Bone resorption

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Bone resorption
Classification and external resources
Osteoclast.jpg
Osteoclast, displaying many nuclei within its "foamy" cytoplasm, above a bone's surface
ICD-10M80
ICD-9733.99
eMedicineent/646
MeSHD001862
 
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Bone resorption
Classification and external resources
Osteoclast.jpg
Osteoclast, displaying many nuclei within its "foamy" cytoplasm, above a bone's surface
ICD-10M80
ICD-9733.99
eMedicineent/646
MeSHD001862

Bone resorption is the process by which osteoclasts break down bone[1] and release the minerals, resulting in a transfer of calcium from bone fluid to the blood.[2]

The osteoclasts are multi-nucleated cells that contain numerous mitochondria and lysosomes. 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. High levels of calcium, magnesium, phosphate and products of collagen will be released into the extracellular fluid as the osteoclasts tunnel into the mineralized bone. Osteoclasts are also prominent in the tissue destruction commonly found in psoriatic arthritis and other rheumatology related disorders.

The human body is in a constant state of bone remodeling.[3] Bone is resorbed by osteoclasts, and is deposited by osteoblasts in a process called ossification. Osteocyte activity also 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 a decrease in ossification.

During childhood, bone formation exceeds resorption, but as the aging process occurs, resorption exceeds formation.

Regulation[edit]

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. Low levels of calcium stimulates the release of parathyroid hormone (PTH) from chief cells of the parathyroid gland. In addition to its effects on kidney and intestine, PTH also 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.[3] Continued elevation of PTH levels increases the abundance of osteoclasts. This leads to a greater resorption of calcium and phosphate ions.[3]

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 track, leading to elevated levels of plasma calcium,[3] and thus lower bone resorption.

Calcitriol (1,25-dihydroxycholecalciferol) is the active form of vitamin D3.[4] It has numerous functions involved in blood calcium levels. Recent research indicates that calcitriol leads to a reduction in osteoclast formation, and bone resorption.[5][6] Although 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,[7] the precursor to 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.[3] Calcitonin has a greater effect in young animals than in adults, and plays a smaller role in bone remodeling than PTH.[3]

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 also arise. This can be caused by conditions such as hypoparathyroidism and hypovitaminosis D or even decreased hormonal 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. Due to the condition of being in a zero-gravity environment, astronauts do not need to work their musculoskeletal system as hard as when on earth. Ossification decreases due to a lack of stress, while resorption increases, leading to a net decrease in bone density.[8]

See also[edit]

References[edit]

  1. ^ Bone Resorption at the US National Library of Medicine Medical Subject Headings (MeSH)
  2. ^ Teitelbaum SL. (2000). "Bone resorption by osteoclasts.". Science 289: 1504–8. doi:10.1126/science.289.5484.1504. PMID 10968780. 
  3. ^ a b c d e f Guyton and Hall Textbook of Medical Physiology, 12th Edition. ISBN 1416045740
  4. ^ Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium; Ross AC, Taylor CL, Yaktine AL, et al., editors. Dietary Reference Intakes for Calcium and Vitamin D. Washington (DC): National Academies Press (US); 2011. 3, Overview of Vitamin D. Available from: http://www.ncbi.nlm.nih.gov/books/NBK56061/
  5. ^ Kikuta J, Kawamura S, Okiji F, Shirazaki M, Sakai S, Saito H, Ishii M. Sphingosine-1-phosphate-mediated osteoclast precursor monocyte migration is a critical point of control in antibone-resorptive action of active vitamin D. Proc Natl Acad Sci U S A. 2013 Apr 23;110(17):7009-13. doi: 10.1073/pnas.1218799110. Epub 2013 Apr 8. PubMed PMID 23569273; PubMed Central PMCID: PMC3637769.
  6. ^ Yamamoto Y, Yoshizawa T, Fukuda T, Shirode-Fukuda Y, Yu T, Sekine K, Sato T, Kawano H, Aihara K, Nakamichi Y, Watanabe T, Shindo M, Inoue K, Inoue E, Tsuji N, Hoshino M, Karsenty G, Metzger D, Chambon P, Kato S, Imai Y. Vitamin D receptor in osteoblasts is a negative regulator of bone mass control. Endocrinology. 2013 Mar;154(3):1008-20. doi: 10.1210/en.2012-1542. Epub 2013 Feb 6. PubMed PMID 23389957.
  7. ^ Stamp TC, Haddad JG, Twigg CA. Comparison of oral 25-hydroxycholecalciferol, vitamin D, and ultraviolet light as determinants of circulating 25-hydroxyvitamin D. Lancet. 1977 Jun 25;1(8026):1341-3. PubMed PMID 69059.
  8. ^ Iwamoto J, Takeda T, Sato Y. Interventions to prevent bone loss in astronauts during space flight. Keio J Med. 2005 Jun;54(2):55-9. Review. PubMed PMID 16077253.