A molecular mechanism that promotes bone destruction could be harnessed to combat osteoporosis, suggests a paper online in Nature Medicine.
Bone formation depends on a balance between cells that create it -- osteoblasts -- and cells that destroy it -- osteoclasts. Understanding the mechanisms that control the origin and function of these cells is crucial for developing treatments for diseases such as osteoporosis.
Kurt Redlich and colleagues report that the C-C chemokine receptor-2 (CCR2) is crucially involved in the regulation of bone mass by promoting the appearance of osteoclasts. The group found that mice lacking CCR2 have high bone mass owing to a decrease in number, size and function of osteoclasts. At the molecular level, activation of CCR2 in osteoclast progenitor cells results in increased expression of a molecule known as RANK, which enabled these cells to respond to signals that drive osteoclast differentiation.
In a model of postmenopausal osteoporosis -- mice that underwent ovary removal and therefore have less oestrogen -- CCR2 levels increased, thereby increasing RANK and the differentiation potential of osteoclast progenitor cells. As a result, mice lacking CCR2 are resistant to bone loss associated with reduced oestrogen. CCR2 activation could therefore be a target to combat postmenopausal osteoporosis.
Kurt Redlich (Medical University Vienna, Austria)
Abstract available online.
(C) Nature Medicine press release.
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