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.

35 peri-implantitis recently referred for 10 years showed four types of inflammatory lesions, such as mild granulomatous lesion(n=5), severe granulomatous lesion(n=4), severe inflammatory fibrous scar tissue(n=15), severe abscess formation(n=11). However, the inflammatory lesions were usually localized at the peri-implant area accompanying compensatory hyperplasia of fibrous connective tissue. The fibrous scar and the necrotic abscess frequently occurred depend on the severity of inflammatory reaction. Among 30 cases of severe inflammatory lesions, only 2 cases involved condensing osteitis in adjacent alveolar bone. Thus, we suppose that the inflammatory progression of peri-implantitis could be partly inhibited by the hyperplastic fibrous stromal tissue stimulated by implant material. And more, the focal abscess formed around the implant can be easily drainaged through the fibrous tract of implant pathway, resulted in the chronic persistent inflammatory granulomatous lesion, that is contrast to the common socket granuloma after tooth extraction. However, depend on the degree of inflammatory reaction in the peri-implantitis the inflamed fibrous collagenous tissues, unregenerated graft materials, necrotic abscess and sequestra should be removed by surgical intervention and followed by antibiotic therapy, because the peri-implant tissue is as vivid as the normal periodontium for the inflammatory defense system. Therefore, we suggest that the inflammatory lesions of peri-implantitis be carefully treated to improve the prognosis for the following dental treatments