Relationship between histological degree of inflammation and epithelial proliferation in macaque gingiva

Abstract

Epithelial proliferation of various regions of macaque gingival epithelium, as measured by uptake of locally injected H«^-thymidine, showed regional differences which could be explained in part by the size and nature of the inflammatory infiltrate invariably found in gingival biopsies. The proliferative activity of oral sulcular epithelium was greater than that of oral epithelium and was negatively correlated with the size of the area of infiltrated connective tissue. On the other hand labelling of oral epithelium was positively correlated with size of infiltrate, the effect decreasing with distance of the epithelium from the infiltrate.

Interleukin‐1β, clinical parameters and matched cellular‐histopathologic changes of biopsied gingival tissue from periodontitis patients

“…Changes in pocket epithelia were especially found in affected tissues with heavy inflammatory infiltration. These findings agree with data of a rapid turnover and mitotic rate of pocket epithelial cells being correlated with increasing cellular infiltrate (47, 48). The presence of ulceration and/or thinning of pocket epithelia in biopsied gingivae have been suggested to be a key factor necessary for the perpetuation of supra‐crestal destruction and alveolar bone loss in experimental periodontitis (49–51).…”

The Permeability of Oral Mucosa

“…126 Epithelium shows a bimodal response to inflammation; a mild degree of inflammation stimulates proliferation, severe inflammation depresses it. 127 Inflammation tends to reduce keratinization, as observed by Riber and Kaaber,125 and this change in differentiation is presumably accompanied with an alteration in the permeability barrier toward the type found in nonkeratinized tissue. In normal oral mucosa, nonkeratinized epithelium may be more than twice as permeable as keratinized regions (see Table 1), which is the same order of difference found by Riber and Kaaber.…”

Oral hygiene and periodontal considerations in preventing and managing dentine hypersensitivity

“…Although the process of recession is not well-understood [4][5] , early histological studies in the rat and monkey showed that periodontal inflammation is essential to the formation of cleft defects principally by the growth and anastomosis of the rete pegs of the oral epithelium and the epithelium lining the periodontal pocket. Since the studies have not been duplicated in the human, it is not known definitively if the pathogenesis of recession is the same for humans.…”

“…Longitudinal studies have provided significant evidence to support the premise that gingival recession is associated with excessive oral hygiene and plaque control habits producing lesions that are exacerbated in the presence of certain anatomic factors [4][5][6][7][8] . The most common anatomic factors that predispose sites to recession [6][7][8][9][10][11][12][13][14][15] include:…”