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The Role of Macrophage in the Pathogenesis of Osteoporosis

Osteoporosis is a systemic disease with progressive bone loss. The bone loss is associated with an imbalance between bone resorption via osteoclasts and bone formation via osteoblasts. Other cells including T cells, B cells, macrophages, and osteocytes are also involved in the pathogenesis of osteop...

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Detalles Bibliográficos
Autores principales: Yang, Deng-Ho, Yang, Meng-Yin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539137/
https://www.ncbi.nlm.nih.gov/pubmed/31035384
http://dx.doi.org/10.3390/ijms20092093
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author Yang, Deng-Ho
Yang, Meng-Yin
author_facet Yang, Deng-Ho
Yang, Meng-Yin
author_sort Yang, Deng-Ho
collection PubMed
description Osteoporosis is a systemic disease with progressive bone loss. The bone loss is associated with an imbalance between bone resorption via osteoclasts and bone formation via osteoblasts. Other cells including T cells, B cells, macrophages, and osteocytes are also involved in the pathogenesis of osteoporosis. Different cytokines from activated macrophages can regulate or stimulate the development of osteoclastogenesis-associated bone loss. The fusion of macrophages can form multinucleated osteoclasts and, thus, cause bone resorption via the expression of IL-4 and IL-13. Different cytokines, endocrines, and chemokines are also expressed that may affect the presentation of macrophages in osteoporosis. Macrophages have an effect on bone formation during fracture-associated bone repair. However, activated macrophages may secrete proinflammatory cytokines that induce bone loss by osteoclastogenesis, and are associated with the activation of bone resorption. Targeting activated macrophages at an appropriate stage may help inhibit or slow the progression of bone loss in patients with osteoporosis.
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spelling pubmed-65391372019-06-04 The Role of Macrophage in the Pathogenesis of Osteoporosis Yang, Deng-Ho Yang, Meng-Yin Int J Mol Sci Review Osteoporosis is a systemic disease with progressive bone loss. The bone loss is associated with an imbalance between bone resorption via osteoclasts and bone formation via osteoblasts. Other cells including T cells, B cells, macrophages, and osteocytes are also involved in the pathogenesis of osteoporosis. Different cytokines from activated macrophages can regulate or stimulate the development of osteoclastogenesis-associated bone loss. The fusion of macrophages can form multinucleated osteoclasts and, thus, cause bone resorption via the expression of IL-4 and IL-13. Different cytokines, endocrines, and chemokines are also expressed that may affect the presentation of macrophages in osteoporosis. Macrophages have an effect on bone formation during fracture-associated bone repair. However, activated macrophages may secrete proinflammatory cytokines that induce bone loss by osteoclastogenesis, and are associated with the activation of bone resorption. Targeting activated macrophages at an appropriate stage may help inhibit or slow the progression of bone loss in patients with osteoporosis. MDPI 2019-04-28 /pmc/articles/PMC6539137/ /pubmed/31035384 http://dx.doi.org/10.3390/ijms20092093 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Yang, Deng-Ho
Yang, Meng-Yin
The Role of Macrophage in the Pathogenesis of Osteoporosis
title The Role of Macrophage in the Pathogenesis of Osteoporosis
title_full The Role of Macrophage in the Pathogenesis of Osteoporosis
title_fullStr The Role of Macrophage in the Pathogenesis of Osteoporosis
title_full_unstemmed The Role of Macrophage in the Pathogenesis of Osteoporosis
title_short The Role of Macrophage in the Pathogenesis of Osteoporosis
title_sort role of macrophage in the pathogenesis of osteoporosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539137/
https://www.ncbi.nlm.nih.gov/pubmed/31035384
http://dx.doi.org/10.3390/ijms20092093
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