Caries is an indirect outcome of the consumption of a ” civilized dietary,” in which the natural or foundation foods are refined and unfavorably altered in the processes of preparation and cooking. In general, incidence of caries is directly proportional to intake of refined carbohydrate. In the process of refining, removal of certain elements from the natural carbohydrate is responsible for a number of changes—oral and alimentary—the end result of which is a greatly facilitated degradation of carbohydrate into lactic and other acids, as indicated in the summary below :
(1) Local or oral effects. (a) Removal of cellulose or fibre : lack of functional stimulus to jaws and teeth during the formative period, resulting in poorly developed arches, crowded teeth, and increased lodgment areas, favoring food stagnation. (b) Insufficient attrition to remove deep fissures, grooves, and other lodgment areas (compared with primitive races). (c) Incomplete insalivation of food, leading to alimentary sequelae (2, below). (d) Refined white-flour products are either salivary depressants or induce flow of thick, viscous, acid saliva, which deposits mucin, and facilitates food lodgment and plaque formation. (2) General or alimentary effects. (a) Food too concentrated in relation to its bulk and the energy requirements of the individual, resulting in loss of peristaltic tone, digestion to a large degree being replaced by fermentation. (b) Loss of vitamin- 13, during refining, causing incomplete metabolism of carbohydrate and accumulation of intermediate catabolic products. (c) Fermentative changes in the alimentary tract, reflecting back to the oral field, produce media suitable for development of acidogenic bacteria, interaction of which with pabulum provided by refined carbohydrates is the causative factor in production of caries. (d) Fermentative changes in the alimentary tract, and accumulation of intermediate breakdown- products, result in excess of acid production. Demineralization of staple foods, in processing and cooking, results in lowered body mineral-reserves. When these reserves are exhausted, as buffers, the body may endeavor to maintain correct acid/base ratio by excretion of excess of acid. When such acid is excreted by the oral mucous-glands, erosion, or erosion plus infection, or gingival caries, may result.
The varying susceptibilities of individuals to caries is determined by the facility and rapidity with which carbohydrate is broken down to acid. This, in turn, is dependent on type of pabulum, presence of certain enzymes, and symbiotic action of streptococcal and acidogenic types of organisms. Acid saliva in caries-susceptibles is the direct result of intrinsic activities of bacteria, and the indirect result of the alimentary condition. The final stage in the carious process is bacterial proteolytic decomposition of the organic dentinal matrix. This action is productive of local alkalosis which, under certain conditions, may protect the approximating tooth from the initial carious attack. Except that poorly calcified teeth may exhibit deep unclosed fissures, and thus offer greater degrees of food lodgement, the cal‑cification of teeth is in no way related to incidence of caries. Until enamel is shown to be possessed of a circulation, there is no method by which the tooth itself could develop intrinsic resistance, either anti-bacterial or anti-acid, to the initial decalcifying lesion resulting in caries.
References: Aus. J. Den., 1936, 1938 (latter contains chart showing interacting factors).