is a periodontal pathogen exacerbating periodontitis by inducing nitric oxide production.

Abstract

Periodontitis, a chronic inflammatory disease, often causes alveolar bone loss.is a Gram-negative bacterium that has been identified in periodontal patients, but its role in periodontitis remains unclear. In the present study, we examined whetherexacerbates periodontitis in a mouse ligature-induced periodontitis (LIP) model and investigated its underlying molecular mechanism. Topical treatment withon maxillary second molar exacerbated alveolar bone loss and worsened epithelial and periodontal ligament damage. Histological analyses showed thatincreases tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts and inducible nitric oxide synthase (iNOS) levels in the gingival tissue. Treatment withinduced nitric oxide (NO) production in RAW 264.7 cells, which was inhibited by polymyxin B, implying thatlipooligosaccharide (LOS) is a major etiologic agent in the inflammatory response. Indeed, LOS purified fromenhanced NO production and iNOS expression, primarily with activating Toll-like receptor (TLR) 4 and partially activating TLR2. LOS administration into the disto-palatal papilla near the molar further aggravated periodontitis in the LIP mouse model. These results suggest thatis a periodontal pathogen that exacerbates inflammation and alveolar bone loss, with its LOS acting as an important virulence factor via TLR2/4 activation, leading to the production of the inflammatory mediator NO.