Abstract
Paget’s disease is a focal disorder of bone in which there is a localized increase in bone remodeling. The cellular actions which constitute normal bone remodeling are complex and require the spatially and temporally coordinated actions of several cell types.1 Remodeling commences with an initiation signal(s) leading to a phase of resorption where bone is excavated from the remodeling site by multinucleated osteoclasts. In pagetic foci, but not in unaffected sites, the osteoclasts exhibit increased multinuclearity and are overactive, resulting in excessive resorption. Normally resorption lacunae are then colonized by osteoblasts which synthesize bone matrix components (osteoid) and the bone is replaced. The mechanism(s) which ensures that the processes of bone resorption and formation remain tightly linked is termed “coupling.”2 The increased osteoclastic activity observed in Paget’s disease is matched by an increase in osteoblastic activity, so bone resorption and bone formation remain coupled.
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Birch, M.A., Gallagher, J.A. (1996). Cytokines and Growth Factors in Paget’s Disease. In: The Molecular Biology of Paget’s Disease. Medical Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-22505-9_5
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