Abstract
Although the skeleton’s principal function is most often associated with the determination of size and shape of vertebrates, it also serves as a reservoir of calcium (and phosphate), from which the body maintains this important divalent cation within a critical range required for membrane polarization, muscle function, and other key physiological processes. Parathyroid hormone (PTH), the most important hormone for the minute to minute regulation of blood calcium levels, regulates the catabolic process of bone resorption. Interestingly, although osteoclasts are the cells responsible for dissolving bone collagen matrix and calcium release, receptors for PTH in bone reside chiefly on osteoblasts, the anabolically active bone cell that produces collagen and the other matrix associated macromolecules that constitute the organic scaffolding of bone and upon which mineral deposition occurs. In order to maintain a structurally intact skeleton, the amount of bone lost through resorption must be matched by an equal amount of bone produced by formation. For more than a decade this concept has been referred to as coupling, and one or more growth factors have been hypothesized to function in this capacity as coupling factors in bone remodelling1.
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McCarthy, T.L., Centrella, M. (1994). Regulation of IGF Activity in Bone. In: Le Roith, D., Raizada, M.K. (eds) Current Directions in Insulin-Like Growth Factor Research. Advances in Experimental Medicine and Biology, vol 343. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2988-0_38
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DOI: https://doi.org/10.1007/978-1-4615-2988-0_38
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