Menopausal osteoporosis

International Journal of Gynecology & Obstetrics 46 (1994) 203-207

Menopausal osteoporosis G. Tang*, H.K. Ma Department of Obstetrics and Gynaecology, The University of Hong Kong Queen Mary Hospital, Hong Kong, Hong Kong

Received28 March 1994;revisionreceived 7 April 1994; accepted 7 April 1994

Keywords: Menopause; Osteoporosis; Diet; Calcium; Exercise; Hormone

Introduction

Pathogenesis of osteoporosis

Postmenopausal osteoporosis is a complex condition caused by a number of factors. Fractures frequently occur in the metabolically normal but fragile bones of menopausal osteoporotic women [l]. The fragility of the bone is related to reduced bone mass, impaired repair of the microdamage caused by normal wear and tear of bone, and falls. Fragile bone may fracture at various sites of the body such as the vertebrae, the hips and the wrists. Bone loss from midlife onwards is inevitable, but the rate of loss is slow before the menopause. Such bone loss is also different in the cortical (appendicular bone) and the trabecular bone (axial bone) components. It has been estimated that bone loss starts about 10 years before the menopause at a rate of approximately 0.3-0.5% per year and 1.2% per year for the cortical and the trabecular bones, respectively. This rate of loss accelerates on an average to 2-3% or more per year after the menopause and lasts for 8- 10 years [2].

Bone is a living tissue, constantly being lost and replaced with healthier new bone. Renewal of bone, and hence its strength, is governed by the bone-remodeling cycle [3]. The bone-remodeling cycle involves the bone resorption cells, the osteoclasts, and the bone formation cells, the osteoblasts. Hormones, such as calcitonin and parathyroid hormone and mechanical stresses influence the adjustment of the bone. It has been said that the activation phase of the boneremodeling cycle takes place every 10 s. During the process of bone resorption, the osteoclasts secrete an acid-like substance which dissolves and digests the organic matrix and mineral of the ‘old’ bone. When the resorption cavity reaches a certain pre-set depth, the process ceases. The osteoblasts are specialized cells capable of forming new bone by synthesizing bone matrix, a collagen-rich ground substance essential for the adherence of hydroxyapatite and other crystals. This is bone formation. The resorption and formation phases are coupled and bone mass can therefore be maintained.

* Corresponding author.

0020-7292/94/$07.00 0 1994 International Federation of Gynecology and Obstetrics SD1 0020-7292(94)02118-I

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J. Gynecol. Obstet. 46 (1994) 203-207

It has been observed that bone loss is greatly accelerated after the menopause because of high bone turnover and enhanced osteoclast activity [3]. The interaction between estrogen and bone resorption and formation has been studied [4]. Estrogen administration has been found to increase calcitonin which has a direct inhibiting effect on osteoclast activity, thus reducing bone resorption [5]. Decreased estrogen level may also lead to an increase in skeletal sensitivity to parathyroid hormone resulting in an increase in bone resorption [6]. The most recent data has elucidated that it is possible that action of estrogen on bone is mediated by the cytokines [7]. Cytokines are locally acting chemical messengers. Bone resorption by the osteoclasts is activated by a specific set of cytokines produced by the osteoblasts. These osteoblasts possess estrogen receptors. Estrogen inhibits osteoblastic secretion of cytokines directly, thereby inhibiting osteoclast formation and so inhibiting bone loss. Monocytes in the peripheral blood are also capable of regulating osteoblastic secretion of cytokines and this action can also be inhibited by estrogen. Clinically, castrated women on hormone replacement therapy have been shown to have a decreased cytokine production with concommittant reduction in bone loss. Some of the mechanisms of estrogen in preventing osteoporosis are now known. Menopausal osteoporosis is a health issue Bone loss from midlife onwards (35-40 years) is inevitable resulting in an age-related reduction of about 0.5% per year in both sexes. However, women in their first 5-10 years after the menopause have an accelerated rate of bone loss of l-8% in the spinal vertebrae and 0.5-5% in the femoral head of the femur. This rapid bone loss is related to the postmenopausal abrupt decrease in estrogen which has been shown to have antiresorption action on bone. As a result of such bone loss, it has been estimated that women could lose up to 50% of their bone mass by the age of 70, whereas men only lose 20% of their bone mass by the age of 90 [8]. Thus, osteoporosis can be considered as a condition specific to the menopause.

Bone loss or osteoporosis, is without symptoms until fractures occur. The three common sites of menopausal osteoporotic fractures are distal radius, vertebral body and femoral neck. Together, 40% of these fractions occur in women over the age of 65. Of the three fractures, hip fracture (femoral neck) is the most serious. Twentyseven percent of women with hip fractures will die within a year and 20% of women will be permanently disabled and will be dependent on others for their daily care [9]. The long-term care for nonfatal hip fracture is expensive and it has been estimated that some 3.8 billion US dollars are spent on treatment and care for these osteoporotic females every year and the expenditure increases rapidly and proportionally with age [lo]. According to ‘The World Aging Situation 1991’, the aging of populations is a global phenomenon. In 1950, 8% of the population was aged 60 and older. By 2025, the percentage is projected to be 14%, i.e. 1.2 billion people. A majority of them, 72% of the total, will be living in developing countries. It is also well known that women are much more likely to survive to an older age than men, with a ratio of about 100:89. The majority of the menopausal women are living in the developing regions of the world where health care emphasis is largely on safe motherhood and on the reduction of perinatal mortality. It is unlikely that attention will be focused on menopausal osteoporosis which is symptomless until fractures occur. As a matter of fact, menopausal symptoms such as hot flushes and night sweats are also found to be present less frequently in Asian women than in the Caucasians [I l] and by 2025 58% of the elderly population in the world will be Asians. From the above figures, it can be seen that menopausal osteoporosis is going to be a health issue particularly in the developing Asian countries in the next millenium. Is osteoporosis a preventable condition? Osteoporosis is preventable and should not be regarded as a disease in the true sense of the word [l]. It is a state of deficiency which can be prevented, identified and remedied.

G. Tang, H.K. Ma /ht.

J. Gynecol. Obstet. 46 (1994) 203-207

Prevention of osteoporosis should start at the time of adolescence. The goal is to maximize bone mineral accrural resulting in optimal peak bone mass which is attained before the age of 30. Although there is a genetic effect on bone mass with important bearing on later development of osteoporosis [12], a combination of exercise, appropriate diet and healthy life-style can influence bone growth behavior from an early age. Exercise is a known initiator of the boneremodeling cycle because mechanical loading, muscular activity and gravity stimulate the bone cells to differentiate and grow. Bone mineral maintenance depends on the type and frequency of exercise and also on gravity. Highly trained tennis athletes had significantly greater lumbar bone mass when compared with age-matched competitive swimmers because tennis increases the weight-bearing of the bones [ 131. In brief, regular weight-bearing exercise should protect against bone loss. The type and frequency of exercise should be appropriate to the individual’s age, physical condition and environment. Exercise may be prescribed according to the individual needs. The exercise should be weight-bearing, vigorous and diverse. Diversity can reduce the boredom to the minimum, an essential ingredient to ensure long-term compliance. The beneficial effect of exercise on bone maintenance is rapidly lost if the frequency and intensity of the exercise is reduced [l]. It may be diRicult for some women to go on some specific exercise program such as tennis or aerobic exercise, but walking upstairs and on level ground instead of taking elevators or motor rides may be equally beneficial and should be encouraged. Calcium is one of the principal bone minerals. Its supply, absorption, deposition and withdrawal from bone determine bone health. Recommended daily requirements of calcium are: 800 mg/day from 1- 10 years of age; 1200 mg/day from 1 1- 18 years; 1000 mg/day for premenopausal women and 1400 mg/day for postmenopausal women because of their less efficient absorption from gut and poorer resorption from kidneys [14]. Women should strive to take a diet that is adequate in calcium. Food items rich in calcium are dairy products, beans, shell fish and green vegetables.

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Obviously, an individual may like food that is deficient in calcium and if that is recognized, a calcium supplement should be given. Will calcium by itself prevent osteoporosis? There has been much debate on this issue, and clinical trials of calcium supplements have shown reduced rates of bone loss [ 151. However, calcium supplements may have a potential side effect, the development of renal stones, which normally is a rare condition in women. Renal stones occur in individuals who do not have the enzymes necessary to keep the calcium in solution in the urine. It is not because of excessive calciwn intake. It should also be noted that high protein diet will lead to increased calcium loss. Large consumption of alcohol, smoking and caffeine have been shown to increase the risk of osteoporosis. Based on the identified risk factors (Table I), an attempt should be made to identify women at risk of osteoporosis [ 11, and appropriate advice should be given to minimise the chance of developing osteoporosis or to delay its occurrence. Notelovitz [l] proposed the use of bone density measurements and biochemical bone markers in an ‘Osteopenia Identification Program’. The program involves repeated bone density measurements as a form of osteoporosis screening. The concept is similar to that of screening for cervical cancer. Unfortunately, osteoporosis screening by bone density

Table 1 Risk factors for osteoporosis Family history of osteoporosis Race: Menstrual status: Diet:

Personal habits: Medical conditions:

White, Oriental Menopause, premature ovarian failure, gonadal dysgenesis Calcium deficiency Increased caffeine, protein, fibre intake Smoking, alcohol consumption Decreased physical activity Gastrectomy Malabsorption syndromes Hyperprolactinemia Hyperparathyroidism Cushing’s Disease Diabetes mellitus Thyrotoxicosis

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measurements is expensive and may not be available in many places. Such screening may be useful for the at-risk group, especially those with a family history of osteoporosis. Estrogen is the most powerful agent which can prevent osteoporosis [ 171 and its action has been discussed. All forms of estrogen are effective and the dose required is small, e.g. 0.625 mg conjugated equine estrogen [ 181. This dosage will not replace bone, but will decrease the rate of loss. Ideally, if estrogen is to be used, its use should be started in the early postmenopausal period and should continue for lo- 15 years. The side effect of estrogen which is most disconcerting to women is the irregular vaginal bleeding, and the regular withdrawal bleeding. Whether the hormone will cause breast cancer is another concern. It must also be mentioned that once the estrogen therapy is discontinued, bone loss will occur. Therefore, estrogen needs to be taken for a number of years. Hormonal replacement therapy, although effective in preventing menopausal osteoporosis, has problems in its practical application. However, if a woman is found to have a bone density that is below 1 S.D. of her age-related norm, then she should consider such therapy [19]. The future and the goal Menopausal osteoporosis is a state of deficiency which is related to genetic makeup, nutrition, exercise and estrogen. All the above factors determine the peak bone mass which plays an important role in the development of this deficiency state in later life. Hence, women should be educated and made aware that they need to build their bone mass to the maximum from adolescence. Currently, only women who are approaching the menopause will begin to realise the health risk of osteoporosis and by that time, the condition may have already become a disease state because of fractures. Much can be done regarding nutrition and exercise. The present day fast food is not conducive to calcium intake. In places where dairy products are not readily available or where the preferred diet is lacking in calcium, its supplementation should be seriously considered. Calcium is relatively inexpensive and is rarely associated with side effects.

Exercise has to be encouraged and the ill effects of a sedentary lifestyle needs to be emphasized. Perhaps the majority of women cannot participate in an exercise program, but they can certainly take simple measures such as climbing up stairs and walking. These are also beneficial to their cardiovascular system. Moreover, these exercises are unlikely to be associated with injury or falls leading to fractures. A healthy lifestyle cannot be over-emphasized. Alcohol, cigarettes and caffeine cause other health hazards in addition to osteoporosis. Women should be advised to avoid them. There are women who may have optimal bone mass but they lose bone more rapidly than others. They may have family history of osteoporosis or other risk factors. For them, bone density measurements and assays of biochemical markers for bone turnover will be useful to monitor their bone loss at the time of menopause. In selected women, estrogen replacement therapy should be considered. Population-wide estrogen therapy is unnecessary when women have understood the role that nutrition, exercise and lifestyle plays in alleviating menopausal osteoporosis. It is realistic to achieve the goal that in the next century and millenium, osteoporosis and fractures in elderly women will become a historic pathological condition that women have conquered. References Ill Notelovitz M. Osteoporosis: Screening, prevention, and management. Fert Steril 59(4): 707, 1993. 121Riggs SL, Wahner HW, Dunn WL, Mazess RB, Offord KP, Melton LJ III: Differential changes in bone mineral density of the appendiclular and axial skeleton with aging: relationship to spinal osteoporosis. J Clin Invest 67: 328, 1981. 131 Parlitt AM: Bone remodeling and bone loss: understanding the pathophysiology of osteoporosis. Clin Obstet Gynecol 30: 789, 1987. I41 Riggs L, Spelsberg TC: Mechanism of oestrogen action on bone. Postgrad Med; Special Report (April): 13,1989. 151 Stevenson JC, Abeyasekerg G, Hillyard CJ, Phang KG, MacIntyre 1: Calcitonin and the calcium regulating hormones in postmenopausal women. Lancet i: 693, 1981. I61 Jasani C, Nordin BEC, Smith DA: Spinal osteoporosis and the menopause. Proc R Sot Med 58: 441, 1965. 171 Horowitz MC: Cytokines and estrogen in bone: antiosteoporotic effects. Science 260: 626, 1993.

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AM, Whedon GD: Calcium nutrition and bone health in the elderly. Am J Clin Nutr 36 Suppl. 5: 986, 1982. I151 Heaney RP: The role of nutrition in prevention and management of osteoporosis. Clin Obstet Gynecol 30: 833, 1987. 1161 Seeman E, Melton LJ III, O’Fallon WM, Riggs BL: Risk factors for spinal osteoporosis in men. Am J Med 75: 977, 1983. I171 Lindsay R: Prevention of postmenopausal osteoporosis. In: The menopause. Obstet Gynecol Clinics of N America Vol. I4 Ch. 5. (ed RO Gambrell), pp. 63-76. WB Saunders, Philadelphia, 1987. I181 Christiansen C, Lindsay R: Estrogens, bone loss and preservation. Osteoporosis Int I: 7, 1990. 1191 Johnson CC Jr, Slemenda CW, Melton LJ III: Clinical use of bone densitometry. N Engl J Med 324: 1105, 1991.