tooth. Therefore we should at 
once, under conductive or general anaesthesia, secure a 
large incision at as low a level as possible. In case of 
subperiosteal parulis, which is particularly liable to cause 
extensive necrosis, especially if it is of long duration, this 
incision should be very extensive so as to give free drain- 
age. Some authors recommend leaving the tooth alone 
until the acute symptoms have subsided, but I prefer to 
remove the cause at once. If conductive or general an- 
aesthesia is used, this may be effected when the abscess is 
incised. An opening should be drilled into the tooth and 
the bulk of the diseased pulp is removed. The incision 
is made on the gum as described. The pus should be taken 
up with a sponge, especially under general anaesthesia. 
The point of a piston syringe or fountain syringe is in- 
serted into the root canal and the whole area is washed 
out thoroughly with normal salt or mild antiseptic solu- 
tion. Under general anaesthesia this solution should be 
taken up by sponges and not left to run into the mouth. 


Under conductive anaesthesia the management is much 
simpler and the whole treatment can be done more success- 
fully. The incision should be kept open by means of a 
wick made of rubber tissue, and the washing should be 
repeated until the discharge of pus stops. The opening 
in the tooth can be closed temporarily after an antiseptic 
dressing has been placed into the root canal. After the 
root canal has been cleaned and sterilized it can be filled, 
and if this is correctly done, the abscess will not recur or 
continue as a chronic lesion unless the periodontal mem- 
brane has been destroyed at the apex of the root or become 
necrosed during the period of suppuration. In such 
cases we have to resort to apiectomy or extraction. 
extraction ^e most radical, but usually also the 
quickest relief is extraction of the offend- 
ing tooth. If the patient's resistance is low so that a 
speedy healing by the application of any one of the above 
methods cannot be expected, or, if high fever or com- 
plications set in, it is almost always advisable to resort 
to more radical means. If extraction is decided upon, it 
should be undertaken at once, because nothing is gained 
by waiting. It is an erroneous idea that a tooth should 
not be extracted during the acute stage. Nothing gives 
a more spontaneous result than elimination of the cause 
and establishment of drainage through the alveolar 
socket. The extraction should be performed under 
general or local conductive anaesthesia. Spray the mouth 
thoroughly and paint the tooth and surrounding gum 
with iodine to prevent secondary infection. The extrac- 
tion should be followed by curettage, after which the 
wound is freely irrigated, treated with iodine, and lightly 
packed with gauze. Antiseptics and anodines can be ap- 
plied on this dressing; iodoform, orthoform, or the fol- 
lowing preparation is of benefit : 

Eur of orm paste : 

Orthoform 40 

Europhen 60 

Add liquid petroleum to make a paste. 


The wound should be irrigated daily and granulation 
should be allowed to fill the cavity from the bottom. An 
antiseptic mouth wash should be used freely and often 
and held in the mouth for five to ten minutes at a time. 
If the socket does not fill in with granulation tissue 
speedily it is advisable to procure a slight hemorrhage 
with a sterilized instrument. The socket is then filled 
with a blood clot which organizes in a very short time. 
In cases where the disease has progressed to the stage of 
parulis, an incision should be made on the gum in addi- 
tion to the extraction and communication established from 
the gum to the socket. Curette the diseased process and 
irrigate profusely. The socket is treated with tincture 
of iodine placed into the wound of the gum to drain the 
abscess and permit the socket to fill in with a blood clot. 
The dressing is changed every day until suppuration is 
stopped, when the wound is left to heal. 

For Palliative Effect. A hot foot-bath 
treatment an( ^ cathartic should be ordered. Pre- 
scribe the foot-bath as follows : A tub is 
partly filled with warm water and the feet immersed. 
Hotter water is added to raise the temperature of the bath 
to the greatest degree that can be tolerated. Powdered 
mustard may be dissolved in warm water and added to the 
foot-bath. (Do not dissolve the powder directly in the 
hot water; it would defeat the action necessary to pro- 
duce the irritant volatile oil.) Keep the feet in the water 
five to ten minutes. The effect is dilation of the blood 
vessels in the lower extremities, reducing the blood pres- 
sure in the head. After the foot-bath the feet should be 
thoroughly dried and the patient should go to bed, which 
has been warmed beforehand. It is essential not to step 
on a cold floor with the bare feet, or to chill the feet in 
any way, because this would contract the vessels again 
and spoil the effect. 

For a cathartic prescribe castor oil in gelatine capsules. 
Six 2y 2 gram capsules should be taken before retiring. 


Other laxatives are: 

Tab. Caseara Sagrada a.a. 0.3 chocolate coated. 
Sig. One to two tablets before retiring. 


Aloini gr. 1/5 

Strychnia gr. 1/120 

Ext. Belladonna Fol gr. 0/8 

S. Take one to two pills before retiring. 
An alternative may also be given in certain cases : 

Potassii iodidi 6.0 g. — 3 jss. 

Syrupi sarsaparillae comp. 90.0 — f3 iij. 

Sig. Take a teaspoonful in water every 2 hours 
till 3 doses are taken, then a teaspoonful after meals. 

For Belief of Pain. Phenacetin and aspirin have 
been found by the author the most effective antipyretic 
for pain in the trigeminal region. Give gr. V of each and 
repeat after one hour if necessary. Trigeminin gr. V or 
pyramidon gr. II s.s. sometimes prove of value. To tide 
the patient over a very severe attack or to give a night's 
rest a hypnotic may be used. Tab. Bromural (Knoll & 
Co.) a.a. 0.3 (gr. V) two to three tablets before retiring 
should be given. In extreme cases : 

Morphiae sulph 0.015 gr. 14 

Kalii Bromid 2.0 gr. xxx 

Aquae 30.0 3i 

Sig. One half to be taken at once ; balance in three 
hours, if needed. 

For prompt relief give % or % E r - morphine hypo- 

Diet. Order a light, easily digestible diet which is 
strengthening at the same time. 


treatment "^ a smus ^° ^ ne ^ ace exists we always 
of sinus have to resort to extraction of the respon- 

TO face s ^ e tooth. The discharging of an ab- 

scess in the face is often invited by 
poultices or hot applications to the face. This should be 
avoided; poultices if used should be applied to the gum 
and cold applications only to the face. If a sinus exists 
it should be curetted and washed. After extraction of 
the tooth and curetting of the diseased area the sinus will 
close up speedily; unfortunately, however, not without 
leaving a permanent mark. This scar can be improved 
somewhat by excision of the fibrous connection which 
fixes the skin to the bone and closing of the wound by a 
plastic operation. 

2. Treatment of Chronic Condition. 

Chronic abscesses in all stages are of very persistent 
character and the fact that they cause none of the car- 
dinal symptoms makes it extremely hard to ascertain in 
a general way whether the lesion is yielding to treatment 
or not. Even the radiograph for this special purpose 
is not always a safe means of finding out, because lighter 
and darker shadows, smaller and larger areas can be 
obtained by variation in the exposure, the quality of the 
ray, the depth of the development and the angle at which 
the exposure is made. Generally we may say that as long 
as there is any area of lessened density at all and as long 
as the root end is necrosed we cannot claim to have cured 
the abscess. 

Antiseptic treatment of chronic abscesses has for a 
long time been the treatment per se. A large number of 
drugs have been and still are in use. They are either 
forced through the apical foramen but more frequently 
are only applied into the root canal of the tooth by 
means of cotton dressings, and it is left to their power of 
evaporation to penetrate into the diseased periapical 
tissue and cure the abscess. Ionic medication has been 
recommended to carry the antiseptic into the diseased 


tissue. Careful experiments with these methods and a 
variety of drugs proved to my satisfaction that there is 
today no antiseptic known that has sufficient penetrating 
and sterilizing power to destroy bacterial life completely 
in the periapical granulomata. I have treated blind ab- 
scesses of medium size from the root canal with all known 
methods and found such treatment extremely uncertain, 
if not entirely insufficient. Grieves,* whom I consider 
one of the most thorough investigators, makes the follow- 
ing statement about treatment of pericemental condi- 
tions: "There is to my knowledge no medicament nor 
method, germicidal, oxydizing or electrolytic, that will 
revivify the pericemental apex. If it be vital, the tooth 
is healthy ; if it be diseased, the tooth is next to doomed. 
This is the point in treatment where materia medica stops 
and good surgery begins. ' ' 

This is exactly my opinion, based upon histopatho- 
logical study, as shown in Chapter VI, and investigations 
especially undertaken to study the value of the different 
popular methods of medication. 

Original Investigation of the Efficiency of Medication 
for the Treatment of Granulomata. 

Five teeth in different patients have been used for ex- 
periments. All cases showed an area of about pea 
size and were of long standing. I first used antiseptic 
dressings until there was no more odor. Teeth 1 and 2 
received no further treatment. Teeth 3 and 4 received 
zinc ions, milliampere for ten minutes on two different 
days, the fifth tooth received iodine ions % to 1 milliam- 
pere for fifteen minutes on two days. Tooth 1 was ex- 
tracted ; on tooth 2 apiectomy was performed. Cultures 
were made both from root apex and abscess and showed 
bacterial growth. Tooth 3 was extracted. No growth 
from the root apex, slight bacterial growth from the ab- 
scess. Apiectomy was undertaken on tooth 4 and bac- 

* Grieves, C. J. : Dental Periapical Infection as the Cause of Systemic Disease. 
Dental Cosmos, January, 1914. 


terial growth was received from both abscess and root. 
Tooth 5 was also a case of root amputation; the abscess 
yielded a culture of staphylococcus albus and a few very 
small chains of streptococci. 

Another case showed the inefficiency of ionic medica- 
tion in the treatment of the chronic abscess ; Mr. R. suf- 
fered with arthritis and especially complained of toxemia 
and decreased mental capacity. He had to stop smoking 
as the system was not able to take care of the nicotine. 
From radiographic examination I concluded that there 
were chronic abscesses on left upper first and second bi- 
cuspids and proliferating periodontitis on the left upper 
cuspid. The root canals were carefully cleaned and 
treated with medicines, zinc ions were used twice and 
iodine ions once, then I filled the canals. Much care was 
taken in condensing the root canal fillings which resulted 
in forcing the root canal cones through the foramina. 
During the treatment the patient received great relief 
and finally got rid of the systemic conditions, his head 
was clear in the morning, and he was especially pleased 
that he could again smoke "like a chimney." After five 
or six months he returned, however, saying that his old 
symptoms were returning. I delayed treatment for four 
or five weeks longer, when he was almost as bad as before. 
Radiographs showed about the same amount of decreased 
density about the two bicuspid roots. Apiectomy was per- 
formed and cultures procured. These yielded a bacterial 
growth and the symptoms disappeared almost entirely 
several days after the operation. 

From these observations I conclude that in cases where 
we do not deal with a purely local condition, but where 
the patient's health is involved, more radical treatment 
than medication is recommendable. 

A chronic alveolar abscess or granuloma looked at from 
the viewpoint of the bone instead of the tooth is, as 
already mentioned, an osteomyelitic condition; the dis- 
ease occurs in the bone and at the expense of the bone, 
and the only reason why the disease does not spread more 


easily is due to the abundant blood supply of the jaws and 
the protecting reaction of the tissues which form a fibrous 
layer at the periphery of the lesion enclosing the seat 
of suppuration. In cases where there is necrosis of the 
root, and necrosis occurs in most all roots surrounded for 
a long time by chronic inflammation, it is impossible to 
cure the condition without getting rid of the diseased 
part by surgical means. In cases where the disease has 
not progressed beyond the apical part, the usual condi- 
tion, we can separate the necrosed part of the tooth sur- 
gically and curette the bone, which will induce prompt 
healing of the condition. This operation permits us to 
extirpate the abscess radically, remove the necrosed root 
end surgically, and still save the tooth. 
removal of J ^ so ™ c ^ ron ^ c di seas e it is imperative to 
the CAUSE remove the primary cause. The principal 

cause of proliferating periodontitis and 
granulomata is the condition of septic and imperfectly 
filled root canals. Our aim therefore ought to be to 
thoroughly cleanse the root canal and remove all infected 
tissue. Root canal treatment and root canal filling are 
operations which require considerable skill and patience. 
The technique will be described in the chapter on pre- 

Antiseptics applied into the root canal 
treatment have, as already discussed, been used for 
with anti- a i on g time to render the tooth aseptic. 
placed ■*■ ^° no ^ think that they ever were meant 

into the to be used for treatment of chronic ab- 

ROOT canal scesses, and their insufficiency for this 

purpose has already been enlarged upon, 
but it may be wise to say also that formaldehyde, 
either alone or combined with other drugs, has never 
been meant to be the cure of all pulp and periapical dis- 
eases. Dr. G-. Y. Black has described at length its irrita- 
ting action and its power of destroying periodontal mem- 
brane, and Buckley himself has stated that formaldehyde 
acts only on the surface and has no penetrating power. 



Ionic medication is advisable in all those 
cases of short standing where the prolif- 
eration of the periodontal membrane is of 
small extent and where the apex has not been affected by 
necrosis nor the periodontal membrane destroyed. The 
effect of ionic medication is to distribute into the sur- 
rounding tissues the antiseptic placed in the root canal. 
The dentinal tubules, as well as accessory foramina, are 
sterilized by this method, which prevents later reinfec- 
tion. The therapeutic action depends on the drug used ; 
zinc, copper, silver, and iodine are most commonly em- 

Zinc Ion. A zinc electrode is used with a three per 
cent, solution of zinc chloride applied on a few fibres 
of cotton. Place the zinc broach into the root canal. 
The positive pole is used in the tooth, the negative pole 
is held in the hand, or applied to the cheek, and one-half 
to three milliamperes are applied for from five to fifteen 
minutes. The action of zinc chloride is tissue destruc- 
tive. It is used by some men to destroy the granuloma, 
which is then thought to be resorbed. 

Copper Ion. A two per cent, solution of copper sul- 
phate is used with a copper anode on the positive pole. 
One milliampere seems to give a good dissociation of ions. 
Its action is similar to zinc chlorid. 

Iodine Ion. Tincture of iodine is used and applied 
on the negative pole, preferably on an iridium platinum 
electrode. Use one half to three milliamperes for five to 
fifteen minutes. To be safe the treatment should be 

Action of Antiseptic Ions. The effect of ionic medica- 
tion is to distribute the antiseptic deeper into the tissues. 
Its action is destructive to bacteria. The zinc ion seems 
to be the most effective, but like the copper ion, it seems 
to have a decidedly irritating and tissue destructive, if 
not escharotic or caustic effect. Symptoms of swelling 
and pain have been observed after the treatment in several 
cases by the author, and for this reason the iodine ions are 
more commendable. It has only a bactericidal action 


and does not destroy the tissue, and is well known as the 
great antiseptic. I have used an aqueous solution of 
iodine lately. It has all the iodine properties minus the 
irritating action, and also penetrates more profusely in 
moist tissue. Ionic medication with iodine is of great 
importance for root canal sterilization and is to be highly 
recommended for routine practice to sterilize in a proper 
way the dentinal tubules and accessory foramina of a 
tooth, as will be described in the chapter on prevention. 
apiectomy Apiectomy is an operation by which we 
can positively eliminate a chronic abscess 
without sacrificing the tooth. It is the only sure method 
of treatment if the apex of the root is diseased, if the 
apical periodontal membrane is destroyed, if the root 
canal cannot be treated and filled to the very end, if the 
side of the root has been perforated near the apex by a 
root-canal instrument, or if an instrument has been 
broken off in the end of the root. It can also be per- 
formed on teeth that carry crowns or bridges if the root 
canal is accessible and properly treated and filled previous 
to the operation. Not all teeth, however, are favorable 
cases. The operation is impossible on third and almost 
always on second molars. The first molars are frequently 
accessible, and all the remaining teeth can easily be 
operated upon. 

The operation consists in opening through the side of 
the alveolar process, amputation and removal of the dis- 
eased root apex and thorough curettage of the diseased 
bone. It is a strictly aseptic, surgical operation. 

Radiographic examination: A careful examination of 
the condition of the occlusion and a study of the length 
and shape of the root by means of a good radiograph is 
imperative. The condition of the root canal should be 
investigated ; from the radiograph we can judge how well 
we shall be able to fill it. Observe also the position of the 
neighboring teeth and how much alveolar process to hold 
the tooth there will be left after the operation. A tooth 
with pyorrhoea or with an apical periodontitis extending 
almost to the alveolar border is not a favorable case, be- 


Fig. 197 

Fig. 198 

Fig. 199 

Fig. 200 

Figs. 197, 198, 199 and 200.— Apiectomy, on the left upper cuspid. Fig. 197 shows incision, 

Fig. 198 gum and periosteum retracted, Fig. 199, cutting of a window into the alveolar process 

to expose the root end, Fig. 200, the root end and granuloma exposed. 


Fig. 205 

Fig. 206 


Fig. 207 

Fig. 208 

me none cavity Figs 206 and 207 show the first horse-hair suture Fio- 208 
shows the completed operation. 


cause after the operation there would not be enough 
periodontal membrane or bone left to give firm attach- 
ment to the tooth ; neither should a tooth be operated on 
if the tooth next to it has also a chronic abscess which 
will either directly or indirectly reinfect the healing 

Treatment of the Root Canal. Apiectomy is only suc- 
cessful if the root canal has been sterilized and properly 
filled previous to the operation. It is not sufficient 
simply to amputate the root where the old filling ends ; but 
the root canal and dentinal tubules have to be sterilized, 
or there will be reinfection from the tubules exposed 
where the root is cut. If it is not worth while to remove 
a crown and treat the root canal, the tooth should be ex- 
tracted or there will be recurrence (with or without 
symptoms) and the patient is as badly off as before. It 
is not justifiable to leave a crown on a tooth because it is 
a masterpiece of art, if the foundation upon which it is 
built ruins the patient's health. The root canal should 
be rendered aseptic by application of antiseptics or by 
ionic medication. It should be filled with the rosin-chlo- 
roform-gutta-percha method, which has the advantage 
of making the point adhere firmly to the root canal. Dr. 
William H. Potter, Professor of Operative Dentistry, 
Harvard University Dental School, inserts root canal 
fillings with pure lead points. That pure lead is accep- 
table to the tissue has been proven by the encapsulation 
of bullets in almost any part of the body. It has the 
advantage of being burnishable from the abscess cavity, 
of not disintegrating, and of safely staying in place dur- 
ing root-canal reaming for fitting of a post and crown. I 
use the following method for lead fillings : Dehydrate the 
root canal with acetone and hot air, dry with electric root 
canal dryer until the patient feels the heat. Fill chloro- 
form and resin (dram I to gr. IY) with a sub-Q syringe 
into the canal and insert a gutta-percha point or cone, 
pumping it forty times up and down. Remove the re- 
mains of the point and insert a lead cone, previously steri- 
lized by boiling it or immersing it for five minutes into 


phenol and five minutes into alcohol. Condense the filling 
as well as possible with root filling condensers so that it 
adapts itself to the walls. Any filling or crowning of the 
tooth is performed before the operation so as not to dis- 
turb the healing process. 

Preparing the Patient for the Operation. If local an- 
aesthesia is used, it sometimes is necessary to use pre- 
operative treatment, especially in nervous, apprehensive, 
and hysteric patients. Bromural-Knoll (alphabrom- 
isovaleryl urea) is an excellent sedative; one tablet is 
given to children, two to adults (in water thirty minutes 
before the operation), or ^4 gram of morphia hypoder- 
mically one hour before the operation. 

Preparing the Field of Operation. The mouth should 
be sprayed out with an antiseptic solution, and the mu- 
cous membrane should be cleaned with a cotton roll in the 
area where we intend to operate. 

Anaesthesia. Local anaesthesia, applied by the im- 
proved technique* with novocain suprarenin is best 
adapted for this operation. The amount of suprarenin 
should not be too large, because too much local anaemia 
is undesirable, making it almost impossible to procure 
enough hemorrhage at the end of the operation to fill the 
bone cavity with blood. 

Radiograph. A new intraoral radiograph can be taken 
at this stage, while we wait for the anaesthesia to take 
effect. This is essential to ascertain the extent of the 
root canal filling. 

Preparation for the Operation. The operation should 
be performed on the principles of aseptic surgery. The 
instruments have been selected beforehand, have been 
boiled and put on a sterile table, and are covered with a 
sterile towel until they are used. A sterile table is pre- 
pared to deposit the instruments for use, the patient is 
covered with a sterile sheet, and in order to exclude the 
hair, the head is covered with a sterile towel except over 

* See Thoma : Textbook on Oral Anaesthesia. 


Fig. 209 

Fig. 210 

Fig. 211 

Figs. 209, 210 and 211. — Radiographs of three cases 

which are not favorable for apieetomy because the bone 

and periodontal membrane has been diseased from the 

apex to the neck of the tooth. 


Fig. 212 

Fig. 216 

Fig. 213 

Fig. 218 

Fig. 217 

Fig. 219 

Fig. 214 

Fig. 215 

Fig. 220 

Fig. 212 and Fig. 216. — The patient has five devital : zed teeth w'th granuloma. Ore 

tooth had to be extracted on each side. The treatment, filling, hr'd^ework nM 

apiectomy which was finally performed is seen in Figs. 213, 214 and 215, for one side, 

Figs. 217, 218, 219 and 220 for the other side. 


the eyes, nose, and mouth. It goes without saying that 
the operator wears sterile gowns and gloves. 

Operation. The saliva ejector is put in place by the 
assistant and the lip is retracted with a lip retractor. One 
sterile syringe is placed on either side of the part that is 
to be operated so as to prevent saliva entering the field 
of operation. The mucous membrane is dried with 
sterile gauze and painted with 3y 2 per cent, iodine or 
aqueous solution of iodine. 

Incision. With a flap knife make a "U "-shaped in- 
cision, as shown in the picture. Lift the periosteum and 
gum from the bone with the sharp periosteal elevator. 
Insert a suitable gum retractor and use sterile gauze to 
remove the blood. 

Amputation of the Root. The alveolar process is now 
visible if it has not been destroyed by the granulation. 
A good-sized opening is cut with the chisel and mallet, or 
by aid of the burr to get a clear view of the apex of the 
root. Resect the apex with a fissure burr at a point fur- 
ther down than the extent of the root-canal filling and as 
far toward the cervical part as is necessary to remove all 
parts which are necrosed. Remove the resected apex 
with a suitable elevator. 

Curetting of the Abscess Cavity. The most important 
part is still ahead. This is the removal of the granulation 
tissue and curetting of the alveolar process with a round 
burr, until all granulation and osteomyelitic bone is re- 
moved and healthy bone is visible on all sides. 

Treatment of the Wound. Smooth carefully with the 
burr all sharp points and margins of the alveolar process. 
Do not shape the distal part of the tooth like the end of 
a root, as it is sometimes advised, because this still de- 
creases the amount of attachment with the bone. Also, 
I prefer to have one round, clean cavity without anything 
projecting into it. Wash with normal salt solution, re- 
move all the debris, sponge, and sterilize the whole cavity 
with 3% per cent, iodine or aqueous solution of iodine. 
Remove the excess with sterile sponges and stimulate 
bleeding with a suitable instrument. When the cavity is 


filled up with a blood clot, draw the flap over the opening 
and sew it carefully with three horse hair stitches. 

Healing. If proper aseptic care has been taken, a 
good union of the gum is obtained in a short time. The 
stitches are removed after three days and if horsehair has 
been used, this causes little or no discomfort. In my 
mind, the sewing in the mouth is of greatest importance ; 
it prevents reinfection from saliva and the fluids of the 
mouth. The healing of the bone cavity occurs by organi- 
zation of the blood clot, and bone is later formed from this 
tissue. In some of the radiographs it can be seen how 
the trabeculae of bone grow into the cavity. Ultimately 
the tooth becomes ankylosed at the end to the newly- 
formed bone. The patient should be told that the face 
may swell up the following day as a result of the mechan- 
ical injury, for which dry heat can be applied. After 
three or four days the face is normal again. After-pain 
is very seldom noticed. 

Failures and Dangers. 

The anatomical relations of the jaw should be kept in 
mind: in the upper jaw the proximity of the antrum, in 
the lower bicuspid region the mental foramen, and if 
operating on the lower molars the relation to the man- 
dibular canal. If the operation is performed with per- 
fect aseptic precautions there is very little danger. 
Failures, however, may occur either because the granu- 
lation tissue has not been entirely removed, because a 
neighboring tooth may be involved, because the tooth has 
not been sterilized, or because the cement of the root may 
be discolored and necrotic almost to the cervical margin. 
The last two reasons are the most important ones and 
always cause reinfection, which can only be cured by 
extraction. I want to make it very plain that this opera- 
tion is not a short cut to save the removal of a crown, and 
proper treatment of the root canal, and it is only success- 
ful if that work has been previously accomplished 


Fig. 221 

Fig. 222 

Fig. 223 

Fig. 224 

Fig. 225 

Fig. 226 

Fig. 227 

Fig. 228 

Fig. 229 

Fig. 230 

Fig. 231 

Fig. 232 

Fig. 233 

Fig. 234 

Fig. 235 

S?ectomv'on 2 »' l^ra^'nw' *l? ^ ? 2 - 7 '~ R adio S r aph? showing the different steps of root canal treatment and 
apiectomy on a lateral incisor, which had imperfect root filling and apical granuloma. Fig. 226, taken directly after 
Vtcs 9o« o9q ,qn a oo-, t> j,- operation. Fig. 227 four months later. 

taken two month* »ft»r tiT « f- ° g *?l ph i S sho ?' in S th .e treatment for apiectomy on another lateral incisor. Fig. 231 is 
taken two months after the operation, the bone is starting to fill in. The excised granuloma of this case is seen in Figs! 

Figs. 232. 233, 234 and 235.— Radiographs showing the process of' apiectomy on two teeth, the lateral incisor and cuspid. 


Fig. 237 

Fig. 239 

Fig. 241 

Fig. 236 

uU: I 

Fig. 238 

Fig. 240 

Fig. 242 

Figs. 236, 237 and 238. — Eadiographs showing apiectomy on a first bicuspid. Fig. 23 
immediately after the operation. Fig. 238 shows the process of healing, six months later. 

Figs. 239, 240, 241 and 242. — Apiectomy on a cuspid. Fig. 241 directly after the 
operation. Fig. 242, nine months after the operation. 


If apiectomy is ruled out as the advisable 
anTT ACT,ON treatment for one reason or another, we 
CURETTAGE still have the most radical treatment 
left; this is extraction of the tooth and 
curettage of the bone. This treatment radically and 
positively removes not only the lesion, but also its cause. 
I lay great stress on the removal of the chronic abscess 
with the curette or surgical burr. After washing the 
wound, the alveolar socket should be inspected and curet- 
ting is repeated if all has not been removed. Very fre- 
quently we find a definite abscess in the radiograph, but 
after the tooth has been extracted, there is no abscess 
attached to the tooth, and if we inspect the socket there 
is only bone to be seen. This may be due to the fact that 
the lamella of the alveolar socket has not been destroyed 
by the disease and that it has to be broken through at the 
bottom if we want to reach the granulation. After the 
curetting has been completed the wound is again in- 
spected, and if all the bone looks healthy, I sterilize the 
wound with 3%% iodine or aqueous solution of iodine, 
and then allow the socket to fill with blood. The blood 
clot will organize and form new tissue. 

After the bleeding is stopped, the patient is instructed 
to use a mouth wash, and is asked to return for inspection 
of the healing wound and for treatment. 

In severe systemic disorders, if the patient has a low 
resistance, or in any weak person, it is necessary to use 
proper judgment in determining the number of teeth that 
are to be extracted at one time. I have in many cases 
noticed an exacerbation after surgical treatment, and 
Hartzel reports that he has noted an exacerbation of 
joint inflammation in all arthritic patients following 
surgical treatment of pyorrhoea or curettage of abscesses. 
A sudden extensive removal of a large number of lesions 
may cause positive harm, especially in weakened patients 
who have suffered a long time, and where the protective 
cells have been worn out from long-continued chronic 
focal infection. It is therefore not advisable to extract 
a large number of teeth at one sitting, or to remove all 


the teeth, and the tonsils the same day, while the succes- 
sive removal of the foci will benefit the patient ; the action 
of this process will be described later under surgical auto- 

FYTiRPATinM ^e ex ^i r P a ^ on °f teeth with chisel or 
OF TEETH burr, or both, is an operation performed 

as the last resort, if extraction by forceps 
and elevator have failed. But often it is indicated as a 
typical primary operation, if the case is diagnosed as a 
difficult one by means of radiographic examination. 

Indication. Extirpation of roots and teeth is specially 
indicated in cases of extensive exostosis of the root apices, 
or in cases of broken down roots, partly or entirely 
covered by the gum, and especially if the distal teeth have 
moved forward so that the root is too large for the space. 

Anaesthesia. Local anaesthesia or local and general 
anaesthesia combined can be used. The decreased bleed- 
ing obtained by local injections is desirable, especially in 
the back of the mouth. 

Preparation. Sensitive and apprehensive patients 
should receive a sedative, such as Bromural-Knoll, two 
tablets to adults, in water, thirty minutes before the 
operation, if local anaesthesia is used. One hour before 
the operation % gram of morphia with or without atropin, 
as required, hypodermically, is used before a general an- 

Preparing the Field of Operation. The mucous mem- 
brane should be dried and the area to be operated on is 
painted with tincture of iodine or aqueous solution of 
iodine. The saliva is taken care of by the saliva ejector. 

Incision. Several types of incisions are used accord- 
ing to location and condition. It should be large enough 
to prevent laceration of the soft tissue and give a clear 
view of the field of operation. 

Operation. After the retractors are inserted remove 
the outer part of the alveolar process, so as to expose the 
entire root or roots ; in molars the roots should next be 
separated, and this is best done with a fissure burr. The 
root or roots are then luxated with an elevator, after 
which the sockets are curetted and the edges of the bone 


Fig. 243 

Fig. 244 

Fig. 245 

Fig. 246 

Fig. 251 

Fig. 252 

Fig. 253 

Figs. 243, 244, 245 and 246. — Apieetomy on a cuspid which is an abutment for a bridge. The 

pulp had died. No root filling. Fig. 244 shows root filling. Fig. 245, immediately after the 

operation. Fig. 246, after eight months. 

Figs. 247 and 248. — Apieetomy on a lateral incisor. 

Figs. 249 and 250. — Apieetomy on a central incisor. 
Figs. 251, 252 and 253. — Apieetomy on two teeth, central and lateral incisors. Fig. 251, 
directly after the operation. Fig. 252 shows the healing process after two months. Fig. 253 

shows the bone completely filled in after ten months. 


Fig. 254 

Fig. 255 

Fig. 256 

Fig. 257 

Fig. 258 

Fig. 259 

Fig. 260 

Figs. 254 and 255. — Apiectomy on a lower incisor. 

Fig. 256. — Apiectomy on two lower incisors. 

Figs. 257 and 258. — Apiectomy on a lower incisor with broken root instrument in 
apical part of the root canal. 

Figs. 259 and 260. — Apiectomy on a lower bicuspid, the molar was extracted at 

the same sitting. 


smoothed with the surgical burr. It is important to re- 
move all pieces of process which are fractured or pro- 
jecting so as not to prolong or hinder the healing process. 
Care of Wound. The gum should be placed back and 
sutured to its original position. The wound is washed 
with normal salt solution until all debris is removed, and 
then treated with 3% per cent, tincture of iodine or 
aqueous solution of iodine. In cases of chronic abscesses 
the wound can be filled in with a blood clot if the curettage 
has been performed properly, but in cases of active sup- 
puration, I prefer to pack the socket with iodoform 
gauze, saturated with orthoform or novocain powder to 
prevent pain. A mixture of orthoform powder, novocain, 
and campho-phenique is also most excellent for this pur- 
pose. The wound should be irrigated and dressed until 
filled in with granulations. 

3. Treatment of Abscesses Due to Diseases of the Gum. 

Abscesses Due to Injury of the Gum. The abscesses 
which start at the gingival part of the gum respond easily 
to treatment as soon as the cause is removed. Foreign 
substances, irritating fillings or crowns should be taken 
care of, the abscesses should be incised and washed out. 
Iodine is most effective as a therapeutic agent. 

Abscesses Due to Pus Pockets. Abscesses caused by 
the closing of a pyorrhoea pocket should be incised to 
evacuate the pus. The tooth is scaled until all debris 
attached to it are removed. After washing with normal 
salt solution, treatment with iodine is found beneficial. 
Ionic treatment is also highly recommended. Most of 
these cases are due to pyorrhoea and the treatment of 
pyorrhoea will not be considered in this book. 

4. Treatment of Abscesses Due to Difficult Eruption, 
Impaction and Unerupted Teeth. 

Radiographic examination is imperative in all cases 
of impacted and unerupted teeth, not only to make sure 
of the diagnosis, but also to find out the position of the 
tooth and to determine the course of treatment. Intraoral 
films often give good results, but generally I prefer a 


plate. With many patients it is hard to use an intraoral 
film on account of trismus or a sensitive throat, and often 
we get only the crown of the tooth in the picture, and 
while it is possible to determine from this how the crown 
is interlocked, it leaves us in doubt about the formation of 
the roots. From this radiograph we should be able to 
ascertain the number of roots, their form, as well as the 
location of the tooth in regard to the ramus and mandi- 
bular canal. 

extirpation -^ i m P ac ted teeth which give rise to 
OF II mp acted pathological conditions, such as abscess 
and pockets or pain caused by pressure, neural 

UN erupted anc [ mental irritation, should be promptly 
teeth extirpated. This involves a difficult and 

serious operation in which sometimes the skill of the oral 
surgeon is taxed to its highest degree. The technique of 
the operation I shall not mention here, but a few words 
about pre-anaesthetic medication, anaesthesia and after- 
treatment may be of use. The physician has not yet gen- 
erally appreciated the difficulty of this operation, and the 
dentist has not until lately recognized the value of proper 
preparation and the after-treatment necessary for the 
extirpation of impacted teeth, as well as other oral sur- 
gical operations. If the operation is performed under 
local conductive anaesthesia, which is the anaesthesia of 
choice, it should be preceded by administration of an 
hypnotic or narcotic, such as Bromural-Knoll, two tab- 
lets in water half an hour before the operation, or in more 
serious cases, morphine gr. 1/6 to gr. *4, or morphine, gr. 
y±, and atropine, gr. 1/150. This stupifies the patient so 
as to take away the terror of the operation, and appre- 
hension of the instrumentation. It also relieves the 
after-pain associated with such an operation. Many pa- 
tients, however, prefer a general anaesthetic, which also 
should be preceded by the usual preanaesthetic medica- 
tion. General and local anaesthesia may be combined 
to great advantage to overcome the physical as well as 
psychic shock. All depends of course a good deal upon 
the attitude of the patient and the difficulty of the case. 
A good many impacted or unerupted teeth can be extir- 


Fig. 261 

Fig. 264 

Fig. 267 

Fig. 262 

Fig. 265 

Fig. 268 

Fig. 263 

Fig. 266 

Fig. 269 

Figs. 261, 262 and 263. — Series of radiographs showing healing of the bone cavity. Fig. 
262, immediately after operation. Fig. 263, after about one year. 

Figs. 264, 265 and 266. — The condition before the operation is seen in Fig. 264. Fig. 265 

shows the healing after a few weeks. Fig. 266 shows complete filling in of the bone 

cavity after about fourteen months. 

Figs. 267, 268, 269. — Radiographs showing the healing process after apiectomy. Fig. 
268 shows bridges of bone growing into the cavity. Fig. 269 the condition after about 

one year. 


Fig. 270. — A selection of curettes. 


pated without great effort, and in a comparatively short 
time, while others call into action the greatest operating 
skill. The easy cases can easily be performed in the 
office, while hard cases, in apprehensive and neurasthenic 
patients, should be done at the hospital, where the patient 
can receive proper preanaesthetic treatment and have 
proper care and medication for a few days. After the 
operation great pain is usually experienced, especially 
after the removal of lower impacted wisdom teeth, which 
frequently extend into the mandibular canal. To com- 
bat the pain, give morphia gr. 1/6 to gr. ^4 hypoder- 
mically, later, if the pain is less severe, the following 
powders have been found excellent by the author : 

Phenacetin 0.7 gr. xii 

Sodium bicarbonate 1.03 gr. xx 

Codeine sulphate 0.06 gr. i 

Caffeine citrate 0.24 gr. iv 

Mx et devide chartulas in powders No2 iv. 

Sig. One powder every three hours until relieved. 

If there is only a small amount of pain prescribe : 

Phenacetin — 

Aspirin aa. 2.0 gr. xxx 

Mx et devide chartulas in powders No2 vi. 

Sig. Take one powder every hour until relieved. 

5. Treatment of Abscesses of the Tongue. 

The treatment of abscesses of the tongue depends very 
much upon the duration of the lesion and the differen- 
tiation of the simple, the phlegmonous, and tubercular 

In simple abscesses of the tongue with 

tuber- on ty moderate infiltration, a small deep 

" incision is all that is necessary. The ab- 

scess cavity is drained and kept open by 

an iodoform wicking, which is changed 

until suppuration has stopped and the wound healed. In 

the severe type of phlegmonous abscess of the tongue, it 


is important to incise as early as possible. General an- 
aesthesia is usually necessary to open the mouth, which 
is locked by muscular trismus, so that the tongue can be 
properly palpitated and the cause ascertained. The an- 
aesthetic should be given by a method which makes 
aspiration of pus and blood impossible. If an abscess 
is the cause of the disease, this should be widely opened 
first, and if due to a tooth or teeth, these should be ex- 
tracted without hesitation. The tongue then is drawn 
forwards and pressed towards the healthy side. Its 
muscle is deeply incised with a crescent-shaped knife by a 
horizontal cut, which should start as far back as possible 
and reach way forward near the point through the thick, 
ungainly, deformed substance of the tongue. There may 
be not much discharge of pus from the tongue, except a 
small amount of badly smelling liquid, which almost al- 
ways flows from the wound. This is, however, enough 
to lessen the dangerous increase of the swelling and give 
relief to the angina, feared more than anything else by 
the patient. The mouth gag should stay in the mouth 
until the patient has awakened, when the danger of aspir- 
ing blood and pus is passed. 

Small tubercular lesions should be 
OFSMALL thoroughly excised and the wound sutured 

tubercular immediately. Lactic acid is used by 
LESSONS Brophy to sterilize the wound, and the use 

of the X-rays is recommended as post- 
operative treatment. 

This operation is recommended by Krause 
E)^siON OF arLC ^ Seymann for tuberculosis, gumma, 
the TONGUE Den ig n tumors and selected malignant 

tumors which involve only the tip of 
the tongue. Under anaesthesia the tongue is drawn 
forward and a thread of heavy silk is then drawn 
through each side as far back as possible. These 
hold the tongue in position . A V-shaped incision is 
now made in the healthy tissue, a good distance 
away from the diseased part. In order to lose 
the least amount of blood, the incision is only made two- 


Fig. 271 

Fig. 272 

Figs. 271 and 272.— Excision of tip of tongue as 
described in text. 


thirds deep, the anterior part is held with a tongue for- 
ceps and drawn forward, and silk sutures are inserted at 
once to draw the two sides together. After several 
stitches are inserted, the incision is continued towards 
the floor of the mouth on one side. When the lingual 
artery is divided, the vessel should be seized with a haem- 
ostatic forceps and ligated. The same thing is done on 
the other side. The sutures are continued while the two 
sides are drawn together. A new tip is thus formed by 
the dorsal part of the tongue; this is drawn up so that 
the lower surface becomes accessible. The diseased part 
of the tongue is now hanging down and the suturing is 
continued while the tip is resected, bringing the surfaces 
in exact contact. Finally the excised part is severed and 
the remaining wound united. The two large pieces of 
silk which served to draw the tongue forward are re- 
moved, but two of the threads from the sutures are left 
and fastened, one on each cheek, to pull the tongue for- 
ward in case of post-operative oedema. Liquid diet 
should be prescribed, which is to be given through a glass 

Large tubercular abscesses of the tongue, especially 
those on the side and extending down to the reflection of 
the mucous membrane of the floor of the mouth, cannot be 
operated upon as just described. These should be curet- 
ted. Brophy recommends application of lactic acid and 
the X-ray. He says that the results of treatment of 
tuberculosis of the tongue are not gratifying, and that 
this is primarily due to the fact that the patient is much 
debilitated by the presence of tuberculosis in other parts 
of the body, therefore one should be guarded in his 

6. Treatment of Abscesses of the Salivary Glands and 


Abscesses of salivary glands and ducts are almost al- 
ways associated with salivary calculi, which are ascer- 
tained and diagnosed by means of radiographs. Surgical 
interference therefore is always necessary. 


Abscesses and calculi, which are formed in the glan- 
dular ducts, can almost always be excised from the inside 
of the mouth, except in Wharton's duct, which we can 
only trace as far back as the myohyoid muscle from this 
region. Also the sublingual gland is accessible from the 
inside of the mouth, while the submaxillary gland, how- 
ever, and the posterior part of its duct, as well as the 
parotid gland, can only be reached by an incision through 
the skin. 

After the mouth has been opened under 
operation ether the tongue is seized with a pair of 
floor T of tongue forceps and drawn towards the 
THE MOUTH corner of. the mouth on the healthy side, 

the lower part turned up. The tongue 
now can be retracted so that we get good access to 
the field of operation. Pack the pharynx with gauze and 
apply iodine for sterilization. Ajo. incision is made half- 
way between the f renum of the tongue and the inner sur- 
face of the jaw, and parallel with the latter. The mucous 
membrane is carefully dissected away and retracted. 
Part of Wharton's duct is now visible, and if it harbors 
the stone it should be dissected (lingual nerve towards 
the mesial side). Split the duct lengthwise directly over 
the stone. This is then removed, after which a fine probe 
may be inserted through the ranuncula salivaris, over 
which the opening of the duct can be closed with a few 
sutures. If the stone, however, is not found to be in 
this duct, or if it had been diagnosed from the beginning 
to be in the sublingual gland, we should first ascertain its 
exact location by puncturing the gland with a straight and 
fine steel needle. If we draw pus or feel hard resistance 
we know that we are near. The way to the stone should 
be secured by a blunt instrument injuring as little of the 
glandular substance as possible. A fine haemostatic 
forceps serves well for taking hold of the stone, and 
after it is removed the pus should be washed out with salt 
solution, tincture of iodine may be applied, after which 
the mucous membrane is closed by catgut sutures. In 


the experience of the author great relief and speedy im- 
provement follows this operation. 

In cases where the stone cannot be re- 
of^the 01 ^ nioved from the inside of the mouth, ex- 

G lands cision of the whole gland is advisable to 

prevent salivary fistulas. The same is 
true in cases of extensive destruction of any of the glands. 
If a fistula exists already it is sometimes due to obstruc- 
tion in the excretory duct, the relief of which has been 
found to cause speedy healing of the fistula. 

7. Treatment of Systemic Complications. 

The important factor in treatment of systemic compli- 
cations is the early removal of the focus. If foci have 
been in an active state for a considerable period of time 
the disease becomes firmly fixed, the secondary infection 
may be well established, and in the persistent stage tissue 
destruction may have occurred ; this condition is beyond 
repair. Elimination of the focus then does little in the 
way of repair, although it prevents reinfection and re- 
moves a septic condition which is a great burden to the 
system, wearing out the organs, the duty of which is to 
protect the body by destroying the bacteria and neutral- 
izing the foreign ferments and protein poisons. 

If a result is expected from the removal of the focus of 
a disease, it is of utmost importance not only to find and 
remove the primary focus, but also others, namely, the 
secondary foci caused by hematogenesis from the primary 
focus, as these are new factors which will continue the 
trouble. A streptococcus infection of the tonsils may, 
for example, have been the primary cause of an endocar- 
ditis or acute arthritis, but they also may have produced 
a streptococcus infection in two chronic alveolar granu- 
lomata which heretofore had been caused by staphylococci 
albi. After the removal of the tonsils, the infection con- 
tinues from the streptococcus infection of the dental 
granulomata and we fail to get a cure. No time there- 
fore should be lost in acute hopeful conditions to ascertain 


all foci, whether primary or secondary, and promptly 
start in with their radical removal. 

This, however, should be undertaken in a 
autSnoc- systematic way, and not as one multiple 
ulation operation, as such procedure could, under 

certain circumstances as we have seen, 
bring positive harm. The surgical interference neces- 
sarily inoculates the patient with a large number of or- 
ganisms, inducing an effect similar to that of an efficient 
vaccine, with the added advantage that the constant 
supply is shut off from the disturbed focus. This sur- 
gical auto-inoculation stimulates the production of anti- 
bodies benefiting the patient after each operation, bring- 
ing about a gradual gain. It can readily be seen that a 
too large inoculation would cause positive harm, 
especially in a patient who is weakened and has lost his 
resistance by long standing disease. The removal of the 
foci should, therefore, be carefully planned; three to six 
days should elapse between each operation. Not only 
should foci in different parts of the body be removed at 
different times, but also foci in one region should, if pos- 
sible, be operated on with intermission. In the mouth, 
for example, abscessed teeth should be extracted and 
curetted one at a time, leaving three to six days between 
each operation, and here again I want to impress the im- 
portance of thorough curettage, because it not only 
removes the principal part, the real focus, which other- 
wise may continue to feed the infection, but also surgical 
auto-inoculation is wholly dependent upon thorough dis- 
turbance of the focus. 

In most diseases treatment of the secondary manifes- 
tations is to be undertaken hand in hand with the removal 
of the focus, because we can not expect that pathological 
changes in the new lesions disappear without the proper 
care and attention. Medical therapeutics, massage, hy- 
drotherapeutics, surgical interference, rest, or exercise, 
fresh air, cheerful surroundings, regulation of diet and 
improvement in digestion and assimilation, all will fur- 
ther improvement and cure of the disease. 


restoration ^ ne °^ ^ e ^ ac ^ ors which improves the 
OF masti- patient's digestive process, and with it his 
gating health and strength, is proper mastication 

efficiency °^ ^* e ^°°d- We cann °t expect that the 
stomach of a weakened patient, whom we 
desire to build up, will digest food which has not been 
properly prepared in the mouth. It is therefore of 
greatest importance to replace all teeth, those which have 
been previously lost and those which had to be sacrificed 
to get rid of a primary or secondary infectious focus. The 
mouth should as soon as possible be restored to its full 
and important physiologic action by plates or removable 
bridge work. 



Gigantic studies have been made both in medicine and 
dentistry in the last twenty or thirty years. The most 
important advances, perhaps, are those of preventive 
medicine and hygiene, and from all the specialties of 
medicine there is none in which prevention is more im- 
portant than in dentistry. Disease of a tooth means 
invariably loss of substance; whether it is hard or soft 
tissue, restoration to normal is seldom possible, a decayed 
tooth will never fill in, an inflamed pulp will not yield 
to any treatment, and the result is always loss of part of 
the tooth or of the whole organ. The treatment is a re- 
placement of the lost organic substance by inorganic 
material, metal or porcelain, and the result is a com- 
promise of a more or less temporary character. 

The importance of the oral hygiene movement has been 
acknowledged by the physician, the schools, and the pub- 
lic, and it is general knowledge that teeth should be saved 
for masticating purposes and that insufficient mastication, 
from lack of teeth, often causes malnutrition. Today, 
however, there is connected with oral hygiene a still 
greater factor than saving teeth for mastication; this is 
prevention of septic conditions in the mouth. We have 
seen that the mouth is the very gateway through which 
disease may enter and proceed through various channels 
to almost any part of the body. In our practical hospitals 
and clinics we have occasion to see patients where disease 
is well on the way, so that it is too late for a cure of the 
secondary chronic disease; we see a large number of 
patients where we can stop disease by removing the septic 
condition, and in still others we shall be able to prevent 
septic oral foci by judiciously selecting favorable cases 


only for root canal treatment, advising extraction of those 
teeth which cannot properly be taken care of. Our great- 
est effort, however, should be directed towards educating 
the public to make them realize the importance of pre- 
serving the vitality of the tooth and prevent decay, which 
is almost always the primary cause of pulp disease and 
dental abscesses. The gums should be kept in healthy 
condition so as to prevent pyorrhoea, which is a disease 
of almost equal frequency. 

Prevention of Secondary Diseases from Oral Abscesses. 

At another place we have discussed the privilege and 
duty of the dentist to participate in the diagnosis of the 
cause of secondary disease and the aid in treatment, by 
judiciously and radically removing such foci, if abscesses 
or other septic conditions are found in the mouth. The 
difficulty in obtaining a speedy cure by the removal of 
the focus after the secondary disease has passed into a 
chronic stage, has been pointed out at various places, and 
the advantage of removing such foci for prevention is 
therefore obvious. Each individual mouth should be 
examined most carefully by means of instrumentation and 
radiographs, and all septic conditions should be radically 
removed. If it seems advisable to treat these teeth in 
a conservative way by carefully sterilizing and filling the 
root canals, subsequent examination by the radiograph 
at regular intervals is indicated to note whether there is 
improvement or whether the condition is getting worse. 
It may be hard for a man who has practised for years the 
saving of every tooth at any cost, to make up his mind 
to advise extraction or expensive root-canal treatment if 
there is no apparent local trouble in the mouth, and it 
will be hard for a patient to understand why this or that 
tooth which does not ache, could be a factor of present 
or future ill-health, and should be treated or removed, 
unless the dentist is able to explain the condition in a con- 
vincing manner, which can only be based upon a thorough 
understanding of the condition. But he who does not 
tolerate septic conditions in his patient's mouth practises 


good dentistry as far as the teeth are concerned, and most 
excellent preventive medicine from the standpoint of the 
whole body. 

Prevention of Periapical Infection. 

The question whether or not abscesses on devitalized 
teeth can be prevented has not yet been entirely solved. 
The men (Ulrich*) who believe that these abscesses are 
caused principally by haematogenous infections of the 
periapical area of pulpless teeth, which represents tissue 
of lower resistance, think that it does not matter how well 
the root canals are filled, abscesses may be caused in any 
case, if there are infectious foci in other parts of the body, 
which cause a mild bacteremia. They claim that it is 
especially the streptococcus to which the lesion may be 
attributed and look at most apical abscesses as secondary 
infections. However, we need not search for very remote 
modes of infection when there are other causes nearer at 
hand. If we consider the anatomy and pathology of the 
dental pulp, if we remember how hard it is to render asep- 
tic the root canal, the dentinal tubules and the apical fora- 
mina, and how often careless methods of technique are 
employed, we find the causes may be practically obvious. 
However, I do not doubt that in some instances abscesses 
start as a secondary infection, and furthermore, that 
subacute attacks of abscesses which have been in the 
quiescent stage of inflammation for many years may per- 
haps be explained in this way, although here again we 
have other factors to consider. 

RADIO- It is well to radiograph a tooth before 

GRAPHIC undertaking to treat a root canal, no 

DIAGNOSIS matter what condition it is in. Abnormal 
before ROOT formation of the roots and obstructions 
CANAL such as deposits of secondary dentine and 

tment pulpstones can in this way be determined 
beforehand, and the patient and the dentist save much 
time and expense if it is determined, whether or not 
we can mechanically achieve a perfect result. 

* Ulrich, Henry L. : The Blind Abscess. Journal of the American Medical As- 
sociation, November 6, 1915, p. 1619. 


Fig. 273. — Microphotograph of the apex of a tooth showing multiple 


Specimen by author and stained with Mallory 's Phosphotungstic 
acid and Hematoxylin. 


Grieves* points out that arsenic used for 
FOR E rulf^ SBA devitalization of a pulp is very apt to 
extirpation cailse necrosis in the periapical tissue on 
account of its vascularity, the drug being 
absorbed by the pulp. Pressure anaesthesia with novo- 
cain or cocaine as first described by Professor Edward C. 
Briggs of Boston, is of greatest value for pulp extirpa- 
tion. Local anaesthesia with novocain suprareninf is 
also very excellent, and many times the only method that 
gives results, as in cases of diseased pulps with persisting 
nerve fibres or partly extirpated pulps. General anaes- 
thesia is not recommended except in front teeth where 
the procedure is comparatively simple. 

If a pulp is infected or disturbed by sur- 
pulp PLETE gi- ca l interference, it strangles itself at 
EXTIRPATION ^ ne a pi ca l foramen on account of the hy- 
peremia produced. It is therefore 
important to remove every particle of it, or later it will 
become a source for periapical infection. 

In pulp extirpation a fine broach should be inserted as 
far into the root canal as possible so that the entire pulp 
is removed at once. A fine wire with a loop should then 
be inserted with the mild antiseptic dressing, and another 
radiograph should be taken to find out whether we have 
reached the end of the root. 

If the root canal is not large enough to 
and A enlarg- a ^ ow eas ^ P assa g e to its end, and if dis- 
ING the " ease d oi" healthy tissue remains, this 
canal should be taken care of by the sulphuric 

acid or sodium potassum method. Both 
of these drugs are valuable for root canal work, but care 
should be taken not to force any through the apical fora- 
men. The sulphuric acid should be neutralized with 
sodium bicarbonate; both drugs are best used in Luer 
syringes with root canal hub. The sodium potassium 
paste is used on smooth broaches; its great affinity for 
organic matter draws the drug through obstructed places, 

* Grieves, Clarence J. : Dental Cosmos, October, 1915, p. 1118. 
t Thojia, Kurt H.: Oral Anaesthesia, p. 107. 


making passage way for the broach. The result, however, 
depends a great deal upon patient and continued instru- 
mentation. The Rhein picks are the most valuable in- 
struments for this purpose. The strong caustic alkali 
which is formed by this process should be neutralized by 
sulphuric acid, and this in turn by sodium bicarbonate. 
An important factor in root canal operations is easy 
access, for the crown of the tooth should be so reduced 
as to allow straight entrance into the canals. 

Failure of achieving the desired results in 
medicatIon root-canal operations has gradually led to 

the use of highly oxidizing, tissue obstruc- 
ting drugs with great penetrating power, in the age when 
older antiseptic methods have almost entirely yielded to 
good surgery, and where it is an important principal to 
destroy as few cells as possible, and where we know that 
any cell which is rendered necrotic adds only another 
place where infection may find media of its liking. 
Drugs, such as formaldehyde and all its numerous prepa- 
rations, should not be placed into a root canal under any 
condition. Formaldehyde preparations should only be 
used as the first dressing upon a putrescent pulp, placed 
into the pulp chamber, and covered with cotton saturated 
in petrol oil or with temporary stopping, as the case re- 
quires. After the pulp has been extirpated, this drug 
should no longer be applied into the pulp chamber nor 
into the root canal, as it would penetrate through the 
foramen and do harm to the periapical tissue. Zinc 
chloride, copper sulphate, concentrated phenol, tri- 
chloracetic acid are other root-canal drugs of great tissue 
destroying action. Their use as well as the use of sul- 
phuric acid and sodium potassium for root-canal cleaning 
should be carefully controlled, and great care should be 
taken to confine their action to the root canal. Gr. V. 
Black* describes at length experiments made by appli- 
cation of the different drugs for use in root canal treat- 
ment. The different medicaments were applied to the 
skin on cotton in small rubber cups, held in position by 

* Black, G. V. : Special Dental Pathology, pp. 291-298. 


Fig. 274. — Microphotograph of the end of a root. 

A, showing root filling extending into a remnant of pulp which 

may give a symptom of pain which often is mistaken for the 

pain caused when emerging through the apical foramen. 

B, Necrosed area of the dentine. D, Pulp remnant. 

C, Secondary dentine filling the canal. 

Specimen prepared by the author. Stained by Mallory's 
Phosphotungstic acid and Hematoxylin. 


court plaster. Oil of cloves and Blackwood creosote each 
produced practically no inflammation, Black's 1, 2, 3 only 
slight irritation, oil of cinnamon a large blister, creosol 
and formalin in each instance a very deep inflammation 
which was painful and so unbearable that it had to be 
removed after seven hours ; the tissue formed no blister 
but was of yellowish color as though it would slough 
away ; needles could be stuck into the tissue one-third of 
an inch before sensation was felt. Six weeks later a scar 
was visible which looked as though the area had been 
burned. It is evident that such an injurious drug should 
not be sealed into root canals. 

To avoid injury of the periodontal membrane and bone 
surrounding the apex of the tooth, the operator should 
put his effort into perfecting his technique rather than 
relying on strong drugs to sterilize what he neglected to 
remove. Mild antiseptics and anodines are sufficient as 
dressings in most cases, ionic application of iodine will 
take care of bacteria in dentinal tubules and accessory 
foramina, and if a healthy condition cannot be obtained 
by mild medication, the cause is to be looked for outside 
the tooth. If a radiograph was not taken beforehand, it 
is now time to find out the condition of the periapical 
tissue, and in most cases it will be found that the reason 
of not making any headway is due to a granuloma or 
chronic abscess, a lesion which does not yield to medicinal 
treatment. Mild antiseptics of reputation are : 

Black's 1, 2, 3. 

01. cassiae 1 part 

Thenolis 2 parts 

01. Gaulteriae 3 parts 

Mx the oils and add melted crystals of phenol. 

Buckley's Modified Phenol. 

Mentholis gr. xx 

Thymolis gr. xl 

Phenolis f 3 iii 


Ionic medication has already been consid- 
medicatson ere( ^ -^ or treatment of periodontitis. Zinc 
chloride and copper sulphate should not 
be used for sterilization of dental structures on account 
of their tissue destroying action, upon which some men 
base the treatment of the apical granuloma. This is be- 
lieved to be dissolved by this method so that it can be 
resorbed by the tissue. Such applications, however, also 
destroy the periodontal membrane, and as we have seen 
that the success of root canal treatment depends upon 
preservation of this most important structure, it would 
be unwise to apply an agent which has exactly the oppo- 
site effect. 

Iodine ions are, however, to be recommended for root 
canal or rather dentine sterilization. Tincture of iodine 
3y 2 per cent, or aqueous solution of iodine, a recent prepa- 
ration without the irritating action of the alcohol, is 
applied into the root canal by means of a Luer syringe. 
The negative pole is applied to a platinum broach, with 
cotton saturated in the same solution attached, the posi- 
tive pole is placed under the rubber dam in the form of a 
sponge electrode, or held in the hand. The circuit of a 
direct current, reduced by a special rheostat (there are 
several well made ionization machines in the market) and 
measured by a milliampere meter is now closed and the 
amount is gradually increased until from % to 3 milliam- 
pere is used. The treatment should be applied for ten 
minutes in each canal. Iodine should be added from 
time to time, as it is used up quickly, which is indicated 
by the white color of the peripheral part of the dressing. 
After ionic medication with iodine the pulp chamber 
should be washed out with alcohol or acetone to remove 
the brown stain. A mild aseptic dressing is inserted and 
the canals filled at another sitting. 

The most important factor which has to do with poor 
root-canal filling and following periapical infection is 
unsuccessful dehydration. Acetone should be applied by 
means of Luer syringe and broach, and dried out with 
hot compressed air. An electric root-canal dryer is then 


Fig. 278 

Fig. 275 

Fig. 279 

Fig. 280 

Fig. 276 

Fig. 281 

Fig. 282 

Fig. 277 

Figs. 275, 276 and 277. — Radiographs showing the process of root canal treatment. 

Fig. 275, shows a wire which was inserted to see whether the apex was reached. 

Fig. 276 shows an unsuccessful root canal filling. Fig. 277 the final filling. 

Figs. 278, 279 and 280. — Radiograph No. 278, showing two teeth not filled to the end. 

Fig. 279, radiographs with wires inserted. Fig. 280 shows the canal fillings. 
Figs. 281, 282. Radiograph No. 281 shows "corkscrew" filling which was replaced 

by filling seen in Fig. 282. 


Fig. 283 

Fig. 284 

Fig. 285 

Fig. 285. — On left root treatment attempted through small 

cavity, the broach does not go around the curve. On right 

mesio-occlusial cavity cut extensively, so as to get proper 

access to canals. 

Fig. 284 and 285. — Specimen of bent and curved roots, the 
root canals of which would be hard to treat and fill. 


inserted and if used for the first time the operator mil be 
surprised to hear a sizzling noise, indicating that there 
was still some moisture left. The heat is applied until 
the patient feels the warmth. For root-canal filling 
the author prefers the chloroform-resin-gutta-percha 
method.* The chloroform and resin (d.i to gr. iv) 
is best applied into the canal by use of an ordinary Luer 
Q syringe ; with a smooth broach carefully remove all air 
bubbles. Select a sterile gutta-percha cone or point and 
pump it into the canal forty times. The chloroform dis- 
solves the gutta percha, which is forced into the fine canals 
and foramina by the pumping action. Other cones follow 
the first until the canal is filled, when the filling is con- 
densed with a root canal condenser. This method has 
several advantages; the most important ones are that 
newly-formed chloro-percha can be forced into the finest 
canals without the evaporation which spoils the result in 
other methods, and that the excess forced through the 
foramina is not a sharp point projecting into the peri- 
apical tissue, but a soft paste which caps the apex, so to 
speak, adapting itself on its surface. A radiograph is 
taken immediately, and in case the filling does not reach 
to the apex it can be removed before it has hardened, when 
the same process is repeated until the filling is satis- 

Sterilization of the instruments and 
Ti on and aseptic methods cannot be too strongly in- 
ASEPSiS sisted upon. If we consider that the bac- 

teriologist sterilizes his smooth platinum 
needle most carefully in the flame before he uses it for 
inoculation of an artificial medium, we must realize how 
much more important it is to sterilize in a most scrupulous 
manner rough instruments, such as broaches, so as not to 
inoculate the human tissue. All root-canal instruments 
should be immersed in alcohol, or in phenol first and 
alcohol secondly, each time before they are used. The 
field of operation should be properly prepared by use of 

* Calahan, J. E. : Eesin Solution in Eoot Canals. Items of Interest, August, 
1915, p. 579. 


rubber-dam and scrubbing of the projecting teeth with 
10% formaldehyde, which is dried off by means of air. 
If cotton dressings are used for root canal work, or if 
broaches wound with cotton are used, a number properly 
prepared and sterilized should be kept on hand. The 
cavity should be most carefully sealed after each treat- 
ment to keep saliva from entering. 
summary OF ^ e important factors which should be 
important borne in mind in operations of pulp re- 
FACTORS TO moval, root-canal work and filling, are, in 
prevent short, the following : 

periapical i Diagnose the condition first by 

means of a radiograph. 

2. Treat only cases which promise a good result. 

3. Observe strict aseptic precautions. 

4. Extirpate all pulp tissue. 

5. Avoid injury and necrosis of the periapical tissue 
as caused by the use of certain irritating drugs. 

6. Avoid infecting of the periapical tissue by instru- 

7. If a root canal does not yield treatment in a short 
time and no radiograph was taken in the first place, take 
one now with an indicator in the root canal and find out 
what is wrong. 

8. Fill the root canals to the very end and ensure a 
successful operation by means of another radiograph. 

Prevention of Devitalised Teeth. 

devitaliza- Our knowledge of the etiology and com- 

tion FOR plications of alveolar abscesses and reali- 

SrSSi'wiyAMrk zation of the uncertainty of root-canal 
DENTINE and . •* .j ,, 

prostheses fillings should impress in our minds the 
notjusti- seriousness of pulp extirpation. He 
fied w h extirpates the pulp of one, two or 

more teeth to restore masticating efficiency by bridge 
work renders poor services if granulomata develop on the 
devitalized teeth, which are apt to endanger the patient's 
health. A pulp for such or similar purposes should not 


be sacrificed except after the most careful consideration 
and prognostic study of the roots and root canals by 
means of radiographs. Prosthetic appliances should be 
constructed which do not require devitalization of healthy 
teeth, and our efforts should be in the direction of devis- 
ing reconstruction work which is not destructive to the 
remaining hard or soft tissues of the mouth. 
tr e ATM E NT Hyperemia and exposures are frequently 
OF hyperemia brought about when excavating cavities 
sures of°" ^ insufficient attention is paid to the 
THE pulp TO approach to the pulp. The pulp horns 
prevent de- are especially liable to become acciden- 
vitalization tally involved. Large metal fillings are 
liable to cause hyperemia because they are good conduc- 
tors of heat and cold. A nonconductor should be placed 
into the deepest parts of the cavity beneath the filling. 
A pulp in the state of active hyperemia can almost always 
be saved if the irritating causes are removed. The 
mildest anodines should be applied, such as oil of cloves 
or modified phenol slightly warmed, until the irritation 
has subsided, when the same treatment as for pulp cap- 
ping is indicated. Pulp capping is performed over deep 
decayed areas which reach very close to the pulp, and 
where there is danger of making an exposure if excavation 
is continued. The action then is that of preservation. In 
actual small exposures made by excavators in fully 
formed teeth in cases where the pulp has previously given 
no symptoms of inflammation, and in exposures of teeth 
the apical foramen of which is wide open, with pulp nor- 
mal or very slightly inflamed, we may attempt to save 
the pulp by the so-called capping method. The patient, 
however, should be informed of the doubtful outcome of 
the undertaking. If there is slight hyperemia of the pulp, 
an anodine such as modified phenol or oil of cloves should 
first be applied, sealing it into the tooth with quicksetting 
cement (not gutta percha) for one week. At the second 
visit zinc oxide and eugenol, mixed to a thin paste, is 
slightly coaxed over the exposed area ; this is covered with 
a layer of quick-setting cement. All depends upon per- 


feet asepsis, skillful manipulation and prevention of any 
pressure or irritation. A temporary filling may be used 
until the result is made sure of. 

early treat- The prevention of hyperemia, which leads 
me NT of to other diseases of the pulp, is best ac- 

c aries and complished by filling the cavities when 
prophylaxis sma ii an d shallow, or better still, in con- 
trolling decay by prophylactic treatment. This is also 
prevention in the highest degree against alveolar abscesses 
and its many and dangerous complications. The teaching 
to the public of oral hygiene, which first was principally 
undertaken to combat the loss of masticating efficiency 
and its sequels, poor digestion, and ill-health, has now 
grown to a still greater importance, namely : the preven- 
tion of systemic diseases of the gravest nature to which 
the unsuspecting individual is liable to fall prey. With 
this point in view, the dentist should educate the public 
to the far-reaching meaning of preventive dentistry, and 
offer his patients prophylactic treatment at such inter- 
vals as seem necessary for each individual case, and teach 
each individual how to keep the teeth in good condition 
by suggestions as to a suitable diet and practical demon- 
strations of how to take care of teeth and gums at home. 

Fig. 288 

Fig. 2i 

Figs. 286, 287, 288 and 289. — Left and right side view and occlusial view of upper 
and lower jaw of a patient's teeth who had the four first molars extracted when sixteen 
years of age. The four illustrations show the condition when the patient was thirty -five 

years of age. 

Reproduced ~by the courtesy of Dr. Eugene H. Smith. 



Dean Smith, of Harvard University Dental School, in 
his timely paper read before the First District Dental 
Society of the State of New York, said: "We all know 
how difficult it is to adjust material values. How much 
more difficult it is to adjust physiological values, in the 
misjudging of which the happiness, health, and frequently 
the life of the people is jeopardized!" It is indeed diffi- 
cult to place the right value on a tooth; the judgment 
depends a good deal on education, education of the dentist 
and education of his patients. The value of a healthy 
tooth in good occlusion is the easier to determine ; it cer- 
tainly cannot be overestimated, but if a tooth is affected 
by any of the various dental diseases, there arises a great 
difference of opinion. Among the various pathological 
conditions I shall consider only those we are especially 
concerned with in this book, namely, the oral abscesses and 
systemic diseases which are caused by them. One cannot 
place too low a value on a devitalized tooth if it causes 
conditions which endanger the patient's health. 

The tooth which is the most frequent cause of abscesses 
is the first permanent molar. This tooth, which plays 
such an important part in the health, decays under our 
very eyes in children who have the best of care, unless the 
fissures are carefully filled as soon as the gum has 
shrunken away from the occlusial surface. In the poor, 
who do not care for their teeth except if so forced by pain, 
this tooth is almost always a ruin when it comes under 
our observation, and its pulp is invariably diseased and 
very often periapical infection has already set in. The 
value of this tooth sinks then from the highest mark to 


the lowest level. Such badly decayed teeth are contin- 
uous expenses, as they would have to be filled and refilled 
and finally crowned, and would be sure, sooner or later, 
to cause periapical infection. The poison which dis- 
charges into the system from such a focus only lowers 
the child's resistance to various illnesses, and hampers 
the development of the body, but, worse than all, may 
cause systemic diseases of the gravest nature from which 
recovery may be impossible. How much better is extrac- 
tion in such cases ; the twelve-year molars will move for- 
ward into place, and while it would not always result in an 
ideal condition, the condition which the orthodontist calls 
" perfect occlusion," it would, if symmetrically carried 
out, be just as good as what the average person has ; per- 
sonally, I would say infinitely better, because a first molar 
with periapical infection would have to be extracted 
sooner or later ; it is only a matter of time ; and when ex- 
tracted in later life it will leave a space which cannot then 
be filled in by nature, the second molars having been firmly 
fixed in the bone at that period of life ; for the patient the 
result is worse from any point of view : that of occlusion, 
masticating efficiency, chance of systemic infection, and 
loss of time and money. 

The saving of teeth in children should be of preventive 
nature, which is the only safe way of securing and keep- 
ing normal occlusion; but if it is too late for prevention, 
we must be satisfied with the next best healthy condition. 
The results obtained from symmetric extraction of the 
badly decayed permanent first molars are very satisfac- 
tory if undertaken before the age of twelve ; the occlusion 
is in the majority of cases very good, as has been named 
" sufficient occlusion" by Dean Smith, a term which ex- 
presses the condition fully. Figures 286 to 293 show 
models of two patients who had the first permanent molars 
extracted at the proper age on account of extensive decay, 
and the results are gratifying. These illustrations have 
been reproduced with Dr. Smith's consent from his 
already mentioned paper. While I want it clearly under- 
stood that I do not believe in the wholesale extraction of 


Fig. 290 

Fig. 291 

Fig. 292 

Fig. 293 

Figs, 290 and 291. — Left and right view of the teeth of a boy aged thirteen. The 
right lower first molar is half decayed, pulp involved, apical foramina open. The left 
lower first molar has an exposed pulp. The upper first molars are decayed. All the 
first molars were extracted, no appliances had been used and already after three years 
the good result shown in Figs. 292 and 293 were obtained. 

Reproduced by the courtesy of Dr. Eugene H. Smith. 


children's teeth, and that neither Dr. Smith nor I would 
advise the above treatment except in cases where the first 
molars are in hopeless condition, I would say this: that 
I for one should much prefer to own any of the mouths 
shown in these pictures with only "sufficient occlusion" 
of twenty-eight healthy teeth, than an ideal occlusion 
with a number of devitalized teeth and arthritic joints. 

The value of healthy teeth is so inestimably high that 
every effort should be made to preserve them. A devital- 
ized tooth diminishes greatly in value if an abscess is 
formed at its roots, but when it becomes a focus of ill- 
health and disease in other parts of the body, its value 
becomes decidedly negative and its ownership a curse. 


Adami & McCrae, Textbook of Pathology. (Lea & Ferbiger, Phila- 

Adloff, P. Zur Frage der Herkunft des Epithels in den "Wurzel- 
zystem. (see Deutsche Monatsschr. f. Zahnheilkunde.) 

Baehr, G. Glomerular Lesions of Subacute Bacterial Endocarditis. 
(see Journal of Experimental Medicine, Vol. 15.) 

Beck, J. C. Chronic Focal Infection of the Nose, Throat, Mouth and 
Ear. (see Journal of American Medical Association, Novem- 
ber, 1914, Vol. LXIII, p. 1636.) 

Bellei, G. A Short Contribution to the Study of General Infection 
produced by Staphylococcus Aureus and by the Steptococcus. 
(see Lancet, March, 1902.) 

Berger, A. Dento Alveolar Abscess, (see Items of Interest, Sep- 
tember, 1914, p. 641.) 

Billings, F. Clinical Aspect and Medical Management of Arthritis 
Deformans, (see Illinois Medical Journal, January, 1914.) 

The Medical Management of Chronic Arthritis, (see 
Illinois Medical Journal, September, 1914.) 

Focal Infection, (see Journal of American Medical Asso- 
ciation, September, 1914, V. LXIII, p. 899.) 

Chronic Focal Infections as a Causative Factor in Chronic 
Arthritis, (see Journal of American Medical Association, 
September, 1913, Vol. LXI, p. 819.) 

Mouth Infection as a Source of Systemic Disease, (see 
Journal of American Medical Association, December, 1914.) 

Bramwell, B. Notes on the Treatment of Pernicious Anemia. 
(British Medical Journal, January, 1909, p. 209.) 

Brophy, T. W. Oral Surgery. (P. Blakiston's Son & Co.) 

Bunting, R. W. The Pathology of the Dental Pulp, (see Dental 
Cosmos, February, 1915, p. 143.) 

Bush, B. E. The Close Relation of the Dentist and the Physician. 
(Journal American Medical Association, 1910, p. 752.) 

Butt, Wm. Redfield. Nose, Throat and Ear as Neighboring Organs 
to the Teeth, (see The Dental Cosmos, August, 1915, p. 837.) 


Cabot, E. C. Analysis of Six Hundred Cases of Heart Disease. 

(Journal of the American Medical Association, 1914, Vol. 

Callahan, J. E. Eoot Canal Preparation, (see Items of Interest, 

August, 1915, p. 567.) 

Camac, C. N. B. Dental Sepsis: Its Eelation to the System, (see 
Journal of the National Dental Association, November, 1915, 
p. 8.) 

Cantani, Prof. Arnaldo. La Clinica Italiana. June and July, 1914. 

Cababelli, G. Elden von Lunkaszprie, Anatomie des Mundes. 
Wien, 1842. 

Caven, "W*. P. The Importance of Oral and Dental Conditions. 
(Dominion Dental Journal, 1912.) 

Colyeb, J. F. Oral Sepsis and its Eelation to General Diseases. 
(Journal British Dental Association, Vol. XXIII, p. 409.) 

Colyeb, J. & S. Dental Disease in its Eelation to General Medicine. 
(London: Longman's, 1911.) 

Corwin, J. W. Fetid Breath, (see Items of Interest, November, 
1914, p. 827 ; also discussion, p. 855.) 

Cbaig, C. Burns. Periodontal Infection as a Causative Factor in 
Nervous Diseases, (see Journal of the American Medical 
Association, December 5, 1914.) 

Dalton. A Case Showing Eelationship to Oral Sepsis. (British 
Medical Journal, November, 1914, p. 1368.) 

Daly, E. E. Eelations of Dental and Ehinologic "Work, (see Dental 
Cosmos, January, 1915, p. 43.) 

Davis, D. J. Bacteriology and Pathology of the Tonsils with Especial 
Eeference to Chronic Articular, Eenal and Cardiac Lesions. 
(see Journal of Infectious Diseases, Vol. X, No. 2, March, 
1912, p. 148.) 

Davis, Wm. T. The Inter-relation of the Teeth and the Eye. (see 
The Dental Cosmos, July, 1915, p. 769.) 

Dependobp, Th. Zur Pathogenese der Zahnwurzel2yzstem. (see 
Deutsche Monatsschr. f. Zahnheilkunde, November, 1912, p. 

DeVecchis, B. New Problems Eegarding Tubercular Infection and 
a Special Treatment for Cervical Adenitis following Oral 
Sepsis, (see Dental Cosmos, July, 1915, p. 737.) 

Dorbance, Geobge Mobbis. Enlarged Cervical Glands, with Special 
Eeference to the Mouth as an Etiological Factor, (see The 
Dental Cosmos, August, 1913, p. 808.) 


Doxtater, L. W. Constitutional Infection due to Chronic Dento- 
Alveolar Abscess and Pyorrhoea Alveolaris. (see Dental 
Cosmos, September, 1915, p. 983.) 

Dreschfeeld, H. T. Dental Diseases and their Relation to Public 
Health. (Journal of London Institution, Vol. XXIII, 1903, 
p. 867.) 

Editorial. Mouth Infection and Systemic Disease, (see Items of 
Interest, December, 1915, p. 943.) 

Eisen, E. J. & Ivy R. H. Origin and Metastatic Importance of 
Chronic Oral Infections, (see Items of Interest, February, 
1916, p. 81.) 

Eustis, R. S. Endocarditis in Children, (see Boston Medical and 
Surgical Journal, September, 1915, p. 348.) 

Fetler, Breslau. Zur Anatomie des Foramen Apicale. (Deutsche 
Monatsschr. f. Zahnheilkunde.) 

Gilberti. Medical Practice Series, 1910, V. Ill, p. 313.) 

Gildersleeve, Nath. Oral Infections, (see The Dental Cosmos, 
December, 1915, p. 1350.) 

Gillett, Henry W. Management of Badly Mutilated Mouths, (see 
Journal of Allied Dental Societies, December, 1915, p. 431.) 

Gilmer, J. L. Chronic Oral Infections, (see Archives of Internal 
Medicine, April, 1912, Vol. 9, p. 499.) 

Gilmer, J. L. and Moody, A. M. A Study of the Bacteriology of Al- 
veolar Abscess and Infected Root Canals, (see Journal of 
American Medical Association, December, 1914, Vol. LXIII, 
p. 2023.) 

Goldthwait, Painter & Osgood. Diseases of the Bones and Joints. 
(Boston: D. C. Heath & Co.) 

Grayson, C. P. The Teeth in Relation to Ear and Throat Diseases. 
(see The Dental Cosmos, June, 1907, p. 555.) 

Grieves, C. J. Systemic Pus Poisoning Associated with Diseased 
Dental Apical Regions, (see Items of Interest, May, 1911, 
p. 339.) 

Dental Periapical Infections as the Cause of Systemic 
Disease, (see The Dental Cosmos, January, 1914, p. 52.) 

Unhygienic Mouths, (see The Dental Cosmos, November, 

1913, p. 1102.) 

The Responsibilities of the Dentist in Systemic Diseases 
Arising from Dento-Alveolar Abscess as Illustrated by the 
Etiology of Periodontal Abscess, (see Dental Cosmos, May 

1914, p. 564.) 


Grieves C. J. — Continued. 

Secondary Infections, (see Journal of Allied Dental So- 
cieties, June, 1914, p. 178.) 

The Eelation of the Vitality of the Periapical Cementum 
and Adjacent Tissues to the Patient's Health, and the 
Status of the Dental Profession, (see The Dental Cosmos, 
October, 1915, p. 1112.) 

Artificial Production of Apical Necrosis by Root Canal 
Drugging, (see The Dental Cosmos, October, 1915, p. 1119.) 

Hamann, C. A. Some of the Complications and Results of Dental 
Infections, (see Wisconsin Medical Journal, March, 1903.) 

Hartzel, T. B. Two Preliminary Reports of Arthritis Caused by 
Dental Abscess, (see Official Bulletin of National Dental 
Association, March, 1914, p. 4.) 

Report of the Minnesota Division of the Scientific Foun- 
dation and Research Commission, (see Journal of National 
Dental Association, November, 1915, p. 333.) 

The Clinical Type of Arthritis Originating about the 
Teeth, (see Journal of American Medical Association, Sep- 
tember, 1915, p. 1093.) 

Secondary Infections having their Primary Origin in the 
Oral Cavity. (see Journal of Allied Dental Societies, June, 
1914, p. 166.) 

Report : Mouth Infection Research Corps of National Den- 
tal Association. (see Official Bulletin, National Dental 
Association, October, 1914, p. 48.) 

Hunter, "William. Pernicious Anaemia. (London: Charles Griffin 
& Co., Ltd.) 

Huschart, J. H. The Relation Diseases of the Teeth Bear to the 
Eye and Ear. (see Dental Brief, Vol. XII, p. 799.) 

Idmann, Gosta. Bakteriologische Untersuchungen von periostalen 
Abszessen (see Arbeiten aus dem Pathologischen Institut 
der Universitdt Helsingfors, Erster Band, Gustav Fischer, 
Jena, 1913.) 

Jones, W. I. Treatment of Impacted Third Molars, (see Items of 
Interest, October, 1915, p. 786.) 

Kauffmann, Joseph Herbert. Abscess and Pyemia? A Case of 
Extensive Alveolar Abscess Associated with Pyemia, (see 
The Dental Cosmos, May, 1915, p. 530.) 

Krause, Heymann. Lehrbuch der chirurgischen Operationen. (Ur- 
ban & Schwarzenberg, Berlin, "Wien.) 

Langwortht, Henry Glover. Some Remarks on the Removal of 
Troublesome Tonsils of Interest to Dentists, (see The Den- 
tal Cosmos, July, 1913, p. 718.) 


Lawrence, Chas. H. Chronic Arthritis. (Paper read before the 
Boston Surgical Fortnightly Club, October, 1915.) 

Lee, R. I. Preventable Heart Disease, (see Boston Medical and Sur- 
gical Journal, July, 1915, p. 157.) 

Lehmann, K. B. & Neumann, R. 0. Bakteriologie und Bakterio- 
logische Diagnose. (Munchen, 1907: Verlag von I. I. 

Lever, J. W. Pneumococcic Arthritis with Eeport of Six Cases. 
(see Boston Medical and Surgical Journal, September, 1915, 
p. 387.) 

Levy, M., Berlin. Statistische Untersuchungen liber den Zusammen- 
hang von Zahnkaries und Rheumatismus und Gicht. (Deu- 
tsche Monatsschr. fur Zahnheilkunde, June, 1914, p. 436.) 

Logan, W. H. G. Blood Findings in 162 Consecutive Cases of Chronic 
Oral Infection Associated with Teeth, (see Items of In- 
terest, December, 1915, p. 912.) 

Lyons, C. J. The Pathological Significance of Impacted and Un- 
erupted Teeth, (see The Journal of the National Dental 
Association, March, 1916, p. 28.) 

Mackee, G. M. and Remer, John. Oral Sepsis as a Focus of Infec- 
tion, (see American Journal of Roentgenology, p. 158.) 

Mallory, Frank B. Principles of Pathologic Histology. W. B. 
Saunders Co. 

May, Charles H. Manual of Diseases of the Eye. (William Wood 
& Co., New York.) 

Mayo, C. H. Mouth Infection as a Source of Systemic Disease, (see 
Journal of American Medical Association, December, 1914, 
Vol. LXIII, p. 2025.) 

Medalia, Leon S. The Use of Bacterial Vaccines in Acute Septic 
Conditions of the Oral Cavity met with by the Dentist, with 
Special Reference to Mandibular and Septic Apical Abscesses. 
(see The Dental Cosmos, January, 1914, p. 12.) 

Mex, P. Beobachtungen iiber den Zusammenhang periodontitischen 
Erkrankungen zu Allgemeinkrankheiten, insbesondere zu 
den Drusenerkrankungen der Kinder. (Deutsche Monatsschr. 
f. Zahnheilkunde, March, 1913.) 

Milne, L. S. Chronic Arthritis, (see Journal of American Medical 
Association, February, 1914, Vol. LXII, p. 593.) 

Miner, L. M. S. Antagonistic Therapy: Its Laboratory Aspects and 
Its Application in Septic Processes of the Oral Cavity, (see 
Journal of Allied Societies, March, 1910.) 


Monieb. Contribution a l'etude pathologique des infections den- 
taires. These de Paris, 1914. (Steinheil.) 

Neumann, R., Berlin. Die Wurzelspitzenresektion an den unteren 
Molaren. Verlag von Hermann Meusser. 

Nodine, A. M. Rheumatic Fever and the Contribution of a Septic 
Mouth and Carious Teeth to its Cause and Cure, (see Items 
of Interest, September, 1912, p. 656.) 

Orton, F. H. Root Canal Filling, (see Items of Interest, November, 
1915, p. 801.) 

Osler, Sir William. The Principles and Practice of Medicine. (D. 
Appleton & Co., London.) 

Park, William Hallock, and Williams, Anna W. Pathogenic 
Microorganisms. (New York: Lea & Febiger.) 

Partsch. Die Chronische Wurzelhautentziindung. (Deutsche 
Zahneilkunde in Vortrdgen, Leipzig.) 

Perkins, A. F. Root Canals Which Cannot be Filled, (see Items of 
Interest, November, 1915, p. 806.) 

Phillips, W. Charles. Diseases of the Ear, Nose and Throat. (Phil- 
adelphia, 1911.) 

Preisweik, Gustav. Zahnheilkunde, J. F. Lehmann. Miinchen, 1908. 

Proell. Weiteres zur Mikroskopie der Granulome und Zahnwur- 
zelzystem. (Deutsche Montsschr. f. Zahnheilkunde, Jan- 
uary, 1913, p. 1.) 

Uber die Mikroskopie der Granulome, Entstehung und 
Wachstum der Zahnwurzelzystem. (Deutsche Monatsschr. 
f. Zahnheilkunde, July, 1911, p. 558.) 

Zur Mikroskopie der Granulome und Zahnwurzelzystem. 
(Deutsche Monatsschr. f. Zahnheilkunde, March, 1911, p. 

Raper, H. R. Bad Canal Work. What Shall We Do About It? 
(see Dental Items of Interest, February, 1916, p. 111.) 

Rhein, M. L. The Dental Aspect of Oral Infection, (see Items of 
Interest, June, 1914, p. 439.) 

Infected Areas Around the Ends of Roots of Teeth, (see 
Journal of American Medical Association, August, 1912, Vol. 
LIX., p. 361.) 

Scientific Treatment of Root Canals, (see Dental Cosmos, 
September, 1911.) 

Deep-seated Alveolar Infections, (see Surgery, Gynecol- 
ogy and Obstetrics, January, 1916, p. 33.) 

Roe, W. J. Surgical Lesions Due to Oral Sepsis and Their Treat- 
ment, (see The Dental Cosmos, February, 1915, p. 174.) 


Rosenow, E. C. Lesions Produced by Various Streptococci, Endo- 
carditis, and Rheumatism, (see New York Medical Journal, 
February, 1914, p. 270.) 

The Production of Ulcer of the Stomach by Injection of 
Streptococci, (see Journal of American Medical Association, 
November, 1913, Vol. LXI, p. 1947.) 

The Newer Bacteriology of Various Infections as Deter- 
mined by Special Methods, (see Journal of American Medi- 
cal Association, September, 1914, p. 903.) 

Mouth Infection as a Source of Systemic Disease. (see 
Journal of American Medical Association, December, 1914.) 
Transmutations within the Streptococcus Pneumococcus 
Group, (see Journal of Infectious Diseases, Vol. 14, Janu- 
ary, 1914.) 

The Etiology of Acute Rheumatism, Articular and Mus- 
cular, (see Journal of Infectious Diseases, Vol. 14, Janu- 
ary, 1914.) 

Rumpel, C. Die Plasmazellen des Zahngranuloms. (see Viertel- 
jahrsschrift fur Zahnheilkunde, January, 1911, p. 60.) 

Sawyer, A. J. Oral Sepsis as the Cause of General or Systemic In- 
fection, and the Dentist's Responsibility, (see The Dental 
Cosmos, March, 1915, p. 272.) 

Schamberg, M. I. Dentistry, a Blessing and a Curse, (see Journal 
of Allied Dental Association, December, 1915, p. 418.) 

Schuster, Ernst. Die Sektion der Zahnwurzel eine Operations- 
methode zur Entfernung abgebrochener Instrumente aus 
Wurzelkanalen. (Deutsche Monatsschr. fur Zahnheilkunde, 
January, 1913, p. 43.) 

Schwabe. Beziehungen zwischen Augen und Zahnkkrankheiten. 
(Deutsche Monatsschr. filr Zahnheilkunde, June, 1914, p. 

Smith, A. H. Some Studies of the Jaws in Health and Disease. 
(see The Dental Cosmos, August, 1913, p. 765.) 

Smith, E. H. The Value of a Tooth. (see The Journal of Allied 
Dental Societies, September, 1915, p. 331.) 

Steinharter, E. C. Gastric Ulcer Experimentally Produced. (Bos- 
ton Medical and Surgical Journal, May 11, 1916.) 

Acute Arthritis Experimentally Produced by Intravenous 
Injection of the Staphylococcus Pyogenes. (Boston Medical 
and Surgical Journal, July 13, 1916.) 

Storck, J. A. Teeth as a Factor in Digestive Diseases and Dis- 
orders, (see New Orleans Medical and Surgical Journal, 
January, 1904, p. 497.) 

Straussberg, M. Successful Treatment of Apical Abscesses by Ioni- 
zation, (see Dental Items of Interest, April, 1915, p. 259.) 


Streitmann, W. H. Oral Sepsis as Kelated to Systemic Disease, (see 
Items of Interest, December, 1915, p. 930.) 

Stueeidge, Ernest. Dental Electro Therapeutics. (Philadelphia: 
Lea & Febiger.) 

Teague, B. H. The Eecognition of Systemic Disturbance in the Treat- 
ment of Oral Lesions, {see The Dental Cosmos, April, 1915, 
p. 428.) 

Thoma, Kurt H. Oral Anaesthesia. (Boston: Hitter & Flebbe.) 

Oral Anaesthesia with Special Eeference to Surgical Op- 
erations for Chronic Alveolar Abscesses, (see American 
Journal of Surgery, Vol. I, No. 3, April, 1915.) 

Oral Abscesses, (see Journal of the Allied Dental Socie- 
ties, March, 1916.) 

Thomas, J. D. The Effects of Prolonged Treatment and Persistent 
Retention of Diseased Teeth, (see Items of Interest, August 
1912, p. 617.) 

Thomson, Sir St. Clair. Diseases of the Nose and Throat. (Lon- 
don: D. Appleton & Co.) 

Ulrich, H. L. Streptococcicosis. (see Journal-Lancet, November, 

The Blind Dental Abscess. (see Jour nal o f American 
Medical Association, November, 1915, Vol. LXV, p. 1619.) 

Some Medical Aspects of Certain Mouth Infections, (see 
Dental Review, December, 1914.) 

Van Doorn, J. W. Relation of Dental Lesions to Insomnia and Nerve 
Strain, (see The Dental Cosmos, June, 1909, p. 677.) 

Vaughan, V. C. Die Phenomena der Infektion und Ergebuisse der 
Immunitatsforschung Experimentellen Therapie, Bakteri- 
ologie und Hygiene. (see Fortsetzung des Jahresberichts 
uber die Ergebuisse der Immunitatsforschung.) 

Vaughan, Walter, Victor C, and Victor C, Jr. Protein Split 
Products in Relation to Immunity and Disease. (Lea & 

Wallace, J. Sim, London. Dental Diseases in Relation to Public 
Health. (Publishing Office of The Dental Record, 1914.) 
(Deutsche Monatsschr. fur Zahnheilkunde, June, 1914.) 

Williger, Fritz. Zahnarztliche Chirurgie, Berlin. (Leitfaden der 
Praktischen Medizen, Band I, 1910.) 

Young, J. H. Tonsillectomy as a Therapeutic Measure in the Treat- 
ment of Chorea and Endocarditis, (see Boston Medical and 
Surgical Journal, September, 1915, p. 356.) 

Zilz, Juljan. Zur Klinik und Pathologischen Anatomie der 
Speichelsteine. (see Zeitschrift fur Mund-und Kierfer- 
chirurgie und Oreuzgebiete, Erster Band, Erstes Heft, p. 32.) 




I Fig. 1. Predynastic Egyptian Skull, showing loss of bone due 

to Abscess 14 

Fig. 2. Occlusial View of Upper Jaw of same Skull 14 

II Fig. 3. Prehistoric Peruvian Skull, with loss of bone from 

acute abscessed condition 15 

III Fig. 4. Apical, Lateral and Interradial Abscess 18 

IV Figs. 5 and 6. Eadiographs of Abscesses caused by Trauma. . . 20 
Figs. 7 and 8. Eadiographs showing Treatment of Case in Fig. 5 20 
Figs. 9, 10 and 11. Eadiographs of Abscesses involving neigh- 
boring teeth 20 

V Figs. 12 and 13. Abscesses due to Pyorrhoea Pockets 21 

Figs. 14 and 15. Abscesses from Temporary Teeth 21 

Figs. 16, 17, 18 and 19. Abscesses due to Decay of Permanent 

Teeth 21 

VI Fig. 20. Acute Periodontitis 24 

Fig. 21. Acute Abscess 24 

Fig. 22. Subperiosteal Parulis 24 

Fig. 23. Subgingival Parulis 24 

VII Figs. 24, 25, 26, 27, 28, 29, 30 and 31. Sinus Formations 25 

VIII Fig. 32. Skull showing Bone Destruction due to Abscesses 26 

IX Fig. 33. Ostitis, caused by a tooth 27 

Fig. 34. Osteomyelitis of Mandible 27 

X Figs. 35 and 36. Photographs of Teeth showing Exostosis of 

Eoot 28 

Fig. 37. Molar with Scar Bone 28 

XI Fig. 38. Central Incisor with Acute Abscess 29 

Fig. 39. Photograph of Subgingival Parulis 29 

XII Fig. 40. Lateral Granuloma 34 

Fig. 41. Apical Granuloma 34 

Fig. 42. Interradial Granuloma 34 

XIII Figs. 43, 44 and 45. Granulomata caused by Decay of Tooth. . 35 
Figs. 46, 47 and 48. Granulomata caused by Incomplete Pulp 

Extirpation 35 

Figs. 49 and 50. Granulomata due to Broken Instruments 35 

XIV Figs. 51, 52, 53, 54, 55 and 56. Granulomata caused by In- 
efficient Eoot Canal Fillings 38 

Figs. 57, 58 and 59. Granulomata from Decay under Filling. . 38 

Figs. 60, 61 and 62. Granulomata on Crowned Teeth 38 



















Fig. 63. Skull showing Bony Destruction Caused by an Apieal 

Granuloma 39 

Fig. 64. Skull showing Bony Destruction due to a Granuloma. . 40 
Figs. 65, 66, 67, 68, 69 and 70. Badiographs showing Exostosis 

of Boots 41 

Figs. 71, 72 and 73. Badiographs showing Teeth with Necrosed 

Apices 41 

Fig. 74 and 75. Badiographs of Teeth showing large Oste- 

omyelitic Areas 41 

Fig. 76 and 77. Badiographs of Teeth showing Small Areas in- 
dicating Periodontitis 44 

Fig. 79, 80 and 81. Badiographs of Teeth showing Large Areas 

indicating Granulomata 44 

Fig. 82 and 83. Badiographs of Teeth with Subacute Abscesses 44 
Fig. 84, 85 and 86. Badiographs showing Pus Pockets caused 

by Mechanical Injury 45 

Fig. 87, 88, 89 and 90. Badiographs of Teeth showing Dark 

Areas at the Alveolar Border 45 

Fig. 91. Badiograph showing Apical Abscess caused by Pus 

Poeket; Tooth Vital 45 

Figs. 92, 93, 94 and 95. Badiographs showing Abscesses caused 

by Impacted Wisdom Tooth 48 

Fig. 96, 97 and 98. Badiographs of Abscesses caused by TTn- 

unerupted Molars 48 

Fig. 99. Badiograph showing Impacted Second and Third Molar 49 
Pig. 100. Badiograph showing Broken Off Impacted Second 

Molar 49 

Figs. 101 and 102. Badiographs showing Impacted Temporary- 
Molars 49 

Figs. 103, 104, 105, 106, 107 and 108. Other Impacted Teeth. . . 49 
Fig. 109. Badiographic Plate showing an Impacted Upper 

Third Molar on Posterior Wall of Antrum 50 

Fig. 110. Badiographic Plate showing Unerupted Lower Third 

Molar at the Angle of Jaw 51 

Fig. 111. Simple Abscess of Tongue 52 

Fig. 112. Tubercular Abscess of Tongue 52 

Fig. 113. Swelling under Tongue on Left Side 56 

Fig. 114. Badiograph showing Salivary Calculus 56 

Fig. 115. Badiograph of Granuloma 58 

Fig. 116. Smear of Bacteria Contained in above Granuloma. . 58 

Fig. 117. Tooth with Large Granuloma 68 

Fig. 118. Microphotograph of Section of Above showing Actin- 
omycoses Colonies 68 

Fig. 119. Microphotograph of Section through Granuloma show- 
ing Actinomycoces Colonies 70 

Fig. 120. Microphotograph of Chronic Myocarditis produced in 

Babbit 72 

Fig. 121. Microphotograph of Acute Myocarditis produced in 

Babbit 72 































































122. Microphotograph showing Infiltration of Leucocytes 
and Lymphocytes in Kidney of Eabbit 74 

123. Microphotograph showing Polymorphonuclear Abscess 
in Medulla of Kidney of Eabbit 74 

124. Microphotograph of Epitheliated Granuloma 76 

125. Microphotograph of Simple Granuloma 78 

126. Microphotograph of Simple Granuloma showing dis- 
tinct Capsule 78 

127. Microphotograph of Simple Granuloma showing 
Active Pus formation 78 

128. Microphotograph of Granuloma with Sinus 78 

129. Lithograph showing Construction of Capsule of 
Granuloma (Fig. 127) 80 

130. Lithograph showing Construction of Granuloma 
(Fig. 124) 80 

131. Lithograph of Inner Part of Granuloma of Fig. 124 80 

132. Lithograph of Inner Part of Granuloma of Fig. 128 80 

133. Radiograph showing Granuloma in Lateral Incisor. . 81 

134. Photograph of Excised Granuloma 81 

135. Microphotograph of same Granuloma 81 

136. Lithograph of High-power Drawing of Granuloma 
(Fig. 135) 82 

137. Lithograph of High-power Drawing of another part 82 

138. Antrum exposed to show Abscess 90 

139. Radiograph of Case 1 91 

140. Radiographic Plate of Case 1 91 

141. Cross Section through Eye 94 

142. Acute Catarrhal Conjunctivitis 95 

143. Simple Ulcer of Cornea 95 

144. Normal Eye, and Iritis 95 

. 145, 146, 147 and 148. Radiographs of Case VI 98 

149. Radiograph of Case VII 99 

150. Radiograph of Case VIII 99 

151. Position of Lymph Glands beneath Lower Jaw 100 

152. Schematic Drawing showing Teeth Drained by Lymph 
Glands 101 

153. Radiograph Case IX 104 

154. Radiograph Case X 104 

. 155 and 155a. Radiographs of Case XI 105 

156. Radiograph of Case XVII 122 

157 and 158. Radiograph of Case XVII 122 

159 and 159a. Radiograph of Case XX 123 

160. Radiographic Plate of Case XXI 130 

161. Radiograph of Case XXII 131 

162. Radiographic Plate of Case XXII 131 




LI Figs. 163, 164 and 165. Eadiographs of Case XXVII 136 

LII Fig. 166. Normal Hand 137 

Fig. 167. Hypertrophic Arthritis 137 

LIII Fig. 168. Gouty Arthritis 138 

LIV Fig. 169. Infectious Arthritis 139 

Fig. 170. Atrophic Arthritis 139 

LV Fig. 171. Eadiographic Plate of Case XXVIII 142 

LVI Fig. 172. Eadiograph of Case XXVIII 143 

Fig. 173. Eadiographic Plate of Case XXIX 143 

LVII Figs. 174, 175, 176, 177, 178 and 179. Eadiographs showing a 

Large Amount of Bridgework and Many Abscesses. . 144 

LVIII Figs. 180, 181, 182, 183, 184 and 185. Eadiographs of a Neg- 
lected Mouth 145 

LIX Figs. 186 and 187. Eadiographs revealing Deep Cavities causing 

Obscure Pain 146 

Fig. 188. Eadiograph shows a large amount of trouble 146 

Figs. 189, 190, 191, 192 and 193. Eadiographs showing the 

Value of X-Eays before undertaking Eoot Canal Work 146 

LX Fig. 194. Eadiographic Examination of a Mouth 147 

Fig. 195. Chart Indicating Granulomata and Eoot Canal Fil- 
lings of the above case 147 

LXI Fig. 196. Eeport Chart as used by Dr. Potter 148 

LXII Figs. 197, 198, 199 and 200. Steps in Apiectomy 162 

LXIII Figs. 201, 202, 203 and 204. Steps in Apiectomy 162 

LXIV Figs. 205, 206, 207 and 208. Steps in Apiectomy 162 

LXV Figs. 209, 210 and 211. Eadiographs of Three Cases not favor- 
able for Apiectomy 164 

LXVI Figs. 212 to 220. Eadiographs showing the Treatment of Five 

Devitalized Teeth 165 

LXVII Figs. 221, 222, 223, 224, 225, 226 and 227. Eoot Canal Treat- 
ment and Apiectomy on a Lateral Incisor 166 

Figs. 228, 229, 230 and 231. Eoot Canal Treatment and Apiec- 
tomy on Another Lateral Incisor 166 

Figs. 232, 233, 234 and 235. Process of Apiectomy on Two 

Teeth shown by Eadiographs 166 

LXVIII Figs. 236, 237 and 238. Eadiographs showing Apiectomy on a 

First Bicuspid 167 

Figs. 239, 240, 241 and 242. Eadiographs of Apiectomy on a 

Cuspid 167 

LXIX Figs. 243, 244, 245 and 246. Apiectomy on a Cuspid which is 

the Abutment of a Bridge 168 

Figs. 247 and 248. Apiectomy on a Lateral Incisor 168 

Figs. 249 and 250. Apiectomy on a Central Incisor 168 

Figs. 251, 252 and 253. Apiectomy on a Central and Lateral In- 
cisor 168 

LXX Figs. 254 and 255. Apiectomy on a Lower Incisor 169 

Fig. 256. Apiectomy on Two Lower Incisors 169 




LXX Pigs. 257 and 258. Apieetomy on a Lower Incisor with Broken 

Eoot Instrument 169 

Figs. 259 and 260. Apieetomy on a Lower Bicuspid 169 

LXXI Figs. 261, 262 and 263. Kadiographs showing Healing of Bone. 170 
Figs. 264, 265 and 266. Kadiographs showing Healing of Bone. 170 
Figs. 267, 268 and 269. Eadiographs showing Healing of Bone. 170 

LXXII Fig. 270. A Selection of Curettes 171 

LXXIII Figs. 271 and 272. Excision of Tip of Tongue 172 

LXXIV Fig. 273. Microphotograph showing Multiple Foramina 180 

LXXV Fig. 274. Microphotograph showing a Boot Canal Filling 182 

LXXVI Figs. 275, 276 and 277. Eadiographs showing the Process of 

Eoot Canal Treatment 184 

Figs. 278, 279 and 280. Eadiographs showing the Process of 

Eoot Canal Treatment 184 

Figs. 281 and 282. Eadiograph showing Poor and Good Eoot 

Canal Filling 184 

LXXVII Fig. 283. Eoot Treatment through Small and Large Cavity 185 

Figs. 284 and 285. Specimen of Bent Eoots 185 

LXXVIII Figs. 286, 287, 288 and 289. Models of a Patient's Mouth (Age 
35) who had the Four Six-year Molars Extracted 

at Age of Thirteen Years 189 

LXXIX Figs. 290 and 291. Models of the Mouth of a Boy Aged Thirteen 190 
Figs. 292 and 293. Models of same mouth Three Years Later, 

All Six-year Molars having been Extracted 190 




acute alveolar 24 

acute alveolar, histological 

pathology of 77 

acute, methods of collect- 
ing bacterial specimens. 59 

alveolar, chronic 27 

bacterial specimens of 59 

clinical signs 30 

general symptoms.... 30 

histological pathology 78 

local symptoms 30 

radiographic examina- 
tion 31 

subacute 28 

alveolar, due to difficult 
eruption, impaction, and 

unerupted teeth 47 

clinical signs 50 

course of disease 47 

diagnosis 49 

etiology 47 

general symptoms .... 50 

local symptoms 49 

radiographic examina- 
tion 50 

alveolar, due to diseases of 

dental pulp 18 

pathological develop- 
ment of 18 

alveolar, due to disease of 

the gum 45 

clinical signs 47 

course of disease 46 

diagnosis 47 

etiology 45 

general symptoms .... 47 

local symptoms 47 

radiographic examina- 
tion 47 

treatment of 169 

of salivary glands and 

ducts 54 

clinical course 56 

clinical signs 57 

diagnosis 56 

etiology 55 

local symptoms 56 

radiographic examina- 
tion 57 


Abscesses of salivary glands and 
ducts. — Continued. 

treatment 173 

excision of glands 175 
operation from floor 

of mouth 174 

of tongue 51 

treatment of 171 

varieties 51 

phlegmonous 52 

clinical signs 53 

diagnosis 53 

etiology 52 

general symptoms. . 53 

simple 51 

clinical course 52 

clinical signs 52 

diagnosis 52 

etiology 52 

local symptoms .... 52 

tubercular 53 

clinical course 54 

clinical signs 54 

diagnosis 54 

etiology 53 

general symptoms. . 54 

local symptoms .... 54 

oral, history and varieties 15 

bacteriology of 58 

histological pathology 

of 77 

review of bacteriologi- 
cal study of 61 

Absorption, channels of 12 

Actinomycosis, investigations of 

Thoma 70 

Action of bacterial ferments 8 

Affections of the nervous system .... 128 

Alimentary canal, diseases of 109 

haematogenous in- 
fection of 110 

Alveolatomy 162 

Anaemia 121 

pernicious 122 

primary and secondary.... 121 

septic 122 

Case XIX 122 

etiology 122 

symptoms 122 




Anaesthesia for pulp extirpation. . . . 181 

local 164 

Angina 53 

Animal inoculation 61 

Antiseptic medication 182 

Antitoxin 6 

Apiectomy 164 

failures and dangers 166 

healing of wound 166 

operation 165 

preparing the patient 164 

Appendicitis 113 

Application of counter-irritants for 

acute abscesses 152 

Arkovy, bacterial table 62 

Arthritis 135 

Asepsis and sterilization in root 

canal 185 

acute infections 135 

Case XXVII 136 

etiology 136 

atrophic 138 

Cases XXVII, XXIX 140,142 

etiology 138 

treatment 139 

chronic infectious 137 

hypertrophic 137 

etiology 137 

Aural disturbances 100 

Author 'a remark 75 

Autoinoculation, surgical 176 


Bacteria, invasion of, causing prolif- 
erating periodontitis .... 38 
aerobic and anaerobic, culti- 
vation of 60 

Bacteremia 11 

Bacterial ferments 2 

action of 8 

Immunity 5 

investigations : 

Arkovy 62 

Author 's remark 75 

Gilmer 70 

Goadby 62 

Hartzel and Henriei 71 

Mayerhof er 65 

Miller 61 

Monier 63 

Partsch 63 

Schreier 61 

Steinharter 75 

Thoma 70 

Vincent 65 

metabolism, by-products of 9 
specimens, method of col- 
lecting 60 


Bacteriological study, importance of 59 

review of 61 

Bacteriology of Oral Abseesses 58 

Biological laws of Vaughan 5 

Black's 1, 2, 3 152 

Blood, changes of, during infection. . 11 

diseases of 115 

Body cell, the 3 

ferments of 3 

sensitization of 9 

Buckley 's modified phenol 151 


Calculi, salivary in glands and ducts 55 

Cards for examination 146 

Case charts, Potter 149 

Cathartics in acute abseesses 145 

Changes in blood from infection. ... 10 
Change in oxygen tension causing 

acute periodontitis 26 

Channels of absorption 12 

Chart, radiographic 149 

Cholesterin, degeneration in granu- 
loma 83 

Chorea 132 

Case XXIV 133 

etiology 132 

Choroiditis 97 

etiology 97 

symptoms 97 

Chronic alveolar abscess 33 

clinical signs 34 

general symptoms 33 

local symptoms 33 

radiographic examination 34 

Chronic conditions, treatment of 157 

Classification of oral abscesses 16 

Clinical picture of infection 9 

Colitis 113 

Collection of bacterial specimens . . 59, 60 

Complications 84 

of acute periodontitis. 26 

secondary 84 

systemic treatment of 178 

Conjunctivitis 95 

infectious 95 

etiology 95 

symptoms 95 

Counter-irritants, application of for 

acute abscess 152 

Cover glass preparations 60 

Cultivation of aerobic and anaerobic 

bacteria 60 

Curettage and extraction in abscessed 

conditions 167 

Cyelitis 97 

Cysts 41 

Cysts in granulomata 83 





Decay of deciduous teeth causing 

acute periodontitis 21 

first molar 189 

permanent teeth causing 

acute periodontitis 22 

the teeth causing prolifer- 
ating periodontitis 36 

Decrease of resistance 4 

Defence of the body, protective 4 

Devitalized teeth, prevention of 186 

Disease, secondary, prevention of . . . 179 
Diseases of soft tissues, examination 

of 147 

the alimentary canal .... 109 

blood 115 

heart 123 

joints 135 

teeth 147 

Diagnosis of condition of devitalized 

teeth 148 

abscesses caused by ab- 
scesses of tongue, sal- 
ivary glands and 

ducts 51, 56 

abscess of the tongue. . 52 
acute periodontitis .... 29 
alveolar abscesses 
caused by diseases of 

the dental pulp 18 

alveolar abscesses due 
to other causes than 
diseases of the dental 

pulp 45 

phlegmonous abscess of 

the tongue 53 

proliferating periodon- 
titis 29 

tubercular abscess of 

the tongue 54 

unerupted and impact- 
ed teeth 49 

Ducts, pathological development of 

salivary abscesses from .... 51 

abscesses from 54 


ulcer (see Ulcer) 113 


Ear (see Aural disturbances) 100 

Efficiency of treatment of granulo- 

mata, original investigations 158 

Electrolytic treatment for abscesses. 161 

for root canal work .... 184 

Endocarditis 125 

acute and chronic 125 

Case XX 127 

treatment 125 


Enteritis, septic 112 

etiology 112 

Case XIV 113 

symptoms 112 

Europhorm paste 155 

Exacerbation 167 

Examination cards 146 

Examination of oral cavity 144 

by dentist 146 

physician 145 

Examination of soft tissue of mouth 145 

the teeth 146 

physical 146 

Excision of salivary glands 175 

small tubercular ab- 
scesses of tongue .... 172 

tongue V-shaped 172 

Exostosis of root 28 

Extirpation of impacted and un- 
erupted teeth 170 

preanaesthetic medication after 

treatment 171 

Extirpation of teeth 168 

anaesthesia 168 

care of wound 169 

indication 168 

operation 168 

Extracellular ferments 2 

toxins 3 

Extraction and curettage of abscessed 

condition 167 

of badly decayed first molars 

in children 190 

teeth in acute abscesses. . . 154 


Ferments, action of bacterial 8 

analytic 2, 3 

bacterial 2 

extracellular 2, 3 

intracellular 2, 3 

of body cell 3 

synthetic 2, 3 

Fever, general effects of local infec- 
tion 10 

Fever in acute abscesses 30 

acute sinusitis 116 

alveolar parulis 33 

pyaemia 117 

from impacted and unerupted 

teeth 50 

rheumatic in acute infectious 

arthritis 135 

Filling teeth with infected pulps 

causing acute periodontitis 30 

Focus of infection 13 

Focus, removal of 176 

Formaldehyde contraindicated 182 





Galvanic current for diagnosis. . .30, 34 

Gilmer, bacterial investigation of . . . 70 

Glands, salivary abscesses 51 

pathological development of 54 

Glaucoma 99 

etiology 99 

primary and secondary. ... 99 

symptoms 99 

Goadby, bacterial investigations of . . 62 

Granuloma 39 

apical 36 

clinical signs 43 

epitheliated 81 

general signs 43 

histological pathology... 79 

interradial 39 

local symptoms 42 

lateral 37 

methods of collecting bac- 
terial specimen 60 

with lumen 82 

Hartzel and Henrici, bacterial inves- 
table of fer- 
mentation... 73 

Heart, diseases of 123 

High frequency current for diagnosis 30 
History and varieties of oral ab- 
scesses 15 

Hyalin degeneration in granuloma.. 83 


Idman, bacteriological investigation 66 

Immunity, acquired 5 

bacterial 5 

natural 5 

toxin 5 

Impacted teeth 48 

extirpation of 170 

Incision in simple abscess of tongue. 171 

Infection, phenomena of 1 

from pus pockets causing 

acute periodontitis 20 

Infections 10 

acute and chronic 10 

clinical picture 9 

continuous 84 

from adjacent teeth caus- 
ing acute periodontitis. . 20 

general 11 

general effects of 10 


Infections, haematogenous 85 

causing proliferating 

periodontitis 39 

influence of quantity on . . . 9 

local 10 

lymphatic 85 

predilection of 13 

prevention of periapical . . 180 

secondarily transported... 11 

virulence 9 

Infection through alimentary canal. 85 

Infective virus, the 1 

Injury of the gum causing alveolar 

abscess 45 

Inoculation 10 

of animals 61 

of artificial media 60 

Instrumentation causing acute peri- 
odontitis 23 

Intracellular ferments 2 

Investigation, original, of the efficien- 
cy of treatment of granulomata. . . 158 
Involvement of neighboring parts ... 86 
Iodine for root canal treatment. . . . 184 

Ionic medication 161, 184 

Iridiohoroiditis 97 

Iridocyclitis 96 

etiology 97 

symptoms 97 

Iritis 97 

etiology 97 

symptoms 97 


Joints, diseases of 135 


Keratitis suppuration 95 

etiology 95 

symptoms 95 


Laxative in acute abscess 156 

Lead points for root canal fillings.. 163 

Lymphadenitis, cervical 104 

acute 104 

Case X 106 

etiology 105 

symptoms 105 

treatment 105 

chronic 106 

etiology 106 

symptoms 106 

treatment 106 




Lymphadenitis, subacute 106 

Case XI 106 

symptoms 106 

# tubercular 106 

Case XII 109 

etiology 107 

symptoms 107 

treatment 107 

Lymphangitis 103 

Case IX 104 

etiology 103 

symptoms 103 

treatment 103 

Lymphatic infection 102 

Lymph glands, enlarged 146 

location 102 


Malaise 119 

treatment of 119 

Manifestations secondary 13 

Mastication efficiency, restoration of 177 
Mayerhofer, bacteriological investi- 
gations 65 

table 66 

Medication, antiseptic 182 

ionic 161 

for root canal treat- 
ment 184 

Melancholia 133 

Case XXVI 135 

Menier, bacterial investigation 63 

bacteriological table 65 

Mental depression 133 

Case XXV 134 

Metabolism, by-products of bacterial 8 

Metastasis 11 

Methods of animal inoculation 61 

bacterial study 60 

collecting bacterial speci- 
mens 59 

Middle ear inflammation 100 

Miller, bacterial investigation 62 

Molar, early decay of first 189 

Myocarditis 121 


Natural Immunity 5 

Necrosis 26 

of root 29 

Nerve communication between ear 

and teeth 100 

communication between eye 

and teeth 94 

reference table 131 

Nervous system, affections of 128 


Neuralgia, trifacial 130 

Case XXII 132 

Case XXIII 132 

etiology 130 

symptoms 132 

Neuritis 128 

Case XXI 129 

etiology 128 

general 129 

symptoms 129 

intraocular optic 98 

etiology 98 

symptoms 98 

retrobulbar optic 98 

Case VI 98 

etiology 98 

symptoms 98 


Occlusion, sufficient 190 

Ophthalmic disturbances 94 

Optic neuritis 98 

Oral abscesses, treatment of 150 

cavity, examination by physi- 
cian 145 

examination of 144 

Osteomyelitis, acute 26 

chronic 41 

Ostitis 26 

Otalgia 101 

Case VIII 101 

Otitis media 100 

Case VII 101 

Overdentistried teeth 146 


Pain in ear (Otalgia) 101 

relief of 156 

Papillitis 98 

Paresthesia 129 

Partsch, bacterial investigation 63 

Parulis, alveolar 24 

clinical signs 33 

differential diagnosis 32 

general symptoms 33 

histological pathology 78 

local symptoms 31 

radiographic examination. . 33 

Parulis, subgingival 25 

subperiosteal 24 

Pathological development of absces- 
ses of tongue and 

salivary glands 51 

development of alveolar 
abscesses caused by 
diseases of the den- 
tal pulp 18 




Pathological development of alveo- 
lar abscesses due to 
other causes than 
disease of the dental 

pulp 45 

Pathology, histological 77 

Peptic ulcer 113 

Periapical infection, prevention of.. 180 

Pericarditis 124 

Periodontitis 19 

acute and its sequels 19 

acute interradial 19 

acute lateral 19 

clinical signs 29 

diagnosis 29 

histological pathology 77 

apical 19 

complication 26 

course of disease 24 

definition 19 

etiology 20 

Periodontitis, proliferating 

clinical signs 42 

diagnosis 42 

general symptoms 42 

local symptoms 42 

radiographic examination 42 

Periodontitis, proliferating and se- 
quels 34 

course of disease 39 

definition 34 

etiology 45 

histological pathology 79 

termination 41 

varieties 35 

Pharyngitis 92 

Case III 92 

symptoms 92 

treatment 92 

Phenomena of infection, the 1 

Physical examination of oral cavity. 145 

Poison, protein 7 

Potter, case charts 149 

Prevention 178 

of abscesses by early treat- 
ment 188 

caries by prophylaxis. . 188 

devitalized teeth 186 

devitalized teeth by 
treatment of hyper- 
emia and exposures 

of the pulp 187 

periapical infection. . . 180 
secondary diseases 

from oral abscesses. 179 

Process of infection, the 6 

Proctitis 113 

Protective defenses of the body .... 4 


Protein poison 7 

poison caused by bacterial 

metabolism 8 

poisons 59 

sensitization 6 

Prognosis before root canal treat- 
ment 148 

Pulp, death of, without access of air, 
causing proliferating peri- 
odontitis 38 

extirpation incomplete caus- 
ing proliferating periodon- 
titis 36 

Pulp extirpation, anaesthesia for. . . 180 

Pus pockets causing alveolar ab- 
scesses 46 

Pyaemia 117 

etiology 117 

illustrative Case XVI 117 

symptoms 117 

treatment 117 


Eadiographic chart 149 

diagnosis before root 

canal treatment .... 181 
diagnosis important in 
secondary infection . 84 

examination 148 

in acute maxillary 

sinusitis 87 

in chronic maxil- 
lary sinusitis... 88 
in trismus of mus- 
cles of mastica- 
tion 93 

of acute alveolar 

abscesses 31 

of alveolar absces- 
ses caused by 
diseases of the 

gum 47 

of alveolar parulis 33 
of chronic absces- 
ses 34 

of granulomata. . . 43 
o f proliferating 

periodontitis ... 42 
of salivary stones. 57 
of subacute attacks 44 
of unerupted and 
impacted teeth. . 50 
Eadiotherapy for tubercular lymph- 
adenitis 108 

Belief of pain 156 

Eemoval of the cause in acute and 
chronic conditions 160 




Eesistance 4 

decrease of 4 

increase of 5 

Resolution of aeute periodontitis. ... 27 
of proliferating periodon- 
titis 41 

Eest of diseased tooth 152 

Restoration of masticating efficiency 177 

Retinitis 97 

etiology 97 

symptoms 98 

Review of bacteriological study of 

oral abscesses 61 

Rheumatic fever (see acute arthritis) 135 

Root exostosis 40, 28 

necrosis 40, 29 

Root canal cleaning and enlarging . . . 181 

filling 185 

drying 185 

radiographic examination 

before apiectomy 164 

treatment, asepsis and 

sterilization 185 

treatment before apiec- 
tomy 148 


Sapremia 118 

Scar bone 27 

Schreier, bacterial investigation .... 61 

bacteriological table 62 

Scleritis 95 

etiology 95 

Case V 96 

symptoms 95 

Sensitization : protein 6 

of body cell 7 

Septicemia 116 

etiology 116 

symptoms 116 

treatment 116 

Sequestrum 27 

Sinus, active 27 

closed 27 

to face, treatment of 157 

Sinusitis maxillary 86 

acute 86 

etiology 86 

clinical signs - 87 

symptoms 86 

treatment 87 

chronic 88 

Case 1 90 

Case II 90 

etiology 88 

clinical signs 88 

symptoms 89 

treatment 89 


Sodium potassium treatment 181 

Steinharter, bacterial investigation. 75 
Sterilization and asepsis in root canal 

treatment 185 

Summary of prevention of periapical 

infection 186 

Systemic complications treatment. . 175 
treatment for acute ab- 
scesses 155 


Table of nerve reference 131 

Teeth, devitalized, examination of . . 148 

examination of 147 

extraction and extirpation. . . 168 
of in acute ab- 
scesses 144 

overdentistried 146 

prevention of devitalized. . . . 186 
unerupted and impacted, 

differential diagnosis 47 

Termination of acute periodontitis . . 27 
Thermal shocks causing acute peri- 
odontitis 21 

Thoma, bacteriological investigations 70 

Thrombosis 117 

Tongue, abscesses, pathological devel- 
opment 51 

abscesses, treatment 171 

excision of small tubercular 

lesions 172 

excision of V-shaped part. . 172 
incision in simple abscess.. 172 

Toxemia 11 

Cases XVII, XVIII 120 

chronic 119 

etiology 118 

symptoms 119 


activity 6 

absorbed from granulomata . . 63 

definition 3 

extracellular 3 

intracellular 7 

Treatment of acute and subacute con- 
ditions 150 

abscesses due to diffi- 
cult eruption, etc. . . . 169 
abscesses due to dis- 
eases of the gum .... 169 
abscesses of salivary 

glands and ducts .... 173 
abscesses on tongue . . . 171 
caries to prevent ab- 
scesses 188 

chronic conditions .... 157 




Treatment of excision of glands .... 175 
hyperemia and expo- 
sures of pulp to pre- 
vent devitalization of 

pulp 187 

operation from floor of 

mouth 174 

root canals in chronic 
conditions before 

apiectomy 163 

sinus to face 157 

systemic complications 176 
systemic complications 
for acute abscess. . . . 155 
with antiseptics applied 

to root canal 160 

Trismus, etiology 93 

Case IV 93 

diagnosis 93 

symptoms 93 

treatment 93 

Tubercular lymphadenitis 106 

Tuberculosis of granuloma 63 


Trigeminal neuralgia (see Neural- 
gia) 130 

True value of a tooth 189 


Unerupted teeth, extirpation (see 

Extirpation) 170 

Ulcers, gastric and duodenal 113 

Case XV 114 

etiology 113 

symptoms 113 


Value of healthy tooth 191 

Value, true, of tooth 189 

Varieties of alveolar abscesses caused 

by diseases of the dental pulp .... 18 
Varieties and history of oral ab- 

sceses 15 

Vincent, bacteriological investiga- 
tions 65 

Virus, the infective 1 


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RD 641 T36 C.1 

Oral abscesses,