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LYSOSOMAL CONCEPT IN DENTAL CARIES DEVELOPMENT JOHN GABROVSEK* Introduction The idea that host factors are involved in dental caries development is not so new. Hippocrates believed that the decay of the teeth was caused partly by phlegm and foods. Galen suggested that dental caries was caused by abnormal conditions in the blood and that bodily humors altered the internal structure of the teeth, causing decay. Borovsky, Prohonchykov, and Kodola [1] reviewed the work of the Nineteenth Congress of European Organization for Caries Research (ORCA) held in Leipzig in June 1972. In their conclusion the authors state that the congress was disappointing because most of the presentations by Western scientists did not reflect the role of the endogenous factors in the pathogenesis of dental caries. In the introductory chapter ofPathobiology, Minckler [2] says that the fallacious notion of a single factor as a "cause" of disease evolved from the field of infectious diseases, perhaps more than from other branches of pathology. For unknown reasons, according to Minckler, people have the tendency to credit some single thing with causing a disease. To disprove this tendency he gives as an example the polio virus and the disease poliomyelitis. Most people carry the virus during epidemics and yet most people do not get the disease. This type of observation has slowly forced the notion that any diseased state is a product not of a single causative agent but of factors emanating from both the agent and the host. I feel that this notion of a single "cause" of disease still persists in the field of dental caries research. Although this notion is not very obvious—because in papers we always read that the role of the host is important—the research and discussions are directed toward diet and bacteria, and almost none is pertinent to the host. It is interesting to note that both periodontologists and cariologists ?Department ofAnatomy, School of Medicine and Developmental Biology Center, Case Western Reserve University, Cleveland, Ohio 44106. I thank Professor Marcus Singer, director of the Department of Anatomy, and Richard Graham, Jr., associate professor of medicine, for their valuable advice and critical comments. Credit for their assistance is also gratefully extended to Dr. Charles Rehor, Mr. Arthur Feher, and Mr. James Epstein. Perspectives in Biology and Medicine · Autumn 1975 I 77 consider dental plaque as a source of evil, and both agree that substances from dental plaque initiate periodontal diseases and dental caries. Although cariologists mention that the host plays a role in the development ofdental caries, most ofthem still have the tendency to favor Miller's old chemicoparasitic theory; their basic position is that diet, bacteria, and bacterial acid production are the main factors in caries development. This theory is not in accordance with modern pathology because it does not take into account the reaction of the living host on infection. On the other hand, some periodontologists have more recently considered the role of Iysosomes and their enzymes derived from the host in disease development. With this concept, in addition to the environmental factors , the role of the host in disease development is very much emphasized . An attempt will be made here to show that bacteria and acids alone are not sufficient for caries development. During growth and remodeling of the bone, a physiological process, osteoclasts play a role in bone resorption, proteolysis, and decalcification without the help of bacteria. Since both neutrophil leukocytes and osteoclasts are known to release lysosomal enzymes upon phagocytosis, they functionally resemble each other in this respect. This may also indicate that neutrophil leukocytes may play a role in proteolysis and decalcification in dental caries development, as osteoclasts play a role in bone resorption. Biochemical evidence showing the involvement ofIysosomes and their enzymes in the processes of bone resorption has been reviewed by Vaes [3]. Bacteria, without doubt, play a major role in the development of dental caries. A problem arises when we ask ourselves why Streptococcus mutans is more associated with dental caries than acidogenic and aciduric lactobacilli, and whether it is possible that the production of acid by bacteria isjust not adequate to induce dental caries. Certainly no one has succeeded—and no one is likely to succeed—in reproducing...