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Cell populations and episodic periodontal attachment loss in humans *
Author(s) -
Zappa U.,
ReinkingZappa M.,
Graf H.,
Espeland M.
Publication year - 1991
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1991.tb00082.x
Subject(s) - periodontal disease , cell , medicine , dentistry , biology , genetics
The purpose of the present study was to assess possible associations between episodic probing attachment loss and cell populations in the supracrestal connective tissue in humans. 10 systemically healthy adult patients with untreated advanced periodontitis were monitored during a period of 10 months. At baseline and every month thereafter, probing attachment levels were measured at 6 sites of every tooth using an electronic pressure sensitive probe and flexible stents. Corresponding contralateral sites were identified where 1 site had lost 2 mm or more attachment within the previous month (P), and the other site had not (C). Supracrestal soft tissue biopsies were taken from these sites, processed and cut into 1 μm sections. Cell populations were identified in superficial and deep connective tissue areas by counting fibroblasts, macrophages, plasma cells, mast cells, granulocytes, lymphocytes, endothelial cells and the total number of inflammatory cells. Analysis of variance assessed differences in cell populations between P‐ and C‐sites. There were statistically significantly higher numbers of fibroblasts in the standard areas of C‐sites ( p < 0.0001). In P‐sites, the numbers of macrophages, plasma cells, mast cells, lymphocytes and total inflammatory cells were significantly higher as compared to C‐sites ( p = 0.05–0.0001). There were no differences in cell populations between superficial and deep connective tissue areas within P‐and C‐sites ( p > 0.2). Clinically assessed episodes of periodontal disease progression may be associated with site‐specific shifts in inflammatory cell populations.