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en: Various roles of calprotectin in periodontal disease and its possibility as a diagnostic marker for periodontal disease

ja: カルプロテクチンの歯周病病態における多様な役割と歯周病診断マーカーとしての可能性

en: Journal of the Japanese Association of Periodontology

ja: 日本歯周病学会会誌


en: 糖尿病と慢性腎疾患(CKD)

ja: 糖尿病と慢性腎疾患(CKD)

en: 月刊糖尿病

ja: 月刊糖尿病


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: Crosstalk of Gingival Fibroblasts and Macrophages in Inflammatory Cytokine Cascade: Potential Mechanisms of Periodontitis

en: Journal of Cell Signaling

ja: Journal of Cell Signaling


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: 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: Basic Research to Clinical Dentistry:Potentiality of plasma IgG antibody titer test against to periodontal pathogens

ja: 基礎研究から歯科臨床へ:歯周病原細菌に対する血漿IgG抗体価検査の可能性


en: The role of caveolin-1 in prostate cancer: clinical implications.

en: Caveolin-1 (cav-1) is reportedly overexpressed in prostate cancer cells and is associated with disease progression. Specific oncogenic activities of cav-1 associated with Akt activation also occur in prostate cancer. A membrane-associated protein, cav-1, is nonetheless secreted by prostate cancer cells; results of recent studies showed that secreted cav-1 can stimulate cell survival and angiogenic activities, defining a role for cav-1 in the prostate cancer microenvironment. Serum cav-1 levels were also higher in prostate cancer patients than in control men without prostate cancer, and the preoperative serum cav-1 concentration had prognostic potential in men undergoing radical prostatectomy. Secreted cav-1 is therefore a potential biomarker and therapeutic target for prostate cancer.

en: Prostate Cancer and Prostatic Diseases

ja: Prostate Cancer and Prostatic Diseases


en: Gingival Fibroblasts-mediated Pathophysiology of Periodontal Diseases, Periodontitis and Drug-induced Gingival Overgrowth

ja: 線維芽細胞を中心とした歯周病・歯肉増殖症の病態形成に関する基礎的研究


en: Gene polymorphisms in periodontal health and disease.

en: Periodontology 2000

ja: Periodontology 2000


en: Perspective of cytokine regulation for periodontal treatment: fibroblast biology.

en: Efforts to understand the pathogenesis of periodontal diseases have been underway for decades. Studies of immunological aspects in addition to the structural components of gingival fibroblasts showed that the fibroblasts actively participate in immune and inflammatory events in periodontal diseases. Future strategies for the prevention and treatment of periodontal diseases should biologically regulate fibroblast activities. These cells are surrounded by monocyte-derived proinflammatory cytokines such as interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and lymphocyte-derived interleukin-6 (IL-6) in inflamed gingival tissue. Recent anti-cytokine therapy for inflammatory diseases including rheumatoid arthritis aimed to inhibit the binding of cytokines to targeted cells such as fibroblasts and condrocytes. IL-1beta and TNF-alpha are thought to be therapeutic targets because these cytokines are essential for the initiation of inflammatory immune reactions and are produced for prolonged periods in inflammatory diseases. IL-6 is also a target, because it is abundantly present in inflammatory lesions and activates fibroblasts in the presence of soluble IL-6 receptor. In addition, these cytokines accelerate gingival fibroblasts to produce collagenolytic enzymes, resulting in tissue destruction. Soluble receptors for IL-1beta and TNF-alpha are suggested to be candidates for therapeutic molecules, but soluble receptor for IL-6 is suggested to be a factor-stimulating fibroblast. This paper will review the utilization of soluble receptors specific to inflammatory cytokines which potentially stimulate fibroblasts to regulate biological events involved in the pathogenesis of periodontal diseases.

en: Journal of Periodontology

ja: Journal of Periodontology


en: 日本歯周病学会 ニュースレター 編集後記

ja: 日本歯周病学会 ニュースレター 編集後記

en: 日本歯周病学会 ニュースレター

ja: 日本歯周病学会 ニュースレター

misc_type: others