Senile osteoporosis: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
No edit summary
Line 26: Line 26:
'''Senile osteoporosis''', has been recently recognized as a [[geriatric]] syndrome with a particular pathophysiology. Senile (involutionary) is a type of primary osteoporosis (type II) which affects men and women equally over the age of 70 years and is accompanied by vitamin D deficiency, body's failure to absorb calcium, and increased parathyroid hormone.<ref>{{cite journal | vauthors = Sotorník I | title = [Osteoporosis - epidemiology and pathogenesis] | journal = Vnitrni Lekarstvi | volume = 62 Suppl 6 | pages = 84–87 | date = 2016 | pmid = 28124937 }}</ref><ref name=":0">{{cite journal | vauthors = Glaser DL, Kaplan FS | s2cid = 40587551 | title = Osteoporosis. Definition and clinical presentation | journal = Spine | volume = 22 | issue = 24 Suppl | pages = 12S–16S | date = December 1997 | pmid = 9431639 | doi = 10.1097/00007632-199712151-00003 }}</ref>
'''Senile osteoporosis''', has been recently recognized as a [[geriatric]] syndrome with a particular pathophysiology. Senile (involutionary) is a type of primary osteoporosis (type II) which affects men and women equally over the age of 70 years and is accompanied by vitamin D deficiency, body's failure to absorb calcium, and increased parathyroid hormone.<ref>{{cite journal | vauthors = Sotorník I | title = [Osteoporosis - epidemiology and pathogenesis] | journal = Vnitrni Lekarstvi | volume = 62 Suppl 6 | pages = 84–87 | date = 2016 | pmid = 28124937 }}</ref><ref name=":0">{{cite journal | vauthors = Glaser DL, Kaplan FS | s2cid = 40587551 | title = Osteoporosis. Definition and clinical presentation | journal = Spine | volume = 22 | issue = 24 Suppl | pages = 12S–16S | date = December 1997 | pmid = 9431639 | doi = 10.1097/00007632-199712151-00003 }}</ref>


It has been pointed out that senile osteoporosis is the product of a [[human skeleton|skeleton]] in an advanced stage of life and also due to a deficiency caused by [[calcium]], but physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together and the product is an osteoporotic bone, regardless of age.<ref>[http://emedicine.medscape.com/article/330598-overview An overview on Osteoarthritis] MedicineNet. Retrieved on 2010-03-05</ref> Elderly are the fastest growing population in the world and since bone mass declines with age so does the risk of fractures. Annual incidence of osteoporotic fractures is more than 1.5 million in the US and notably 20% of people die during the first year after a hip fracture.<ref name=":2">{{cite journal | vauthors = Lane NE | title = Epidemiology, etiology, and diagnosis of osteoporosis | journal = American Journal of Obstetrics and Gynecology | volume = 194 | issue = 2 Suppl | pages = S3-11 | date = February 2006 | pmid = 16448873 | doi = 10.1016/j.ajog.2005.08.047 }}</ref>
It has been pointed out that senile osteoporosis is the product of a [[human skeleton|skeleton]] in an advanced stage of life and also due to a deficiency caused by [[calcium]], but physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together and the product is an osteoporotic bone, regardless of age.<ref>[http://emedicine.medscape.com/article/330598-overview An overview on Osteoarthritis] MedicineNet. Retrieved on 2010-03-05</ref> Elderly are the fastest growing population in the world and since bone mass declines with age so does the risk of fractures. Annual incidence of osteoporotic fractures is more than 1.5 million in the US and notably 20% of people die during the first year after a hip fracture.<ref name=":2">{{cite journal | vauthors = Lane NE | title = Epidemiology, etiology, and diagnosis of osteoporosis | journal = American Journal of Obstetrics and Gynecology | volume = 194 | issue = 2 Suppl | pages = S3-11 | date = February 2006 | pmid = 16448873 | doi = 10.1016/j.ajog.2005.08.047 }}</ref>


==Cause==
==Cause==
Line 45: Line 45:


==== Genetic: ====
==== Genetic: ====
Maternal body build, life style, and 25(OH) vitamin D status are some of the genetic and epigenetic effects that have been found to affect the BMD, specifically the developmental plasticity. <ref>{{Cite journal|last=Aspray|first=Terry J.|last2=Hill|first2=Tom R.|date=2019|title=Osteoporosis and the Ageing Skeleton|url=https://www.ncbi.nlm.nih.gov/pubmed/30888662|journal=Sub-Cellular Biochemistry|volume=91|pages=453–476|doi=10.1007/978-981-13-3681-2_16|issn=0306-0225|pmid=30888662}}</ref>
⚫
Studies have found that race, age, body mass, and gender have played a role in contributing to the risk of osteoporosis. Although the incidence of developing osteoporosis and hip fractures vary from different population groups, the increase in age have been consistent in showing increased rates of incidence.<ref name=":2" />

⚫
Additionally, other studies have found that race, age, body mass, and gender have played a role in contributing to the risk of osteoporosis. Although the incidence of developing osteoporosis and hip fractures vary from different population groups, the increase in age have been consistent in showing increased rates of incidence.<ref name=":2" />


==== Social Factors/Nutrition: ====
==== Social Factors/Nutrition: ====

Revision as of 20:18, 2 August 2020

Senile osteoporosis
Other namesOsteoporosis type II

Senile osteoporosis, has been recently recognized as a geriatric syndrome with a particular pathophysiology. Senile (involutionary) is a type of primary osteoporosis (type II) which affects men and women equally over the age of 70 years and is accompanied by vitamin D deficiency, body's failure to absorb calcium, and increased parathyroid hormone.[1][2]

It has been pointed out that senile osteoporosis is the product of a skeleton in an advanced stage of life and also due to a deficiency caused by calcium, but physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together and the product is an osteoporotic bone, regardless of age.[3] Elderly are the fastest growing population in the world and since bone mass declines with age so does the risk of fractures. Annual incidence of osteoporotic fractures is more than 1.5 million in the US and notably 20% of people die during the first year after a hip fracture.[4]

Cause

Bone remodeling, or the absorption and resorption of bone, is a natural mechanism that occurs to repair and strengthen bones in the body. However, an imbalance between the resorption and formation of bone occurs as people age, contributing to the development of senile osteoporosis. The aging of cortical and trabecular bones in particular cause the decrease in bone density in the elderly population.[5] Although most of the etiologic considerations regarding senile osteoporosis are not very clear for physicians yet, risk factors of osteoporosis have been identified. These factors include gender, age, hormone imbalances, reduced bone quality, and compromised integrity of bone microarchitecture.[5]

Based on the current evidence attached to clinical experimentation, there is some evidence that the pathogenesis of the disease is related to a deficiency of zinc.[6] Such deficiency is known to lead to an increment of endogenous heparin, which is most likely caused by mast cell degranulation, and an increase in the bone resorption (calcium discharge in the bones) reaction of prostaglandin E2, which constrain the formation of more bone mass, making bones more fragile. These co-factors are shown to play an important role in the pathogenetic process attached to senile osteoporosis as they enhance the action of the parathyroid hormone.[7]

The intake of calcium in elder people is quite low, and this problem is worsened by a reduced capability to ingest it. This, attached to a decrease in the absorption of vitamin D concerning metabolism, are also factors that contributes to a diagnosis of osteoporosis type II.

Risk Factors

Though senile osteoporosis (type II) is attributed to age this does not exclude other risk risk factors such as medical, pharmacological, genetic, and environmental. Peak bone mass is a major determinant of bone density which starts in the utero and is typically done by the age 40. [4]

Medical:

Secondary osteoporosis can be present in pre- and post-menopausal women and in men and have found to be factors contributing to osteoporosis in both sexes (50-80% of men and 30% of post-menopausal women).[8] Therefore, when treating patients, it is important to exclude secondary causes of osteoporosis which include endocrine disorders (e.g. hyperthyrodism and diabetes mellitus), gastrointestinal, hepatic and nutritional disorders (e.g. celiac disease and inflammatory bowel disease), hematological disorders (e.g. systemic mastocytosis), renal disorders (e.g. chronic kidney disease), and autoimmune disorders (e.g. rheumatoid arthritis and systemic lupus erythematosus).[8]

Pharmacological:

Medications that can contribute to bone loss include aluminum (found in antacids), aromatase inhibitors, cyclosporine, depo-medroxyprogesterone (premenopausal), glucocorticoids, lithium, proton pump inhibitors, serotonin reuptake inhibitors, tacrolimus, and tamoxifen (premenopausal). These medications can contribute to bone loss and can increase risk for osteoporotic fractures.

Genetic:

Maternal body build, life style, and 25(OH) vitamin D status are some of the genetic and epigenetic effects that have been found to affect the BMD, specifically the developmental plasticity. [9]

Additionally, other studies have found that race, age, body mass, and gender have played a role in contributing to the risk of osteoporosis. Although the incidence of developing osteoporosis and hip fractures vary from different population groups, the increase in age have been consistent in showing increased rates of incidence.[4]

Social Factors/Nutrition:

There are several environmental and social factors that can contribute to the risk of developing osteoporosis. Smoking tobacco can increase the risk by decreasing the ability for the intestine to absorb calcium. Caffeine intake and heavy alcohol were also correlated with the decrease in bone density in the elderly population.[4]

Without proper intake of vitamin D and calcium, it can increase the risk of osteoporosis in the elderly. These vitamin deficiencies pose as a risk factor, as it can decrease bone mass, decrease calcium absorption, and increase in bone turnover. There are various medications can that interfere with the absorption of calcium such as anticovulsants, diuretics, corticosteroids, and NSAIDS. [4]

Diagnosis

Because the diagnosis of osteoporosis is made only after a pathologic fracture has occurred, it is best to take serial bone density (also known as bone mineral density or BMD) measurement scans for high risk patients (elderly).[2] The World Health Organization (WHO) has established a diagnostic criteria for osteoporosis using BMD T-scores which describes a patient's BMD in terms of the number of SDs by which is differs from the mean peak value in young, healthy persons of the same sex--currently more than 2.5 SDs below the mean as the criterion for osteoporosis.[4] For osteopenia (low bone mass) the range is 1.0 SD to less than 2.5 SDs below the mean. However, T-scores were initially used as an estimation of the prevalence of osteoporosis across populations not to assess osteoporosis prevalence in specific patients which lead to the National Osteoporosis Foundation and the International Society for Clinical Densitometry to consider using dual-energy X-ray absorptiometry (DXA) of the hip and/or spine as the preferred measurement diagnosis of osteoporosis.[4]

Treatment

Calcium and Vitamin D3 intake from diet or supplementation are crucial in the ethiopathogenesis of this disease; therefore, the effective treatments should comprise of non pharmacological methods (such as a modified diet with more calcium and vitamin D3, exercising, smoking cessation, and alcohol restriction), fall prevention, and individually chosen pharmacological intervention (such as estrogen replacement therapy).[10] Given bone fracture (hip, vertebrae, and colles) is a devastating complication of osteoporosis, vitamin D3 combined with calcium are used as primary prevention, along with alendronate, residronate, strontrium and zoledronic acid which have proven efficacy in primary and secondary hip fracture prevention.[11] The Institute of Medicine recommends a daily allowance of 800 IU of Vitamin D for people 71 and over, to get to a level of serum 25-hydroxyvitamin D (25OHD) of at least 20 ng/ml (50 nmol/liter) in addition to a daily allowance of 1,200 mg of calcium.[12]

One study of pharmacological agents on postmenopausal woman age 65 found alendronate to be more efficacious in improvement of bone marrow density compared to calcitonin.[13] In addition to bisphosphanates, pharmacological treatments for osteoporosis can include calcitonin, parathyroid hormone 1-34, hormone replacement therapy, and monoclonal antibody therapy.[14] Another study showed that among 7,868 women aged 60-90, monoclonal antibody therapy reduced the incidence of vertebral fractures by 68% and reduced the incidence of hip fractures by 40%.[15]

Even though more studies are necessary for an efficient evaluation of the role played by zinc in senile osteoporosis, doctors recommend a proper supplementation of dietary zinc in addition to calcium and vitamin D3.[6]

Replacement estrogen has proved to be an efficient way to combat the loss of bone mass in women when such treatment is started in the menopausal stage of their lives. John R. Lee, a Harvard graduate who wrote a book on the subject, came to the conclusion that by adding supplementation with natural progesterone to an existing natural osteoporosis treatment program, bone density was increased every year by 3-5% until it stabilized at the bone density levels expected for a 35-year-old woman, this after studies in 100 women between 38 and 83 with an average of 62 years old.[16] The addition of replacement estrogen has been shown to be especially protective against fractures in postmenopausal women for the first two years following initiation of estrogen.[17]

Complications: Fracture Risk

Because senile osteoporosis is caused by the loss of bone mass due to aging, the bones are more fragile and thus more prone to fractures and fracture-related complications. These complications can include a more than doubled risk increase for future fractures and a lower quality of life resulting from chronic pain or disability, sometimes needing long-term nursing care.[5] Depending on the site, pathologic fractures can also increase relative mortality risk. Hip fractures alone are particularly debilitating and have a nearly 20% higher mortality rate within one year of the fracture.[18] Other fractures are more subtle and can go undetected for some time. For example, vertebral compression fractures in the spine, often noticeable by a loss of vertical height, can occur even during routine motions like twisting, coughing, and reaching.[19]

In addition to decreased bone mineral density, there are other factors that contribute to fracture risk such as advanced age, lower body mass index, fracture history, smoking, steroid use, high alcohol intake, and fall history.[5] Studies linking alcohol and fracture risk define high intake as three or more drinks per day.[20] High caffeine intake may also play a role in fracture risk.[21] Many healthcare organizations also utilize a Fracture Risk Assessment Tool (FRAX) that can estimate a 10-year probability of having an osteoporotic fracture based on an individual's health information and the criteria listed above.[22]

Fall Prevention

Of the risks listed above, falls contribute most significantly to the incidence of osteoporotic fractures. There are precautions that can be taken at home to reduce the risk of falling. These include anchoring rugs to the floor, minimizing clutter, improving overall lighting and visibility, and installing handrails in stairways and hallways.[5] Regular exercise is another way to further decrease fall risk. Back and posture exercises as well as weight-bearing exercises such as walking can slow bone loss, improve balance, and strengthen muscles.[23]

References

  1. ^ Sotorník I (2016). "[Osteoporosis - epidemiology and pathogenesis]". Vnitrni Lekarstvi. 62 Suppl 6: 84–87. PMID 28124937.
  2. ^ a b Glaser DL, Kaplan FS (December 1997). "Osteoporosis. Definition and clinical presentation". Spine. 22 (24 Suppl): 12S–16S. doi:10.1097/00007632-199712151-00003. PMID 9431639. S2CID 40587551.
  3. ^ An overview on Osteoarthritis MedicineNet. Retrieved on 2010-03-05
  4. ^ a b c d e f g Lane NE (February 2006). "Epidemiology, etiology, and diagnosis of osteoporosis". American Journal of Obstetrics and Gynecology. 194 (2 Suppl): S3-11. doi:10.1016/j.ajog.2005.08.047. PMID 16448873.
  5. ^ a b c d e Sözen T, Özışık L, Başaran NÇ (March 2017). "An overview and management of osteoporosis". European Journal of Rheumatology. 4 (1): 46–56. doi:10.5152/eurjrheum.2016.048. PMC 5335887. PMID 28293453.
  6. ^ a b Yamaguchi M (May 2010). "Role of nutritional zinc in the prevention of osteoporosis". Molecular and Cellular Biochemistry. 338 (1–2): 241–54. doi:10.1007/s11010-009-0358-0. PMID 20035439. S2CID 35574730.
  7. ^ National Center for Biotechnology Information. "Etiology of senile osteoporosis" 2010-03-05.
  8. ^ a b Mirza, Faryal; Canalis, Ernesto (2016). "Management of endocrine disease: Secondary osteoporosis: pathophysiology and management". European Journal of Endocrinology. 173 (3): R131–151. doi:10.1530/EJE-15-0118. ISSN 1479-683X. PMC 4534332. PMID 25971649.
  9. ^ Aspray, Terry J.; Hill, Tom R. (2019). "Osteoporosis and the Ageing Skeleton". Sub-Cellular Biochemistry. 91: 453–476. doi:10.1007/978-981-13-3681-2_16. ISSN 0306-0225. PMID 30888662.
  10. ^ Wawrzyniak A, Horst-Sikorska W (2008). "[Senile osteoporosis]". Polskie Archiwum Medycyny Wewnetrznej. 118 Suppl: 59–62. PMID 19562973.
  11. ^ Duque G, Demontiero O, Troen BR (February 2009). "Prevention and treatment of senile osteoporosis and hip fractures". Minerva Medica. 100 (1): 79–94. PMID 19277006.
  12. ^ Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. (January 2011). "The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know". The Journal of Clinical Endocrinology and Metabolism. 96 (1): 53–8. doi:10.1210/jc.2010-2704. PMC 3046611. PMID 21118827.
  13. ^ Downs RW, Bell NH, Ettinger MP, Walsh BW, Favus MJ, Mako B, et al. (May 2000). "Comparison of alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women". The Journal of Clinical Endocrinology and Metabolism. 85 (5): 1783–8. doi:10.1210/jcem.85.5.6606. PMID 10843152.
  14. ^ Cosman F, de Beur SJ, LeBoff MS, Lewiecki EM, Tanner B, Randall S, Lindsay R (October 2014). "Clinician's Guide to Prevention and Treatment of Osteoporosis". Osteoporosis International. 25 (10): 2359–81. doi:10.1007/s00198-014-2794-2. PMC 4176573. PMID 25182228.
  15. ^ Cummings, Steven R.; Martin, Javier San; McClung, Michael R.; Siris, Ethel S.; Eastell, Richard; Reid, Ian R.; Delmas, Pierre; Zoog, Holly B.; Austin, Matt; Wang, Andrea; Kutilek, Stepan (2009-08-20). "Denosumab for Prevention of Fractures in Postmenopausal Women with Osteoporosis". New England Journal of Medicine. 361 (8): 756–765. doi:10.1056/NEJMoa0809493. ISSN 0028-4793.
  16. ^ Natural Progesterone And Osteoporosis Treatment Archived 2010-03-08 at the Wayback Machine Retrieved on 2010-03-05
  17. ^ Kiel, Douglas P.; Felson, David T.; Anderson, Jennifer J.; Wilson, Peter W.F.; Moskowitz, Mark A. (1987-11-05). "Hip Fracture and the Use of Estrogens in Postmenopausal Women". New England Journal of Medicine. 317 (19): 1169–1174. doi:10.1056/NEJM198711053171901. ISSN 0028-4793.
  18. ^ Melton LJ, Achenbach SJ, Atkinson EJ, Therneau TM, Amin S (May 2013). "Long-term mortality following fractures at different skeletal sites: a population-based cohort study". Osteoporosis International. 24 (5): 1689–96. doi:10.1007/s00198-012-2225-1. PMC 3630278. PMID 23212281.
  19. ^ "Osteoporosis and Spinal Fractures - OrthoInfo - AAOS". www.orthoinfo.org. Retrieved 2020-07-31.
  20. ^ Kanis JA, Johansson H, Johnell O, Oden A, De Laet C, Eisman JA, et al. (July 2005). "Alcohol intake as a risk factor for fracture". Osteoporosis International. 16 (7): 737–42. doi:10.1007/s00198-004-1734-y. PMID 15455194. S2CID 10303026.
  21. ^ Hallström H, Wolk A, Glynn A, Michaëlsson K (2006-06-06). "Coffee, tea and caffeine consumption in relation to osteoporotic fracture risk in a cohort of Swedish women". Osteoporosis International. 17 (7): 1055–64. doi:10.1007/s00198-006-0109-y. PMID 16758142. S2CID 19735422.
  22. ^ "Fracture Risk Assessment Tool (FRAX®)". APTA. Retrieved 2020-07-31.
  23. ^ Kelley GA, Kelley KS, Tran ZV (September 2002). "Exercise and lumbar spine bone mineral density in postmenopausal women: a meta-analysis of individual patient data". The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 57 (9): M599-604. doi:10.1093/gerona/57.9.M599. PMID 12196498.

Further reading

Retrieved from "https://en.wikipedia.org/w/index.php?title=Senile_osteoporosis&oldid=970855154"