The role of cytokines in inflammatory bone loss

Author(s)

Souza, Pedro P. C. ^[1] ; Lerner, Ulf H. ^{[2, 3]}

Affiliation

^[1] Univ Estadual Paulista, UNESP, Araraquara Sch Dent, Dept Physiol & Pathol, Araraquara - Brazil

^[2] Umea Univ, Dept Mol Periodontol, SE-90187 Umea - Sweden

^[3] Univ Gothenburg, Sahlgrenska Acad, Inst Med, Ctr Bone & Arthrit Res, Gothenburg - Sweden

• Document type: Journal article
• Source: IMMUNOLOGICAL INVESTIGATIONS; v. 42, n. 7, p. 555-622, 2013.
• Web of Science Citations: 102

Abstract

Chronic inflammatory processes close to bone often lead to loss of bone in diseases such as rheumatoid arthritis, periodontitis, loosened joint prosthesis and tooth implants. This is mainly due to local formation of bone resorbing osteoclasts which degrade bone without any subsequent coupling to new bone formation. Crucial for osteoclastogenesis is stimulation of mononuclear osteoclast progenitors by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL) which induces their differentiation along the osteoclastic lineage and the fusion to mature, multinucleated osteoclasts. M-CSF and RANKL are produced by osteoblasts/osteocytes and by synovial and periodontal fibroblasts and the expression is regulated by pro-and anti-inflammatory cytokines. These cytokines also regulate osteoclastic differentiation by direct effects on the progenitor cells. In the present overview, we introduce the basic concepts of osteoclast progenitor cell differentiation and summarize the current knowledge on cytokines stimulating and inhibiting osteoclastogenesis by direct and indirect mechanisms. (AU)

• FAPESP's process: 08/07221-4 - Kinins and prostaglandins in inflammatory bone resorption
• Grantee: Pedro Paulo Chaves de Souza
• Support Opportunities: Scholarships in Brazil - Post-Doctoral