Tumor Necrosis Factor-a and its Receptors, p55 and p75, in Gingiva of Adult Periodontitis

Abstract

Tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine, can stimulate matrix metalloproteinase synthesis and osteoclastic bone resorption. We hypothesized that elevated expression of TNF-alpha and its p55 and p75 receptors (TNF-R) in gingival tissue might associate with periodontitis. Immunohistochemistry was used for the study of the localization of TNF-alpha and its p55 and p75 TNF-R in adult periodontitis (AP) gingival tissue, in comparison with that in healthy control specimens. TNF-alpha and p55 TNF-R were detected in sulcular epithelial basal cells and in monocyte/macrophages, fibroblasts, and endothelial cells in the AP gingival tissue specimens, but mainly in fibroblasts and endothelial cells in control specimens. P75 TNF-R was occasionally found in monocyte/macrophage-like cells in gingival tissue specimens. The percentage of TNF-alpha-containing cells was not increased in AP compared with controls (13.2%+/-6.1% vs. 12.8%+/-7.6%), but, due to the increased cellularity of AP samples, the number of TNF-alpha positive cells/mm2 was clearly increased (1621+/-663 vs. 664+/-191, p > 0.001). Thus, AP gingival tissue has an elevated expression of TNF-alpha and especially its p55 receptor, suggesting that TNF-alpha may contribute to tissue degradation in periodontitis.

Mutations in the ELANE Gene are Associated with Development of Periodontitis in Patients with Severe Congenital Neutropenia

“…In addition, the mean and median levels of IL-17, IL-6, and TNF-α in patients with ELANE mutations were higher than in HAX1 or unknown mutations although these differences did not reach statistical significance, most likely due to the small size of the cohort and great variations within groups. It is known that elevated levels of IL-1β [39, 40], IL-6 [41], TNF-α [42], and IL-17 [43] in GCF are associated with severe periodontal disease, and that these cytokines may also be elevated in chronic periodontitis tissue [44–46]. Thus, the GCF from patients with ELANE mutations displays the presence of the strong proinflammatory cytokine IL-1β, which might be expected in the inflamed periodontium.…”

Macrophage-Elicited Osteoclastogenesis in Response to Bacterial Stimulation Requires Toll-Like Receptor 2-Dependent Tumor Necrosis Factor-Alpha Production

“…Since our BMMs were exposed to FBS prior to incubation with CS fluids and since it is known that TGF-␤ is present in FBS, we cannot definitively rule out a role for TGF-␤ in P. gingivalis-induced osteoclastogenesis in our macrophage system. TNF-␣ is frequently detected in inflamed tissues from patients with periodontal disease (36). TNF-␣ has been demonstrated to contribute to oral bone loss in a P. gingivalis-induced inflammatory oral bone loss mouse model (13).…”

The role of water channel aquaporin 3 in the mechanism of TNF‐α‐mediated proinflammatory events: Implication in periodontal inflammation

“…2A,B), indicating an early kinetics response of this water channel protein in the presence of an inflammatory event. Periodontal infection is associated with both TNFR I and II, which are not usually expressed on healthy gingival epithelial cells (Tervahartiala et al, 2001;Ikezawa et al, 2005). Furthermore, TNF-a and its receptor type 1 (TNFR I) have prominent effects on increased edema formation, and subsequent plasma protein extravasation (Mizgerd et TNFR neutralization study, the absence of TNFR I partially but significantly attenuated TNF-a-induced AQP3 expression, suggesting that TNF-a acts through the plasma membrane receptor TNFR I, leading an alteration of AQP3 protein expression (Fig.…”