jsafoms 10.5005/jp-journals-10032-1065
Urvashi Verma et al
Review article
Menopausal Osteoporosis 1
Urvashi Verma, 2Ruchika Garg, 3Rekha Rani
ABSTRACT Every woman faces menopause and many dread its approach fearing the onset of uncomfortable physical side effects and loss of their youth. With the increasing longevity (life expec tancy), more women are liable to live more years with meno pause. Menopausal women spend one-third of their life after menopause amounting to almost 30 years. The menopause should be the time for new learning, development, more free dom and to look forward with more confidence. Its management should start before its arrival with the practice of healthy habits and minor modifications in life style. Keywords: Bone mineral density, Menopause, Osteoporosis, T-score. How to cite this article: Verma U, Garg R, Rani R. Meno pausal Osteoporosis. J South Asian Feder Menopause Soc 2015;3(1):24-26. Source of support: Nil Conflict of interest: None Date of submission: 10 Jan 2015 Date of acceptance: 28 Mar 2015 Date of publication: June 2015
Introduction Menopause is defined as a time of cessation of ovarian function resulting in permanent amenorrhea. It is a retrospective diagnosis. Word menopause is derived from Greek word ‘menos’ meaning mensuration and pause means stop, i.e. cessation of period. Menopause occurs when spontaneous mensuration ceases for 6 months to 1 year at approximate age of 45 years or above. About 60 million women in India are above 55 years. Due to increase in life expectancy, women spend one-third of their life in the postmenopausal age. Many hormonal, metabolic and anatomical changes take place during this time. Management of menopause should be such that a woman can say ‘For me no pause.’
Epidemiology Menopausal osteoporosis is a major global public health problem. More than 20 million individuals are 1-3
Assistant Professor
1-3 Department of Obstetrics and Gynecology, SN Medical College, Agra, Uttar Pradesh, India
Corresponding Author: Ruchika Garg, Assistant Professor Department of Obstetrics and Gynecology, SN Medical College Agra, Uttar Pradesh, India, Phone: 09720004485, e-mail: ruchika
[email protected]
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suffering from osteoporosis in the USA. Postmenopausal osteoporosis (PMO) is a chronic, progressive disease characterized by low bone mass, microarchitectural bone deterioration, and decreased bone strength that lead to increased bone fragility and a consequent increase in fracture risk.1 It is a silent disease in most cases, with no symptoms until fractures occur.2 One in three women will sustain a vertebral fracture after age 65 years. One of three women will sustain hip fracture (5–30% mortality rate). Trabecular bones are affected earlier than cortical bone. Common sites of fractures are vertebrae, distal radius and femoral neck. Half of all postmenopausal women will have an osteoporosis-related fracture during their lives, including one-quarter with vertebral deformity and 15% with a hip fracutre.3 Research suggests that about half of all women over the age of 60 will experience at least one fracture due to osteoporosis.4 Studies have also shown that Caucasian and Asian women are more likely to develop osteoporosis.5 The World Health Organization (WHO) has identified osteoporosis as a major public health concern due to its high prevalence and the serious consequence of osteoporotic fractures.2
Risk Factors for Osteoporosis • • • •
Elderly age Diet—decrease in dairy products Smoking Age, race, small body frame, early menopause, multi parity, prolonged period of lactation with inadequate calcium, family history of osteoporosis • Lifestyle—smoking, excessive alcohol use, sedentary lifestyle • Associated medical conditions—hyperthyroidism, hyperparathyroidism, chronic renal disease • Drugs—systemic corticosteroids, heparin and anti convulsants.
Pathophysiology of Menopausal Osteoporosis The skeleton consists of two types of bones: Cortical bone constitutes 80% of the total bone, while 20% is cancellous (spongy or trabecular) bone. The trabecular bone consists of active osteoblasts, inactive osteoblasts and osteoclasts. Cortical bone is in the shafts of long bones and outer layers of virtually all bones. Cancellous bone is in the bones of axial skeleton and in the ends of long bone.
jsafoms Menopausal Osteoporosis
Skeleton mass gradually increases during growth and is at its maximum between 18 and 35 years of age. It is known as peak adult bone mass which is 25 to 30% higher in males. Bone remodeling occurs throughout life. It consists of regeneration, degradation and repair, allowing damaged bones to be replaced by new bone. Bone consists of a large collagenous matrix which is impregnated with mineral salts and populated by cells. The matrix is composed of type I collagen lying in a mucopolysaccharide ground substance there also small amount of noncollagenous protein mainly in the form of proteoglycans and the bone-specific proteins osteocalcin and gamma carboxyglutamic acid (GLA) protein, whose function is unknown. Gamma carboxyglutamic acid protein is produced only osteoblasts and its concentration in the blood is to some extent a measure of osteoblastic activity. The unmineralized matrix is known as osteoid. Bone mineral, which occupies almost half the bone volume, consists mainly of calcium and phosphorus in the form of crystalline hydroxyapatite. In mature bone, the proportion of calcium and phosphorus is constant and the molecule is firmly bound to collagen. Bone cells are of four kinds as follows: 1. Osteoblasts 2. Osteocytes 3. Osteoclasts 4. Lining cells Peak adult bone mass is reached at about the age of 30 to 35 years for cortical bone and earlier for trabecular bone. Rate of bone formation and resorption is relatively low and approximately equal. Beyond the age of 40 years, resorption begins to exceed formation by 0.3 to 0.5% per year in both sexes. In women around menopause, accelerated loss of cortical bone is superimposed on the age-related loss. Up to 5% of trabecular bone loss per year and 1 to 1.5% of cortical bone mass loss occur after menopause. Bone loss that occurs in the first 15 years after menopause is attributable to estrogen deficiency rather than aging. After that, it continues age-related loss and menopause-related bone loss, results in 40 to 50% reduction in trabecular bones (spine, distal radius) and 30% reduction in cortical bone.
Relation between Osteoporosis and Menopause/ Pathogenesis of Osteoporosis Exact mechanism of menopausal osteoporosis has not been completely defined. Protein and micronutrient deficiency are thought to contribute to this disease. Calcium absorption decreases with age. High salt in Indian diet is likely to increase urinary calcium excretion. Increase absorption of calcium probably secondary to estrogeninduced enhancement of the ability of 1, 25 (OH) 2D.
There is a direct relationship between the lack of estrogen after menopause and the development of osteoporosis. After menopause, bone resorption outpaces the building of new bone. Early menopause and any prolonged periods in which hormone levels are low and menstrual periods are absent or infrequent can cause loss of bone mass.5 Menopause increases a woman’s risk of developing osteoporosis. It is estimated that 10% of bone mass is lost in the first 5 years after menopause.3
Clinical Manifestations The most common clinical manifestations of PMO are backaches, fractures of the hip, vertebrae of wrist. Osteoporosis-related fractures are responsible for excess mortality, morbidity, chronic pain, reduction in quality of life, admission to long-term care, and health and social care costs.6
Diagnosis Following investigations are helpful in making diagnosis: • Radiology single photon absorptiometry • Dual proton absorptiometry • Dual energy X-ray absorptiometry (DEXA) provides good precision for all sides of osteoporosis it measures three sides—the radius, the hip and the spine. This is gold standard for measuring bone mineral density. • Quantitative computed tomography (CT) • Bone densitometry by ultrasound Bone mineral density (BMD) is essential for the diagnosis. WHO T-score is measured in three sides, lumbo sacral, hip and wrist joint. T-score is the number of stan dard deviations from mean for a young healthy woman. Fracture risk assessment tool developed by WHO Task Force in 2008 to evaluate the 10 year probability of bone fracture risk. Normal T-score within one SD (1 or –1), osteopenia T-score between 1 and 2.5 SD (–1 or 2.5 SD). It signifies an increase fracture risk but does not meet the criteria for osteoporosis. Osteoporosis T-score below 2.5. So, it has higher frac ture risk than osteopenia. US preventive services task force (USPSTF) recom mendation for osteoporosis screening advice the scree ning for women 65 years or older and also in women with the risk of osteoporosis similar to that of a 65-year-old or women to be screened with one or more risk factors inclu ding advance age, low body weights, alcohol or tobacco intake, a parent with osteoporosis fractures. Evaluation of BMD by DEXA is recommended for all women above 65 years and for younger postmenopausal women with one or more risk factors.
Journal of South Asian Federation of Menopause Societies, January-June 2015;3(1):24-26
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Urvashi Verma et al
PREVENTION AND TREATMENTS FOR OSTEOPOROSIS Prevention • Patient education is indicated in all ages. • Emphasis should be on prophylaxis rather than treatment. – Preventions start from childhood. – Good bone mass should be ensured right from the age of puberty. – Dietary intake of milk with vitamin D supplementation (200 ml of milk gives 420 gm calcium). Avoid aerated drinks. Cessation of smoking and decreasing alcohol intake should be promoted long before the menopause. – Physical activity and weight-bearing exercises should be encouraged. – Avoidance of certain drugs, e.g. long courses of corticosteroids, etc. will help. – Prevention of fall in old age is very important to reduce morbidity and mortality. Chain slippery floors at home install adequate lightening. Sides’ supports in bathrooms will help to prevent falls.
Treatments Indications for pharmacological therapy of osteoporosis are as follows: • Women with fragility fracture or T-score 2.5 or below • Borderline BMD with risk factors • For established osteoporosis, calcitonin and alendro nate are approved and recommended • Fractures must be managed by orthopedic surgeons: – Drugs – Calcium – Bisphosphonates – Selective estrogen receptor modulators (SERMs) – Calcitonin – Parathyroid hormone – Teriparatide – Strontium ranelate – Estrogen therapy – Fluorides – Calcitriol
Management of Postmenopausal Osteoporosis Management of PMO involves pharmacological and nonpharmacological approaches.
Pharmacological Approaches Most of the pharmacological agents are associated with an increase risk of adverse health outcomes in the long-term. Hence, their usage is left to the physician and patient discretion.2 Some of the approaches are as follows:
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• Selective estrogen receptor modulators (SERMs) are, in general, well-tolerated but with transient occur rence of hot flashes and leg cramps in certain patients. Consequently, they are not recommended to symptomatic postmenopausal women. Other new SERMs have been developed in recent years, but some were discontinued because of unacceptable efficacy, safety and/or tolerability profile. • Hormone replacement therapy is associated with an increased risk of adverse health outcome (stroke and venous thromboembolic events) in the long-term therapy. Women receiving estrogen and progestrogen showed a small but significant increase in breast cancer in the women’s health initiative study. • Bisphosphonates—causes of gastroesophageal intole rance, femoral shaft fractures, and atrial fibrillation have been reported in patients receiving long-term bisphosphonates. Osteonecrosis of the jaw has been reported primarily in patients with cancer who have received large and cumulative doses of intravenous bisphosphonates.2
Nonpharmacological Approaches Peak bone mass, determined by genetic influence and modif iable aspects in lifestyle and health status, is achieved during the third decade of life. Factors, such as nutrition, hormonal status, physical exercise, medical conditions, drug abuse, alcohol or tobacco, can interfere with the peak of bone mass. Patients should be encou raged to stop smoking and reduce excessive alcohol and caffeine intake.2 For prevention, strategies should be discussed with the patients and some medical conditions, such as dizziness, postural hypotension, poor vision and inadequate footwear, need to be addressed.2 Several studies demonstrate that physical exercise programs, including impact exercises, specific strength training, balance and coordination training, may maintain or increase spine and hip bone mineral density as well as decrease the frequency of falls among osteoporotic and osteopenia patients.
References 1. Karen FM, Bart LC. Diagnosis, screening, prevention and treatment of osteoporosis. Mayo Clin Proc 2006;81(5):662-672. 2. Maeda SS, Lazaretti-Castro M. An overview on the treatment of postmenopausal osteoporosis. Arg Bras Endocrinol Meta 2014;58(2):161-171. 3. USPSTE. Available at: http://ww.wuspreventiveservicestask force.org. Accessed on: May 26, 2014. 4. Better Health Channel. Available at: http://www.betterhealth. vic.gov.au/. Accessed on: May 26, 2014. 5. Cleveland Clinic. Available at: http://myclevlandclinic.org. Accessed on: May 26, 2014. 6. Wiley Online Library. Available at: http://onlinelibrary.wiley. com. Accessed on: May 26, 2014.
