A text-book of dental pathology and therapeutics for students and practitioners, based upon the original of Henry H. Burchard ...

Front matter

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A TEXT-BOO I

Preface To Sixth Edition

In revising this work for a new edition, the editor has endeavored to maintain the original idea of a text-book, furnishing a description of each dental disease and its treatment in such manner that teachers may find it a useful adjunct in the presentation of the subject of dental pathology and therapeutics to their students. Since the last edition a reprint has been necessary, owing to an unexpectedly large demand by the Government, and in consequence of this and the almost revolutionary changes which have occurred in the professional thought and because of natural developments from scientific investigations many changes have had to be made. It has been thought advisable to omit certain chapters dealing with subjects which are better covered in other approved text-books and to include new chapters upon subjects which are germane to dental pathology. Thus, chapters on Prophylaxis, Radiography, Plantations, The Uses of Electricity in Therapeutics and Root Amputation have been inserted. Many new illustrations have been added to take the place of some omitted and to enhance the elucidation of the subjects.

Wherever quotations appear an endeavor has been made to credit the author, the idea to be presented has been the compelling motive rather than the writing of a history. Quotations have generally been made from current literature and from as limited a bibliography as possible in order that this work may have value added to it by reference to books and journals within easy reach of any who desire further details. The editor desires to thank those who have kindly loaned illustrations, and the publishers for their generous treatment, also the profession for its continued favor. O. E. Inglis.

1524 Chestnut Street, Philadelphia.

Chapter I. General Principles

General pathology (pathos, disease, and logos, & discourse) is that branch of science which treats of the modifications in function and changes in structure occurring in disease. It embraces all pathological processes occurring in the human body, and as many of these occur in and about the teeth, modified only by the peculiar anatomy of the parts, Dental Pathology may be said to be that branch of dental science which treats of modifications in function and changes in structure occurring in the diseases of the teeth and associate parts.

This being true, it follows that the study of dental pathology must be preceded by a study of the general disease processes which affect the tissues of the body, and such of these as are applicable to the study are known as the General Principles.

The word Therapeutics is derived from the Greek therapeuein, to take care of, meaning the measures adopted to remedy or remove the changes induced by pathological processes.

The study of the pathology of a part begins with a study of its anatomy and histology, then naturally follows a study of its physiology and embryology. These form the basis from which degrees of abnormal function and altered structure may be judged by comparison with similar processes occurring in other parts of the body.

This altered function and structure theoretically go hand in hand, as whichever begins first the other surely follows even if only to a microscopic degree. Disease, in its broad sense, is therefore an alteration of nutrition, resulting in changes in function and structure. The term Disease refers to the various classified pathological con- 2 (17)

18 GENERAL PRINCIPLES

ditions. each occurring in a more or less definite way and having sufficiently defined characteristics to render them distinct from each other. The sequence of cause, effect upon the circulation and the cells, the alterations in the function and structure of the cells and of the part or body as a whole, together with the terminations of disease, are embraced in the term Pathology. The term Morbid Anatomy refers more particularly to the changes in structure.

A disease cause may be defined as any influence of whatsoever nature which is capable of disturbing the nutritive balance of any portion of the body.

The study of disease causes is called Etiology. The signs of disease obtainable by vision, hearing, touch, smell, taste, microscopic examination or chemical analysis are termed the Objective Symptoms. Such sensations or effects as are described by the patient are the Subjective Symptoms. The study of both kinds is Symptomatology.

The grouping of all the clinical phenomena of a particular disease is its Clinical History.

The distinction of a present disease from all others by means of its symptoms is Diagnosis, and its probable outcome judged from the existing phenomena and the usual clinical history under such circumstances is Prognosis.

The cause which directly produces a disease is known as the exciting cause, while a condition, either local or systemic, which favors its action is known as a predisposing cause (see those of Dental Caries). A Proximate Exciting Cause is one which exerts its effect directly upon the cells, while a cause back of this and to which the proximate cause may be due, is a Primary Exciting Cause.

The proximate exciting causes may be conveniently grouped into:

1. Abnormal Food Supply, a condition of the blood which contains substances improper for the cells, or lacks constituents they need, or the cells are supplied with too much or too little lymph (food).

2. Abnormal Waste Removal, either due to circulatory disturbance causing retention of the waste of cells about them when it should be removed, or as a fault of some excretory organ (primary cause) retaining waste of cells in the blood as a whole.

3. Abnormal Physical Conditions, such as direct injuries, mechanical interference with the cells or their circulation, or chemical effects including the action of microorganisms.

4. Abnormal Nerve Supply, such as excessive or defective innervation.

In a general way all living cells, including microorganisms, have common life conditions which may be grouped as follows:

PATHOGENESIS 19

1. A proper food supply, including water and oxygen, though some bacteria seem to do better in the absence of oxygen and plants require carbon dioxid.

2. A proper removal of waste products.

3. Proper physical conditions, including a proper temperature.

4. Possibly a proper innervation, though this does not apply to microorganisms.

As disease conditions are alterations of nutrition, due mainly to change in life conditions, the above classification of proximate exciting causes is justifiable.

From the standpoint of dental pathology, exciting causes may again be divided into (1) septic or those due to bacteria or protozoa and

(2) aseptic or non-septic, such as the mechanical, chemical and nervous, the resulting diseases being also broadly classifiable into septic and non-septic, each class having many dental representatives.

In the production of pathological conditions by a disease cause the part may (1) be injured directly after which the process of pathology starts in the tissue injured if death of all cells be not immediately produced, but if death of cells occurs, the process begins in the adjoining living cells or (2) the cells may be stimulated, all their functions being increased either within semi-physiological bounds or stimulated to the point of weariness and exhaustion. The substance of the cells is lost in overwork, and if not promptly replaced, degeneration ensues.

(3) The cells may be reduced in activity by lessened temperatures, retained waste products or lack of food supply, lessened innervation, etc., and all of their functions reduced. They gradually pass through atrophy, degeneration and death, owing to altered metabolism. (4) Cells may be altered in character by infiltration of materials derived from other sources into their substance or they may be individually injured by microorganisms.

The origin and progress (Pathogenesis) of a disease being known, intelligent efforts may be made for its prevention. This is Prophylaxis.

The science of prevention of disease upon the broad basis of a knowledge of disease causes and observance of laws of health is Hygiene.

It will be seen that a knowledge of special pathology can only be obtained from (1) a knowledge of pathology in general or at least of those principles of general pathology which underlie all disease processes; (2) a knowledge of the local anatomy and histology; (3) a knowledge of local embryology and physiology; (4) a study of local pathology and morbid anatomy. To this must be added a study of materia medica arid special therapeutics.

20 GENERAL PRINCIPLES

"When treatment is based on pathogenesis and a parallel knowledge of the action of drugs and remedies, it is termed Rational Therapeutics. When based upon known good effects of a drug or remedy, without knowledge of its action, it is termed Empirical Therapeutics.

In this work merely the most important general principles are included, the reader being referred to works on general pathology for subjects not touched upon.

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BLOOD.

(Ehrlich triple stain.) (Prepared by Dr. I. P. Lyon.)

Fig. I. TYPES OF LEUCOCYTES.

a. Polymorphonuclear Neutrophile. b. Polymorphonuclear Eosinophile. c. Myelocyte (Neutrophilic), d. Eosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). /. Small Lymphocyte (small Mononuclear).

Fig. II. NORMAL BLOOD, field contains one neutrophile. Reds are normal.

Fig. III. AN/EMIA, POST-OPERATIVE (secondary).

The reds are fewer than normal, and are deficient in haemoglobin and somewhat irregular in form. One normoblast is seen in the field, and two neutrophiles and one small lymphocyte, showing a marked post-hsemorrhagie anaemia, with leucoeytosis.

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY.

The reds are normal. A marked leucoeytosis is shown, with five neutrophiles and one small lymphocyte. This illustration may also serve the purpose of showing the leucoeytosis of malignant tumor.

Fig. V. TRICHINOSIS.

A marked leucoeytosis is shown, consisting of an eosinophilia.

Fig. VI. LYMPHATIC LEUKAEMIA.

Slight anaemia. A large relative and absolute increase of the lymphocytes (chiefly the small lymphocytes) is shown.

The reds show a secondary anaemia. Two normoblasts are shown. The leucoeytosis is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelocytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations from the typical in size and form.

Fig. VIII. VARIETIES OF RED CORPUSCLES.

a. Normal Red Corpuscle (normocyte), b, c. Anaemic Red Corpuscles, d-g. Poikiloeytes. ft. Mieroeyte. i. Megaloeyte. j-n. Nucleated Red Corpuscles. j,k. Normoblasts. I. Microblast, to, n. Megaloblasts.

Chapter II. Disturbances Of The Vascular System

A suitable amount and quality of blood normally flows through the arteries, capillaries and veins, and is in close relation to processes of nutrition occurring in the lymph channels or adjunct circulatory apparatus.

The amount of blood in the vessels may be increased (plethora), though not permanently. It may be decreased rapidly in quantity, as by hemorrhage, or its red corpuscles may be gradually lessened in number (acute or chronic anemia) . The proportion of white corpuscles to red ones may be increased abnormally (leukemia). The hemoglobin of red corpuscles may be deficient (chlorosis). Locally the amount of blood in a part may be increased (hyperemia or inflammation) or diminished (ischemia).

Normally the blood contains floating in the plasma 5,000,000 red corpuscles, or erythrocytes, and from 5000 to 10,000 (1 to 500 red) white corpuscles, or leukocytes, to each cubic millimeter. (See Plate, Fig. II.) A marked increase in the number of erythrocytes is termed polycythemia; a marked decrease, oligocythemia. The temporary increase in number of white corpuscles is leukocytosis, a temporary fall is leukopenia; a persistent increase, leukocythemia or leukemia.

The blood corpuscles may be classified as follows:

See Plate, Fig. 1 Fig. VIII

Normocytes (normal size) .

Erythrocytes (non-nucleated red corpuscles)

Normal to blood.

Microcytes (small size) h

Pathological I Macrocytes (large size)

indicators. | Megalocytes (very large size) i

Poikilocytes (irregular form) d e f g

Erythroblasts (nucleated ( red corpuscles derived J Pathological indicators.

from red marrow bones)

of

{Normoblasts (normal size) Microblasts (small size) Megaloblasts (large size) .

I m n

Leukocytes (white corpuscles) .

Normal to blood.

Fig

Lymphocytes (small) 22%

Lymphocytes (large) 6 "

Polymorphonuclear neutrophiles . . 70 "

Polymorphonuclear eosinophiles . . 2 "

See Plate, 1 Fig. I

5 /

6 e

7 a

8 b p , . . . j Basophilic leukocytes or mast cells.

... -j Neutrophilic myelocytes from bone-marrow . [ Eosinophilic myelocytes

DISTURBANCES OF THE VASCULAR SYSTEM Fig.

Normal blood (triacid stain): 1, normal red cell, flatly spread and evenly stained; 2, normal rouleau; 3, normal red cells varying slightly in size, thickly spread, showing central clear areas; 4, normal red cell, of slightly altered shape; 5, lymphocyte, medium size; 6, large mononuclear leukocyte, incurved nucleus; 7, polynu clear neutrophile leukocyte; 8, eosinophile leukocyte. Separate nuclear lobes. (Schmaus and Ewing.)

ANEMIA.

Anemia is a condition in which the blood is lessened in quantity or partly deprived of its essential constituents — i. e., red corpuscles and hemoglobin — in consequence of which the tissues receive less oxygen and the general nutrition is impaired.

Acute Traumatic Anemia occurs as a result of copious hemorrhage. The individual becomes temporarily pale and weak. The arterial pressure is lessened, the circulation slowed, and the pulse is frequent and small. Recovery is, as a rule, prompt, the water being first restored and later the corpuscles being regenerated. 1 Frequent hemorrhages cause the blood to become watery and debility results from impaired nutrition. (See Plate, Fig. III.)

1 Ziegler, General Pathology.

ANEMIA 23

Symptomatic Anemia. — A diminution in the number of red corpuscles may occur as a result of protracted overwork, anxiety, study, or long-continued illness, such as a fever.

The number of red blood corpuscles may be reduced to one-half the normal amount, and there is a corresponding debility. The condition may disappear with appropriate removal of the cause.

Chlorosis. — This is a form of anemia occurring, for the most part, in girls and young women, and characterized by a great deficiency in the hemoglobin of the red corpuscles without a corresponding reduction in the number of the red corpuscles. In the watery blood very small red corpuscles (microcytes) are seen; also a few very large ones (macrocytes), and some of irregular outline (poikilocytes). 1 Myelocytes are occasionally seen. (Stengel.) The pathology is uncertain. If prolonged, the red corpuscles may sink in numbers to 3,000,000 or 2,000,000 per cubic millimeter and 20 per cent, of hemoglobin.

Being, as a rule, readily cured by a course of iron, it is inferred that the body is starved of iron, an essential constituent of hemoglobin. It is often associated with gastric disturbances, constipation, defective hygiene, and irregular habits, and also has been associated with oral sepsis, which apparently have a casual relation. The skin and mucous membranes are pale and have a slightly greenish tinge. 2 In recovery the number of corpuscles is first increased, then the hemoglobin.

Leukocytosis. — This is not a form of anemia, but a temporary increase in the number of multinucleated leukocytes, apparently derived from the lymphoid structures of the body in response to some demand for leukocytes. Thus it occurs normally after a full meal, in the later months of pregnancy (13,000) or in the postpartum state [15,000], pathologically after hemorrhage, in acute fevers, in tuberculosis, in sarcomas and in conditions accompanied by suppuration. 3 Its presence during the course of surgical disease has been held to be diagnostic of pus formation 4 — e. g., in abdominal surgery from 8000 to 40,000 per cubic millimeter. In general above 10,000 is regarded as leukocytosis 20,000 to 50,000 as hyperleukocytosis. (See Plate, Fig. IV.) In its opposite leukopenia the white cells may be about 4000 per cubic millimeter, 6000 being about the dividing line. Infectious diseases are usually accompanied by it. 5

Leukemia. — Leukemia is a disease characterized by a considerable increase in the number of white corpuscles of the blood, by a

1 Green, Pathology and Morbid Anatomy.

2 Ibid. s ibid.

4 Cabot, Boston Medical and Surgical Journal. 5 See works on General Pathology.

diminution in the number of the red corpuscles, and by enlargement of some of the lymphatic organs. The proportion of one white to ten red corpuscles is common (1 to 5 often, occasionally 1 to 1). The spleen may be hypertrophied (splenic leukemia). The lymphatic glands may be hypertrophied (lymphatic leukemia). In these latter cases the blood contains an excess of uninuclear leukocytes. It is rare except when combined with other forms. When the marrow of bones is hypertrophied (myelogenic leukemia) large mononuclear leukocytes with neutrophile granules are found 1 (myelocytes) and the lymphocytes and polymorphonuclear forms are increased. 2 The blood contains toxic substances generated by the destruction of leukocytes, xanthin bodies, and acids (lactic, acetic). The urine frequently contains an excess of xanthin bases and lactic acid. (See Plate, Figs. VI and VII.)

Pernicious Anemia. — This is a comparatively rare but generally fatal disease, characterized chiefly by a great fall in the number of red corpuscles to one million or less per cubic millimeter, those remaining being altered in form and size and showing evidences of degeneration. The total hemoglobin is reduced, but the relative amount may be increased. Degeneration is shown by peculiarities of staining. Normal red corpuscles (normocytes), nucleated red corpuscles (megaloblasts), large nucleated red corpuscles (gigantoblasts), microcytes, and poikilocytes are found. The blood platelets and leukocytes are somewhat diminished. 3 The oxygen-carrying power is markedly lessened and all tissues suffer from malnutrition. The power of coagulation of the blood is lessened. Marked fatty degeneration of the heart muscles is apt to occur 4 as well as fatty changes in the kidneys and liver.

The causes are obscure, but gastro-intestinal disorders, intestinal parasites, pregnancy and lactation, hemorrhages, malaria, syphilis, tuberculosis, and infections are the chief causes supposed to produce it.

Aplastic anemia is a severe type of progressive pernicious anemia, in which the bone-marrow fails to develop myelocytes and erythroblasts owing to lack of marrow cells (hypoplasia of bone-marrow.)

COAGULATIVE DISTURBANCES AND HEMORRHAGE.

The blood when drawn from the body or in contact with a wounded surface of injured vessel wall undergoes a process of solidification

1 Ziegler, General Pathology.

2 Stengel, A Text-book of Pathology.

3 Green, Pathology and Morbid Anatomy. * Ibid.

called coagulation. The nature of the process is in some doubt, but it is now thought that the following reactions occur: 1

Thrombogen + Thrombokinase = Thromboplastin

(in leukocytes and platelets.) (in platelets and tissue.)

Thromboplastin + Antithrombin = Prothrombin Prothrombin + Calcium salts = Thrombin

Thrombin + Fibrinogen = Fibrin

(in the plasma.)

Fibrin entangling corpuscles = Clot.

Fibrin forms a network, in the open spaces of which the corpuscles are entangled (Fig. 2). Occurring after an accident or surgery opening bloodvessels, coagulation causes the cessation of hemorrhage by plugging the vessels with a thrombus (or clot within the living vessel). In the case of a ligated artery this extends to the next anastomosing branch. The filling of vacant spaces such as abscess cavities or alveoli of teeth after extraction, also assists, not only in checking hemorrhage, but also acts as a scaffold for the granulation tissue, which brings about regeneration of the part. The clot is gradually absorbed (see page 56) . In inflammation the lymph exudate may coagulate in the tissue spaces, apparently an effort to limit or define the area by blocking up the lymphatics. Coagulation may occur in the living vessel, as a thrombus, or in the interstitial tissue, as in inflammation and infarction.

Thrombosis. — The formation of thrombi or clots within the living vessel may occur in the heart, arteries, veins, or capillaries. If the blood stream be somewhat retarded, an increased number of white corpuscles and blood platelets occupy the peripheral zone and adhere to the vessel wall. If the vessel wall be injured, the blood platelets become attached to it. With these platelets the white corpuscles and sometimes the red become deposited. Fibrin forms and the corpuscles are included. The thrombus is red when red corpuscles are included in it; white when only white corpuscles are present. The causes of thrombosis are these: (1) a retardation of the blood current at some point from some cause; (2) local changes in the walls of the vessels and (3) probably pathological changes in the blood. 2

Older thrombi are firmer than those recently formed. Thrombi are also formed in the capillaries, a circumstance which favors the spontaneous cessation of hemorrhage. 3 They may form in the vessels in inflammation. 4 Remaining in the situations in which they were formed, they either undergo simple or puriform softening or are

1 Howell, Text-book of Physiology.

2 Ziegler, General Pathology.

3 See above. 4 See page 38.

calcified, or are resorbed and replaced by connective tissue. (See Regeneration.) The calcified varieties are called phleboliths in the

veins; arterioliths in the arte- Fig. 2 ries. The effect of a thrombus

is to obstruct circulation in the degree in which it closes the lumen of the vessel. Thus in o o ft M o, o *-o \° ^it-

Fibrin filaments and blood tablets.

A, network of fibrin, shown after washing away the corpuscles from a preparation of blood that has been allowed to clot; many of the filaments radiate from small clumps of blood tablets; B (from Osier), blood corpuscles and elementary particles or blood tablets within a small vein.

Fig. 4

A thrombus in the saphenous vein, showing the projection of the conical end of the thrombus into the femoral vessel: S, saphenous vein; T, thrombus; C, conical end projecting into femoral vein. At v, v, opposite the valves, the thrombus is softened. (Virchow.)

Diagram to show phenomena of venous thrombosis: v, v, valves of veins, a, b, primary thrombus (white); c, d; s, /, g, secondary white thrombi connected with primary white thrombus by various red thrombi; h, piece of white thrombus becoming detached by blood current. If septic this would be a possible cause of septic infarction (or pyemic metastasis) . (Green, modified from Thoma.)

(1) trauma it plugs it completely, obstructing hemorrhage; (2) occurring in an artery (not by trauma) it tends to cause ischemia of a part supplied by it and may cause necrosis (dry gangrene) by lack of food supply (nutrition) ; (3) in a vein it tends to prevent return of blood to the heart (venous hyperemia) and if this is partial, degeneration is produced, if total, necrosis (moist gangrene) . A clot in a vessel may extend a great distance (Figs. 3 and 4).

Embolism. — Portions of the softened varieties of thrombi may become detached and float about in the blood; these are called emboli. Other foreign substances may act as emboli — e. g., air or fat globules. In important parts it may cause local anemia, paralysis, or slow or rapid death (Fig. 5).

Fig. 5

Fig. 6

Embolus impacted at the bifurcation of a branch of the pulmonary artery, showing the formation of thrombi behind and in front of it, and the extension of these as far as the entrance of the next collateral vessels: E, embolus; t, V ', secondary thrombi. (Virchow.)

Diagram of a hemorrhagic infarct: a, artery obliterated by an embolus (e) ; v, vein filled with a secondary thrombus (th); 1, centre of infarct which is becoming disintegrated; 2, area of extravasation; 3, area of collateral hyperemia. If caused by an infective embolus an abscess may result. (O.

Weber.)

If the thrombus be septic, as in the case of puriform softening, the emboli may lodge in small vessels and cause secondary septic disease processes, as, for example, in the cases of pyemia accompanied by infarctions in which multiple metastatic (or miliary) abscesses are formed, each causing local injury and acting as a fresh focus of infection as well (see page 47 and below).

Infarction. — When an embolus occludes a terminal artery, that is, an artery whose branches spread like those of a tree without anastomosis, the part first becomes ischemic, but soon the backward pressure from the vein upon the blood in the capillaries causes an extravasation of blood into the interstitial tissue of the wedge-shaped area, forming what is called a hemorrhagic infarct. A clot forms degeneration of the clot occurs, and if aseptic it is absorbed and replaced by connective tissue (see Regeneration); if caused by a septic embolus, it may be involved in the resulting septic process — e. g., in pyemic metastatic abscess. Infarction has been held by Black to occur in the dental pulp, but he has not proved the case as he distinctly describes infarction as the stasis of venous hyperemia, quite a different condition. 1 A demonstration has been made by Hopewell-Smith of a pulp disease which might be infarction, yet having from the description certain characteristics of venous hyperemia. (See Infarction of Dental Pulp.) (Fig. 6.)

Hemorrhage.— By hemorrhage is meant the escape of blood from the vessels. It may be arterial, venous, or capillary. If the vessel is ruptured, it is hemorrhage by rhexis. If it occurs by diapedesis, as in infarction (into the tissue spaces), it is hemorrhage by diapedesis. The diapedesis occurs through the capillary wall rather than the stomata; pressure is the cause. Hemorrhage usually ceases spontaneously through thrombosis, as previously described.

If hemorrhage occurs into the tissues it receives the following designations, the escape itself being called an effusion or extravasation:

Ecchy?nosis, an effusion of moderate extent into tissue beneath a surface, as into subcutaneous tissue.

Petechia the same, but small and circumscribed.

Suffusion the same when an extensive area is involved. The term also covers the staining of bone or dentin by hemoglobin, e. g., suffusion of dentin of the crown and root in venous hyperemia of the pulp.

Infarction, when the area involved is that supplied by terminal and non-anastomosing arteries as above described.

Hemorrhage involves an injury to vessels by traumatism, or disease rendering them incapable of retaining the blood, or by increased internal pressure, as in violent exertion, or in congestion of local vessels, as in venous hyperemia, or as the result of diminished external atmospheric pressure, as in high altitudes. The extra vasated blood may be absorbed or deposited in the tissues, as in a bruise; or excite inflammation or cyst formation (extravasation cyst) . Acute hemorrhages or repeated extravasations lead to anemia (which see). The extravasated corpuscles may be disintegrated and the hemoglobin broken up into varying compounds having various colors. This is hematogenous pigmentary infiltration and may be seen in a bruise. The colors are often permanently deposited. The color changes may occur in some degree in teeth suffused through venous hyperemia or the hemoglobin may be modified by pulp putrefaction (see Pulp

» Special Dental Pathology, p. 257 (Ed. 1915).

Putrefaction and Bleaching of Teeth) . As seen in a bruise the extravasations produce the following pigmentary infiltrations:

(a) Hemoglobin, dark red.

(b) Hemin, reddish-brown or bluish-black.

(c) Methemoglobin, brownish-red.

(d) Hematin, dark-brown or bluish-black.

(e) Hematoidin, orange or reddish-brown (light pea green (Jakob)). (/) Hemosiderin, yellowish or brownish.

Hemorrhagic Diathesis. — This is a condition, largely hereditary, in which coagulation does not close wounds readily, and ordinarily trivial wounds may, in spite of surgical aid, induce death by hemorrhage. Hereditary hemorrhagic diatheses (hemophilia) is usually transmitted through the female to the male descendants — i. e., from grandfather to grandson through the grandfather's daughter — and seven or more generations of hemophilics have been recorded. 1 Males suffer more than females in the ratio of about 11 to 1.

In a family of 207 members, in four generations, 37 were hemophilics, all of the male sex; almost half died from hemorrhages, usually in infancy, while in the living the tendency to bleed lessened as they grew older. 2

According to Legg, 3 "It is of three degrees of severity:

"1. Characterized by external and internal bleedings of every kind, and by joint affections.

"2. By spontaneous hemorrhages from mucous membranes, but no traumatic bleeding or ecchymoses, and no joint affections.

"3. A tendency simply to ecchymoses. The first seen most frequently in men, the second in women; the third may appear in either sex."

The joint affections are due to hemorrhage, and simulate rheumatic affections. Hemophilics are apt to be thin-skinned, neurasthenic, and liable to sudden flushings and vasomotor disturbances. 1 Blondes suffer more than brunettes. 4

The injured part may bleed from the first, or a normal clot may form and secondary hemorrhage or capillary oozing occur. Death may rapidly occur, or the patient bleed to fainting or until almost dead, and hemorrhage then cease. This may require any period, even weeks. One case is said to have continued for a year. 5

The pathology of the condition is uncertain. Fillebrown 6 reports a fatal case in which the arteries were excessively thin. Porter 7 points

1 Porter, International Dental Journal, 1900.

2 Losser, International Journal of Surgery.

3 Musser, Medical Diagnosis. 4 Thompson, Practical Medicine.

6 Scott, Dental Cosmos, 1912, p. 60. P International Dental Journal, 1900.

7 Porter, Loc. cit.

out that the blood may clot in the receptacle, yet not in the small vessels of the wound, and infers that some hereditary deficiency exists which interferes with the action of the vasoconstrictors.

Hemophilics usually manifest a history of bleeding before puberty, and hemophilic infants have died from hemorrhage due to gumlancing, circumcision, etc. Certain surgical cases in which secondary hemorrhages have been due to the action of the continuous use of acetanilid have been reported.

Treatment of Hemorrhage.— Hemorrhages in general are controlled or prevented upon four local and three systemic principles which may be combined for more rapid effect.

1 . Mechanically obstructing the flow of blood by ligatures, hemostatic forceps, compression of the artery leading to the part, pressure of tampons upon the open bleeding vessels which may be reinforced by compresses and in case of the jaws forcible closure of the teeth upon the compress by a Barton or other bandage. Elevation and rest of the part counteract gravity and muscular propulsion. In a severe hemorrhage upon the palate, as after lancing, finger pressure may be used or a vulcanite or even a modelling compound plate, made to produce pressure. 1 In alveolar hemorrhage clots about which hemorrhagic leakage occurs, should be removed before packing the alveolus.