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It is the cells in tissues that are responsible to mechanical forces. It is now well recognized that mechanical forces play a fundamental role in the regulation of cell functions, including gene induction, protein synthesis, cell proliferation, migration, death, and differentiation, which are essential to maintain tissue homeostasis and functions such as in muscle, bone, tendon, periodontium, and the cardiovascular system (REF).
A typical example is bone, which changes its shape, density, and stiffness when its mechanical loading conditions are altered (Turner and Pavalko, 1998); (Mullender et al, 2004). When bone receives mechanical force, this force is transmitted to the fluids and cells within bone. The forces on the fluids are then transferred through the canaliculi down to the osteocytes.
Osteocytes in bone tissue act as mechanical strain sensors called mechanosensors to convert information about mechanical force into chemical messages. These chemical messages control osteoblast and osteoclast activity and can result in either bone deposition or bone resorption. In response to mechanical force, a two-step process occurs. First, mechanical sensitive membrane proteins on the surface of the osteocytes are activated. Second, chemical pathways within the osteocytes are activated. Activation of these intracellular pathways stimulates osteoblast activity and inhibits osteoclast activity (REF).
When tissue containing smooth muscle is subjected to chronic increases in mechanical stress, smooth muscle content and contractility is increased (Smith et al, 1994). Conversely, abnormal mechanical loading conditions alter cellular function and change the structure and composition of the extracellular matrix (ECM), eventually leading to tissue or organ pathologies such as osteoporosis, osteoarthritis, tendinopathy, atherosclerosis, and fibrosis in the bone, cartilage, tendon, vessels, heart, lung, and skin (Ross 1986; Chicurel et al. 1998; Grodzinsky et al. 2000; Ireland et al. 2001; Riley et al. 2002; Ingber 2003; Bag et al. 2004; Borer et al. 2004; Eckes and Krieg 2004; Lammerding et al. 2004).
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