Bone reabsorption is resorption of bone tissue, the process by which osteoclasts destroy tissue in bone and release minerals, resulting in the transfer of calcium from bone to blood tissue.
Osteoclasts are multi-nucleated cells containing many mitochondria and lysosomes. These are the cells responsible for bone resorption. Osteoclasts are generally present in the outer layer of the bone, just below the periosteum. The osteoclast attachment to the osteon begins the process. Osteoclasts then induce infolds of their cell membranes and secrete collagenases and other enzymes that are important in the resorption process. High levels of calcium, magnesium, phosphate, and collagen products will be released into the extracellular fluid as osteoclast tunnels to mineralized bone. Osteoclasts stand out in the tissue damage found in psoriasis arthritis and rheumatological disorders.
The human body is in a state of constant bone remodeling. Bone remodeling is a process that maintains bone strength and ion homeostasis by replacing the old parts of the old bone with a newly synthesized protein protein matrix packet. The bone is directed by osteoclasts, and deposited by the osteoblasts in a process called ossification. The activity of osteocytes plays a key role in this process. Conditions resulting in decreased bone mass may be due to increased resorption or by decreased ossification. During childhood, bone formation exceeds resorption. When the aging process occurs, resorption exceeds the formation.
Bone resorption rates are much higher in older post-menopausal women due to estrogen deficiency associated with menopause. Common treatments include drugs that increase bone mineral density. Bisphosphonates, RANKL inhibitors, SERMs - selective estrogen receptor modulators, hormone replacement therapy and calcitonin are some common treatments. Light weight training tends to eliminate the negative effects of bone resorption.
Video Bone resorption
Rule
Bone resorption is strongly stimulated or inhibited by signals from other parts of the body, depending on the demand for calcium.
The calcium membrane receptor membrane in the parathyroid gland monitors the levels of calcium in the extracellular fluid. Low levels of calcium stimulate the release of parathyroid hormone (PTH) from the main cells of the parathyroid gland. In addition to its effects on the kidney and intestines, PTH increases the amount and activity of osteoclasts. Increased activity of an existing osteoclast is the initial effect of PTH, and begins within minutes and increases for several hours. Increased levels of PTH are increasing increasing osteoclast abundance. This leads to greater resorption of calcium and phosphate ions.
High levels of calcium in the blood, on the other hand, cause decreased release of PTH from the parathyroid glands, decreasing the amount and activity of osteoclasts, resulting in reduced bone resorption. Vitamin D increases the absorption of calcium and phosphate in the intestinal tract, leading to increased plasma calcium levels, and thus decreases bone resorption.
Calcitriol (1,25-dihydroxycholecalciferol) is an active form of vitamin D 3 . It has many functions involved in blood calcium levels. Recent research has shown that calcitriol leads to reduced osteoclast formation, and bone resorption. Therefore, an increase in vitamin D 3 intake should lead to decreased bone resorption - it has been shown that oral vitamin D administration is not linearly correlated with elevated serum levels of calcifediol, a precursor for calcitriol.
Calcitonin is a hormone secreted by the thyroid in humans. Calcitonin decreases osteoclast activity, and decreases the formation of new osteoclasts, resulting in decreased resorption. Calcitonin has a greater effect on children than adults, and plays a smaller role in bone remodeling than PTH.
In some cases where bone resorption goes beyond ossification, bone breaks down much faster than can be updated. The bones become more porous and fragile, exposing people to the risk of fractures. Depending on where in the bone resorption of the body occurs, additional problems such as tooth loss may arise. This can be caused by conditions such as hypoparathyroidism and hypovitaminosis D or even decreased hormone production in the elderly. Some diseases with symptoms of decreased bone density are osteoporosis, and rickets.
Some people who experience increased bone resorption and decreased bone formation are astronauts. Because the conditions are in the environment without gravity, astronauts do not have to work their musculoskeletal system as hard as on earth. Osification decreases due to lack of stress, while resorption increases, causing a net decrease in bone density.
Maps Bone resorption
Alcoholism
The effects of alcohol on bone mineral density (BMD) have been well-known and studied in both animal and human populations. Through both direct and indirect pathways, prolonged exposure to ethanol increases the risk of fracture by decreasing bone mineral density and promoting osteoporosis. The indirect effects of alcohol abuse occur through growth hormones, sex steroids, and oxidative stress.
Growth hormone is an important regulator of bone growth and remodeling in adults, and it acts through growth factor I such as insulin (IGF1) to stimulate osteoblastic differentiation. Chronic alcoholism lowers IGF1 levels, which suppresses the ability of GH to increase bone mineral density.
Increased alcohol intake is associated with decreased testosterone and serum estradiol levels, which in turn leads to the activation of RANK protein (a TNF receptor) that promotes osteoclast formation. Oxidative stress occurs when ethanol induces the expression of NOX, resulting in the production of ROS in osteoblasts that can eventually lead to cell aging. The immediate effects of chronic alcoholism are evident in osteoblasts, osteoclasts and osteocytes. Ethanol suppresses activity and osteoblast differentiation.
At the same time, it has a direct effect on osteoclast activity. This results in increased bone resorption rate and decreased bone mineral density due to increased number of pits and bone pit areas. Studies have shown that a viable osteocyte (another type of bone cell) can prevent osteoclastogenesis, whereas osteocytes apoptosis tends to induce osteoclast stimulation. Stimulation of osteocyte apoptosis by exposure to alcohol may explain the decrease in bone mineral density in chronic drinkers.
See also
- Bone remodeling
- Nuclear factor-kappa B
References
Source of the article : Wikipedia
0 Comments