Studies on the bone resorption of radicular cyst

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Although the expansion of radicular cyst has been attributed to osmotic pressure, more physiological explanation, in terms of cellular resorption ob bone and connective tissue destruction, has emerged. Recently, several kinds of anareobic microorganisms have been isolated from infected dencal root canals and odontogenic abscesses. In this study, protease activities of various microorganisms isolated from infected root canals and odontogenic abscesses were evaluated using synthetic protease substrates, and the effect of microorganism on the secretion of prostaglandin E2 NPGE2) and proteased from monolayer culture cells of gingival fibroblasts and endotherial cells were examined. B. endodontalis (B.e) produced gly-pro peptidase and kallikrein-like protease, B. gingivalis produced trypsin-like protease, kallikrein like protease, and gly-pro peptidase, and B. intermedius produced cathepsin H-like protease and gly-pro peptidase. B.e, a putative pathogen of radicular cyst, induced monolayer cultures of human gingival fibroblasts to synthesize PGE2, but those of human gingival carcinoma cell line (Ca 9-22: squamous endothelial cell) did not synthesize PGE2. Furthermore, B.e stimulated the secretion of plasmin from human gingival cells in monolayer cultures, and also stimulated the secretion of elastase from Ca 9-22. These data suggests that one way in which pathogens of microorganisms might directly mediate connective tissue destruction through production of various proteases, furthermore indirect way, B.e stimulated the production of PGE2 and plasmin from gingival fibroblasts and elstase from gingival endothelial cells. Since PGE2 is a potent mediator of bone resorption and elastase inhibits the activity of TIMP, an inhibitor of collagenase, from polymorphonuclear cells, this microorganism may play an important role in the formation or growth of radicular cysts.