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Osteoclast-derived activity in the coupling of bone formation to resorption
The cells of bone and the immune system communicate by means of soluble and membrane-bound cytokines and growth factors. Through local signalling mechanisms, cells of the osteoblast lineage control the formation and activity of osteoclasts and, therefore, the resorption of bone. Both T and B lymphoc...
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Published in: | Trends in molecular medicine 2005-02, Vol.11 (2), p.76-81 |
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description | The cells of bone and the immune system communicate by means of soluble and membrane-bound cytokines and growth factors. Through local signalling mechanisms, cells of the osteoblast lineage control the formation and activity of osteoclasts and, therefore, the resorption of bone. Both T and B lymphocytes produce activators and inhibitors of osteoclast formation. A local ‘coupling factor’ linking bone resorption to subsequent formation in the bone multicellular unit (BMU) has long been proposed as the key regulator of the bone remodelling process, but never identified. There is evidence in support of the view that the coupling mechanism is dependent on growth factors released from the bone matrix during resorption, or is generated from maturing osteoblasts. We argue that osteoclasts contribute in important ways to the transiently activated osteoclast, and stimulate osteoblast lineage cells to begin replacing the resorbed bone in each BMU. |
doi_str_mv | 10.1016/j.molmed.2004.12.004 |
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John</creatorcontrib><creatorcontrib>Sims, Natalie A.</creatorcontrib><title>Osteoclast-derived activity in the coupling of bone formation to resorption</title><title>Trends in molecular medicine</title><addtitle>Trends Mol Med</addtitle><description>The cells of bone and the immune system communicate by means of soluble and membrane-bound cytokines and growth factors. Through local signalling mechanisms, cells of the osteoblast lineage control the formation and activity of osteoclasts and, therefore, the resorption of bone. Both T and B lymphocytes produce activators and inhibitors of osteoclast formation. A local ‘coupling factor’ linking bone resorption to subsequent formation in the bone multicellular unit (BMU) has long been proposed as the key regulator of the bone remodelling process, but never identified. There is evidence in support of the view that the coupling mechanism is dependent on growth factors released from the bone matrix during resorption, or is generated from maturing osteoblasts. We argue that osteoclasts contribute in important ways to the transiently activated osteoclast, and stimulate osteoblast lineage cells to begin replacing the resorbed bone in each BMU.</description><subject>Animals</subject><subject>Bone Remodeling - physiology</subject><subject>Bone Resorption - metabolism</subject><subject>Bone Resorption - therapy</subject><subject>Cell Communication</subject><subject>Humans</subject><subject>Mice</subject><subject>Osteoclasts - physiology</subject><subject>Osteogenesis - physiology</subject><subject>Parathyroid Hormone - pharmacology</subject><subject>Parathyroid Hormone - physiology</subject><subject>Receptors, Calcitonin - genetics</subject><subject>Receptors, Calcitonin - physiology</subject><issn>1471-4914</issn><issn>1471-499X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkF9LwzAUxYMobk6_gUiffGtN2jRpXwQZ_sPBXhR8C2lyqxltM5NssG9vysYe9SUn955z74UfQtcEZwQTdrfKetv1oLMcY5qRPItygqaEcpLSuv48Pf4JnaAL71cYk5Lz6hxNSMlqWnE8RW9LH8CqTvqQanBmCzqRKpitCbvEDEn4hkTZzbozw1di26SxAyStdb0MxkbbJg68deuxukRnrew8XB10hj6eHt_nL-li-fw6f1ikipY8pAWTtCw4ZtA2kpVQSZmzVrG8rnLVyBKzXCtZMh1fHXuy0EXVENVCPdqsmKHb_d61sz8b8EH0xivoOjmA3XjBOMWc1vzfIOGc0rqkMUj3QeWs9w5asXaml24nCBYjbbESe9pipC1ILqLEsZvD_k0zesehA94YuN8HIOLYGnDCKwODAm0cqCC0NX9f-AUye5Qq</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Martin, T. 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John</creatorcontrib><creatorcontrib>Sims, Natalie A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Trends in molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martin, T. John</au><au>Sims, Natalie A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osteoclast-derived activity in the coupling of bone formation to resorption</atitle><jtitle>Trends in molecular medicine</jtitle><addtitle>Trends Mol Med</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>11</volume><issue>2</issue><spage>76</spage><epage>81</epage><pages>76-81</pages><issn>1471-4914</issn><eissn>1471-499X</eissn><abstract>The cells of bone and the immune system communicate by means of soluble and membrane-bound cytokines and growth factors. Through local signalling mechanisms, cells of the osteoblast lineage control the formation and activity of osteoclasts and, therefore, the resorption of bone. Both T and B lymphocytes produce activators and inhibitors of osteoclast formation. 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subjects | Animals Bone Remodeling - physiology Bone Resorption - metabolism Bone Resorption - therapy Cell Communication Humans Mice Osteoclasts - physiology Osteogenesis - physiology Parathyroid Hormone - pharmacology Parathyroid Hormone - physiology Receptors, Calcitonin - genetics Receptors, Calcitonin - physiology |
title | Osteoclast-derived activity in the coupling of bone formation to resorption |
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