Peri-implantitis (PI) is bacteria-induced inflammatory condition which affects the alveolar bone and soft tissue around implants and may result in the loss of supporting bone. Attenuation of the P. gingivalis lipopolysaccharide (LPS)-induced inflammatory response can be a new therapeutic approach in the treatment of PI. This study was conducted to evaluate the anti-inflammatory effect of 635-nm light-emitting diode (LED) irradiation over MG63 osteoblast-like cell. Scratch was made on MG63 cells with or without LPS, then 635-nm irradiated. The expression of the cyclooxygenase-2 (COX-2) proteins was evaluated with western blot. The production of the prostaglandin E2 (PGE2) and expression of the receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) was measured with enzyme-linked immunoassay, and the cytokine profile was evaluated with the human inflammation antibody array. Wound closure effect presented in the cells treated with LPS was observed more significantly in the cells with 635-nm irradiation than the cells without irradiation. The 635-nm irradiaiton reduced LPS-induced expression of the COX-2 and production of the PGE2. Also, 635-nm irradiation affect the expression of RANKL, OPG, and proinflammatory cytokines. These results indicate that 635-nm irradiation could reduce the alveolar bone resorption induced by LPS stimulation through the inhibition of COX-2 expression and PGE2 production, the suppression of proinflammatory cytokine, and the modulation of RANKL/OPG balance in MG63 cells.

Topoisomerases are essential enzymes involved in all processes of DNA metabolism, and their inhibitors have been identified as potential anti-cancer agents. The present study examined the effect of linoelaidic acid (C18 polyunsaturated fatty) compounds derived from Gardenia jasminoids Ellis extract on the activity of eukaryotic topoisomerases inhibition. The present study identified linoelaidic acid compounds using open column fraction, HPLC, NMR and LC/MS which have effects on cell death in oral cancer cell line, FaDu, but not in immortalized normal cell line, HaCaT. Subsequent studies revealed linoelaidic acid-induced autophagy through LC3 activation. Finally, its inhibition of topoisomerase I and selectively induction of oral cancer cell death possibly implies that linoelaidic acid can be a role as potenial agents in the prevention and therapy of oral cancer.