Although it has been documented that exogenous antigens of microbial origin are involved in the induction of the local inflammatory responses in human adult periodontitis (AP), endogeneous antigens may contribute to the chronicity of this common disease. In this study, we used the enzyme‐linked immunospot (ELISPOT) test to enumerate antibody‐secreting cells to human collagen Types 1‐VI by cells isolated from the gingivae and peripheral blood of AP patients. Analyses of dissociated cells from gingivae of 39 AP patients revealed the presence of high numbers of cells that secrete antibodies to Type I collagen, and to a lesser extent, Type III. Although the majority of such cells produced specific antibodies of the IgG class, IgA‐ and IgM‐ anti‐collagen ‐secreting cells were also detected. When compared to the total antibody‐producing cells, the numbers of cells forming specific antibodies to collagen Type I were surprisingly high. In contrast, anti‐collagen antibody‐producing cells were rarely detected in the peripheral blood of patients with adult periodontal disease and only low levels of anti‐collagen antibodies were present in the serum. The finding of local production of anti‐collagen antibodies in AP suggests that autoimmunity may contribute to the pathogenesis of this common disease.
The enzyme-linked immunospot assay was used to enumerate both the number and the frequency of spontaneous IgG, IgA, and IgM immunoglobulin-secreting cells and IgA- and IgM-rheumatoid factor (RF)-producing cells present in the gingivae and peripheral blood of adult periodontitis patients. Cells from 29 patients were incubated on plates coated with human IgG, Fc, or F(ab')2 fragments and on plates coated with class-specific anti-human antibodies and secreted antibodies were subsequently visualized by means of an immunoenzymatic procedure. The data indicate that (1) IgA-RF- and IgM-RF-secreting cells are frequently present in the gingiva of adult periodontitis patients; (2) production of RF in gingivae of adult periodontitis patients occurs in the absence of demonstrable RF production by simultaneously obtained peripheral blood mononuclear cells, suggesting that local autoimmune reactions may occur in this disease; and (3) lack of correlation between IgA-RF and IgM-RF production in diseased gingiva suggests that the two RF isotypes are regulated independently of each other.
The presence of HNK‐1 (Leu‐7)‐positive cells and natural killer (NK) cell activity was determined in human periodontal tissues. Gingival tissues obtained from 25 adult patients were processed for analysis utilizing a HNK‐1 (Leu‐7) mouse monoclonal antibody. A subpopulation of non‐adherent lymphoid cells obtained by collagenase digestion of inflamed gingival tissues from 10 patients was examined for the presence of large granular lymphocytes (LGL) by May‐Grünwald‐Giemsa staining and for NK cell activity against K562 cells by a 51Cr release cytotoxicity assay. HNK‐1+ cells were identified in gingival tissue sections of 21 patients, and were present in or close to discrete foci of plasma cells. HNK‐1+ cells were scarce in mildly inflamed or uninflamed tissues sections. LGL were identified in 9 of 10 gingival single‐cell suspensions and constituted approximately 5% of the gingival cell population. NK cell‐mediated cytolysis, at varying effector/target cell ratios, was observed for 3 of 4 enriched gingival mononuclear cell populations. Gamma‐interferon (INF‐γ) preincubation of enriched gingival effector cells from 5 additional patients resulted in a 43% increase in NK cell activity. The finding of increased HNK‐1+ cells with gingival inflammation suggests that these cells may play a role in tissue damage, as well as in modulation of B cell activity, in gingivae of patients with periodontal disease.
This case report describes the placement of a large-diameter implant at the time of a maxillary molar extraction in conjunction with a simultaneous oroantral communication (OAC) repair and an intraosteotomy lift and the 5-year postloading follow-up. Literature exists supporting the efficacy of immediate implant placement using both conventional and modified insertion techniques. However, no reports detail the repair of an OAC concomitantly with immediate implant insertion. The OAC was repaired by first placing multiple layers of a collagen matrix through the socket, followed by grafting with a mixture of freeze-dried demineralized bone and calcium sulfate, simultaneous obliteration and reshaping of the socket using implant shape-specific osteotomes, and immediate placement of a Frialait-2 6.5-mm-diameter implant. No flap elevation was performed and no membranes were placed. A radiograph taken 5 year after loading showed a stable implant in conjunction with a new maxillary sinus bony floor.
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