Osteoporosis Pathogenesis

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The underlying mechanisms, in any case Osteoporosis is a kind of imbalance in bone resorption and bone formation. In normal bone, there is a fixed bone matrix remodeling up to 10% of bone mass may be undergoing remodeling at any point in time. This process took place in bone multicellular units (Bachelor of Music) first described in 1963 by Frost. Bone re-absorption of bone cells (ie, from the bone marrow), the deposition of new bone osteoblasts.

Three main mechanisms for the development of osteoporosis is not enough to peak bone mass (bone development lack of strength, quality and growth process), excessive bone resorption and inadequate formation of new bone remodeling process. One of the three mechanisms of interaction between the fragile foundation for development of bone tissue.  a strong hormonal factors determine the rate of bone resorption, the lack of estrogen (as a result of menopause) and bone resorption increased, and reduction of new bone deposition usually occurs in load-bearing bone. The amount of estrogen need to stop this process is lower than normally required to stimulate the uterus and mammary glands. In the α-type estrogen receptor seems to be the most important regulator of bone metabolism.  In addition to estrogen, plays an important role in calcium metabolism, bone turnover, and lack of calcium and vitamin D lead to impaired bone deposition; In addition, low levels of parathyroid response to calcium-parathyroid hormone secretion (thyroid side gland, Mandarin), increased bone resorption in order to ensure adequate calcium in the blood. The role of calcitonin, a hormone produced by the thyroid is to increase the deposition of bone, it is not clear, may not be of great significance that the Mandarin.

Activation of osteoclasts is affected by a variety of molecular signals, which ligand (receptor activator of nuclear factor-κB ligand) is one of the best learning. Such molecules are by osteoblasts and other cells (eg lymphocytes), and to stimulate the clerk (receptor activator of nuclear factor κB). Osteoprotegerin (OPG) ligand binding in order to have the opportunity to combine staff, so it can inhibit bone resorption increased. Ligand, rank, and OPG is closely related to tumor necrosis factor and its receptor. The role of the Wnt signaling pathway is recognized, but not yet very clear. Locally produced peanuts and interleukin be considered involved in the regulation of bone turnover, and excess or reduced production of these mediators basis for the development of osteoporosis.

Trabecular bone is the spongy ends of long bones and spine. Cortical bone is a hard shell and bone in long bones. Because osteoblasts and osteoclasts surface of living bone, trabecular bone is more active, more subject to bone turnover, in order to restore. Not only the bone density decreased, but the micro-bone destruction. Weak trabecular bone needles break ( “micro”), and replace weak bones. Common sites of osteoporotic fracture, wrist, hip and spine, there is a relatively high trabecular bone cortical bone ratio. These areas depends on the strength of trabecular bone, and therefore the intense remodeling will lead to the degradation of these areas the most when the remodeling imbalance

2 Responses to “Osteoporosis Pathogenesis”

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