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

Abstract

The deposition of bacterial plaques on tooth surfaces appears to be responsible for the initiation and progression of periodontal disease. In this study, human peripheral blood polymorphonuclear leukocytes (PMNs) actively released lysosomal constituents upon in vitro exposure to either viable or irradiated, supragingival or subgingival dental plaque. Plaques were obtained from the PMN donors (autologous plaque) or from pooled samples (homologous plaque) secured from patients with periodontal lesions. Fresh sera from PMN donors amplified the release reactions to supragingival and subgingival plaques. Heated (56 degrees C, 30 min) sera also enhanced release reactions, but not as consistently as fresh serum. It was postulated that modulation of PMN release by serum is mediated by complement components and/or antibodies to plaque bacteria. Electron microscopic observations indicated that degranulation and discharge of PMN lysosomal enzymes may be associated with phagocytosis of gram-positive and gram-negative plaque bacteria and with reverse endocytosis of lysosomes from cells contacting relatively large masses of aggregated plaque bacteria. These data suggest that PMN lysosome release in response to plaque may serve as a potential mechanism of tissue injury in the pathogenesis of gingival and periodontal inflammation.

The relationship of serum IgG antibody titers to periodontal pathogens to indicators of the host response in crevicular fluid

“…The results also indicate a negative correlation between serum IgG antibody titer to periodontal pathogens and the level of BG in GCF. Lysosomal BG is considered a marker for primary granule release from PMN (Taichman et al, 1977, Miller &Russel 1986, In previous reports a positive relationship between elevated BG in GCF and disease progression as measured by clinical attachment loss was observed (Lamster et al 1988). Therefore, the presence of a serum IgG antibody titer to periodontal pathogens in chronic adult periodontitis IS consistent with a protective host response.…”

Correlation analysis for clinical and gingival crevicular fluid parameters at anatomically related gingival sites

“…In a previous longitudinal trial , we described a relationship between elevated BG activity in GCF and clinical attachment loss in patients with chronic adult periodontitis. BG is a lysosomal acid hydrolase that can serve as a marker for primary granule release from PMN (Taichman et al 1977, Miller & Russell 1986. One of our observations in that study was elevated BG activity in mesiobuccal samples frequently could be used to identify clinical attachment loss occurring at one of the sites within the adjacent papillae.…”

Host responses in maintaining periodontal health and determining periodontal disease

“…Polymorphonuclear leukocytes synthesize and release a number of substances, such as lysosomal enzymes including tissue-destructive proteases [18, 125,135,172,173,213,242] that are associated with the breakdown of periodontal tissues. Interactions of polymorphonuclear leukocytes with bacteria have been shown to damage a variety of crucial cell types, including fibroblasts, endothelial cells, and keratinocytes [241].…”