الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Osteoporosis is a progressive disease that has physical and psychosocial consequences; It is the most common bone disease in humans, characterized by low bone mass, deterioration of bone tissue, disruption of bone architecture, compromised bone strength, and increased bone fracture risk over time (Sadat-Ali et al., 2011). The estrogen deficiency accompanying menopause induces bone loss and increased risk of fracture. Osteoporotic fractures are associated with high morbidity, increased mortality risk, and major economic impact (Autier et al., 2000).
Osteoporosis treatment too often consists of drug prescription (anti resorption drugs e.g. bisphosphonate, estrogen replacement therapy) (body et al., 2010). While current osteopenia treatment guidelines include exercise, vitamin D and recently vitamin K supplementation (Cheung et al., 2008).
Despite it is generally thought that disuse (prolonged periods of inactivity) and unloading of the skeleton (e.g.in cases of paralysis) promotes reduced bone mass whereas mechanical loading through exercise increases bone mass (dolbow, 2011), exercise provides an osteogenic stimulus to the bones by increasing serum concentrations of bone formation markers as well as decreasing bone resorption markers (Bakhtyar et al., 2011).
A significant body of evidence has been published over the last 10 years indicating that all major bone cells have the capacity to metabolize 25-OH D to 1,25-(OH)2 D, which in turn exerts autocrine/paracrine actions to regulate bone cell proliferation and maturation, as well as bone mineralization and resorption. In vivo and in vitro studies indicate that these autocrine/paracrine activities of 1,25-dihydroxyvitamin D in bone tissue contribute to maintain bone mineral homeostasis and enhancing skeletal health (Lamb et.al., 2011).