You just celebrated your seventieth birthday. It was a grand occasion, but a few days after you devoured your second piece of birthday cake, you went in for your yearly physical. At the doctor's office, you got some confusing news. You've been 5' 7" tall since high school, but now your doctor says you're 5' 6". Were you standing straight? Is the doctor's height instrument wrong? Or. . . do you have osteoporosis?
Osteoporosis is a progressive condition that causes the loss of bone over time. The gradual weakening of bones caused by osteoporosis may eventually result in fractures (broken bones), most commonly of the hip and spine. Particularly in elderly people, broken bones are often disabling. Serious breaks can lead to other illnesses, or even death.
Although bone is often considered to be stable, it is actually changing continually. New bone cells are formed after old bone cells are broken down into components, such as calcium, which are taken out of the body in the blood. Osteoporosis is believed to be caused by an imbalance in two types of cells, osteoblasts and osteoclasts. Osteoblasts are responsible for making bone while osteoclasts break down bone. The process of bone break down and rebuilding is often called bone turnover, and the breakdown of bone may be known as resorption. When osteoclasts break bone down faster than osteoblasts build bone, osteoporosis occurs. The following factors can contribute to the disease:
The latest estimates from the National Osteoporosis Foundation state that about 8 million American women and 2 million American men have osteoporosis. As many as 34 million more Americans may have osteopenia (lower than average bone density as compared to others of the same age and gender). Only one-third of all people with osteoporosis have been diagnosed with it and only one-seventh of those diagnosed receive treatment according to the National Osteoporosis Foundation. As the number of older individuals increases, the number of Americans who have osteoporosis or who have increased risk for getting osteoporosis is expected to increase. Osteoporosis contributed to about 2 million broken bones in 2005, according to the National Osteoporosis Foundation. In 2005, the National Osteoporosis Foundation reported that more than $19 billion are spent annually on broken bones related to osteoporosis.
In humans, the amount of bone in the body is highest between the ages of about 25 and 40. During pregnancy, the developing baby gets calcium from the mother's bones, but the mother usually regains bone density after she finishes breast-feeding. Both men and women begin to lose bone density permanently in their forties and fifties. By the age of 80, nearly 90% of women and 50% of men have osteoporosis. Because women experience more rapid bone loss in the years following menopause, they usually have an earlier risk of fractures. Approximately one-half of women over 50 years of age will experience a fracture related to osteoporosis as compared to about one-eighth of men over the age of 50 years. For a woman, the risk of a hip fracture is equal to the risk of breast, uterine, and cervical cancer combined.
Risk factors are characteristics that may increase the chance of developing a condition. Being female greatly increases the chances of having osteoporosis. For women, other osteoporosis risk factors include:
Men who have had their testicles removed surgically or who have lower than average levels of the male hormone, testosterone, may be at greater risk for having osteoporosis.
Other factors that may contribute to osteoporosis are not well defined. For example, studies by the U.S. National Institute of Child and Human Development (NICHD) have shown that irregular menstrual periods in young women may signal a hormonal shortage that could lead to osteoporosis. A separate study has found that individuals with major depression may be at higher risk for developing osteoporosis. Other research suggests that abnormally elevated stress hormone levels may also contribute to bone loss. Another recent study reported that women who needed bed rest to control problem pregnancies lost more bone density than other pregnant women (averages of 4.6% as compared to 1.5%).
Click on the link below to access a checklist of risks for osteoporosis.
Ordinary x-rays are not sensitive enough to reveal bone loss until more than 30% of the highest amount of bone is already gone. The only sure way to determine the true condition of bone is to have a bone mineral density (BMD) test. Also called bone mass measurements, BMD tests are more readily available than they were a few years ago. BMD testing is recommended for postmenopausal women with osteoporosis risk factors and for all postmenopausal women age 65 or greater (medscape). A series of BMD tests may be performed about once a year to measure the rate of bone loss, to estimate the risk of bone breaks due to osteoporosis, and to check whether or not treatments are working.
Various methods are used for the assessment of bone density - usually based on the part of the body that needs to be assessed. The tests, all painless and safe, measure bone density in the bones that break most often due to osteoporosis of the spine (back), hip and/or wrist. Among the most common BMD tests are:
The measured bone density is compared to two standards, or norms, known as "age matched" and "young normal." The age-matched reading compares an individual's measured bone density to what is expected in someone of the same age, sex, and size. The young normal reading compares the measured density to the best peak bone density of a healthy young adult of the same sex as the individual being tested.
Osteoporosis is often called a silent disease because it can progress gradually for many years without any symptoms. When symptoms do appear, the most common ones are:
Although osteoporosis has no cure, several types of medications are available to reduce the rate of bone loss, increase bone density, and reduce the number of fractures. In general, they work in two main ways: they lessen bone break down (anti-resorptive agents) or they stimulate the formation of new bone (anabolic agents). Experts recommend that these medications be taken continuously in order to gain their full benefits. Generally, bone loss resumes if the medications are stopped.
Most of the medications used to treat osteoporosis are also used to help prevent it. They include:
Often, calcium alone is not enough to improve bone density. Supplementing with vitamin D has been shown to help maintain bone strength and increase calcium absorption into bones. A daily intake of 400-800 IU of vitamin D for those people found to be deficient is recommended by the osteoporosis guidelines published in 2003.
Learn more about calcium and vitamin D by clicking on the link below.
To learn more about the drugs used to prevent and/or treat osteoporosis, click on the links below.
With the number of individuals who have osteoporosis expected to increase dramatically as members of the large post-World War II generation reach old age, researchers are taking several approaches to prevent and treat this condition.
Although lifestyle and environmental factors play important roles in delaying or preventing osteoporosis, for an estimated 50% to 90% of individuals, bone mineral density is determined primarily by heredity. Therefore, researchers are also trying to approach treatment and prevention of osteoporosis through isolation of the gene or genes responsible for osteoporosis. Currently, genetic research for osteoporosis takes two tracks. First, researchers are working to determine what specific genes may play a key role in determining and maintaining bone density. A second focus is to identify genetic differences in natural body receptors that may contribute to decreased bone density. Current research centers on estrogen receptors alpha (ERS1s) and vitamin D receptors (VDRs), but several other receptor types are also being studied.
Potential new drug therapies for osteoporosis include some medications already approved for other conditions.
New agents are under study among drug classes already being used to prevent or treat osteoporosis. New bisphosphonates that are in development - such as clodronate and minodronate - may need fewer doses, have different dosing schedules, and come in different dosage forms. PTH is also being developed in non-injected forms, such as transdermal patches. SERMs under study for treating osteoporosis include arzoxifene, bazedoxifene, lasofoxifene, and opsemifene. Because many SERMs seem to reduce the chance of getting breast cancer for women using them for osteoporosis, SERMs are also being studied for preventing breast cancer. They may also have cholesterol-lowering effects. Also under study is combination therapy involving treatment with an agent that builds bone (such as PTH) followed by a drug like a bisphosphonate or a SERM that lessens bone loss.
Potential new classes of drugs for preventing and/or treating osteoporosis include both agents that decrease or delay the rate of bone break down (anti-resorptive agents) and those that increase or speed up the rate of bone formation (anabolic agents). Some investigational agents may do both and some may offer additional health benefits, as well. Among some of the drug classes under various stages of investigation are:
Cathepsin K inhibitors - A type of enzyme that breaks down a body protein known as cysteine, cathepsin K is believed to activate osteoclasts. Agents that block the effects of cathepsin K may slow down bone resorption while bone formation continues at a normal rate.
Insulin-like growth factor-1 (IGF-1) - a substance produced in the liver, IGF-1 is stored in bone. Released during bone break down, it encourages the production of osteoblasts to rebuild bone cells. IGF-1 deficiencies have been associated with lower-than-expected bone density and an increased risk of osteoporosis-related fractures.
Integrin receptor inhibitors (also called disintergins) - Investigational drugs in this class (including contortrostatin, echistatin, and SC56631) block the attachment of osteoclasts to bone. Osteoclasts are prevented from beginning the process of bone break down. Integrin receptor inhibitors may also prevent or slow down the production of osteoclasts, thereby decreasing the number of osteoclasts available to break down bone. Of particular interest are integrin alphavbeta3 receptors, which may also be called vitronectin receptors.
Nitrosylated non-steroidal anti-inflammatory drugs (NO-NSAIDs) ? Certain pain-relievers known as NSAIDs (such as flurbiprofen) may be modified to release nitric oxide (NO) in the body. NO, a byproduct of body processes, has many potential effects. In particular, low levels of NO are associated with increased bone break down, but high levels of NO seem to lessen the rate of bone resorption. In theory, increasing amounts of NO in the body could help to prevent and/or treat osteoporosis.
Osteoprotegerin (OPG) - OPG is a cytokine (a protein produced within the immune system to help control immune function). Laboratory animals with low levels of OPG also tend to have faster bone turnover, poor attachment of new bone cells to old cells, and a less stable bone structure. Increasing OPG may help to normalize bone turnover.
Src inhibitors - By limiting the effectiveness of Src tyrosine kinase (STK), an enzyme that triggers osteoclast activity and inhibits osteoblasts, Src inhibitors are thought to lessen bone break down and encourage bone formation.
Strontium ranelate - An oral drug, which has been tested in laboratory studies and at least two large studies of postmenopausal women with osteoporosis, strontium ranelate appears to decrease the rate of bone break down. It also increases the rate of bone formation. Using it may actually restore lost bone density, if bone-building osteoblast activity replaces bone cells faster than osteoclasts break down bone. Strontium ranelate was recently approved for use in Europe, but is not currently approved in the United States.
References
American Association of Clinical Endocrinologists. Osteoporosis Guidelines. Updated 2003. Available at: http://www.aace.com/pub/pdf/guidelines/osteoporosis2001Revised.pdf. Accessed: October 2007 and October 2008.
American Academy of Orthopedic Surgeons. AAOS On-Line Service- Osteoporosis. Available at: http://orthoinfo.aaos.org/brochure/thr_report.cfm?Thread_ID=13&topcategory=Osteoporosis&searentry=osteoporosis. Accessed: October 2007 and October 2008.
Amizuka N, Shimomura J, Li M, et al. Defective bone remodelling; in osteoprotegerin-deficient mice. Journal of Electron Microscopy (Tokyo). 2003;52(6):503-513.
Ammann P. Strontium ranelate: A novel mode of action leading to renewed bone quality. Osteoporosis International. Published online ahead of print. December 2, 2004.
Anderson HC. An antagonist of osteoclast integrins prevents experimental osteoporosis [editorial]. Journal of Clinical Investigation. 1997;99(9):2059.
Ansbacher R, Carson DS, Lourwood DL, et al. Pharmacist's guide to managing menopause. Amherst, NJ: Center for Pharmaceutical Care at Amherst. 1995.
Bezerra FF, Laboissiere FP, King JC, Donangelo CM. Pregnancy and lactation affect markers of calcium and bone metabolism differently in adolescent and adult women with low calcium intakes. Journal of Nutrition. 2002;132(8):2183-2187.
Biermasz NR, Hamdy NA, Pereira AM, Romijn JA, Roelfsema F. Long-term skeletal effects of recombinant human growth hormone (rhGH) alone and rhGH combined with alendronate in GH-deficient adults: a seven-year follow-up study. Clinical Endocrinology (Oxford). 2004;60(5):568-575.
Biskobing DM. Novel therapies for osteoporosis. Expert Opinion on Investigational Drugs. 2003;12(4):611-621.
Boyce BF, Xing L, Shakespeare W, Wang Y, Dalgarno D, Iuliucci J, Sawyer T. Regulation of bone remodeling and emerging breakthrough drugs for osteoporosis and osteolytic bone metastases. Kidney International. 2003;(85 Suppl):S2-S5.
Burgaud JL, Riffaud JP, Del Soldato P. Nitric-oxide releasing molecules: a new class of drugs with several major indications. Current Pharmaceutical Design. 2002;8(3):201-213.
Canalis MD E. Growth hormone, skeletal growth factors and osteoporosis. Endocrine Practice. 1995;1(1):39-43.
Carbone LD, Tylavsky FA, Cauley JA, et al. Association between bone mineral density and the use of nonsteroidal [sic] anti-inflammatory drugs and aspirin: impact of cyclooxygenase selectivity. Journal of Bone and Mineral Research. 2003;18(10):1795-1802.
Celiker R, Arslan S. Comparison of serum insulin-like growth factor-1 and growth hormone levels in osteoporotic and non-osteoporotic postmenopausal women. Rheumatology International. 2000;19(6):205-208.
Colon-Emeric CS, Caminis J, Suh TT, et al; HORIZON Recurrent Fracture Trial. The HORIZON Recurrent Fracture Trial: design of a clinical trial in the prevention of subsequent fractures after low trauma hip fracture repair. Current Medical Research and Opinion. 2004;20(6):903-910.
Cruz AC, Gruber BL. Statins and osteoporosis: can these lipid-lowering drugs also bolster bones? Cleveland Clinic Journal of Medicine. 2002;69(4):277-278, 280-282, and 287-288.
Cushenberry LM, de Bittner MR. Potential use of HMG-CoA reductase inhibitors for osteoporosis. Annals of Pharmacotherapy. 2002;36(4):671-678.
Delmas PD. Clinical effects of strontium ranelate in women with postmenopausal osteoporosis. Osteoporosis International. Published online ahead of print. December 2, 2004.
Devogelaer JP. A review of the effects of tibolone on the skeleton. Expert Opinion on Pharmacotherapy. 2004;5(4):941-949.
Dickman PW, Adolfsson J, Astrom K, Steineck G. Hip fractures in men with prostate cancer treated with orchiectomy. Journal of Urology. 2004;172(6, Part 1 of 2):2208-2212.
Dodds RA. A cytochemical assay for osteoclast cathepsin K activity. Cell Biochemistry and Function. 2003;21(3):231-234.
Doggrell SA. Present and future pharmacotherapy for osteoporosis. Drugs Today (Barcelona). 2003;39(8):633-657.
Doggrell SA. Recent important clinical trials of drugs in osteoporosis. Expert Opinion on Pharmacotherapy. 2004;5(7):1635-1638.
Dresner-Pollak R, Rosenblatt M. Blockade of osteoclast-mediated bone resorption through occupancy of the integrin receptor: a potential approach to the therapy of osteoporosis. Journal of Cellular Biochemistry. 1994;56(3):323-330.
Engleman VW, Nickols GA, Ross FP, et al. A peptidomimetic antagonist of the alpha(v)beta3 integrin inhibits bone resorption in vitro and prevents osteoporosis in vivo. Journal of Clinical Investigation. 1997;99(9):2284-2292.
Ensom MH, Liu PY, Stephenson MD. Effect of pregnancy on bone mineral density in healthy women. Obstetrical and Gynecological Survey. 2002;57(2):99-111.
Evista [package insert]. Indianapolis, IN: Eli Lilly and Company; July, 2002.
Falchetti A. Genetics of osteoarticular disorders, Florence, Italy, 22-23 February 2002. Arthritis Research. 2002;4(5):326-331.
Fleisch H. Bisphosphonates in osteoporosis. European Spine Journal. 2003;12(Suppl 2):S142-S146.
FORTEO [package insert]. Indianapolis, IN: Eli Lilly and Company; September, 2004.
Gambacciani M, Ciaponi M, Cappagli B, Monteleone P, Benussi C, Bevilacqua G, Genazzani AR. A longitudinal evaluation of the effect of two doses of tibolone on bone density and metabolism in early postmenopausal women. Gynecology and Endocrinology. 2004;18(1):9-16.
Gamero P, Sornay-Rendu E, Delmas PD. Low serum IGF-1 and occurrence of osteoporotic fractures in postmenopausal women. Lancet. 2000;355(9207):898-899.
Garrett IR, Gutierrez G, Mundy GR. Statins and bone formation. Current Pharmaceutical Des. 2001;7(8):715-736.
Gennari C. Analgesic effect of calcitonin in osteoporosis. Bone. 2002;30(5 Suppl):67S-70S.
Geusens P, Hochberg MC, van der Voort DJ, et al. Performance of risk indices for identifying low bone density in postmenopausal women. Mayo Clinic Proceedings. 2002;77(7):629-637.
Grey A. Emerging pharmacologic therapies for osteoporosis. Expert Opin Emerg Drugs. 2007;12(3):493-508.
Grigorie D, Neacsu E, Marinescu M, Popa O. Circulating osteoprotegerin and leptin levels in postmenopausal women with and without osteoporosis. Romanian Journal of Internal Medicine. 2003;41(4):409-415.
Haguenauer D, Welch V, Shea B, Tugwell P, Wells G. Fluoride for treating postmenopausal osteoporosis. Cochrane Database Systematic Review. 2000;(4):CD002825.
Helen Hays Hospital and the State of New York. Osteoporosis risk assessment for men. November 2003. Available at: http://www.health.state.ny.us/nysdoh/osteo/men.htm. Accessed October 2007.
Holmes SJ, Shalet SM. Role of growth hormone and sex steroids in achieving and maintaining normal bone mass. Hormone Research. 1996;45(1-2):86-93.
Horton MA. Integrin antagonists as inhibitors of bone resorption: implications for treatment. Proceedings of the Nutrition Society. 2001;60(2):275-281.
International Osteoporosis Foundation. Available at: http://www.osteofound.org/ Accessed: October 2007.
James IE, Lark MW, Zembryki D, et al. Development and characterization of a human in vitro resorption assay: demonstration of utility using novel antiresorptive agents. Journal of Bone and Mineral Research. 1999 Sep;14(9):1562-1569.
Javaid MK, Godfrey KM, Taylor P, Shore SR, Breier B, Arden NK, Cooper C. Umbilical venous IGF-1 concentration, neonatal bone mass, and body composition. Journal of Bone and Mineral Research. 2004;19(1):56-63.
Jehle S, Zanetti A, Muser J, Hulter HN, and Krapf R. Partial neutralization of the acidogenic western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia. J Am Soc Nephrol. Oct 2006.
Kalkwarf HJ, Specker BL. Bone mineral changes during pregnancy and lactation. Endocrine. 2002;17(1):49-53.
Kawahara TN, Krueger DC, Engelke JA, Harke JM, Binkley NC. Short-term vitamin A supplementation does not affect bone turnover in men. Journal of Nutrition. 2002;132(6):1169-1172.
Keeble JE, Moore PK. Pharmacology and potential therapeutic applications of nitric oxide-releasing non-steroidal anti-inflammatory and related nitric oxide-donating drugs. British Journal of Pharmacology. 2002;137(3):295-310.
Kelley GA et al. Efficacy of resistance exercise on lumbar spine and femoral neck bone mineral density in premenopausal women: a meta-analysis of individual patient data. Journal of Women?s Health. 2004. 13:293-300.
Khan AN, Macdonald S. Osteoporosis, involutional. E-Medicine. Last Updated October 4, 2004. Available at: http://www.emedicine.com/radio/topic503.htm. Accessed October 2007 and October 2008.
Klein BY, Tepper SH, Gal I, Shlomai Z, Ben-Bassat H. Opposing effects of tyrosine kinase inhibitors on mineralization of normal and tumor bone cells. Journal of Cellular Biochemistry. 1997;65(3):420-429.
Kloosterboer HJ. Tissue-selectivity: the mechanism of action of tibolone. Maturitas. 2004;489Suppl 10:S30-S40.
Kurabayashi T, Matsushita H, Kato N, et al. Effect of vitamin D receptor and estrogen receptor gene polymorphism on the relationship between dietary calcium and bone mineral density in Japanese women. Journal of Bone and Mineral Metabolism. 2004;22(2):139-147.
Lark MW, Stroup GB, Hwang SM, et al. Design and characterization of orally active Arg-Gly-Asp peptidomimetic vitronectin receptor antagonist SB 265123 for prevention of bone loss in osteoporosis. Journal of Pharmacology and Experimental Therapeutics. 1999;291(2):612-617.
LeBoff MS et al. Occult vitamin D deficiency in postmenopausal US women with acute hip fracture. JAMA 1999; 281:1505-1511.
Lim LS, Harnack LJ, Lazovich D, Folsom AR. Vitamin A intake and the risk of hip fracture in postmenopausal women: the Iowa Women's Health Study. Osteoporosis International. 2004;15(7):552-559.
Liu YZ, Liu YJ, Recker RR, Deng HW. Molecular studies of identification of genes for osteoporosis: the 2002 update. Journal of Endocrinology. 2003;177(2):147-196.
Long JR, Zhang YY, Liu PY, et al. Association of estrogen receptor alpha and vitamin D receptor gene polymorphisms with bone mineral density in Chinese males. Calcified Tissue International. 2004;74(3):270-276.
Lourwood DL. Hormone replacement therapy. In Carter B, Angaran D, Sisca T (eds.) Pharmacotherapy self-assessment program: Module 5. Nephrology, endocrinology, and immunology. Kansas City: American College of Clinical Pharmacy 1993:189-202, 216-19 (Book A), and 41-46 (Book B).
Marie PJ. Strontium ranelate: a novel mode of action optimizing bone formation and resorption. Osteoporosis International. Published online ahead of print. December 2, 2004.
Medscape Medical News. Osteoporosis Guidelines Updated. Available at URL: http://www.medscape.com/viewarticle/533846. Accessed: October 2007 and October 2008.
Mehta NM, Malootian A, Gilligan JP. Calcitonin for osteoporosis and bone pain. Current Pharmaceutical Design. 2003;9(32):2659-2676.
Mercer B, Markland F, Minkin C. Contortrostatin, a homodimeric snake venom disintegrin, is a potent inhibitor of osteoclast attachment. Journal of Bone and Mineral Research. 1998;13(3):409-414.
Metcalf CA 3rd, van Schravendijk MR, Dalgarno DC, Sawyer TK. Targeting protein kinases for bone disease: discovery and development of Src inhibitors. Current Pharmaceutical Design. 2002;8(23):2049-2075.
Meunier PJ, Roux C, Seeman E, et al. The effects of strontium ranelate on the risk of vertebral fracture in women with postmenopausal osteoporosis. New England Journal of Medicine. 2004;350(5):459-468.
Michaelssan K, Lithell H. Serum retinol levels and the risk of fracture. New England Journal of Medicine. 2003; 4(348):287-294.
Miller WH, Keenan RM, Willette RN, Lark MW. Identification and in vivo efficacy of small-molecule antagonists of integrin alphavbeta3 (the vitronectin receptor). Drug Discovery Today. 2000;5(9):397-408.
Miyauchi A, Notoya K, Taketomi S, et al. Novel ipriflavone receptors coupled to calcium influx regulate osteoclast differentiation and function. Endocrinology. 1996;137(8):3544-3550.
Mousa SA. Anti-integrin as novel drug-discovery targets: potential therapeutic and diagnostic implications. Current Opinion in Chemistry and Biology. 2002;6(4):534-541.
National Institutes of Health. Osteoporosis and Related Bone Diseases. Osteoporosis overview. Revised November 2006. Available at http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/default.asp. Accessed: October 2007 and October 2008.
National Osteoporosis Foundation home page. Available at:http://www.nof.org/. Accessed: October 2007 and October 2008.
National Osteoporosis Foundation. America's bone health: the state of osteoporosis and low bone mass. No date given. Highlights available at: http://www.nof.org/advocacy/prevalence/. Accessed November 16, 2004.
National Osteoporosis Foundation. Medications to prevent and treat osteoporosis. No date given. Available at: http://www.nof.org/patientinfo/medications.htm. Accessed October 2007.
NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. Osteoporosis prevention, diagnosis, and therapy. Journal of the American Medical Association. 2001;285:785-795.
Office of the Surgeon General. Bone health and osteoporosis: a report of the Surgeon General. Rockville, Md.: Department of Health and Human Services, 2004.
Osteoporosis and Related Bone Diseases National Resource Center. National Institute of Arthritis and Musculoskeletal and Skin Diseases. National Institutes of Health. What is bone? Revised August 2005. Available at: http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/default.asp. Accessed: October 2005 and October 2008.
Oursler MJ, Spelsberg TC. Echistatin, a potential new drug for osteoporosis. Endocrinology. 1993;132(3):939-940.
Prelevic GM, Markou A, Arnold A, Bartram C, Puzigaca Z, Ginsburg J. The effect of tibolone on bone mineral density in postmenopausal women with osteopenia or osteoporosis--8 years follow-up. Maturitas. 2004;47(3):229-234.
Promislow JH, Hertz-Picciotto I, Schramm M, Watt-Morse M, Anderson JJ. Bed rest and other determinants of bone loss during pregnancy. American Journal of Obstetrics and Gynecology. 2004;191(4):1077-1083.
Ralston SH. Genetic control of susceptibility to osteoporosis. Journal of Clinical Endocrinology and Metabolism. 2002;87(6):2460-2466.Recker RR, Deng HW. Role of genetics in osteoporosis. Endocrine. 2002;17(1):55-66.
Reginster JY, Lecart MP, Deroisy R, Lousberg C. Strontium ranelate: a new paradigm in the treatment of osteoporosis. Expert Opinion on Investigational Drugs. 2004;13(7):857-864.
Riera-Espinoza G, Ramos J, Carvajal R, et al. Changes in bone turnover during tibolone treatment. Maturitas. 2004;47(2):83-90.
Ringa V. Alternatives to hormone replacement therapy for menopause: an epidemiological evaluation. [Article in French] Journal of Gynecology, Obstetrics and Biological Reproduction (Paris). 2004;33(3):195-209.
Rodan GA, Reszka AA. Bisphosphonate mechanism of action. Current Molecular Medicine. 2002;2(6):571-577.
Rosen CJ, Bilezikian JP. Clinical review 123: Anabolic therapy for osteoporosis. Journal of Clinical Endocrinology and Metabolism. 2001;86(3):957-964.
Rosen Clifford J M.D. Postmenopausal Osteoprosis. The New England Journal of Medicine. August 11, 2005. 323(6):595-603.
Rubin MR, Bilezikian JP. New anabolic therapies in osteoporosis. Endocrinology and Metabolism Clinics of North America. 2003;32(1):285-307.
Rymer J, Robinson J, Fogelman I. Ten years of treatment with tibolone 2.5 mg daily: effects on bone loss in postmenopausal women. Climacteric. 2002;5(4):390-398.
Schlienger RG, Meier CR. HMG-CoA reductase inhibitors in osteoporosis: do they reduce the risk of fracture? Drugs and Aging. 2003;20(5):321-336.
Schweiger U, Deuschle M, Korner A, et al. Low lumbar bone mineral density in patients with major depression. American Journal of Psychiatry. 1994;151(11):1691-1693.
Setchell KD, Lydeking-Olsen E. Dietary phytoestrogens and their effect on bone: evidence from in vitro and in vivo, human observational, and dietary intervention studies. American Journal of Clinical Nutrition. 2003;78(3 Suppl):593S-609S.
Shakespeare WC, Metcalf CA 3rd, Wang Y, et al. Novel bone-targeted Src tyrosine kinase inhibitor drug discovery. Current Opinion in Drug Discovery and Development. 2003;6(5):729-741.
Solomon DH, Finkelstein JS, Wang PS, Avorn J. Statin lipid-lowering drugs and bone mineral density. Pharmacoepidemiology and Drug Safety. 2004 Jul 20.
Susva M, Missbach M, Green J. Src inhibitors: drugs for the treatment of osteoporosis, cancer or both? Trends in Pharmacological Sciences. 2000;21(12):489-495.
Suzuki A, Sekiguchi S, Asano S, et al. Pharmacological topics of bone metabolism: recent advances in pharmacological management of osteoporosis. J Pharmacol Sci. 2008; 106:530-535.
Swegle JM, Kelly MW. Tibolone: a unique version of hormone replacement therapy. Annals of Pharmacotherapy. 2004;38(5):874-881.
Tang QO, Tran GT, Gamie Z, et al. Statins: under investigation for increasing bone mineral density and augmenting fracture healing. Expert Opin Investig Drugs. 2008;17(10):1435-63.
Tas N, Aricioglu A, Erbas D, Ozcan S. The effect of calcitonin treatment on plasma nitric oxide levels in post-menopausal osteoporotic patients. Cell Biochemistry and Function. 2002;20(2):103-105.
Tiegs RD, Body JJ, Wahner HW, Barta J, Riggs BL, Heath H 3rd. Calcitonin secretion in postmenopausal osteoporosis. New England Journal of Medicine. 1985;312(17):1097-1100.
U.S. Department of Agriculture. Agricultural Research Service. USDA Database for Standard Reference. Release 17. Calcium, Ca (mg) content of selected common foods, sorted by nutrient content. 2004. Available at: http://www.nal.usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17w301.pdf Accessed October 2007 and October 2008.
U.S. Food and Drug Administration. FDA Talk Paper. FDA approves teriparatide to treat osteoporosis. November 6, 2002. Available at: http://www.fda.gov/bbs/topics/ANSWERS/2002/ANS01176.html. Accessed: October 2007 and October 2008.
Ueland T. Bone metabolism in relation to alterations in systemic growth hormone. Growth Hormone and IGF Research. 2004;14(6):404-417.
van't Hof RJ, Ralston SH. Nitric oxide and bone. Immunology. 2001;103(3):255-261.
Violette SM, Shakespeare WC, Bartlett C, et al. A Src SH2 selective binding compound inhibits osteoclast-mediated resorption. Chemistry and Biology. 2000;7(3):225-235.
WHO Study Group. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. WHO Technical Report Series 843. Geneva, Switzerland: World Health Organization; 1994.
Osteoporosis Health Condition Last Updated: October 2008
Note: The above information is intended to supplement, not substitute for, the expertise and judgment of your physician, pharmacist, or other healthcare professional. It is not intended to diagnose a health condition, but it can be used as a guide to help you decide if you should seek professional treatment or to help you learn more about your condition once it has been diagnosed.
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