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at what age does bone breakdown generally begin to occur more rapidly than bone formation?

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Medical condition

Os Resorption
Osteoclast.jpg
Low-cal micrograph of an osteoclast displaying typical distinguishing characteristics: a large jail cell with multiple nuclei and a "foamy" cytosol.
Specialty Rheumatology Edit this on Wikidata

Os resorption is resorption of bone tissue, that is, the procedure by which osteoclasts break down the tissue in bones[1] and release the minerals, resulting in a transfer of calcium from os tissue 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. Osteoblasts are mostly present on the outer layer of bone, just below the periosteum. Attachment of the osteoclast to the osteon begins the procedure. The osteoclast so induces an infolding of its jail cell membrane and secretes collagenase and other enzymes important in the resorption procedure. Loftier levels of calcium, magnesium, phosphate and products of collagen volition be released into the extracellular fluid as the osteoclasts tunnel into the mineralized os. Osteoclasts are prominent in the tissue devastation plant in psoriatic arthritis and rheumatological disorders.[3]

The human torso is in a abiding country of os remodeling.[4] Os remodeling is a process which maintains os strength and ion homeostasis past replacing discrete parts of old bone with newly synthesized packets of proteinaceous matrix.[5] Bone is resorbed by osteoclasts, and is deposited by osteoblasts in a process called ossification.[6] Osteocyte activity plays a key role in this procedure. Weather condition that outcome in a decrease in bone mass tin can either be acquired by an increase in resorption or by a subtract in ossification. During babyhood, bone formation exceeds resorption. As the aging procedure occurs, resorption exceeds formation.[five]

Os resorption rates are much higher in mail-menopausal older women due to estrogen deficiency related with menopause.[vii] Mutual treatments include drugs that increase bone mineral density. Bisphosphonates, RANKL inhibitors, SERMs—selective oestrogen receptor modulators, hormone replacement therapy and calcitonin are some of the mutual treatments.[8] Light weight bearing exercise tends to eliminate the negative effects of bone resorption.[nine]

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.[4] In addition to its effects on kidney and intestine, PTH increases the number and activeness of osteoclasts. The increment in activity of already existing osteoclasts is the initial issue of PTH, and begins in minutes and increases over a few hours.[4] Continued elevation of PTH levels increases the abundance of osteoclasts. This leads to a greater resorption of calcium and phosphate ions.[4]

High levels of calcium in the claret, 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 abdominal tract, leading to elevated levels of plasma calcium,[4] and thus lower os resorption.

Calcitriol (ane,25-dihydroxycholecalciferol) is the active form of vitamin D3.[10] Information technology has numerous functions involved in claret calcium levels. Recent research indicates that calcitriol leads to a reduction in osteoclast formation, and bone resorption.[11] [12] It follows that an increment in vitamin D3 intake should lead to a decrease in bone resorption — it has been shown that oral administration of vitamin D does non linearly correlate to increased serum levels of calcifediol,[13] the forerunner to calcitriol.

Calcitonin is a hormone secreted past the thyroid in humans. Calcitonin decreases osteoclast activity, and decreases the formation of new osteoclasts, resulting in decreased resorption.[4] Calcitonin has a greater effect in young children than in adults, and plays a smaller role in os remodeling than PTH.[4]

In some cases where os resorption outpaces ossification, the bone is broken down much faster than information technology can be renewed. The os becomes more porous and fragile, exposing people to the take chances of fractures. Depending on where in the body bone resorption occurs, additional issues like tooth loss can ascend. This tin be caused by conditions such every bit hyperparathyroidism 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 os resorption and decreased os formation are astronauts. Due to the status of being in a zero-gravity environment, astronauts do non demand to work their musculoskeletal system as hard every bit when on world. Ossification decreases due to a lack of stress, while resorption increases, leading to a net decrease in bone density.[xiv]

Alcoholism [edit]

The effects of alcohol on bone mineral density (BMD) are well-known and well-studied in animal and human populations. Through straight and indirect pathways, prolonged ethanol exposure increases fracture risk past decreasing bone mineral density and promoting osteoporosis. Indirect effects of alcohol abuse occur via growth hormone, sexual practice steroids, and oxidative stress.

Growth hormone is an important regulator of os growth and remodeling in adults, and it acts via insulin-like growth factor I (IGF1) to stimulate osteoblastic differentiation.[xv] Chronic alcoholism decreases the levels of IGF1, which suppresses the power of GH to increase bone mineral density.[15]

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.[16] Oxidative stress results when ethanol induces NOX expression, resulting in ROS production in osteoblasts which can ultimately effect in jail cell senescence.[17] Direct effects of chronic alcoholism are apparent in osteoblasts, osteoclasts and osteocytes. Ethanol suppresses the activity and differentiation of osteoblasts.

At the aforementioned time, it has a straight upshot on osteoclast activity. This results in an increased os resorption charge per unit and a decreased bone mineral density due to increased pit numbers and pit areas in the bone.[18] [19] [twenty] Research has shown that feasible osteocytes (some other blazon of bone cell) may prevent osteoclastogenesis, whereas apoptotic osteocytes tend to induce osteoclast stimulation. Stimulation of osteocyte apoptosis by alcohol exposure may explicate decreased bone mineral density in chronic drinkers.[20] [21]

See too [edit]

  • Os remodeling
  • Nuclear factor-kappa B

References [edit]

  1. ^ Bone+Resorption at the U.s.a. National Library of Medicine Medical Subject area Headings (MeSH)
  2. ^ Teitelbaum SL. (2000). "Bone resorption by osteoclasts". Science. 289 (5484): 1504–eight. Bibcode:2000Sci...289.1504T. doi:10.1126/science.289.5484.1504. PMID 10968780.
  3. ^ Mensah, Kofi A.; Schwarz, Edward G.; Ritchlin, Christopher T. (2008-08-01). "Altered Bone Remodeling in Psoriatic Arthritis". Current Rheumatology Reports. 10 (four): 311–317. doi:10.1007/s11926-008-0050-five. ISSN 1523-3774. PMC2656567. PMID 18662512.
  4. ^ a b c d east f g Guyton and Hall Textbook of Medical Physiology, twelfth Edition. ISBN 1416045740
  5. ^ a b Clarke, Bart (2008-11-01). "Normal Bone Anatomy and Physiology". Clinical Journal of the American Society of Nephrology. iii (Suppl 3): S131–S139. doi:ten.2215/CJN.04151206. ISSN 1555-9041. PMC3152283. PMID 18988698.
  6. ^ Maurel, D. B.; Jaffre, C.; Rochefort, G. Y.; Aveline, P. C.; Boisseau, Northward.; Uzbekov, R.; Gosset, D.; Pichon, C.; Fazzalari, Northward. L. (2011-09-01). "Depression os accrual is associated with osteocyte apoptosis in alcohol-induced osteopenia". Os. 49 (iii): 543–552. doi:10.1016/j.bone.2011.06.001. ISSN 1873-2763. PMID 21689804.
  7. ^ Feng, Xu; McDonald, Jay M. (2011-01-01). "Disorders of Bone Remodeling". Annual Review of Pathology. vi: 121–145. doi:ten.1146/annurev-pathol-011110-130203. ISSN 1553-4006. PMC3571087. PMID 20936937.
  8. ^ Russell, Chiliad.; Mueller, G.; Shipman, C.; Croucher, P. (2001-01-01). "Clinical disorders of bone resorption". Novartis Foundation Symposium. Novartis Foundation Symposia. 232: 251–267, discussion 267–271. doi:10.1002/0470846658.ch17. ISBN9780471494331. ISSN 1528-2511. PMID 11277085.
  9. ^ Shanb, Alsayed A.; Youssef, Enas F. (2014-01-01). "The impact of adding weight-bearing practice versus nonweight bearing programs to the medical treatment of elderly patients with osteoporosis". Journal of Family and Community Medicine. 21 (3): 176–181. doi:10.4103/2230-8229.142972. ISSN 1319-1683. PMC4214007. PMID 25374469.
  10. ^ 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. three, Overview of Vitamin D. Available from: https://www.ncbi.nlm.nih.gov/books/NBK56061/
  11. ^ Kikuta J, Kawamura Southward, Okiji F, Shirazaki M, Sakai S, Saito H, Ishii M (April 2013). "Sphingosine-1-phosphate-mediated osteoclast precursor monocyte migration is a critical point of control in antibone-resorptive activeness of active vitamin D." Proceedings of the National Academy of Sciences of the United States of America. 110 (17): 7009–13. Bibcode:2013PNAS..110.7009K. doi:10.1073/pnas.1218799110. PMC3637769. PMID 23569273.
  12. ^ Yamamoto Y, Yoshizawa T, Fukuda T, Shirode-Fukuda Y, Yu T, Sekine K, Sato T, Kawano H, Aihara M, Nakamichi Y, Watanabe T, Shindo M, Inoue K, Inoue East, Tsuji N, Hoshino K, Karsenty G, Metzger D, Chambon P, Kato South, Imai Y (Mar 2013). "Vitamin D receptor in osteoblasts is a negative regulator of bone mass control". Endocrinology. 154 (3): 1008–twenty. doi:ten.1210/en.2012-1542. PMID 23389957.
  13. ^ Postage TC, Haddad JG, Twigg CA (Jun 1977). "Comparison of oral 25-hydroxycholecalciferol, vitamin D, and ultraviolet light as determinants of circulating 25-hydroxyvitamin D.". The Lancet. 1 (8026): 1341–3. doi:10.1016/s0140-6736(77)92553-3. PMID 69059. S2CID 9326591.
  14. ^ Iwamoto J, Takeda T, Sato Y (Jun 2005). "Interventions to foreclose os loss in astronauts during space flight". The Keio Periodical of Medicine. 54 (ii): 55–9. doi:x.2302/kjm.54.55. PMID 16077253.
  15. ^ a b Maddalozzo, G. F.; Turner, R. T.; Edwards, C. H. T.; Howe, K. S.; Widrick, J. J.; Rosen, C. J.; Iwaniec, U. T. (2009-09-01). "Alcohol alters whole trunk composition, inhibits os formation, and increases bone marrow adiposity in rats". Osteoporosis International. twenty (nine): 1529–1538. doi:ten.1007/s00198-009-0836-y. ISSN 1433-2965. PMID 19238309. S2CID 11502836.
  16. ^ Ronis, Martin J. J.; Wands, Jack R.; Annoy, Thomas M.; de la Monte, Suzanne M.; Lang, Charles H.; Calissendorff, Jan (2007-08-01). "Booze-induced disruption of endocrine signaling". Alcoholism, Clinical and Experimental Enquiry. 31 (8): 1269–1285. doi:ten.1111/j.1530-0277.2007.00436.x. ISSN 0145-6008. PMID 17559547.
  17. ^ Chen, Jin-Ran; Shankar, Kartik; Nagarajan, Shanmugam; Badger, Thomas M.; Ronis, Martin J. J. (2008-01-01). "Protective effects of estradiol on ethanol-induced bone loss involve inhibition of reactive oxygen species generation in osteoblasts and downstream activation of the extracellular point-regulated kinase/bespeak transducer and activator of transcription 3/receptor activator of nuclear factor-kappaB ligand signaling cascade". The Journal of Pharmacology and Experimental Therapeutics. 324 (ane): 50–59. doi:ten.1124/jpet.107.130351. ISSN 1521-0103. PMID 17916759. S2CID 27152788.
  18. ^ Robling, Alexander 1000.; Bonewald, Lynda F. (10 February 2020). "The Osteocyte: New Insights". Annual Review of Physiology. 82 (1): 485–506. doi:10.1146/annurev-physiol-021119-034332. ISSN 0066-4278. Retrieved 8 March 2022.
  19. ^ Bonewald, Lynda F. (2011-02-01). "The astonishing osteocyte". Journal of Bone and Mineral Research. 26 (2): 229–238. doi:10.1002/jbmr.320. ISSN 1523-4681. PMC3179345. PMID 21254230.
  20. ^ a b Verborgt, Olivier; Tatton, Nadine A.; Majeska, Robert J.; Schaffler, Mitchell B. (2002-05-01). "Spatial distribution of Bax and Bcl-2 in osteocytes afterward bone fatigue: complementary roles in bone remodeling regulation?". Periodical of Os and Mineral Research. 17 (five): 907–914. doi:10.1359/jbmr.2002.17.five.907. hdl:10067/1033580151162165141. ISSN 0884-0431. PMID 12009022. S2CID 22428635.
  21. ^ Maurel DB, Jaffre C, Rochefort GY, Aveline PC, Boisseau N, Uzbekov R, Gosset D, Pichon C, Fazzalari NL, Pallu S, Benhamou CL (September 2011). "Low bone accrual is associated with osteocyte apoptosis in booze-induced osteopenia". Bone. 49 (3): 543–52. doi:10.1016/j.bone.2011.06.001. PMID 21689804.

External links [edit]

camfieldwrecertrecan.blogspot.com

Source: https://en.wikipedia.org/wiki/Bone_resorption

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