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The interpretation of studies aimed at understanding the pathophysiology of periodontal breakdown has been hampered by an insufficient understanding of the physiology of host responses in clinically healthy gingiva. This investigation was aimed at the evaluation of the in situ phenotype and topographic distribution of the inflammatory cells in clinically normal gingiva and peri-implant keratinized mucosa (PIKM). Soft tissue biopsies were obtained from clinically healthy gingiva or PIKM in 14 patients. Acetone fixed, cryostat sections were stained with a panel of monoclonal antibodies with a three stage avidin-biotin immunoperoxidase technique. Numbers of positive cells/mm2 were determined with a calibrated image analysis system. The major findings of the study were: (i) the presence of significantly higher densities of phenotypically characterized mononuclear cells in the ICT than in the JE in both gingiva and PIKM; (ii) the absence of a significant difference in PMN densities between JE and ICT in both gingiva and PIKM; (iii) the absence of statistically significant differences in densities of phenotypically characterized leukocytes associated with gingiva and PIKM; (iv) the presence of regional differences in the relative proportions of immunocompetent cells in both the gingiva and PIKM. It is concluded that inflammatory cells are selectively distributed in gingiva and PIKM. Unique functional compartments could be identified. The observed compartmentalization requires selective regulatory mechanisms.
Tonetti et al. (Sun,) studied this question.