Caries is a bacterial disease, subject to interpretation in terms of laws of bacteriology and immunology. It is a relatively specific disease, occurring in those who partake of modern diet and have oral food-retention areas. It is caused by dissolution of calcium salts in enamel by acetic acid formed by streptococcic fermentation of cereals. Increase in susceptibility to caries is caused by relative or absolute increase in pathogenicity of oral flora and ensuing accelerated formation of acid, rather than by any change in the affected tooth that makes it less resistant to the action of caries-producing acids. Incidence of caries is determined by the number of food-retention areas ; speed of the process is limited by the thickness and density of the affected enamel, and the degree and rapidity of reaction of underlying dentin. Formed enamel cannot be altered by dietary means, but resistance to and progress of caries in dentin can be influenced by increased intake of vitamin D and mineral fortification. Dentin continues under dietary influence and physiologic control throughout life, but formed enamel is never subject to these influences. Regardless of the state of systemic calcium-metabolism there is no physiologic mechanism by which calcium can be abstracted from, or deposited in, formed enamel. Adequate diet is essential for the development and ‘formation of sound teeth, but nutritional deficiency cannot be considered as the chief nor even as an important factor in causing the excessive caries incidence of civilization. In addition to diet per se there are many predisposing, accelerating, and limiting factors—such as ultraviolet radiation, proportions of calcium and fluorine in drinking water, intercurrent disease, etc.—which directly or indirectly affect metabolism and therefore influence nutritional development of teeth. Modern diets, and their purported effects upon the acid/base balance in the body, cannot be related to caries, for the alkaline buffers of the blood and saliva are identical in caries-susceptibles and caries-immunes. The teeth, from the time of their formation, progress unilaterally in the direction of increased density and resistance to caries. Any agent that interferes with normal metabolism—or any other factor that depresses resistance, local or general—relatively increases the pathogenicity of oral flora.
Much confusion concerning the etiology of caries has been caused by failure to understand that enamel dissolution and dentin destruction are distinct and unrelated phenomena. The situation would be clarified if the term ” caries ” were not applied until the physiologically inert enamel had been disintegrated and the viable and reactive dentin attacked.
Clean saliva is always alkaline in reaction, and there is no relationship between its buffer content and incidence or progress of caries ; and none between blood and salivary buffers in the same individual. Stagnant salivas from caries-susceptibles are always acid, similar salivas from caries-immunes are generally alkaline, in reaction. When salivas from caries-susceptibles and caries-immunes are added to carbohydrate media and incubated, the characteristic and striking difference in reaction is the acceleration of fermentation and acid production in the ” susceptible ” salivary mixtures. In persons showing hypersusceptibility to caries, metastatic decalcification—s’mooth-surf ace decay and erosion—frequently results from acid produced by bacteria on buccal mucosa.
Caries is a disease of civilized man and all others who partake of his diet, being entirely absent among people who subsist upon meat diets, and rare among persons whose carbohydrate is derived from such simple agricultural products as tubers, cane sugar, and fruits. Incidence of caries has paralleled spread of civilization, development of agriculture, and ingestion of agricultural products, particularly cereals. When modern diet is consumed, regardless of racial stock, incidence of caries—in absence of hypersusceptibility—is limited by the number of oral food- fermentation areas. Incidence of food-lodgment areas is not significantly different in caries-immune and caries-susceptible races. Pits and fissures occur frequently among primitive people, but such areas do not undergo early, rapid, and extensive decay unless the individual comes in contact with and consumes the ” diet of civilization.” In civilized races, individuals who have anatomically perfect teeth—no food-lodgment areas—seldom develop caries and are therefore called caries immune, while those who exhibit the greatest number of enamel defects are caries-susceptible because they develop the greatest amount of caries.
Cereals and cereal products in modern diets—consumed in small amounts if at all by primitive people—(a) are fermented with great rapidity (both in mouth and test-tube) by oral bacteria, which produce large amounts of acid ; therefore they (b) are the caries-producing factor of the modern diet, if that disease is due to chemicoparasitic activity. Staple products of primitive diets, such as tubers, potatoes, fruits, and sucrose and other sugars, are fermented so slowly, and with formation of so little acid, that they could not be influential in causing caries. Highly refined cereals are fermented more slowly by oral streptococci than are crude grains, but in whole saliva milled products are converted into acid more rapidly. Processing makes cereal less suitable for the growth of oral alkali-producing bacteria, and prevents them from limiting the development of acidogenic organisms. Refined cereal does not constitute a balanced bacterial diet ; antibiotic relationships cannot be maintained ; and this condition permits selective and unimpeded growth of streptococci. Thus milling greatly increases the caries-inducing qualities of cereals. Staple articles of primitive diets, such as cane sugar, bananas, fruits and other non- cereal carbohydrates, are antagonistic to growth of streptococci and elicit in them profound evolutionary changes characteristic of a complex life-cycle ; and smooth acidogenic strains are converted into rough slow-growing forms which produce little acid. If the evolutionary forms induced by sucrose are incubated in cereal media, they become smooth and regain to an undiminished extent their ability to produce acid. Thus consumption of cereals, particularly in the refined form, causes increase both in relative and absolute streptococcic pathogenicity. This is probably the chief cause of the excessively high caries-rates of civilization.
Streptococci, normally present in all mouths, are chiefly responsible for oral fermentation. For streptococci and cereals to be effective in producing caries, an adequate incubator would have to be provided ; namely, food-lodgment areas,
wherein fermentation would proceed without interruption. The constituent members of the oral flora lead a competitive existence, and normally inhibit free growth of each other ; but when environmental conditions become more favorable for the ubiquitous acid-producing streptococci—by ingestion of an easily fermented diet and presence of numerous incubation zones—the streptococci tend to outgrow all other forms, and to become relatively and absolutely more pathogenic for the hard structures of teeth.
Factors for control of caries: (a) There should be adequate diet, mineral fortification and sufficient vitamin D at all times, particularly during development and formation of teeth ; such means accelerate deposition of secondary dentin and thereby retard progress of caries. (b) So long as fermentable carbohydrates are eaten, caries cannot be prevented by dietary effort, because it will be impossible by any means to prevent occurrence of food-retention areas on teeth. (c) Food- retention areas should be eradicated or immunized by mechanical or chemical means ; and Black’s axiom, ” extension for prevention,” should be practised. (d) Growth of oral flora should be inhibited by mechanical, chemical, and hygienic means. (e) Ingestion of all grains—particularly breakfast foods, bread, pastry, and other materials containing partially or completely refined cereals—should be limited, or the unstable carbohydrate fractions should be destroyed or removed prior to human consumption.
References: Den. J. Australia, 1937; Den. Items Int., 1937, 1938.