Interaction of inflammatory cells and oral microorganisms. IV. In vitro release of lysosomal constituents from polymorphonuclear leukocytes exposed to supragingival and subgingival bacterial plaque.

leukocytes (PMNs)actively released lysosomalconstituents uponinvitro exposure toeither viable orirradiated, supragingival orsubgingival dental plaque. Plaques wereobtained fromthePMN donors (autologous plaque) orfrompooled samples (homologous plaque) secured frompatients withperiodontal lesions. FreshserafromPMN donors amplified therelease reactions tosupragingival andsubgingival plaques. Heated (56°C, 30 min)seraalsoenhanced release reactions, butnotasconsistently asfresh serum.Itwaspostulated thatmodulation ofPMN release byserumismediated bycomplement components and/or antibodies toplaque bacteria. Electron microscopic observations indicated that degranulation anddischarge ofPMN lysosomal enzymes maybeassociated withphagocytosis ofgram-positive andgramnegative plaque bacteria andwithreverse endocytosis oflysosomes fromcells contacting relatively large massesofaggregated plaque bacteria. Thesedata suggest thatPMN lysosome release inresponse toplaque mayserveasa potential mechanism oftissue injury inthepathogenesis ofgingival andperiodontal inflammation. Inflammatory lesions oftheperiodontium are seeninthevastmajority oftheadult population andcanresult inprogressive destruction of thesoft tissues andbonethatsupport teeth in their sockets (19). Theaccumulation ofadherent,heterogenous bacterial plaques onthe crownsandrootsurfaces ofteeth hasbeen linked asthemajoretiological eventinthe initiation andprogression ofgingival andperiodontal disease (16, 31,42). Polymorphonuclear leukocyte (PMN)emigration fromconnective