内毒素と歯周疾患 : 歯周炎および歯髄炎の体液性免疫

Micro-organisms and their products, as toxins and enzymes, in dental plaque cause periodontal disease. Especially their endotoxins are thought to be direct and indirect inducers of periodontal disease. Endotoxin (lipopolysaccharide, LPS) was inoculated into gingival tissue, dental pulp, and extraction wound and induced inflammation and focus in tooth and periodontal tissues. In the advance of the lesion, humoral factors such as immunoglobulins and complements and induced cells such as macrophages and osteoclasts were studied quantitatively. The purpose of this article is to review the effect of endotoxin on the level of the humoral factors and the number of induced cells from the above experiments. After gingival inoculation of endotoxin, complements in gingiva were activated soon and that activation elicited cell infiltration and triggered off succeeding immunological response. The activation of complements was decreased soon and increased again. This biphasic activation of complements in periodontal tissue will reflect temporal local imbalance between the supply from systemic humor and the consumption as a result of activation by endotoxin. In endotoxin-inoculation into dental pulp, from the time of establishment of inflammation in the pulp to the time of formation of focus of apical crest, the level of anti-LPS immunoglobulin G increased greatly, while the level of the other humoral components changed slightly. Antibodies of this class seemed to play a protecting role in the case of infection in dental pulp. In the extraction wound, macrophages appeared soon after tooth extraction and began to decrease in number after 12 hr. Instead of macrophages, osteoclasts began to increase in number at that time. These results showed that endotoxin activated complement directly, elcited the cell infiltration, and rose the level of specific antibody. Endotoxin also induced indirectly repair of inflammation and increased the number of osteoclasts.