Is Caries Caused by Infection

Back to Bacteria in the Hunt for

Caries Causes

A Disciple of Dr. G. V. Black and Dr. W. D. Miller

Finds Their Chemico-Parasitic Theory, Slightly Modernized, Still of Great Import.

He is Dr. Mathew Podolin, writing on



                Dental literature is saturated with opinions and hypotheses concerning caries. Although there are a good many interesting and rational conclusions among the lot, there is not enough evidence to justify their acceptance as a scientific axiom.

Of the many investigations past and present, the studies and observations made by W.D. Miller and G.V. Black seem to hold fast and are gaining momentum with every new discover made in the effort to ascertain the etiology of caries.

Miller’s theory is based on the assumption that certain bacteria are instrumental in producing an acid which decalcifies the hard dental tissue and prepares the tooth for subsequent invasion by micro-organisms resulting in the production of dental caries.

G.V. Black conducting his investigation on some similar lines observed that non-vital teeth and even artificial teeth are subject to caries. He concluded that caries begin externally and are caused by bacterial colonies that in some way attach themselves to the area of invasion. The bacteria form an acid that decalcifies the tooth structure making further invasion possible with the subsequent formation of caries.

Exactly what bacteria cause dental decay they did not know, and to this day it is still the subject of many conflicting opinions.

R.W. Bunting (A.D.A. Journal, Feb. 1929) and his associates have presented evidence to support their contentions that dental caries is an infective disease and that Bacillus Acidophilus is the specific etiologic factor.

M.M. Johnston and associates (A.D.A. Journal, Oct. 1933) in their bacteriologic research find that etiologic significance of Lactobacillus Acidophilus in the production of dental caries is diminished by the demonstration of a high incidence of this species in the mouth of caries-free rats, as well as in those rats in which caries was produced experimentally.

The specific etiologic importance of this species is further minimized by lack of consistent correlation of a high incidence of Lactobacillus Acidophilus with dental caries and a low incidence with the caries in human beings. Nevertheless, they conclude that lowered resistance of the teeth due to some disturbance in their nutrition provides suitable opportunity for the lactobacilli, as well as other bacteria present in the mouth to attack the tooth structure resulting in carious processes.

Hanke (A.D.A. Dec., 1929) points out that the actual number of bacteria in patients afflicted with pyorrhea is far greater than can be found in the average mouth in which active decay is going on. The bacteria, largely streptococci and spirochetes are acid producers. Why then do not the teeth in pyorrhea patients decay more rapidly in the presence of this increased number of bacteria?

Thus he, like many others, questions the bacteria acid theory. However, the majority of investigations are centered around Miller’s and Black’s bacterio-chemical theories. Directly or indirectly they are all working on the theory of immunity.

According to the chemico-parasitic theory the first step in caries is decalcification caused by the lactic acid produced in the fermentation of starchy and carbohydrates foods, clinging to the teeth. This is followed by a general invasion of organisms with a subsequent disintegration of the softened residue.

The modified chemico-parasitic theory implies that the acid is actually produced by the specialized acid-producing bacteria. Assuming that the etiology of caries is parasitic in origin, it is nevertheless likely that there are many predisposing factors that influence the formation of caries. There are many exciting causes that make possible the parasitic activity which terminates in the disintegration of the tooth structure.

Saliva, diet, metabolism, systemic and calcium phosphorus, all seem to play a part according to the undisputed contention of their proponents. Many of these of these opinions are based on honest and conscious research but lack adequate supportive evidence.

Minerals, a Possible Factor in Development

At one time it was regarded that the amount of calcium in the diet should exceed the amount of phosphorus. Today these same authorities insist that phosphorus should overbalance calcium. Again there are some, who claim that minerals such as iron, iodine, sodium, chlorine, copper, magnesium and manganese are very essential in the immunologic process against caries.

The body can get its calcium and other elements from so many different foods that unless the person is actually starving there is hardly any reason to suspect a nutritional deficiency. The phosphorus mineral is not quite as abundant as is the calcium, but then it is much easier to assimilate phosphorus then calcium. Perhaps it is not the deficiency in the diet but rather the inability of the body to assimilate properly the foods that are normally utilized to form and maintain the tooth structure.

M. Mellanby (J., A.D.A.P. 1456-1480, Aug., 1930) through an exhaustive research on dogs, rabbits and to a lesser degree on children comes to the conclusion that caries is fundamentally a problem of metabolism. She believes that defective tooth structure caused by nutritional deficiency is largely responsible for the high incidence of caries in children.

Structural Faults May Contribute

Clinical evidence seems to support the contention that defective tooth structure is a contributing factor, although perhaps not as important in the etiology of caries as some investigators would have it believed. It is not at all uncommon to observe that pits and fissures, normally regarded as areas of susceptibility are perfectly free from caries, while adjacent teeth more perfectly constructed develop caries. The opponents of this hypothesis contend that caries also occur on smooth areas, so that while defective tooth structure may increase the susceptibility to caries it cannot be regarded as an etiologic factor.

We admit that caries are also found on what may obviously be a smooth surface, like on the gingival third and proximal areas. But if we are to follow the theories of Miller and Black the supposed-to-be-smooth areas are no longer smooth when attacked by the acid forming bacteria.

It is quite possible that caries begin where there is a break in the continuity of the enamel and that this defect is common to most pits and fissures which, of course, accounts for the high incidence of caries in these areas. Even if we were to disregard the chemico-bacterial theory of Miller and Black is it not possible that there are microscopic cracks in the enamel in these areas normally regarded a smooth surface? This irregularity in tooth structure probably enables the bacteria to concentrate their acid activity which incidentally may answer E.H. Hatton’s problem of “How are the bacterial colonies and the associated acid confined to the teeth?” (J.A.D.A., Aug., 1932.)

The structure of the tooth may offer resistance or be susceptible to decay but does not necessarily determine the occurrence of dental caries, and while there is a possible relation of nutrition to the etiology of caries the essential nutritional factor producing sound teeth has as yet not been demonstrated.

The effect saliva has on tooth decay has occupied the mind of many investigators. H.P. Pickgrill (B.D.J., 1934, P. 1401) believes that the saliva influenced perhaps by diet has an important effect on the teeth. He calls attention to the fact that the rate of flow of saliva may have a tendency to change its chemical constituents. He points out that an analysis of saliva might contain 5 per cent of a certain substance, but if the rate of flow was only 1 cc per minute, the substance would not have so much influence as it would have in a concentration of 2 per cent but entering the mouth at the rate of 5 cc per minute. The rate of flow of saliva is an important factor and should be given more consideration. Clinical observations seem to support the contention that the incidence of caries is less where there is an excess salivation. Normally saliva is alkaline and a steady flow will neutralize any acid concentration without changing its own reaction.

Every dentist is fully aware of the fact that in pyorrhea there is a marked tendency to form salivary calculus, also that there are fewer caries in these mouths. A careful analysis of the saliva of pyorrhea patients shows a marked increase in the calcium and phosphorus content over those that have no pyorrhea but an abundance of caries. This would naturally lead us to an assumption that a high salivary calcium is associated with immunity, not by any possible absorption of the calcium from the saliva, but by the possibility to form certain plaques about the teeth. The unknown plaque, according to Black, retains the bacteria colonies on the surfaces that subsequently become carious. These unknown plaques differ in character from the known salivary calculus in that they permit bacterial activity.

Grove and Grove (J.A.D.A., Feb., 1935) in their report on a chemical study of saliva mention that the effect of the plaques is dependent on its character. some plaques are permeable and some are impermeable, and it is the latter type that protects the acid producing bacteria in their destruction of tooth structure. They emphasize that their findings indicate that ammonia is an important immunizing factor.

B.G. Bibby (J.A.D.A., Feb., 1935) suggests that the ptyalin of the saliva may play an important part in the production of acids on the teeth. He also points out that the role of saliva in keeping the teeth free from food accumulation is important. There are no doubt many other facts about the saliva that merit consideration and will be taken up from time to time by our enthusiastic research men.

Nutritional Claims Not Substantiated

Our logic leads us to conclude that the incidence of caries is not dependent so much on diet, hygiene or saliva, as it is on defective development in tooth structure. It is likely, however, that those structural defects are caused by an abnormal calcium metabolism. Whether any of the nutrient principles as classified by McCollum are in any way responsible for the calcium deficiency is another story. As yet there is not adequate proof to substantiate any one of these claims. We, however, are primarily interested in caries as an infectious process and aim to treat this subject from this angle.

We fully appreciate that the literature is already over-burdened with theories and claims that are not supported by scientific evidence and may be adding another burden by submitting our philosophy on the subject. But we are in full accord with C.N. Johnson (J.A.D.A., June, 1932) who said, “that in the ultimate, while laboratory experimentation is of immense value, the thing that really counts is our clinical experience.”

In our discussion on infections and resistance in a previous paper, we have shown that the whole process is dependent on the balance of the resistant host and the invading organism. For the present we shall assume that this holds true in all human tissues, not excluding teeth. We are, therefore, quite confident that this unorganized conglomeration of hypotheses, facts and opinions now centered about the etiology of caries, will finally crystallize to the same conclusion that governs pathology and infection all over the body.

Caries is an infection and like infections elsewhere in the body is caused by micro-organisms. We do not deny that the possibility of a constitutional disturbance intensified by a nutritional imbalance facilitates the bacterial activity in its destructive efforts, but we are inclined to be I accord with Miller and Black that caries begin from without the tooth and are very likely caused by micro-organisms, the products of micro-organisms or both. The dental tissues are a part of the entire organism and are interdepended with every other tissue of the human anatomy. Disease of one tissue invariably exerts its influence on the entire organism.

That caries is an infection can hardly be disputed on the grounds that it fails to conform with Koch’s postulate. The fact that Bacillus Acidophilus failed to produce caries in media other than its environment is no criterion, for we are not so sure that Bacillus Acidophilus is not a secondary invader and that the real culprit has as yet not been discovered. There are still some micro-organisms and viruses that evade detection even by the most expert bacteriologist. Furthermore assuming that Bacillus Acidophilus is the offending organism, the fact that it failed to reproduce caries can be explained in the lack of environmental adaptation. If we assume that caries is an infection we must also acknowledge the fact that nature has several ways of resisting of saliva, tooth structure, or systemic, thru nutritional disturbance, whether is influenced by the endocrine glands. Heredity or perhaps some obscure factor is our real problem. It would be more logical to accept the chemico-parasitic theories of Miller and Black and look for the cause of immunity.

Accepting the theory does not mean that we should cease all further investigations. On the contrary, all research should be correlated in an effort to prove or disprove conclusively one of the outstanding and most logical chemico-parasitic theory.

If We Cannot Prevent Caries, Let Us Control It

Since at this time we seem to be unable to prevent its occurrence it would be better that we control caries in its incipiency, the same as cancer, pyorrhea, or any other disease where the cause has not been definitely established.

Just what is caries? How can we recognize it when we see it in its incipiency, and how shall it be treated?

As brought out in the first part of the paper, caries is a molecular destruction of tooth structure of an infectious nature brought about by highly specialized acid-producing bacteria. These organisms through some unknown manner produce an acid that is held concentrated presumably by a plague, until decalcification of the tooth structure permits further invasion and further destruction. If the balance of resistance is greater than the offending organisms or their products, caries may not make much headway and become arrested in their incipiency.

However, nature is sometimes dependent upon artificial resistance in its battle with infection. We frequently have to evacuate pus from an abscessed area to facilitate healing of a wound or reinforce the patient’s strength so that the natural resistance will have a better chance to fight the invading organisms. So must we do in dental caries by excavating the decay and sterilizing the cavity, thus preventing further decay, then filling the space with some suitable filling material. When we learn what constitutes immunity to decay we shall be able to build up the patient’s resistance against this disease.

Vitality of Dental Pulp Should be Retained

E.H. Hatton (J.A.D.A., Dec., 1930) states that within the limitation of its structure the pulp is like any other similar organ of the body, it reacts as do other tissues of the body to stimuli irritation and injury. Our efforts should, therefore, be directed towards the preservation by early attention to a carious tooth.

In the incipient stages caries may sometimes be recognized by feeling the surface of the suspected area with a sharp explorer. The surface is almost always rough and irregular. The enamel will appear chalky and opaque. The patient may complain that cold or hot, salt, sweet, or acid substance taken into the mouth cause pain. This symptom is frequently misleading especially when the pain is unlocalized. There are many conditions about the teeth and gums that may cause pain, and should be taken into account.

Cervical hypersensitiveness, pericemental irritation, and other manifestations may not be carious in nature and should be very carefully considered. The radiogram will identify the caries by an increased radiolucency. As the disease progresses the caries assume a brown stain and are more easily recognized.

At this time the explorer point catches slightly as it passes the involved area. With the disappearance of tooth structure, there follows a rough irregular excavation filled with disintegrated tooth structure mingled with bacteria and food debris. Along with this process there is usually a rarefield condition of the structure forming this excavation which we may rightfully term “dentoporosis.”

At the same time there is a definite deposit of new dentin from the inside of the tooth, which apparently is nature’s effort to fight its destruction. Whether there is any additional density in the tooth adjoining the carious portion has not been established, but we rather suspect that the lymphatic system in the enamel if at all present is undoubtedly inefficient and very slow in response. Within the pulp the reaction is obviously more easily accomplished. In the carious portion of the dentin the lymph circulation is very likely blocked by necrotic material so that its function is considerably inhibited or completely arrested.

Hence nature’s only chance to build its defense is within the pulp chamber, providing of course that the pulp is still unattacked. Should the decay continue uninterrupted and the secondary layer of dentin become invaded, nature will set up a tertiary deposit and will continue to deposit layer after layer until the pulp becomes involved. Thus nature has its own defensive method against the battle against the destructive elements could be won. But unfortunately nature’s wonderful self defensive mechanism is but little understood, consequently many teeth that could possibly be saved meet their premature death.


Mathew Podolin, D.D.S.,

560 Delaware Ave., Buffalo, N.Y.