Bone resorption is resorption of bone tissue, that is, the process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood.
These are the cells responsible for the resorption of bone.
Osteoclasts are generally present on the outer layer of bone, just beneath the periosteum.
Attachment of the osteoclast to the osteon begins the process.
The osteoclast then induces an infolding of its cell membrane and secretes collagenase and other enzymes important in the resorption process.
Osteoclasts are prominent in the tissue destruction found in psoriatic arthritis and rheumatological disorders.
The human body is in a constant state of bone remodeling.
Bone remodelling is a process which maintains bone strength and ion homeostasis by replacing discrete parts of old bone with newly synthesized packets of proteinaceous matrix.
Osteocyte activity plays a key role in this process.
Conditions that result in a decrease in bone mass can either be caused by an increase in resorption or by a decrease in ossification.
During childhood, bone formation exceeds resorption.
As the aging process occurs, resorption exceeds formation.
Bone resorption rates are much higher in post-menopausal older women due to estrogen deficiency related with menopause.
Common treatments include drugs that increase bone mineral density.
Light weight bearing exercise tends to eliminate the negative effects of bone resorption.
Bone resorption is highly stimulated or inhibited by signals from other parts of the body, depending on the demand for calcium.
Calcium-sensing membrane receptors in the parathyroid gland monitor calcium levels in the extracellular fluid.
In addition to its effects on kidney and intestine, PTH increases the number and activity of osteoclasts.
The increase in activity of already existing osteoclasts is the initial effect of PTH, and begins in minutes and increases over a few hours.
Continued elevation of PTH levels increases the abundance of osteoclasts.
This leads to a greater resorption of calcium and phosphate ions.
High levels of calcium in the blood, on the other hand, leads to decreased PTH release from the parathyroid gland, decreasing the number and activity of osteoclasts, resulting in less bone resorption.
Vitamin D increases absorption of calcium and phosphate in the intestinal tract, leading to elevated levels of plasma calcium, and thus lower bone resorption.
Calcitriol (1,25-dihydroxycholecalciferol) is the active form of vitamin D3.
It has numerous functions involved in blood calcium levels.
Recent research indicates that calcitriol leads to a reduction in osteoclast formation, and bone resorption.
It follows that an increase in vitamin D3 intake should lead to a decrease in bone resorption — it has been shown that oral administration of vitamin D does not linearly correlate to increased serum levels of calcifediol, the precursor to calcitriol.
Calcitonin decreases osteoclast activity, and decreases the formation of new osteoclasts, resulting in decreased resorption.
Calcitonin has a greater effect in young children than in adults, and plays a smaller role in bone remodeling than PTH.
In some cases where bone resorption outpaces ossification, the bone is broken down much faster than it can be renewed.
The bone becomes more porous and fragile, exposing people to the risk of fractures.
Depending on where in the body bone resorption occurs, additional problems like tooth loss can arise.
Some people who experience increased bone resorption and decreased bone formation are astronauts.
Ossification decreases due to a lack of stress, while resorption increases, leading to a net decrease in bone density.
The effects of alcohol on bone mineral density (BMD) are well-known and well-studied in animal and human populations.
Through direct and indirect pathways, prolonged ethanol exposure increases fracture risk by decreasing bone mineral density and promoting osteoporosis.
Indirect effects of alcohol abuse occur via growth hormone, sex steroids, and oxidative stress.
Growth hormone is an important regulator of bone growth and remodeling in adults, and it acts via insulin-like growth factor I (IGF1) to stimulate osteoblastic differentiation.
Chronic alcoholism decreases the levels of IGF1, which suppresses the ability of GH to increase bone mineral density.
Increasing alcohol consumption is linked with decreasing testosterone and serum estradiol levels, which in turn lead to the activation of RANK (a TNF receptor) protein that promote osteoclast formation.
Direct effects of chronic alcoholism are apparent in osteoblasts, osteoclasts and osteocytes.
Ethanol suppresses the activity and differentiation of osteoblasts.
At the same time, it has a direct effect on osteoclast activity.
This results in an increased bone resorption rate and a decreased bone mineral density due to increased pit numbers and pit areas in the bone.
Research has shown that viable osteocytes (another type of bone cell) may prevent osteoclastogenesis, whereas apoptotic osteocytes tend to induce osteoclast stimulation.
Stimulation of osteocyte apoptosis by alcohol exposure may explain decreased bone mineral density in chronic drinkers.
Credits to the contents of this page go to the authors of the corresponding Wikipedia page: en.wikipedia.org/wiki/Bone resorption.