WEST, EDWARD S., and JUDY, FREDERICK R.: Medical School, University of Oregon, Portland, Ore. (Aug. 19, 1938).


Solutions of commercial acidified hard candies (4o percent) having low pH values-2.5 to 2.8 in water and 3.4 to 3.7 in saliva—exert markedly de‑structive action upon enamel when teeth are exposed to them for several hours. The destruction is due to solution of mineral salts; also to replacement of phosphate ions by citrate ions. Repeated use of acidified candies probably causes many cases of acute caries.

References: J. Biol. Chem., 1938; J. Den. Res., 1938.

WESTIN, GOSTA : Dental Institute, Stockholm, Sweden (Jan. 12, 1939).

Caries, pulpitis and apical osteitis are, in the main, a single, uniform, and homogeneous inflammation of the dental organ induced by toxins from sub­sequently ingrowing acidifying and pathogenic bacterial matter from the oral cavity. This inflammation begins with the enamel reactions beneath the cuticle, which in turn result from the primary irritation of the odontoblastema via the enamel cuticle, interprismatic protoplasm and lamellae through the Tomes canaliculi, and ends with the chronic reaction of the tissues adjacent to the apex of the tooth. The absence of collateral circulation and the ana­tomical confinement of the pulp have an adverse effect on the inflammatory re­action, and lead to necrosis and decomposition of the enamel block and of the dentin wall. The pulpitis, whose latent forms are the primary ones, sim­ilarly results in the final stage, which is pulpal gangrene (equivalent to caries in the enamel and dentin). Ultimately there arise acute, then chronic, peri­apical osteitis. Here the inflammatory process comes to an end, owing to the ” defensive works ” opportunely put up by the periapical bone-tissue with its collateral circulation. When osteitis of this kind terminates in a root cyst, with a fistular passage opening into the oral cavity, the vicious circle is complete.

Caries research may be divided into three fields: (1) caries in the true sense of the term; (2) exogenous causal factors ; (3) endogenous factors. Field 1 has already been thoroughly investigated. Within field 2 the main interest attaches to the question of a possible unknown virus. Field 3 still exhibits the greatest num­ber of unknown factors. Even if knowledge of field 2 were complete, the vast and intricate complexity of the causes underlying caries would remain to be discovered. In this respect caries is comparable with tuberculosis, the etiology of which, despite the knowledge of the tubercular bacteria, has not been fully elucidated.

True caries, i.e., the calcifying and dissolving zones subject to acid-forming and proteolytic bacteria, does not affect dental tissues only—it attacks all dead hard tissues, whether inside or outside the oral cavity, which may be exposed in saliva to the influence of acids of fermentation and bacterial proteolytic enzymes. For this reason most histopathological investigations, bacteriological and chemical researches, experimental studies on animals, etc., never succeed in getting at the core of the problem of caries, but merely explain peripheric phenomena inherent in the disease. The solution of the problem of caries consists in elucidating that



equilibrium between exogenous injury and endogenous reaction (dentitis) which is a prerequisite for prophylaxis of caries. The exogenous injurious factors—acid­formation, B. acidophilus, pathogenic streptococci, unknown virus ( ?), etc.—may show wide variations, but in a majority of cases within present-day civilized com­munities they are constant. Thus, the decisive factor, from the pathogenic point of view, is the dental tissue’s capacity for reaction and the ability of the reactive process to avoid necrobiotic disintegration within the sphere of reaction—to main­tain equilibrium against exogenous injury. When there is a constant exogenous injury, high caries-frequency occurs during periods when a tooth is best able vigorously to react, when the embryonal pulp contains an abundance of vessels with free dentin walls, and the blastema is undergoing active metabolism. But the frequency is lowered as a tooth ages, when the pulp is subject to atrophy and to ob­literation, in cases of secondary-dentin production, chronic pulpitis, scorbutic dental changes, D-hypervitaminosis—in all physiological and pathological conditions within the hard structures and pulp that result in alterations of the tissues, con­forming in principle to the ” protective steps ” in the local development of the carious dentitis. On the same general assumption of constant exogenous injury, high caries-frequency should likewise be probable under conditions in which special demands are made on the organism and its sensitiveness is increased, e.g. during puberty, pregnancy, lactation, the climacteric years, in hyperergic and allergic states, or general pathological conditions involving increased local reaction to exogenous irritations.

The predominant histological changes caused by inflammation are : (a) altera­tion or degeneration, (b) proliferation and (c) exudation-infiltration. In in­flammation in bone these histological changes invariably appear first in the soft tissue, blastema and connective tissue in canals and marrow-spaces, the exudation- infiltration constituting the primary injurious process in the development of the pathological picture. Only at a later stage of the osteitis does the hard substance participate in degeneration and proliferation (so-called de-differentiation). Owing to the peculiar anatomy of a tooth, the hard substance without any protective blastema is exposed to the exterior, while the marrow cavity and dental canal con­taining the odontoblastema fill the interior. Consequently the inflammatory proc­ess in dental tissues demonstrates the histological changes in reverse chronological order—degenerative processes appear first in the hard portions, followed by pro­liferation, then by exudation-infiltration, when the histological reaction is mor­phologically discernible in the vascular pulp-tissue. Each inflammatory affection is determined by the relation between quality and quantity of the injurious factors and reactive powers of the organ. The inflammation may lead to elimination of the injury, and to healing and restoration of the diseased tissue; if the inflammatory process fails to do so, different necrobiotic processes and death of the organ or part thereof result. Dental carious inflammation affects the organ in places that are exposed to chemico-toxico-bacterial attacks, i.e., fissures and foramina, approximal surfaces and gingival thirds. The inflamed area extends, in a circular, pointed



cone, by the shortest protoplasmic route toward the pulp ; the alteration consists of calcification and fatty degeneration of the transparent zone ; the proliferation con­sists of secondary irregular dentin or cement-bone production from the odontoblas­tema in its inflammatory de-differentiation; and exudation-infiltration character­izes the first latent pulpitic changes at the pulpal point of the dentin cone. As inflammation penetrates deeper, superficial parts affected by the necrobiotic proc­esses of the dentitis gradually reach the necrotic state, whereupon the devitalized portions of tissue disintegrate under the influence of acids of fermentation and of bacterial proteolytic enzymes (true caries).

References: Viertjschr. Zahnh., 1926, 1928 ; Svenska Tandl. Tidskr., 1926 ; Nord. Bokh., 1931; Svenska Tand1.-Siillskapets Festsk., 1935; Nor. Tannlaeg. Tid., 1938 ; Odon. Tidskr., 1938 ; An investigation into questions of social hy­giene in the Counties of Vdsterbotten and Norrbotten, Sweden—Part III : Condi­tion of the teeth and dental diseases in Upper Norrland, 1929-31 (Royal Medical Board).

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