Abstract
The skeleton acts as a support for the rest of the body, and it has long been known that bone tissue adapts to its local mechanical environment: mechanical loading leads to an increase in the bone mass and density, whereas disuse results in a net loss of bone. It has been found that bones respond primarily to dynamic rather that static loads1. Mechanical loading of bone cells is associated with increased prostaglandin E2 (PGE2) production2, and inhibition of prostaglandin synthesis suppresses the osteogenic response3. Inhibition of nitric oxide synthase (NOS) also abolishes the loading response, indicating that nitric oxide (NO) production has an essential early role in bone remodeling, too4.
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Smalt, R., Mitchell, F.T., Howard, R.L., Chambers, T.J. (1997). Mechanotransduction in Bone Cells: Induction of Nitric Oxide and Prostaglandin Synthesis by Fluid Shear Stress, but Not by Mechanical Strain. In: Sinzinger, H., Samuelsson, B., Vane, J.R., Paoletti, R., Ramwell, P., Wong, P.YK. (eds) Recent Advances in Prostaglandin, Thromboxane, and Leukotriene Research. Advances in Experimental Medicine and Biology, vol 433. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1810-9_66
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DOI: https://doi.org/10.1007/978-1-4899-1810-9_66
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