Osteoporosis
Osteoporosis is a systemic disease of the skeleton characterized by a low bone density and alterations in bone microarchitecture, responsible for the exaggerated bone fragility therefore, for a high risk of fracture. Biomechanical studies show that bone mineral density (BMD) is the essential factor for bone fragility. Fractures are signs of complications and seriousness of the disease. Currently, the diagnosis of the disease can be done before the first fracture with the BMD and examination of risk factors (Kelman &Lane, 2005)
Pathophysiology
Bone is constantly remodeled in response to microtrauma. This remodeling occurs discretely in the skeleton and bone resorption is always followed by bone formation, a phenomenon called coupling. Architecturally, cortical bone differs from spongy trabecular bone, but their molecular compositions are similar. They both have an extracellular matrix with mineralized and nonmineralized components. Mechanical properties of a bone are mainly directed by the constitution and architecture of the extracellular matrix. Collagen and minerals play a great role on bone strength (Rossouw et al, 2002).
This permanent remodeling maintains the phosphocalcic homeostasis. Bone resorption is carried out by multinucleated cells called osteoclasts. The formation of osteoid tissue which will subsequently mineralize under the action of vitamin D is controlled by osteoblasts. They are both dependent on each other for the bone production and remodeling. Osteocytes, which are differentiated osteoblasts implanted in mineralized bone, control the timing and location of bone remodeling. There is a strict balance between bone resorption and bone formation. In osteoporosis, the coupling mechanism between osteoclasts and osteoblasts is thought to be unable to keep up with the constant microtrauma of trabecular bone. Osteoclasts need weeks to resorb bone, whereas osteoblasts require months to generate new bone. As a result, any mechanism that enhances the
Pathophysiology
Bone is constantly remodeled in response to microtrauma. This remodeling occurs discretely in the skeleton and bone resorption is always followed by bone formation, a phenomenon called coupling. Architecturally, cortical bone differs from spongy trabecular bone, but their molecular compositions are similar. They both have an extracellular matrix with mineralized and nonmineralized components. Mechanical properties of a bone are mainly directed by the constitution and architecture of the extracellular matrix. Collagen and minerals play a great role on bone strength (Rossouw et al, 2002).
This permanent remodeling maintains the phosphocalcic homeostasis. Bone resorption is carried out by multinucleated cells called osteoclasts. The formation of osteoid tissue which will subsequently mineralize under the action of vitamin D is controlled by osteoblasts. They are both dependent on each other for the bone production and remodeling. Osteocytes, which are differentiated osteoblasts implanted in mineralized bone, control the timing and location of bone remodeling. There is a strict balance between bone resorption and bone formation. In osteoporosis, the coupling mechanism between osteoclasts and osteoblasts is thought to be unable to keep up with the constant microtrauma of trabecular bone. Osteoclasts need weeks to resorb bone, whereas osteoblasts require months to generate new bone. As a result, any mechanism that enhances the