Bone remodelling is an active and dynamic process that relies on the correct balance between bone resorption by osteoclasts and bone deposition by osteoblasts. Moreover, these two func- tions must be tightly coupled not only quantitatively, but also in time and space. When the coupling is lost, the correct bone mass could be compromised, leading to several skeletal pathologies. Indeed, bone loss and osteoporosis are the result of an increased osteoclast function and/or a reduced osteoblast activity. In contrast, other pathologies are related to osteoclast failure to resorbe bone, such as osteopetrosis, a rare genetic disorder characterized by an increased bone mass and also linked to an impairment of bone marrow functions. Starting from these assumptions, it is necessary to more deeply under- stand the molecular mechanisms regulating bone cell func- tions. Indeed, recent studies evidenced a complex interplay be- tween the immune and skeletal systems, which share several regulatory molecules including cytokines, receptors and tran- scription factors. These data allowed to more deeply under- stand the mechanisms underlying bone mass regulation and could open new avenue to identify target molecules for alteran- tive therapies more efficacious against bone diseases. KEY
CITATION STYLE
Kingsley, L. A., Fournier, P. G. J., Chirgwin, J. M., & Guise, T. A. (2008). Molecular Biology of Bone Metastasis. AACR Education Book, 2008(1), 443–457. https://doi.org/10.1158/aacr.edb-mct-07-0234
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