This document summarizes osteoporosis, including its definition, prevalence, risk factors, pathogenesis, diagnosis, and treatment options. It discusses how osteoporosis is a widespread condition characterized by compromised bone strength and increased fracture risk. Diagnostic tools like DXA scans and emerging methods like multi-detector CT are used to assess bone mineral density and structure. Treatment involves lifestyle changes as well as pharmacotherapy like bisphosphonates, calcitonin, PTH, and emerging drugs. Overall the document provides a comprehensive overview of osteoporosis from causes and diagnosis to current and novel treatment approaches.
Way forward in osteoporosis: emerging diagnostic and therapeutic measures
1. Way forward in osteoporosis: a disease which is no longer silent
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4. Fractures in Women Are Common: Incidence of Chronic Diseases 1. Riggs BL, Melton LJ III. Bone. 1995;17(suppl):505S–511S. 2. American Stroke Association. Heart disease and stroke statistics––2005 update. Available at: http://www.americanheart.org. Accessed August 24, 2005. 3. American Cancer Society. Cancer facts & figures; 2005. Available at: http://www.cancer.org. Accessed August 24, 2005. 1,500,000 345,000 373,000 211,240 250,000 0 0.5 1.0 1.5 2.0 Fracture 1 Heart attack 2 Stroke 2 Breast cancer 3 Annual Incidence, million Risk of osteoporotic fracture in 1 year is greater than combined risk of heart attack, stroke, and breast cancer. Hip fracture 1 Women with osteoporosis All women
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7. Pathogenesis of Osteoporosis-Related Fractures Reference: Cooper C, Melton LJ. Epidemiology of osteoporosis. Trends Endocrinol Metab. 1992;3(6):224-229.
19. Pyramid for Osteoporosis Prevention and Treatment Leading the Effort to Help Prevent and Treat Osteoporosis US Department of Health and Human Services. Bone Health and Osteoporosis: A Report of the Surgeon General . US Department of Health and Human Services, Office of the Surgeon General; 2004. Pharmacotherapy (antiresorptives and anabolics) Address Secondary Factors (drugs and diseases) Lifestyle Changes (nutrition, physical activity, and fall prevention)
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27. Osteoporosis Current pharmacotherapy options Source: Alexander I, Andrist L. Menopause. In: F Likis, K. Shuiling, eds. Women’s Gynecologic Health. Sudbury, MA: Jones and Bartlett, 2005:249-289.
28. Source: Alexander I, Andrist L. Menopause. In: F Likis, K. Shuiling, eds. Women’s Gynecologic Health. Sudbury, MA: Jones and Bartlett, 2005:249-289. Osteoporosis Current pharmacotherapy options (Continued…)
29. Source: Alexander I, Andrist L. Menopause. In: F Likis, K. Shuiling, eds. Women’s Gynecologic Health. Sudbury, MA: Jones and Bartlett, 2005:249-289. Osteoporosis Current pharmacotherapy options (Continued…)
30. FDA Indications for Osteoporosis Ann Babbitt. Osteoporosis Update 2010 Drug PMO GIO (Women, Men) Men Prevention Treatment Prevention Treatment Estrogen Alendronate PO Risedronate PO Ibandronate PO Ibandronate IV Zoledronate IV Calcitonin IN Raloxifene PO Teriparatide SC
Fractures in Women Are Common: Incidence of Chronic Diseases This slide demonstrates that the incidence of new cases of osteoporotic fracture in women each year is far greater than the incidence of heart attack, stroke, and breast cancer combined. 1 – 3 Hip fracture incidence alone exceeds that of breast cancer. 1 This information, with the information on the previous slide, further emphasizes that osteoporosis should be considered a major health concern among postmenopausal women in the United States. The point is not to suggest that osteoporosis is more important than the other diseases but that it should be managed as routinely as are the other diseases. References: 1. Riggs BL, Melton LJ III. The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone . 1995;17(suppl):505S – 511S. 2. American Stroke Association. Heart disease and stroke statistics––2005 update. Available at: http://www.americanheart.org/downloadable/heart/1105390918119HDSStats2005Update.pdf. Accessed August 24, 2005. 3. American Cancer Society. Cancer facts & figures: 2005. Available at: http://www.cancer.org/downloads/STT/CAFF2005f4PWSecured.pdf. Accessed August 24, 2005.
Am J Clin Nutr. 2010 Jul;92(1):101-5. Epub 2010 May 19. Phosphate and carbonate salts of calcium support robust bone building in osteoporosis. Heaney RP , Recker RR , Watson P , Lappe JM . Osteoporosis Research Center, Creighton University, Omaha, NE, USA. rheaney@creighton.edu Abstract BACKGROUND: Calcium is an essential cotherapy in osteoporosis treatment. The relative effectiveness of various calcium salts for this purpose is uncertain. Many older women with osteoporosis have phosphorus intakes of <70% of the Recommended Dietary Allowance. OBJECTIVE: Our objective was to test the hypothesis that calcium phosphate would better support anabolic bone building than would calcium carbonate. DESIGN: This study was a 12-mo, randomized, positive-comparator, 2-arm, single-blind clinical trial in 211 patients treated with teriparatide who consumed <1000 mg phosphorus/d. Participants were randomly assigned to receive, in addition to teriparatide and 1000 IU cholecalciferol, 1800 mg calcium/d as either tricalcium phosphate or calcium carbonate. The primary endpoints were changes in lumbar spine and total hip bone mineral densities (BMDs); secondary endpoints were changes in bone resorption biomarkers and serum and urine calcium and phosphorus concentrations. RESULTS: In the combined group, the lumbar spine BMD increased by 7.2%, and total hip BMD increased by 2.1% (P < 0.01 for both). However, there was no significant difference between calcium-treatment groups, and there were no significant between-group differences in serum calcium and phosphorus concentrations or in urine calcium concentrations. Bone resorption biomarkers increased in both groups, as expected with teriparatide, but the increases in the 2 calcium groups did not differ significantly. CONCLUSIONS: Tricalcium phosphate and calcium carbonate appear to be approximately equally effective in supporting bone building with a potent anabolic agent; phosphate salt may be preferable in patients with restricted phosphorus intakes. This trial was registered at clinicaltrials.gov as NCT00074711.
Abstract Zinc is known as an essential nutritional factor in the growth of the human and animals. Bone growth retardation is a common finding in various conditions associated with dietary zinc deficiency. Bone zinc content has been shown to decrease in aging, skeletal unloading, and postmenopausal conditions, suggesting its role in bone disorder. Zinc has been demonstrated to have a stimulatory effect on osteoblastic bone formation and mineralization; the metal directly activates aminoacyl-tRNA synthetase, a rate-limiting enzyme at translational process of protein synthesis, in the cells, and it stimulates cellular protein synthesis. Zinc has been shown to stimulate gene expression of the transcription factors runt-related transcription factor 2 (Runx2) that is related to differentiation into osteoblastic cells. Moreover, zinc has been shown to inhibit osteoclastic bone resorption due to inhibiting osteoclast-like cell formation from bone marrow cells and stimulating apoptotic cell death of mature osteoclasts. Zinc has a suppressive effect on the receptor activator of nuclear factor (NF)-κB ligand (RANKL)-induced osteoclastogenesis. Zinc transporter has been shown to express in osteoblastic and osteoclastic cells. Zinc protein is involved in transcription. The intake of dietary zinc causes an increase in bone mass. β-Alanyl-L-histidinato zinc (AHZ) is a zinc compound, in which zinc is chelated to β-alanyl-L-histidine. The stimulatory effect of AHZ on bone formation is more intensive than that of zinc sulfate. Zinc acexamate has also been shown to have a potent-anabolic effect on bone. The oral administration of AHZ or zinc acexamate has the restorative effect on bone loss under various pathophysiologic conditions including aging, skeletal unloading, aluminum bone toxicity, calcium- and vitamin D-deficiency, adjuvant arthritis, estrogen deficiency, diabetes, and fracture healing. Zinc compounds may be designed as new supplementation factor in the prevention and therapy of osteoporosis.
Adherence - Osteoporosis The 2 primary types of pharmacotherapy for osteoporosis are antiresorptive agents that reduce bone loss and anabolic agents that build bone Antiresorptive agents work by reducing bone loss and include Bisphosphonates estrogen (hormone replacement therapy, or HRT) Selective estrogen receptor modulators (SERMs) Calcitonin Anabolic agents work by building bone and include synthetic parathyroid hormone US Department of Health and Human Services. Bone Health and Osteoporosis: A Report of the Surgeon General. Rockville, MD: US Department of Health and Human Services, Office of the Surgeon General; 2004.