Pyorrhea Alveolaris

Periodontal Disease is a Complex Disorder

It May be a Reflection of Systemic Ills or may be a Cause of Remote Disturbances

Dr. W. Y. Hayden discusses



                Pyorrhea alveolaris bears a double relationship to systemic disease. We have periodontal lesions acting as foci of infection. We have also certain definite periodontal symptoms that are manifestations of systemic disease, such as the proliferative gingivitis, with suppuration, of diabetes, as stressed by Hirschfeld1, and the rapid alveolar atrophy with extensive periodontal pocket formation, sometimes accompanying anaemia, also noted by Hirschfeld2.

All investigators seem agreed that there is no specific organism, although infection is invariably present in all periodontal disturbances; but the periodontal pocket is the primary factor, the inflammation and the bacterial activity being secondary. The infection, however, plays an important part in the pathological tissue changes.

In the outline by a dentist before a medical organization, it does not seem appropriate to touch upon the metastasis nor upon the types of bacteria involved,—other than to repeat the statement of Bloodgood3 that, “Disease of any organ or tissue in the body may be the result of infection that had its origin in the mouth of sinuses.” Nor does it seem necessary to include the treatment of pyorrhea.

Rather does it seem advisable, since the subject is so large, to limit our attention to the purely local changes, in an endeavor to demonstrate why these morbid areas should be considered a menace to the general health.

It would appear that the most effective way to deduce the possible relationship of periodontal lesions to systemic disease, in the short time available, is to summarize the disease under the conventional headings.


Riggs’ disease, periodontitis, periodontoclasia, periclasia, paradentitis, paradentosis.

The term pyorrhea alveolaris is a misnomer. It suggests only one of the symptoms, and that, by no means a constant one. We do find pus often but it is from the gingival crevice, not from the alveolus. However, the name pyorrhea alveolaris seems to persist.


Pyorrhea alveolaris is a breaking-down with pocket formation, of the periodontium, or the tissue investing the teeth. The periodontium includes,—the periodontal membrane, the gingivae, and the alveolar process.


Periodontal disease has been widespread throughout the various civilizations,—Roman, Greek, Hebrew, Egyptian, Chinese. It has been traced back to the middle Palaeolithic period, as the Neanderthal skull shows evidence of it. It was first described in 1550 by Paree; Toirez in 1779 gave it the name pyorrhea alveolaris; and Riggs in the last century devoted considerable attention to it.

Although observed and treated for centuries it has been only during the last fifteen or twenty years that really scientific progress has been made in its study and treatment, but one would conclude that for thousands of years pyorrhea alveolaris must have influenced general health.


It is chiefly a disease of middle age and later life, seldom being found in children. When present in young adults it is usually associated with extreme traumatogenic occlusion, or with a lowered resistance caused by systemic disease. Both sexes seem to be equally subject to it. Usually patients very susceptible to caries do not develop periodontitis and vice versa. Some lower animals are affected; Box4 has studied and experimented upon domestic sheep, which have pyorrhea similar to the human form.


It seems essential to review briefly a few points of the present conception of periodontal histology, in order to elucidate the development and characteristics of these potential foci of infection.


Reprinted from the Journal of the Canadian Dental Association.


Pericementum: The pericementum, or periodontal membrane, is the elastic tissue that fills the space between the root of the tooth and the alveolar process, and whose fibres attach the cementum of the root to the periosteum of the alveolus. It is of varying width increased by function and is made up of, connective tissue fibres, blood vessels, nerves, fibroblasts, cementoblasts, osteoblasts, osteoclasts, and epithelial structures.5

The blood vessels are numerous and run parallel to the long axis of the tooth, but with branches anastomosing with the vessels of the alveolar process, and with those of the gingivae, periosteum, and alveolar mucosa. The nerves follow the course of the blood vessels.

The fibres, in bundles, are of five kinds, according to Black’s6 classification—apical, oblique (constituting by far the greatest bulk), horizontal, alveolar crest, transeptal. The last named attach the neck of each tooth to that of its neighbor, from cementum to cementum. The transeptal fibres therefore do not form part of the pericementum; the others do. The fibres suspend the tooth in its socket so that there is a “pull” on the alveolar bone, not a “push,” thus creating normally a stimulus to the bone.

Regarding the attachment of the fibres to the tooth, Gottlieb7 says. “The maintenance of a tooth in functional activity requires the continual deposition of new cementum on the surface of the root.” This deposition of cementum also retards the downward growth of epithelium, and it prevents enlargement of the alveolar space.

Gingivae: the gingivae5, comprising the cemental gingivae, and the marginal gingivae, are the soft tissues resting upon the crests of the alveolar process, investing the cervical portion of the teeth, and continuous with the alveolar mucosa. The cemental gingivae are attached to the cementum, from the level of the alveolar crest to the base of the gingival crevice.

Through this tissue pass the transeptal and other fibres. The marginal gingivae are wedge-shaped and extend from the cemental gingivae, creating the gingival crevice about each tooth. The gingival epithelium is of the stratified squamous type, on a thin basement membrane, invaginated by deep papillae of connective tissue. Box5considers the crevicular surface of the marginal gingivae, “the weakest link in the chain of the epithelial cordon of the mouth.” It is unusually thin, often with breaks, he finds, and frequently with very few cells separating the flora of the mouth from the capillary loops of this highly vascular tissue, whose blood supply is derived from the pericemental, the periosteal, and the alveolar mucosal blood vessels.

EPITHELIAL ATTACHMENT: The acceptance of Gottlieb’s7 theory of the epithelial attachment, and the continuous eruption of the teeth has somewhat changed the viewpoint of periodontists.

Gottlieb’s investigations seem to prove that instead of having, as formerly thought, a line of epithelium attached to the tooth at the cement-enamel junction, there is, in reality, in the adult, a band of epithelium of varying width (though probably averaging about one half m.m.) and of varying curvature, encircling every tooth.

This band is in organic union with the cuticle of the tooth, whether it be enamel or cementum with which it is in contact. This band of epithelium Gottlieb calls the “epithelial attachment.” Similar in form, it unites the oral epithelium with the tooth, and lies rootward from the bottom of the gingivae crevice.

The deeper rootward border of the epithelial attachment gradually proliferates and grows apically, while along the crownward border, the cells degenerate, thus separating the attachment from the cement-enamel junction. But this does not necessarily mean a deepening of the crevice. With this slow downward movement of the epithelial attachment, there normally is concurrently a resorption of the alveolar crests, a corresponding atrophy of the gingival margin, a deposition of cementum at the apex of the root, and usually abrasion of the occlusal surface.

In other words we have a continuous eruption of the teeth all through life, but at a greatly varying rate of progress in different individuals, in different teeth in the same individual, and on different sides of the same tooth. Thus it is not essentially considered pathological if the clinical crown of a tooth display a portion of the root, as well as the enamel of the anatomical crown.

To show that this is a physiological process, as claimed by Gottlieb, and not pathological, Kronfeld8 describes studies he and Ullik made on wild hedgehogs of different ages, and on other omnivorous wild animals in the natural state, having teeth resembling histologically those of man, and he has found in them the same kind of continuous eruption, with the typical epithelial attachment.


If, due to inflammatory or morphological causes, the gingival margin cannot follow the bottom of the crevice, as it recedes, then the crevice necessarily deepens. Inflammation, as well as trauma, destroys the connective tissue fibres. Calculus, a mechanical and infective irritant, which is formed by the saliva, is almost invariably deposited on the root surface as the crevice deepens, causing further inflammatory hypertrophy and further deepening.

First the cemental gingiva is detached; then the fibres of the pericementum are gradually destroyed, leaving their broken organic ends to putrefy on the denuded cementum surface. The pocket thus formed, with its pure drainage, is ideal for the retention and development of the micro-organisms always present in the mouth.

In the meantime, the inflammatory process in the gingivae has resulted in activity of the osteoclasts, with resorption of the adjacent bone. Kronfeld8 does not agree that this bone resorption is a true osteitis. “Necrosis of the alveolar bone under inflamed gingivae or under pyorrhea pockets,” he states, “has of the pericemental fibres, the functional stimulation is lost, and there is no further deposition of bone.

Independently of this evolution, the periodontium of teeth in traumatogenic occlusion is further attacked by a lesion, named and described in detail by Box5, as “rarefying pericementitis fibrosa,” in which the pericemental structures undergo change, and, enlarged, assume the form of a fibrillar connective tissue, accompanied by the rarefaction and destruction of the alveolar bone. Thus the lamina dura is lost and the pericemental space is widened, with the resultant mobility of the tooth.

As soon as this deeper condition is complicated by gingival infection, with its constant cellular infiltration, there is rapid and deep pocket formation. By enlargement of the medullary spaces and Haversian canals, there is further bone destruction, with its ultimate conversion into granulation tissue. This new infective granulation tissue always becomes covered to the baseof the pocket with epithelium, but this epithelium is of poor quality and often of broken continuity.

“The presence of pus in the periodontal pocket,”Box9 states, “is occasioned by the superimposition of secondary inflammatory processes, pyogenic infections, upon the primary non-suppurative inflammatory process,” and Gottlieb7 assures us that, “Any death of living elements without its necessarily leading to suppuration with abscesses.”


Broderick10 goes to great length to show that the fundamental cause of all true pyorrhea is alkalosis.

Mead11 states, that, “while general systemic disturbances play a great part in the progressive pathologic change of periodontal disease, their effect is usually considered secondary to some predisposing cause. They render the tissues more susceptible to local irritation.”

Merritt12 says, “It is never one condition, or group of conditions, that is directly responsible for the development of periodontoclasia, but he combination of metabolic disturbance, lowered resistance and bacterial infection.” He also quotes Jones and Simonton13for authority that, “of all the bones, the alveolar process is the most sensitive to dietary faults.”

There are two main types of Periodontitis, classified by Box9, as, Periodontitis Simplex and Periodontitis Complex. Periodontitis Simplex is caused by lack of care. Periodontitis Complex is usually associated with some form of traumatogenic occlusion, which is defined by Box, as, “a condition in which the systems of forces acting upon the tooth during occlusion are not in equilibrium.” A horizontal overloading is particularly harmful to the supporting structures of the tooth. Gottlieb7 says, “a tooth is overloaded when the tensile strength of the suspensory apparatus is exceeded.”

Associated with traumatogenic occlusion as local causes of periodontal disturbance are the following:—


Loss of teeth and subsequent drifting of others.

Lack of proper contact and consequent food impaction.

Overhanging and defective fillings.

Faulty bridgework, crowns and other restorations.

Uneven and excessive wear.

Dental caries.

Lack of sufficient exercise of the tissues.

Insanitary mouth conditions.

Holding of pipe stems, etc.



Frequently there is very little apparent evidence of periodontal disease, even when thelesions are fairly well advanced.

The absence of pain is characteristic.

Often in the earlier stages a more or less irregular purplish line can be seen, following the outline of the gingival margin. This is usually accompanied by bleeding on the slightest provocation, such as by brushing, or by pressure of any kind. This form of gingivitis, usually the forerunner of periodontitis simplex, is due to the deposition of serumal calculus beneath the gingival margin. Any cyanosis or hypertrophy of the gingival tissues should be viewed with suspicion. Sometimes on pressure, pus exudes at the neck of the tooth, indicating an ulcer on the crevicular surface of the epithelium.

Mobility of any of the teeth, even slight, indicates resorption of the alveolar bone.

Anterior teeth protruding abnormally are often indicative; they have probably been forced forward by the lower incisors, due to an extreme overbite.

Extruding teeth as well as teeth out of alignment are frequently a sign.

A gingival “flap,” especially one partly covering a third molar, almost invariably conceals a seat of infection.

There is characteristic breath in the later stages.

Box5 enumerates among others, the following clinical signs of incipient periodontitis:—

  1. Asymmetric recession of the marginal gingival line.
  2. Sharply drawn linear depressions in the alveolar mucosa, parallel to the long axis of the root.
  3. Clefts in the gingival border commonly to one side of the tooth.
  4. Absence of stippling,—a smooth, shiny surface instead of the normal stippled gingiva.
  5. Festoons,—a hyperplasia of the marginal gingiva.
  6. A dilatation of the blood vessels in the gingival margin.
  7. Increased depth of the gingival crevice. Any increase much beyond two millimeters is to be regarded as a sign of pocket formation.


The periodontal probe, in several angles, and preferably graduated in millimeters, is the prime requisite in diagnosing. The probe should be passed all around the neck of every tooth, and if it drops three millimeters or more beneath the gingival margin, there is pocket formation, and consequently a potential focus of infection. The orifice of the pocket may be very narrow.

Test the teeth between the two index fingers for mobility.

Digital pressure on the gingivae usually reveals the presence of pus, if present.

The tissues should be carefully examined for any of the signs enumerated above (under symptoms).

A dirty moth does not necessarily denote periodontitis, although it will likely lead to it eventually.

It is best to make a full radiodontic examination. The radiograph is not infallible, but it is an indispensable assistance. There is, however, a tendency to put too much dependence upon it. Without a thorough clinical examination the radiograph is apt to be misleading. Not infrequently, a tooth, having a pocket extending well toward its apex, will appear perfectly clear in the radiograph; the narrow tortuous pocket may be in such a position that the x-ray misses it. A periodontal abscess in the bifurcation of the roots of an upper molar often does not show in a radiograph. On the other hand, the radiologist sometimes condemns a perfectly good tooth, because the alveolar bone supporting that particular tooth is of poor structure, when the clinical explanation is, that the tooth is out of function, and nature has not found it necessary to build up so strong a bony support for it as for the others, which are in occlusion.

Frequently the radiograph shows a general resorption of the alveolar crests. Pathologically this may mean nothing. If the patient is past middle age, it usually denotes just a physiological sensile atrophy. If the patient is younger, it may mean merely that the rate of progress of the later and continuous eruption of the teeth, has been unusually rapid. Only a clinical examination can decide this. If there is a corresponding atrophy of the gingivae, with the gingival crevice of normal depth, there is no infection. If, on the other hand, the clinical examination discloses pockets, and no marked recession of the gingival margin, then we have a pathological condition.

Moreover, the patient may have had previous periodontal treatment and the periodontium be now free from infection, but this may not be shown radiographically. However, the radiograph reveals details of the condition of the periodontal structures that can be learned in no other way. And it is a necessary means of ascertaining the extent of bone loss. It serves as a check in diagnosing, and it also confirms the clinical findings.

The Focus

Box14 maintains that the periodontal pocket is more important as a focus of infection than is the encapsulated apical granuloma, or the apical abscess with a fistula. We have in the periodontal lesion9 an area of soft tissues showing definite chronic reaction to pathogenic micro-organisms, with the presence of a rich capillary bed, with the irritation of calculus to excite capillary response, and with the mobility of the tooth in its alveolus, under occlusal stress, to mechanically aid the passage of bacteria from this focus into the blood stream. He also directs our attention to the large area14 of infected soft tissue exposed in these pockets,—sometimes, he states, as in one patient, an area great enough to cover the palm of the hand.

In treatment, the objective that must be attained is the total elimination of the pockets. Here, against we encounter a double, though indefinite, relationship; a lowered general vitality retards periodontal response to local treatment, whereas, after the clearing of the pockets, there is usually reported an improved systemic condition. Would that there might be demonstrated a more definite relationship between the oral focus and the systemic disease, in the individual case!

Dr. W. Y. Hayden

260 Queen’s Ave.

London, Ontario.




  1. Hirschfeld, Isador: Periodontal Symptoms Associated with Diabetes, Journal of Periodontology, Jan., 1934.
  2. Idem: Proliferating Hypertrophic Gingivitis: Report of Two Cases Accompanied by Severe Anaemia, Jour. Am. Dent. Ass’n, Dec., 1928, p. 2305.
  3. Bloodgood, J.C.: As quoted by Cook, Thos. J., J.A.D.A., May, 1930, p. 881.
  4. Box, Harold Keith: Experimental Traumatogenic Occlusion in Sheep, Oral Health, Jan., 1935.
  5. Idem: Studies in Periodontal Pathology, Can. Dent. Research Foundation, May, 1924.
  6. Black, G.V.: Quoted by Box5 and by Kronfeld8.
  7. Gottlieb, Bernard: Tissue Changes in Pyorrhea, Jour. AM. Dent. Ass’n. Dec., 1927, p. 2178.
  8. Kronfeld, Rudolf: Histopathology of the Teeth and Their Surrounding Structures, Philadelphia: Lea and Febiger, 1933.
  9. Box, Harold Keith: Treatment of the Periodontal Pocket, Toronto: University of Toronto Press, 1928.
  10. Broderick, F.W.: Dental Medicine, London, Eng.: William Heineman, Ltd.
  11. Mead, Sterling V.: Diseases of the Mouth, St. Louis: The C.V. Mosby Co., 1932, p. 246.
  12. Merritt, Arthur H.: Periodontoclasia” Aetiology and Treatment Jour. Am. Dent. Ass’n, Feb., 1934, p. 255.
  13. Jones, Martha and Simonton, F.V.: Mineral Metabolism in Relation to Alveolar Atrophy in Dogs, Jour. Am. Dent. Ass’n, May, 1928, p. 911.
  14. Box, Harold Keith: The Pyorrhea Pocket and Focal Infection, Oral Health, Sept., 1934.