Caries results entirely from the action of bacteria, and of acids formed by bacteria from foods—especially sweets and sugary foods—which periodically lodge in various retention areas on teeth. Sugary food induces proliferation of microorganisms that promote gummy fermentation. To attain the concentration of acid necessary to attack enamel, a retained food-and-saliva mixture must be in a location and of a nature that will not permit the acid to be counteracted by ingress of fresh saliva. Viscid or gummy foods or bacterial products tend to prevent both ingress of fresh saliva and egress of acid formed by bacteria. Excepting as results of disease, the qualities of enamel and dentin, or of saliva and mucus, have little or no influence on the initiation or progress of caries. Formed enamel is inert and cannot be changed by metabolic processes. Such changes as occur in formed enamel are due to chemical or physical processes. The prevalence of caries in modern times, especially among the more highly civilized, is not due to deficiencies in essential elements of nutrition. Tastes, or dietetic habits—e.g., modes of mastication and movements of tongue, lips and cheeks—which tend to keep the mouth in a hygienic state, by physiological means, are highly important in averting caries. The sequence of foods in a meal may influence control of caries to some extent, if the meal is not wholly composed of detergent foods. When sugary foods are eaten, a cleansing food at the end of the meal tends to act as a liberating stimulus to the self-cleansing processes, both mechanical and chemical. In the human mouth, if the teeth are unbroken and the arch normal, even carbohydrate foods of a granular or reticulate nature, through which saliva can pass easily, do not have much opportunity to cause caries. Consequently vegetable foods including cereals, when fresh (or even though cooked without sugar), seldom tend to induce caries. Even when not of a consistency that stimulates mastication, they may help to avert the disease. When vegetable foods are associated with substances which stimulate mastication and salivary secretion, e.g., those firm in texture, or containing acid, aromatic or tasty principles, the likelihood that caries will result is still further decreased.
Enamel cuticle protects enamel from food acids in transit through the mouth, but does not prevent acid (formed by bacteria) in prolonged contact with it from initiating caries. The residual organic fibrils which pass from enamel cuticle through interprismatic enamel-substance facilitate percolation of acid from surface to dentin. This is specially noticeable in lamellae, which may also be regarded as remains of guy-ropes maintaining correct relationship of the limiting membrane,
160 SUMMARIES ON CARIES
or sheet of cells on the outer surface of the forming enamel, to the dentin. The proteolytic bacteria are primarily outside enamel and act antagonistically to acid- producing organisms. Proteolytic products do not decalcify enamel but, after a breach has been made, proteolytic bacteria take a share in the destructive carious process. Chromogenic microorganisms tend to be associated with proteolysis or putrefaction, and with formation of tartar, so that teeth strikingly dirty in appearance are, so far, well protected from caries. In addition to foods of an albuminous nature, serum, phagocytes and salivary corpuscles are antagonistic to the action of acid-forming bacteria.
Supplementary personal statement. On taking tip the study of dentistry in 1890, after previous years in biology and medicine, the author found that leading dental authorities did not appreciate the significance of conclusions of progressive biologists (Weissmann, Galton, A. R. Wallace) and of the bearings of the theory of acquired characters on dental problems. The theory of the non-inheritance of acquired characters gave a clue to dental explanations different from those then current. The supposed hereditary degeneracy of enamel—which being inert, and caries in the initial stages being simply a mutilation—could not, owing to diminished use (Lamarckian doctrine), influence development of enamel. The undoubted fact that caries ran in families was believed by the author to result from what may be in the nature of a legal inheritance, not a biological one. He claimed that, in civilized communities, inasmuch as there were hereditary variations only in the form of the surface of enamel—e.g., depth and shape of cusps, and crevices or pits—which might rightly be considered predisposing causes of caries, the prevalence of the disease was almost wholly attributable to dietetic habits and tastes developed as the result of refinement of food, and to such other conditions as led to mal-hygiene in stagnation areas about the teeth. This, as recent dental literature shows, is now even more universally accepted as true than was the belief in the mechanical use of the tooth-brush, and the control of destructive bacteria by antiseptics, forty years ago.
Primarily, therefore, the author’s methods were deductive but, being in active practice as a dentist, continual clinical observations compelled recognition of facts and of the theories of his predecessors. He made experiments on the relative lodgeability of different foods, in his own mouth especially. Laboratory methods, such as involved use of a biological incubator, were used ; and an experiment on a monkey—perhaps the first animal experiment in the attempt to elucidate the cause of caries—was made. But though fairly closely related to man, it became obvious that even this type of animal was not suitable, its tastes and dietetic habits being markedly different from those of human beings. The author had, therefore, to rely on finding the truth from investigations of, and experimental methods in, the feeding of children, directly or indirectly under his control, which were repeated and confirmed by many dentists and others.
References: Twelve books, 1900-1929; Den. Mag. Oral Topics, 1936; Sir Norman Bennett’s Science and practice of dental surgery, Chapter on Aetiology, 1st ed., 1914, 2nd ed., 1931.