Ultrastructural evidence of large granular lymphocyte (LGL) activity in lesions of chronic adult periodontitis

Relevance of FcγRIIIa-158V-F polymorphism to recurrence of adult periodontitis in Japanese patients

“…Actually, inflamed human gingival tissue contains activated macrophages [23][24][25], NK cells [26][27][28][29] and gd T cells [30]. Recently, two-colour flow cytometric analysis demonstrated that CD16 þ NK cells were increased in PB from periodontitis patients compared with healthy controls [36].…”

“…Kobayashi et al found a significant overrepresentation of the FcgRIIIb-NA2 allotype in patients with AP recurrence [22]. In contrast, inflamed human gingival tissue contains fewer neutrophils but significant numbers of activated macrophages [23][24][25], NK cells [26][27][28][29] and gd T cells [30], which may express FcgRIIIa. In human inflammatory gingival tissues, the major IgG subclass expressed in cells is IgG1 [31].…”

Cell-Mediated Immune System Regulation in Periodontal Diseases

“…Pre-treatment of gingival fibroblasts with sonic extracts of dental plaque increases NK cell cytotoxicity against these cells (Seymour et al, 1984). Ultrastructural changes in fibroblasts indicative of NK-mediated cytotoxicity have also been observed histologically (Cobb et al, 1990). NK cells may also regulate B-cell activity and proliferation (Wynne et al, 1986), which is a hallmark histological feature of the advanced periodontal lesion.…”

“…Although few if any NK cells are seen in healthy tissues, their numbers increase from health to gingivitis to periodontitis (Wynne et al, 1986;Cobb et al, 1989;Fujita et al, 1992). Typically, these cells are located subjacent to the epithelium, and commonly in association with foci of B-cells or plasma cells (Wynne et al, 1986;Komiyama et al, 1988;Cobb et al, 1990). Although the number of NK cells increases with disease severity, the proportion of these cells relative to total lymphocyte counts actually decreases (Cobb et al, 1989).…”

Presence of natural killer cells in human chronic periapical lesions

“…Periodontal studies have reported several significant observations. Patients with recurrent aphthous ulceration have significantly higher peripheral cell covmts (Pedersen et oi, 1991) than normal controls, NK cells and their activity were equally distributed in a patient group demonstrating lichen planus compared with a healthy patient population (Yamamoto et al 1990), A Qow-cytometric analysis of peripheral lymphocyte subsets, including NK cells, in 36 patients with advanced periodontitis and 34 healthy individuals showed no significant differences between the groups (Zafiropoulos et d. 1990), These authors interpreted the results to indicate that local infiammatory reactions and immunoregulatory dysfunction were limited to the periodontium of the patients, with no significant quantitative effects on peripheral lymphocyte populations, Cobb et al (1990) studied eight adults with chronic adult periodontitis and found 3-7% of the total monocytic infiltrated cells were NK cells. These tended to occur singly or in small clusters of 3-12 cells and were in intimate contact with fibroblasts that exhibited morphologic changes consistent with cellular damage or degeneration.…”