title: [Secondary osteoporosis or secondary contributors to bone loss in fracture. The relevance of immune system to bone metabolism].
abstract: Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts. It is also regulated by immune system and its imbalance often results in pathological processes such as secondary osteoporosis. For instance, Th1 and Th17 are involved in activation of immune system and also induce maturation of monocytes to osteoclasts, which leads to osteoporosis. Contrarily, Treg (regulatory T cells) suppresses immune function, but suppresses osteoclast differentiation. Proinflammatory cytokines such as TNF cause an imbalance in bone metabolism via direct and/or indirect effects on osteoclasts. These inflammatory signals originate from the immune system, the largest source of cell-derived regulatory signals and such immunological signals to the bone results in secondary osteoporosis and bone destruction. Based on an improved understanding of immune signals, investigation of the suppression of cell functions may lead to improved understanding and better treatment of bone destruction and osteoporosis.
authors.affiliation: The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.
authors.forename: Yoshiya
authors.initials: Y
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D015519:Bone Density; D001862:Bone Resorption / Q000276:immunology*; D001842:Bone and Bones / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D010006:Osteoblasts / Q000166:cytology / Q000378:metabolism; D010010:Osteoclasts / Q000166:cytology / Q000378:metabolism; D010012:Osteogenesis / Q000502:physiology*; D010024:Osteoporosis / Q000209:etiology / Q000276:immunology*