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en: Biological effects of interleukin-6 on Gingival Fibroblasts: Cytokine regulation in periodontitis.

en: Periodontitis is a bacterial infectious disease, and many inflammatory cytokines regulate periodontitis pathophysiology through a crosstalk between tissue cells and immune cells. Interleukin (IL)-6 is an important cytokine involved in the regulation of host response to bacterial infection. Human Gingival Fibroblasts (HGFs) are the most abundant cells in gingival connective tissues. Various HGF responses to periodontal pathogens or inflammatory cytokines contribute to the development of periodontitis. Lipopolysaccharide derived from Porphyromonas gingivalis (Pg LPS) and IL-1 significantly increase IL-6 production in HGFs. However, IL-6 cannot function in HGFs without the soluble form of the IL-6 receptor (sIL-6R), because HGFs do not express sufficient cell surface IL-6R to bind appreciable levels of IL-6. Importantly, sIL-6R is essential for IL-6 signaling in HGFs, and the sIL-6R is produced by differentiated THP-1 cells treated with IL-6. Calprotectin, a heterodimer of S100A8 and S100A9, is released during inflammation and significantly induces IL-6 production in HGFs via toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-B) signals. Calprotectin also induces sIL-6R production in differentiated THP-1 cells. IL-6 induces vascular endothelial growth factor (VEGF), matrix-metalloproteinase-1 (MMP-1), and cathepsin L production in HGFs in the presence of sIL-6R. Taken together, calprotectin-induced IL-6 production in HGFs may cause periodontitis progression through a crosstalk of fibroblasts and macrophages. There are many reports that examine how cytokines are released from HGFs to cause beneficial or harmful effects in inflamed periodontal lesions. This review explores the pathophysiology of periodontitis by focusing IL-6-mediated crosstalk of HGFs and macrophages.

en: Journal of Cellular Physiology

ja: Journal of Cellular Physiology


en: Etiology of drug-induced gingival overgrowth

en: Current Issues in Periodontics

ja: Current Issues in Periodontics


en: 全顎的な歯肉のびらん・接触痛

ja: 全顎的な歯肉のびらん・接触痛

en: DENTAL DIAMOND

ja: デンタルダイヤモンド


en: 最新の知見から攻める!①歯周病と腎疾患はどう関係するの?

ja: 最新の知見から攻める!①歯周病と腎疾患はどう関係するの?

en: The Journal of Dental Hygiene

ja: デンタルハイジーン


en: 下顎前歯部の動揺

ja: 下顎前歯部の動揺


en: 歯周病が生活習慣病に及ぼす影響

ja: 歯周病が生活習慣病に及ぼす影響

en: The Japanese Journal of Clinical Nutrition

ja: 臨床栄養


en: Effects of advanced glycation end-products on pathogenesis of diabetes-associated periodontitis

ja: 糖尿病関連歯周炎の病態に及ぼす最終糖化産物の影響

en: Journal of the Japanese Association of Periodontology

ja: 日本歯周病学会会誌


en: 下顎前歯部の歯肉腫脹

ja: 下顎前歯部の歯肉腫脹


en: Periodontal conditions in dialysis patients

ja: 透析と歯周病 (2)透析患者の歯周組織所見

en: The Japanese Journal of Clinical Dialysis

ja: 臨牀透析


en: 2.各論 1)歯周病 (特集 透析患者の口腔衛生)

ja: 2.各論 1)歯周病 (特集 透析患者の口腔衛生)

en: 透析フロンティア

ja: 透析フロンティア


en: Establishment of Examination for Judgment of Effects of Prevention and Treatment for Periodontal Treatment According to Clinical Database

ja: 歯周病臨床データベースに基づき歯周病原細菌感染度を指標とした 予防・治療の効果判定検査の確立

en: Journal of the Japanese Association for Dental Science

ja: 日本歯科医学会誌


en: Drug-induced Disorders in Oral Tissues

ja: 薬剤関連の口腔疾患

en: Progress in Medicine

ja: Progress in Medicine


en: 糖尿病における歯周組織破壊の特徴 --- 歯槽骨代謝に及ぼす影響を中心に

ja: 糖尿病における歯周組織破壊の特徴 --- 歯槽骨代謝に及ぼす影響を中心に

en: Diabetes Frontier

ja: Diabetes Frontier


en: Bisphosphonate-related osteonecrosis of the jaws

ja: ビスフォスフォネート関連顎骨壊死をめぐる話題 (特集 すべての医師のための骨粗鬆症診療ガイド2010)

en: Clinic All-Round

ja: 綜合臨牀


en: Root coverage procedures

ja: 根面被覆術について

en: Shikoku Dental Research

ja: 四国歯学会雑誌


en: Relationship between periodontal disease and renal disease

ja: 歯周病と腎臓病の関連

en: Journal of Clinical and Experimental Medicine

ja: 医学のあゆみ


en: Alveolar bone resorption in animal models of periodontitis

ja: 実験的歯周炎動物モデルにおける歯槽骨吸収の動態

en: CLINICAL CALCIUM

ja: クリニカルカルシウム


en: Ca拮抗薬による歯肉増殖症の治療

ja: Ca拮抗薬による歯肉増殖症の治療

en: Dental Diamond

ja: Dental Diamond


en: Drug-Induced Gingival Overgrowth a Review

en: Drug-induced gingival overgrowth is a side effect associated with 3 types of drugs: anticonvulsants (phenytoin), immunosuppressive agents (cyclosporine A), and various calcium channel blockers for cardiovascular diseases. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. Although the mechanisms of these disorders have not been elucidated, recent studies suggest that these disorders seem to be induced by the disruption of homeostasis of collagen synthesis and degradation in gingival connective tissue, predominantly through the inhibition of collagen phagocytosis of gingival fibroblasts. The integrins are a large family of heterodimeric transmembrane receptors for extracellular matrix molecules. alpha2beta1 integrin serves as a specific receptor for type I collagen on fibroblasts, and alpha2 integrin has been shown to play a crucial role in collagen phagocytosis. Actin filaments, which are assembled from monomers and oligomers, are involved in collagen internalization after binding to integrins. Furthermore, the implication of intracellular calcium in the regulation of integrin-mediated binding activity and gelsolin activity, known as a calcium-dependent actin-severing protein, is also described. In this review, we focus on collagen metabolism in drug-induced gingival overgrowth, focusing on the regulation of collagen phagocytosis in fibroblasts.

en: Biological & Pharmaceutical Bulletin

ja: Biological & Pharmaceutical Bulletin