A Consideration Of Periodontal Disease

BY The Recognition of Gingivitis as a Precurser Of Pyorrhea is discussed by Paul H. Belding, D. D. S., AND Leland J. Belding, M. D., in

Successful Pyorrhea Treatment Dependent on Early Diagnosis

Dentistry has made remarkable progress within the last fifty years in practically every phase of its art and science with the exception of periodontal disease. In that field, the tenets of Rigg’s are still Gospel and his primitive methods of traumatic therapy, or their modifications, have been accepted as the sine qua non of pyorrhea therapeutics. As a result of this passive acceptance the scientific energies of the profession were never directed to the solution of this problem. However, following the discovery of the vitamins the supremacy of Riggs was challenged; chaos developed, and interest in gingival disease was so rudely awakened that in continues to be a focal point of dental thought.

This is quite proper for pyorrhea is an important disease. It causes a vast amount of hideousness, and claims eighty percent of the population for its victims. When the esthetic and cosmetic aspects of this disease and the inconvenience of artificial dentures are considered, it is apparent that no stone should be left unturned in the search for the solution of this problem.

Important as these enumerations are, they are the superficial, the less serious aspects of this disease. The systematic sequelae of pyorrhea are manifold. Primarily the function of gastro-intestinal system is impaired by the ingestion of purulent exudates and improperly masticated foods. This disturbs the general metabolism, and the efficiency of the entire organism is vitiated. Further, it is known that a large percentage of the disease and conditions which are caused by foci of infection, such as heart disease, chorea, arthritis, iritis, etc., result directly or indirectly from pyorrhetic activity. It is only when the secondary manifestations of this disease are taken into consideration that its full significance becomes apparent and the necessity for its control obvious. There can be no question but that this problem is one of the most important facing the medico-dental fraternity today.

It is generally accepted that gingivitis and pyorrhea are to all intents and purposes the same disease, the essential difference being of degree wherein the latter condition is distinguished by the presence of pocket formation and the appearance of frank pus. It is equally well accepted that if the original gingivitis could be prevented, pyorrhea would not develop.

We accept the unity of gingivitis and pyorrhea and trust that we will not confuse an already overburdened nomenclature by speaking of this disease entity, gingivitis-pyorrhea, as specific gingivitis.

Before discussing the newer concept of this disease we wish to briefly review the present generally accepted theories concerning its evolution. Generally speaking, the profession is well agreed as to the causes, method of development and pathogenesis of pyorrhea. It is believed that there are many primary causes, some fifty odd being listed: among them are traumatic occlusion, calculus formation, atrophy of disuse, dietary deficiency, gingival trauma, hygienic neglect and irritation. It is believed that as the result of the irritating activity of one or more of these agents, inflammation is produced and gingivitis precipitated. This irritates the classical gingival destruction which eventuates as pyorrhea.

At the onset the gingivae are inflamed and lose their delicate knife edge and this is followed by bulging of the soft structures, particularly in the interdental areas. This hypertrophy of the gingival sulcus; thus intensifying the activity of the precipitating factors and making the gingivae more susceptible to trauma. A pernicious cycle is set up on which gingival destruction and irritation go hand in hand and mutually accelerate the progress of the other. As this reaction continues the soft tissues become congested and pressure develops in the region of the gingival margin. In that the alveolar bone is extremely sensitive to pressure, osteoclasis sets in and the crest becomes honeycombed and resorbed. As this progresses the inflammation and the swelling cause the destruction of the gingival ligament, and the base of the gingival sulcus is further deepened with the epithelial lining migration bodily down the side of the tooth. This pernicious cycle continue and if left alone the gingival sulcus becomes deeper and deeper until a pocket is formed.

Chronic Gingivitis, Precursor of Pyorrhea

In order to present the currently accepted thought concerning the relationship of bacteria to periodontal disease we wish to quote the following: “The pathologic changes described up to this point are those of chronic gingivitis, the invariable precursor of marginal pyorrhea. Now, with the chronic inflammation greatly prolonged and exaggerated and the crevice deepened to the proportions of a pocket, a new factor enters the picture. The crevice epithelium insulted for so long by the mechanical irritation of the adjacent calculus and injured by the action of the omnipresent bacteria of the mouth finally succumbs to the attack of the latter,” and suppuration results, “with the first drop of plus that is established . . . . the condition becomes pyorrhea.”Warren William “Periodontal Disease” – Journal A.D.A. Sept. 1933 pp. 1617-1630

To briefly summarize, it is accepted that mechanical and other irritations, unassisted, cause the initial gingival destruction and continue the process up to and including the stage of pocket formation. After the pocket has been developed it is believed that the bacteria are for the first time able to establish themselves in a pathologic relationship to the process. At this late stage, the bacteria cause the flow of pus and assist in carrying on the destruction. Therapeutic measures compatible with that understanding of the development of pyorrhea are standard measures of prevention and treatment in use today. They consist essentially of attempting to prevent the development of pockets by mechanical stimulation, curettement and cleansing or the obliteration of the pocket by gingivectomy. In the hands of the trained periodontist these methods are surprisingly effective in controlling the symptoms of the disease. The average practioner, however, relies upon the forceps as the only satisfactory method for dealing with pyorrhea.

The accepted theories and the pictorial representation of the destructive forces at work in the production of periodontal disease are fundamentally correct, but the conception that the initiating factor is of mechanical or chemical nature is grossly untenable. As we have previously reported, we have conclusively proved that the initiating factor in the production of gingival destruction is always bacterial activity. In the past there has been considerable conjecture as to the relationship between bacterial activity and the production of pyorrhea but the problem has never been settled and at the present time there is no satisfactory or clinically applicable solution which explains the intimate details in the etiogenesis of this disease. It is the purpose of this paper to explain the roles of the various actors in the oral theater as they develop that dramatic tragedy, pyorrhea.

The various pathological reactions of the gingivae can, for clinical purposes, be grouped under the following headings:

  1. Gingival recession
  2. Gingivitis (hypertrophic).
  3. Vincent’s infection (acute and chronic).
  4. Pyorrhea.

This is a somewhat needless classification for at their inception it is, with the exception of acute Vincent’s infection, impossible to differentiate them. The gingivae are delicate, highly vascular, sensitive end organs, and as such have an excellent terminal arterial blood supply. These structures are very sensitive to both external and internal change and their appearance in many ways reflects the condition of the general health. As the old country practitioner used to look at the tongue, the modern physician feels that the inspection of the gingivae is an integral part of every physical examination.

Nutritional unbalance affects gingival tissues

It is then a well-established fact that the gingivae are sensitive to nutritional, abnormalities, toxic products in the blood stream, metallic poisons, calculus deposits, traumatic occlusion, systemic disease, heat, cold, trauma, dessication and etc. it is equally well established that gingivitis and pyorrhea follow in the wake of these abnormalities.

However, irrespective of the type of abnormality present, the gingival reaction, within limits, is constant. That is, the microscopic tissue changes are identical and it is impossible to tell grossly or from the slide, the nature of the precipitating cause. The exposure may cause by diabetes, nephritis, trauma, calculus, diet, pregnancy, etc. of course after the initial gingival reaction the pathological picture varies and is limited by the care, treatment and constitutional reaction of the individual. In a neglected case the progress is remarkably constant.

The early mild symptomless inflammation is followed by a destructive reaction in the contiguous structures. By direct extension the tissues are destroyed, the periodontium involved and the alveolus absorbed. This is associated with recession of the gums, loosening of the teeth and the formation of pus.

Practically any factor can precipitate gingivitis but only bacteria can initiate it. The oral cavity is filled with bacteria and whenever the various predisposing causes lower the gingival resistance to a sufficient degree to make bacterial invasion possible, disease results. Exposure stands in the same relationship to the development of pneumonia as the various predisposing factors have to the development of pyorrhea; both are caused by bacteria which are normal residents in the mouth but which are unable to produce disease until fortuitous circumstances lower the resistance and make their invasion possible. Thus pyorrhea is a germ disease and represents an activation of the normal bacteria flora which is present in every mouth.

Understanding of oral bacteria essential to problem

In order to appreciate this problem one must have an understanding of the oral bacteria and an appreciation of infectious disease in general. After birth bacteria enter the mouth and some of them, finding conditions suitable for their growth, persist. When the teeth erupt air-tight spaces are formed in the base of the gingival sulcus and bacteria which cannot exist in the presence of air (anaerobes) are able to take up their residence. The spirochetes belong to this group and can be found in the gingival sulci of practically every individual where they are constant, so long as the teeth are retained. These organisms are potentially pathogenic, but not particularly so and endure on the whole as opportunists, awaiting a time in the life of the host when the resistance is lowered that they can initiate their destructive reaction.

Occasionally a virulent strain of these spirochetes develop which is able to initiate disease in every person who comes in contact with it and produces what is commonly called an epidemic of Vincent’s infection. More generally there is a nice balance between the virulence and the resistance with the first one and then the other in ascendency. This gives the characteristic reaction of chronic periodontal disease with its slowly progressive nature and its intermittent exacerbations and remissions.

At one time or another pneumococci can be found in every mouth but in the absence of clinical evidence of disease they have no particular significance. Likewise spirochetes can be found in practically every dentulous mouth and in the absence of clinical evidence of disease they mean nothing. Thus it can be seen how absurd it is to attempt to make a diagnosis of Vincent’s infection or gingival disease by the microscopic studies of smears alone. Further, we can see that contrary to general opinion, no matter how Vincent’s infection is treated, the spirochetes can never be completely eradicated from the mouth and the smears will never become consistently negative. Once the spirochetes gain a pathologic relationship to the gingivae their complete dislodgment is improbable. This is fundamental, for those individuals who have been severely infected will for ever after require a certain amount of treatment for the balance of their dentulous lives.

In the past there has been a great deal of pointless debate upon which was more important in causing pyorrhea, the bacteria or the predisposing factors. Such debate is futile; both are important and generally speaking neither one alone can cause disease. Many years ago Pasteur, Koch and others believed that pathogenic bacteria plus a host spelled disease. Fortunately for mankind this proved to be untrue and with the development of the science of immunology, it was found that many factors enter into the production of disease. More recent studies have emphasized that the maintenance of the physiologic integrity of the individual was of vital importance for the prevention of disease. Thus if the normal physiologic relationships of the gingivae could always be maintained, bacterial invasion would become difficult and gingivitis and pyorrhea would become rare diseases.

The profession must understand that there are two factors in the production of disease: lowered resistance followed by bacterial invasion. The physiochemical-mechanical factors such as diet, traumatic occlusion, and pregnancy, are of vital importance but only in the connection that they predispose to bacterial invasion. The most important causes of lowered gingival resistance are: excessive smoking, hygienic neglect, dietary deficiency and traumatic occlusion.

Toxic materials lower resistance

Many toxic materials such as lead and mercury are excreted through the gingivae. On contact with the air they are oxidized, become insoluble and remain in the tissues as irritating foreign bodies. Tobacco smoke contains a similar toxic material which on excretion injuries the gingivae. In passing it is interesting to note that the incidence of gingival disease among those who chew tobacco is very low. This is not surprising for as Miller demonstrated, tobacco juice is an excellent antiseptic.

The importance of the relationship between diet and gingival disease cannot be overestimated. It is absolutely vital for the preservation of the gingivae in health that the individual be on an adequate dietary intake. Gingivitis is the invariable response to Vitamin C deficiency. The absence of this factor is accredited by many prominent authorities as being the most important predisposing cause of pyorrhea and it is contended that it is possible to prevent the development of this condition in the majority of the cases by an adequate daily ingestion of orange juice or other Vitamin C containing products.

In the blood discrasias we have the finest example of bacterial response to lowered resistance. In agranulocytosis and the acute leukemias activation of the oral bacterial is the almost invariable response and frequently the reaction is so severe that it is the actual cause of deaths. In an acute febrile disease particularly pneumonia with the associated oral desiccati on incident to mouth breathing, is usually accompanied by some degree of gingivitis. However, with recovery and the return of normal resistance the process generally subsides into latency without any particular treatment.

Traumatic occlusion does include osteoclasis by the action of the same principle utilized by the orthodontist, namely pressure, either intermittent or continuous. This osteoclasis not only depresses local resistance but mechanically assists bacteria in their penetration. The two processes working together cause a more rapid destruction than either could alone, and present a greater treatment problem, for a rocking tooth actually milks the bacteria into the gingival space.

Symptoms of periodontoclasia should be recognized

The symptoms of periodontoclasia are so well known that they need no elaboration, but in passing it is proper to mention them. The chief ones are: inflammation of the gingivae, recession, alveolar absorption, loosening of the teeth, pericementitis, suppuration and pocket formation. By definition, with the exception of the latter two symptoms, the others may be present in gingivitis.

The characteristic and deciding factors in making a diagnosis of pyorrhea is the presence of pockets and suppuration. This seems to us to be an unnecessary arbitrary separation and it would seem better to include every pathological gingival manifestation under the heading of periodontoclasia, which it rightly is. Most periodontists agree that pyorrhea is but an advanced gingivitis or gingivitis plus pocket formation. Let us then consider the evolution of this process.

Following an initial gingival involvement an inconspicuous depression appears which if unchecked progressively enlarges into a pocket. This may advance horizontally or vertically, destroying the alveolar process and the pericementum. The advance at the onset is horizontal but as soon as the gingival ligament is destroyed, it passes vertically in the line of least resistance. Thus only one surface of the tooth root may be involved.

It has been the observation of most workers that the pocket formation occurs on those surfaces of the tooth root which are the most protected and the most difficult to clean; the surfaces which show bacterial, calculary and filth deposits. For this reason pocket formation is more common in the proximal spaces and the lingual surfaces, especially in the molar regions. There are of course exceptions to this but even in these cases a careful study will generally show the reason why some such factors as filth, occlusal stress and lack of functional activity has created a local lowered resistance. This is entirely logical, for the basic principle of mouth hygiene teaches that the greatest protection against gingival disease is cleanliness.

Value of oral hygiene cannot be minimized

Recently there has appeared in the literature some ill-advised opinions which tend to minimize the importance of oral hygiene. In the face of it we wish to state emphatically that the parts of the mouth which are kept the cleanest are the most resistant to disease and conversely, the filthy areas are the most subject to it. The importance of oral hygiene within limits cannot be over-emphasized, for one of the greatest aids in the prevention of gingivitis is the thorough daily cleansing of the gingival space by means of a toothbrush.

In health this should be stiff, and it is absolutely essential for effectiveness that two brushes be used, one for night and one for morning. Even the best brush does not sufficiently recover its stiffness in twelve hours to be completely effective. However, many exaggerate the importance of diet and the toothbrush to such an extent that they fail to give that honest personal attention to detail which is essential for the maintenance of normal physiologic tone. No toothbrush or diet can ever supplant the part which must be played by the practitioner in the field of preventive dentistry. Mechanical normality and mechanical cleansing can only be accomplished in a dental office.

There are many phases of this problem which will never be solved by the clinician, the bacteriologist, the nutritionist or the biochemist working alone. The time has come when each must inhibit his selfish desire to add prestige to this particular line of endeavor and whole-heartedly pool their efforts for the common good of science.


Gingivitis and pyorrhea are specifically caused by bacteria; namely the oral spirochetes.

There are many predisposing factors which enable the bacteria to establish themselves in a pathologic relationship to the gingivae.

The treatment of this disease should consist essentially of prevention and curing the early gingivitis by the eradication of the predisposing factors and the destruction of the spirochetes by the topical application of the specifics, bismuth and arsenic.

By the use of specifics in association with the standard practices of periodontia, results can be secured which have hitherto been considered impossible.

The public must be taught, not that pyorrhea can be cured, but what is more important, that it can be prevented.

January 6, 2018 · jagdish1 · Comments Closed