Bone is lost with advancing age in men as in women, leading to an increased incidence of osteoporotic fractures of the fore-arm, vertebral body and femoral neck. By the ninth decade of life, 4% of men will have sustained a fore-arm fracture, 7% a vertebral fracture and 5% a femoral neck fracture. The absolute number of osteoporotic fractures is rising in men, because of the ageing population and an increase in the age-specific incidence of fractures. Even if the age-specific incidence of fractures stabilizes, demographic trends suggest that a further increase in the number of men with osteoporotic fractures is inevitable. Peak bone mass in men is influenced by race, hereditary, hormonal factors, physical activity and calcium intake during childhood and adolescence. Bone loss in men starts at about the age of 35 years and is regulated by genetic, endocrine, mechanical and nutritional factors. Secondary causes of osteoporosis may be detected in about 55% of men with vertebral crush fractures. The major causes are steroid therapy, hypogonadism, skeletal metastases, multiple myeloma, gastric surgery and anticonvulsant treatment. Hypogonadism is found in up to 20% of men with vertebral crush fractures, although the clinical features of testosterone deficiency may not always be present. Hypogonadal osteoporosis is associated with increased bone resorption and decreased mineralization, which is reversed by treatment with testosterone, leading to an increase in bone density. There is little published information on the treatment of primary osteoporosis in men. Although calcitonin, bisphosphonates and testosterone may be effective in the management of osteoporosis in men, confirmation is required in formal clinical trials.

Glucocorticoids produce osteoporosis via a number of mechanisms, the most important of which is probably inhibition of bone formation. This results in reduction in bone mass of 10-20% at commonly assessed sites, but the bone loss is 30-40% when predominantly trabecular bone is measured. The dosage and duration of steroid treatment influence the extent of bone loss, but other factors are not predictive. At the present time, a patient who has demonstrable sex hormone deficiency should receive appropriate replacement therapy. Optimization of calcium intake is advisable. If bone loss is severe or continues in spite of these measures, the addition of a bisphosphonate, calcitonin, fluoride or a vitamin D metabolite may be appropriate, according to local availability. Thiazide diuretics can be combined with all of these regimens. If combined with vitamin D or its metabolites, careful monitoring of serum calcium levels should be undertaken. Bone density should be monitored annually until such time as it is stable.

This review has highlighted important preventive measures for falls and fractures in elderly osteopenic patients, and has discussed the therapeutic possibilities after an osteoporotic fracture has occurred. Assuming that a large proportion of osteoporotic fractures are a consequence of traumatic falls, and are not spontaneous, due to osseous weakness, preventive measures in elderly people are best directed to counteract muscular weakness, improve agility and correct visual impairment. It is also important to guard against unnecessary obstacles in the home and the reflex habits of doctors to prescribe hypnotics and tranquillizers, as well as their occasional tendency to overtreat hypertension. Practical examples of rational measures to protect against these causes of fractures have been given. In the second part of the review, the treatment of fractures has been delineated. The goals are adequate pain relief, early immobilization of the patient, avoidance of overtreatment and fast restoration of the quality of life. Three stages of pain relief by drugs are outlined. The first consists of a simple non-narcotic analgesic, such as paracetamol. In a second stage, either the combination of paracetamol with a muscle relaxant or the administration of a narcotic analgesic of medium potency is proposed. As a third stage, several therapeutic approaches to the administration of potent narcotic analgesics have been discussed. Non-drug measures, such as the use of heat, ultra-soft mattresses, walking frames, crutches and sticks, as well as active forms of physiotherapy, have been discussed both in terms of pain relief and early mobilization.

Oestrogen hormone replacement therapy remains the first choice for the treatment and prevention of osteoporosis in postmenopausal women, but for patients who are unsuitable for this therapy, which of course includes men, other satisfactory treatments are available. Several placebo-controlled studies have demonstrated that bisphosphonates and calcitonin prevent bone loss or perhaps increase bone density over 2-3-year periods, and reduce the rate of fracture. It is not known whether these treatments will increase bone density over longer periods of time. Cyclical etidronate has recently become licensed in the UK for use in the treatment of osteoporosis, and it is hoped that other bisphosphonates and intranasal calcitonin will soon be added to the available treatments. Fluoride appears to increase bone density but, at doses above a very narrow therapeutic window, it increases the fracture rate, either because of bone redistribution, formation of poor quality bone or a toxic effect on osteoblasts. At present, fluoride remains a treatment to be used only under expert supervision or within the context of controlled clinical trials. Anabolic steroids may be of value in selected elderly patients with osteoporosis. The patient may be able to contribute to the prevention of osteoporotic fracture by exercising, which will improve dexterity and may have a small effect to increase bone density, and by avoiding the factors that predispose to falls, such as icy paths and excess alcohol. Changes in the diet are unlikely to play a major role in the maintenance of bone density in women living in the Western world.

Hormone replacement therapy is well documented to reduce the increased bone turnover induced by oestrogen deficiency and, as a result, it prevents bone loss after the menopause. It has been shown that this effect leads to a significant reduction in osteoporotic fracture rates. There is a dose threshold effect, the duration of therapy influences the degree of benefit and, after the cessation of HRT, postmenopausal bone loss resumes. Women take HRT for many reasons, most for relief of menopausal symptoms, and 10-20% show poor compliance. The nature of HRT preparations is discussed and the current understanding of benefits and risks described.

Osteoporosis with attendant increased fracture risk is a common complication of many other diseases. Indeed, almost all chronic diseases make some impact on life-style, usually by restricting physical activity and hence reducing the anabolic effect of exercise and gravitational strains on the skeleton. Restricted appetite and modified gastrointestinal tract function is another commonplace finding that has an impact on bone nutrition and synthesis, as on other systems. Sex hormone status is of particular importance for the maintenance of the normal skeleton, and the postmenopausal woman is at particular risk for most causes of secondary osteoporosis. In dealing with secondary osteoporosis in the hypo-oestrogenic woman, the question of giving hormone replacement therapy in addition to other disease-specific therapy should always be considered, as, for example, in a young amenorrhoeic woman with Crohn's disease. Similarly, in hypogonadal men the administration of testosterone is useful for bone conservation. The wider availability of bone densitometry ought to make us more aware of the presence of osteoporosis in the many disease states discussed above. This is particularly important as the life span of such patients is now increased by improved management of the underlying disease process in many instances. Even in steroid-induced osteoporosis--one of the commonest and most severe forms of osteoporosis--we now have some effective therapy in the form of the bisphosphonates and other anti-bone-resorbing drug classes. The possibility of prophylaxis against secondary osteoporosis has therefore become a possibility, although the very long-term effects of such drug regimens are still unknown. In some situations, such as thyrotoxicosis, Cushing's syndrome and immobilization, spontaneous resolution of at least part of the osteoporosis is possible after cure of the underlying problem. The shorter the existence of the basic problem, the more successful the restoration of the skeleton appears to be. A useful credo for clinicians with respect to secondary osteoporosis is: to think of it; to use specific therapy for the underlying disease; to reduce or remove completely any relevant drug or toxic material; to optimize physical activity and general nutrition; to treat hypogonadism if present and feasible; and to consider the use of specific anti-bone-resorbing or other bone active drugs.

Osteoporosis is a disorder of ageing that shares with other disorders of ageing a multifactorial pathogenesis. The important factors for osteoporosis include the diet, life-style and intercurrent factors such as disease. However, it is clear that loss of ovarian function is an important determinant of bone loss, and oestrogen appears to be the key factor involved. Thus, not only does loss of ovarian function result in bone loss, it can be stopped by adequate oestrogen intervention. Numerous techniques are available to measure bone mass non-invasively and to estimate the risk of future fracture. Thus, for the postmenopausal woman who is concerned about osteoporosis, and who is willing to accept intervention to prevent the disease, bone mass measurement allows the clinician to determine the risk of future osteoporotic fracture and to provide intervention if required. Future studies may elucidate whether determination of skeletal remodelling using biochemistry adds significantly to risk determination. This may be required when considering agents other than oestrogen for intervention among asymptomatic women, as these agents primarily affect the skeleton, while the effects of oestrogen are wide ranging in the body.

Bone mass is the most important determinant of fracture risk. Current bone mass of an individual will be determined by the peak bone mass achieved in early adult life and the subsequent duration and rate of bone loss. In attempting to predict an individual's future risk of fracture it is therefore logical to attempt to assess both of these parameters. Serial measurements of bone mineral density and estimation of the rate of bone turnover may also be used to determine the response to treatment. In this chapter we review the currently available methods of measuring BMD and bone turnover, and discuss their place in the diagnosis and management of osteoporosis.

Bone can be divided into two kinds of tissue, cortical and trabecular bone. The skeleton comprises approximately 80% cortical bone, mainly in peripheral bones, and 20% trabecular bone, mainly in the axial skeleton. Bone density increases with skeletal growth to a peak in late adolescence or early adulthood. Bone loss subsequently occurs with ageing in both sexes, and in females accelerated loss occurs at the menopause. The risk of osteoporotic fracture in later life is the result of peak bone mass achieved at skeletal maturity and subsequent age-related and postmenopausal bone loss. Peak bone mass is largely genetically determined but is also influenced by environmental factors such as dietary calcium and physical activity. Bone loss with ageing occurs at different rates and different times in different skeletal sites. Femoral neck bone loss probably occurs in a linear fashion throughout life from early adulthood but may be accelerated at the menopause. Spinal bone loss may commence before the menopause but is rapidly increased in the immediate postmenopausal years. Bone strength is directly related to bone density, but the loading force is also relevant to risk of fracture.

Bone remodelling and repair are accomplished by the co-ordinated activity of cells of the osteoclast and osteoblast lineages. Small changes in the balance between formation and resorption will, when magnified by repeated cycles, lead to significant reduction in bone mass and strength, ultimately resulting in fracture. This review focuses on the cellular features of bone remodelling and the known regulators of bone cell function. These include systemic and local factors, both soluble and contained within the complex extracellular matrix of bone.

The extent of disability attributable to arthritis is briefly summarized and the World Health Organization's (WHO) classification scheme for progression from pathology to disability described. The types of outcomes that have been examined in evaluations of psychological and educational interventions aimed at preventing arthritis disability are described and classified according to the WHO scheme where appropriate. Next, the most common components included in psychological and educational interventions for arthritis are reviewed. These are (1) providing general information, (2) teaching illness self-management skills, (3) training in biofeedback, (4) applying cognitive-behavioural techniques, (5) using other psychotherapeutic techniques, and (6) enhancing social support. This is followed by a discussion of issues pertinent to assessing the efficacy of various intervention components, citing specific examples of intervention research. Finally, the conclusion that certain types of psychological interventions appear to be effective in mitigating arthritis disability is drawn and the contribution of social science theory to intervention efficacy acknowledged.

A case for studying the psychological aspects of pain is made through a discussion of the problems resulting from investigations of the so-called rheumatoid personality. Following a review of the current theory about pain mechanisms, proposals are made about the best ways of measuring pain in the rheumatological disorders. Later sections tackle issues about the many meanings of pain. Discussion particularly focuses on expectations about pain, on lay beliefs about the rheumatic diseases and on beliefs about pain control. Recommendations are made about the ways in which some of these psychological features might profitably be incorporated into the management of clinical pain.