アブストラクト（32巻3/4号：神奈川歯学）

神奈川歯学

Japanese

Title　： LPSによる破骨細胞活性化機構の検討
Subtitle　： 原著
Authors　： 上村恭弘, 窪田道男, 飯田正人, 梅本俊夫
Authors（kana）　：
Organization　： 神奈川歯科大学口腔細菌学教室
Journal　： 神奈川歯学
Volume　： 32
Number　： 3/4
Page　： 241-248
Year/Month　： 1997 / 12
Article　： 原著
Publisher　： 神奈川歯科大学学会
Abstract　： 「緒言」 歯周炎における最も特徴的な臨床病態は骨吸収をともなうポケット形成であり, 治療の目標はポケットの除去と骨組織を含む歯周組織の再生にある. 成人性歯周炎は, 歯肉縁下における偏性嫌気性のグラム陰性細菌の増加により生じる感染症であり, その局在や特異抗体価の上昇からPorphyromonas gingivalis(P.gingivalis)が歯周病原性細菌として注目を浴びている. その作用については, 菌体成分, 代謝産物, 酵素などによる宿主組織の直接的破壊作用と感染に伴う炎症反応や免疫反応を介して, 組織障害を及ぼす間接的作用とが考えられる. グラム陰性菌の外膜成分であるリポ多糖体(Lipopolysaccharide ; LPS)は, 多彩な直接的および間接的生物活性を有しており, 歯周病原細菌のLPSは, 歯周病における炎症の進展, 免疫応答の活性化および歯槽骨吸収の促進物質の一つと考えられている. しかし, LPSによる骨吸収機構については不明な点が多い.
Practice　： 歯科学
Keywords　： 破骨細胞, Lipopolysaccharide (LPS), コロニー形成法

English

Title　： Analysis of the Mechanism of Osteoclast Activation Caused by Bacterial Lipopolysaccharides
Subtitle　： Original article
Authors　： Yasuhiro KAMIMURA, Michio KUBOTA, Masato IIDA, Toshio Umemoto
Authors（kana）　：
Organization　： Department of Oral Microbiology, Kanagawa Dental College
Journal　： Kanagawa Shigaku
Volume　： 32
Number　： 3/4
Page　： 241-248
Year/Month　： 1997 / 12
Article　： Original article
Publisher　： Kanagawa Odontological Society
Abstract　： [Abstract] A fundamental clinical feature of periodontal disease is pocket formation with alveolar bone loss. Therefore, periodontal tissue regeneration with pocket elimination is a major goal of periodontal treatment. Lipopolysaccharide (LPS) plays an important role in periodontal tissue breakdown. LPS, a cell-surface component of periodontopathic Gram-negative bacteria, induces bone resorption via osteoclast activation, though exactly how is not clear. We attempted to clarify the mechanism of osteoclast activation caused by bacterial LPS using a colony formation method, in vitro. Mouse bone marrow cells (non-adherent cells), passed through a nylon wool column, were suspended in collagen solution. The non-adherent cells were incubated with rIL-3 and cultured in the presence of LPS, PGE2 or autoclaved bacterial cells. The colony cells were stained with tartrate-resistant acid phosphatase (TRACP ; a marker enzyme of osteoclasts) and non-specific esterase (NSE ; a marker enzyme of macrophages). IL-3 was an essential growth factor for osteoclast activation by LPS in haemopoietic cells. LPS caused a significant increase in the number of TRACP positive colonies. The initial addition of LPS supported the differentiation to TRACP positive osteoclasts from TRACP negative precursor cells in this culture system with IL-3. The addition of PGE2, suppressed the colony formation in the presence of rIL-3. The above findings were confirmed by single cell manipulation. Both E.coli. LPS and P.gingivalis LPS potently induced the formation of TRACP positive colonies. Autoclaved P.gingivalis cells increased by 1.5 fold the number of TRACP positive colonies relative to P.gingivalis LPS. These results suggest that P.gingivalis LPS promote the differentiation of osteoclasts, and is implicated in the direct destruction of alveolar bone in periodontitis.
Practice　： Dentistry
Keywords　： Lipopolysaccharide (LPS)