Mechanosensation and Transduction in Osteocytes

Abstract

There may be no single mechanoreceptor in osteocytes, but instead a combination of events that has to be triggered for mechanosensation and transduction of signal to occur. Possibilities include shear stress along dendritic processes and/or the cell body, cell deformation in response to strain, and primary cilia. These events could occur independently or simultaneously to activate mechanotransduction. Signal initiators include calcium channel activation and ATP, nitric oxide, and prostaglandin release. Means of signal transfer include gap junctions and hemichannels, and the release of signaling molecules into the bone fluid. Questions remain regarding the magnitude of strain necessary to induce an osteocyte response, how the response propagates within the osteocyte network, and the timing involved in the initiation of bone resorption and/or formation on the bone surface. Mechanical loading in the form of shear stress is clearly involved not only in mechanosensation and transduction, but also in osteocyte viability. It remains to be determined if mechanical loading can also affect mineral homeostasis and mineralization, which are newly recognized functions of osteocytes.

Figure 1

Cartoon showing potential ways that an osteocyte may sense fluid flow shear stress. (A). Fluid flow shear stress could perturb tethering elements between the canalicular wall and the cell membrane. (B). Fluid flow shear stress may also affect the cell body, causing cell deformation. (C). Fluid flow may perturb primary cilia leading to mechanosensation. Both matrix and cell deformation are also proposed to play a role in osteocyte mechanosensation.