Expression of prostaglandin E synthases in periodontitis immunolocalization and cellular regulation.

The inflammatory mediator prostaglandin E(2) (PGE(2)) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammation-induced PGE(2) synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE(2) production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE(2) synthesis. In response to tumor necrosis factor (TNF-α), IL-1ß, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE(2), whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-α increased PGE(2) production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE(2) enzyme expression or PGE(2) production. Furthermore, PGE(2) production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE(2) production in the inflammatory condition periodontitis.

Production of transforming growth factor beta1 and prostaglandin E2 by osteoblast-like cells cultured on titanium surfaces blasted with TiO2 particles.

The surface roughness of an implant to which osteoblasts attach may influence endogenous expression of growth factor and cytokines at the implant-tissue interface, modulating the healing process and affecting the quality of bone formation. The present study, using cells derived from human mandibular bone, investigated the effect of varying roughness of titanium surfaces on production of transforming growth factor beta1 (TGF-beta1) and prostaglandin E2 (PGE2). The titanium surfaces were turned (control) and then roughened by blasting with 63-90 micro m, 106-180 micro m or 180-300 micro m TiO2 particles. The cells were cultured onto the surfaces till confluence was achieved. Fresh media were added in the presence or absence of 1,25-dihydroxyvitamin D3[1,25-(OH)2D3], the stimulator of osteogenic differentiation, and aliquots of conditioned cell media were used for assay 24 h later. Cellular morphology was determined by scanning electron microscopy. Cellular production of TGF-beta1 and PGE2 on each surface was assessed by enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA), respectively, using commercially available kits. All blasted surfaces showed significantly higher production of TGF-beta1 than the turned surfaces (P < 0.05). In response to stimulation by 1,25-(OH)2D3 cellular production of TGF-beta1, was also significantly greater (P < 0.05) on the blasted surfaces than on the turned one. The total amount of PGE2 in the conditioned media was higher than on the turned surfaces in the presence or absence of 1,25-(OH)2D3. There were no significant differences among the three blasted surfaces with respect to production of the local factors. However, we could not show a synergistic effect of surface roughness and vitamin D on the production of both TGF-beta1 and PGE2 using primary cell culture model.