Causative Factors in Dental Caries

Regurgitation of Pepsin, Digested in Mouth, May Destroy Teeth

Dr. James Logan Shanklin Points Out a New Thought in the Consideration of Dental Disease ‘CAUSATIVE FACTORS IN DENTAL CARIES” (Suspected, in Primary Lesions)

                We wish to present for serious consideration of the profession, a theory that the “primary lesion in true dental caries is due to the digestive action of regurgitated pepsin.”

In so far as we know this is a new theory, and if it should prove tenable, it may result in a constructive approach to this most perplexing problem of dentistry. Were it to become the means of isolating the etiology of dental caries, the cure would probably be in sight. Exhaustive research would then undoubtedly discover some means to control through dieting or otherwise, the greater amount of regurgitation of digestive fluids from the stomach.

A sensible, deliberate approach to this thesis necessitated a tentative reconsideration of at least two previously accepted premises of ours. We had to concede the probability that at least some parts of dental enamel are devital, particularly those parts that are the points of vulnerability to carious lesions. We also had to concede that Miller’s and Black’s theory of “acid-solubility of enamel structure” is wrong in so far as the primary lesion is concerned, while it is probably at least partially right in the secondary stage: i.e., in the progressive action of the disease after it penetrates the periphery of the tooth.

Further doubt as to correctness of the “acid-solubility theory” in primary lesions, is justified by the reflection that bodies of men and animals, long buried in climates that are so warm and moist as to approach the ideal conditions of an incubator, resolve into their primal elements with the enamel protected teeth the last to so resolve.

The conclusion that ordinary processes of decay affect tooth enamel less than they do any other body tissue, seem to lay down a law that “solubility is in inverse ratio to the density of such tissue.” In contemplating dental caries in living subjects with the above “law” in mind, we were forced to conclude that extraordinary processes are at work that seem to conversely order such dissolution in view of the fact that the most dense tissue in the body dissolves first, thus reversing the ratio, and that there must be some logical reason for this reversal.

Permit us to remind you that all living organic (protein) substances are immune to the digestive action of the enzymes, pepsin and trypsin; that pinworms, bacteria, and a host of other anaerobic organisms will survive in a medium that is rich in pepsin; that the walls of the stomach are organic but, being vital, are immune to digestion, and that if we destroy the vital spark of life in any of these organisms, they will be promptly digested in the presence of pepsin either in a test-tube or in the human stomach.

Our paucity of knowledge as to the exact structure of tooth enamel may be the principal reason why we have, so far, failed to discover and establish a satisfactory law governing primary carious lesions. We describe it, vaguely, as consisting of “enamel rods of mineral salts, cemented together with a cement-like substance.” No doubt this cement-like substance is protein, and it is not illogical to suspect that the body of the enamel rods themselves is shot through and through with similar protein cement-like substances.

Such organic animal matter composing this cement-like substance, whatever its exact nature, must very closely approximate devital tissue because it is as far removed from functioning lymph channels as is the periphery of a mature tooth crown. Dissolution of this allegedly devital cement-like substance, through digestive processes would destroy the matrix of the enamel structure and would undoubtedly permit the whole of the mineral portion, so involved, to collapse.

With very limited research facilities, and using extracted teeth, we have for some time been conducting a series of experiments in the hope and with the conviction that we will discover that enamel-cement will positively, albeit very slowly, digest in the presence of pepsin. We feel that we will find that the greatest amount of such action will be noticeable in the fissures and faults of the periphery of the tooth. Since these points, plus the inter-dental-contact points in living mouths, afford mechanical means of retaining quantities of regurgitated pepsin over long periods of time, we expect to be able to correlate the location and the progress of these experimentally induced caries to the usual points of susceptibility and progress of natural carious lesions.

It is our intention to soon conduct exacting digestive tests on the enamel of living teeth in situ, and also to compile a comparative chart of our findings in regard to the amount of pepsin found in the mouths that are afflicted with carious lesions as against mouths that are free of such lesions.

Most of us have been frankly puzzled over the easily recognizable differences between dental caries which occur in enamel protected surfaces, and those cavities, called erosions, that frequently occur at the gingivae of a tooth in exposed dentine beyond the enamel crown. In the event the above “digestive theory” should prove acceptable as a basis for further reasoning, it will open up interesting vistas for research, in an effort to definitely differentiate these two types of cavities in teeth. In this connection we must not fail to keep in mind the premise that the organic matrix in dentine is, probably, entirely vital and therefore immune to digestive action.

To the ingenuity of those who tentatively accept our hypothesis we temporarily consign the problem of “why approximating surfaces of different teeth develop these primary lesions at widely divergent periods.” We have considered the probability that due to the fact that years often separate their embryonic stages, conditions of general health must surely play an important part in perfecting the complex mechanism of enamel. Probably we will find that a closer approximation of enamel-rods in some teeth, with a consequent reduction of bulk in the matrix of the cement-like substance, is a common rule, and that when this matrix is dissolved through digestion, the more constricted spaces would offer less opportunity for the invasion of mineral-dissolving acids.

We all acknowledge that carious activity seems to be no respecter of age. Many individual’s teeth are largely destroyed in youth, carious activity becoming practically static after they reach maturity. In other cases the disease first appears well into adult life; and in other cases this destructive activity seems to be confined to intermittent indefinite periods. These facts seem to point to the likelihood that they are contemporary to, and associated with, gastric disturbances which, in turn, are not necessarily confined to any particular age of the individual.

We sincerely hope that other investigators will become interested enough in this theory to assist in this experimentation, and that some means of comparing our methods and results can be arranged.

JAMES LOGAN SHANKLIN,
6528 Harrisburg Blvd.,
Houston, Texas.

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