OSSG Osteoporosis Sydney Support Group

THE AUSTRALIAN NATIONAL CONSENSUS STATEMENT

on The Prevention and Management of Osteoporosis

The conference on The Prevention and Management of Osteoporosis was held in Canberra on 23-24 October 1996 and was supported by the Pharmaceutical Education Program. The co-supporters were the Australian and New Zealand Bone and Mineral Society, the Australian Pharmaceutical Manufacturers' Association, Osteoporosis Australia, the Australasian Menopause Society, the Royal Australian College of General Practitioners, the Royal Australasian College of Physicians and the Royal Australian College of Obstetricians and Gynaecologists.

The objectives of the conference were to produce a consensus statement that would:

  • form the basis for development of clinical guidelines on the appropriate prevention, diagnosis and treatment (drug and non-drug) of osteoporosis;
  • provide advice to the Pharmaceutical Benefits Advisory Committee (PBAC) about the listing on the Pharmaceutical Benefits Scheme of pharmaceuticals for the prevention and treatment of osteoporosis; and
  • provide advice to health policy makers about interventions for the prevention, diagnosis and management (drug and non-drug) of osteoporosis.

The Australian National Consensus Conference 1996 used a consensus development process to achieve these objectives.

At the conference, a faculty of speakers expert in preventing and managing osteoporosis presented evidence to a Consensus Panel and conference delegates. The Panel included experts in osteoporosis-related fields, including epidemiology, endocrinology, rheumatology, orthopaedics, obstetrics and gynaecology, biochemistry, general practice, dietetics, physiotherapy, and the consumer movement. The speakers were asked to rate the strength of the evidence, from meta-analysis of all relevant randomised controlled trials through to expert opinion. From this evidence, the Panel drafted a statement as a set of answers to questions posed to it by the organising committee. The draft statement was then discussed and debated on the floor of the conference, and the resulting amendments and additions were considered for the final consensus statement.

The Consensus Statement is intended to guide medical practitioners in preventing and managing osteoporosis. The continuing uncertainty in many areas of prevention and management highlights the need for further research.

In July 1997, the Medical Journal of Australia (MJA) published the resulting report.

Included herein are excerpts from that statement. 

What is Osteoporosis?

OSTEOPOROSIS is a condition of increased skeletal fragility. Clinically it is usually defined in relation to bone density. The strength of bone in later life depends on two factors - the peak strength of bone achieved in early adulthood and subsequent age-related and hormone deficiency-related bone loss. In osteoporosis, bones can fracture with trauma that would normally be withstood by the skeleton

At menopause, bone turnover increases. In women, bone loss occurs by thinning, perforation and loss of connectivity. In men, there is no midlife acceleration of bone turnover; trabecular bone loss proceeds by thinning due to reduced bone formation.

A variety of other medical conditions, either by themselves or in relation to therapy, can lead to further and accelerated bone loss (secondary osteoporosis). A particular example of this is corticosteroid osteoporosis.

Although osteoporotic fractures are often thought of more specifically in terms of wrist, hip or spinal fractures, it is important to remember that virtually any bone can fracture in an individual with osteoporosis. Fractures of bones in the upper and lower limbs, ribs, spine and pelvis are more numerous and generally occur in younger individuals than do hip fractures. Although osteoporotic fractures heal normally, from middle age onwards each is associated with significant morbidity and varying degrees of long term disability, since the skeletal deformity may be permanent. Moreover, the occurrence of one fracture is associated with an increased risk of further osteoporotic fractures.

What is the magnitude of the problem of osteoporosis in Australia?

OSTEOPOROSIS can affect any age group and either sex.

It is estimated that the proportion of women with osteoporosis (low bone mineral density) increases from 15% in those aged 60 to 64 years up to 71% in those over 80 years of age. The incidence is much lower in men, ranging from 1.6% of those aged 60 to 64 years up to 19% of those aged over 80 years.

The Dubbo Osteoporosis Epidemiology Study involved a large cohort of elderly men and women studied prospectively from 1989 onwards. Its findings indicate that after the age of 60 years about 60% of women and 30% of men suffer from an osteoporotic fracture.

Direct costs associated with osteoporotic fractures were assessed, and the total annual cost for Australia was estimated to be $779,000,000 (in 1992 Australian dollars).

Rehabilitation comprised the largest proportion of costs for hospital-treated fractures, and community services were the largest cost for outpatient-treated fractures. These estimates do not include the personal costs of loss of independence and mobility.

There is more information available about hip fractures than any other fracture type, because virtually all patients with hip fracture are hospitalised. In the Dubbo Osteoporosis Epidemiology Study only 10% of fractures in people aged 60 to 79 years were hip fractures, compared with 40% in those aged over 80 years. In a recent study conducted in the northern Sydney area, mortality after hip fracture was 24% at 12 months, about five times higher than that in an age-matched group who did not suffer a hip fracture. Between 20% and 26% of people with hip fractures remain in nursing homes for the rest of their lives. Numerous studies in the United States, Europe and Australia have found that around 50% of people who suffer a hip fracture never regain their prefracture mobility.

The problem of osteoporotic fractures is already large and is increasing with the ageing of the population. In 1994, there were 14,600 hip fractures in Australia.

If nothing is done to reduce risks, it is estimated that in 2010 there will be 20,900 hip fractures in Australia.  

What is the relationship between bone density and fracture risk; are there any other useful predictors of fracture risk?

Bone density and fracture risk

There is a continuous inverse relationship between bone density and the risk of fracture, comparable to that between serum cholesterol and the risk of coronary heart disease and that between blood pressure and the risk of stroke.

Measuring bone density

Bone densitometry measures the average density of bone mineral within the region scanned. It is currently the best available measure of bone strength.

Single and dual energy absorptiometry and quantitative computerised tomography are techniques for measuring bone mineral density. The four sites of measurement commonly used in Australia (the forearm, spine, proximal femur and total body) all have merit, but some are more suitable for diagnostic purposes and some for longitudinal studies.

Other tests for prediction of fracture risk

A World Health Organization Study Group in 1994 concluded that tests to predict fracture risk would be improved by the ability to assess bone mass accurately in conjunction with more specific biochemical measures of bone turnover. At present such measures remain research tools, but recent evidence indicates that they provide an independent predictor of fracture risk. Ultrasound is promising but currently remains a research tool also.

Other useful predictors of fracture risk

In addition to the fragility of bone, fracture risk is determined by the interaction of several other factors, including the risk of falls and other trauma, the adequacy of protective responses and the adequacy of soft tissue to absorb impact.

In making decisions about investigation and treatment, the individual's full risk profile should be taken into account. The most clinically useful of these predictors include:

  • Age, sex and family history
    With ageing there is a decrease in bone mineral density, muscle strength, balance and other factors that increase the risk of fracture. In older individuals, fracture risk doubles every five to ten years. Among women who have a history of fracture in close family members (maternal or paternal), the risk of osteoporotic fracture is almost doubled.
  • Prior fracture
    The occurrence of one fracture increases the risk of further fractures. This is partly because those whose bones fracture have low bone mineral density, but it also indicates an increased risk beyond this of about two or three-fold.
  • Falls
    Even in a simple fall, enough energy may be generated to fracture the femur. In young people, protective responses, the strength of the bone and the quantity of soft tissue generally prevent fractures from occurring. In elderly people, other factors, such as increased body sway and reduced muscle strength, Parkinson's disease, poor vision, physical inactivity and psychotropic medications, may have an important influence on the risk of falling.
  • Low body weight
    Low body weight is associated with low bone mineral density and decreased soft tissue protection, both of which are associated with increased fracture risk.
  • Other risk factors
    There is reasonable evidence of several other risk factors for fracture: very low calcium intake, smoking, menstrual irregularity/absence and some medications, particularly corticosteroids.  
What diagnostic evaluations are needed in patients with presumed osteoporosis?

THE CHOICE of appropriate diagnostic technique is influenced by the aetiology of the presumed osteoporosis. Depending on the clinical assessment, one or more of the following diagnostic procedures will be required.

Radiographic assessment

X-rays will usually be necessary to confirm a fracture but are not suitable for use in the diagnosis of low bone density.

Bone densitometry

As discussed this is currently the single best in-vivo estimate of bone strength. Densitometry technology has advanced to such a degree that it measures apparent bone mineral density with acceptably high accuracy and precision. It is now relatively widely available and inexpensive. Dual energy x-ray absorptiometry (DXA) can provide a rapid assessment of both whole body and regional bone mass (and calculated "areal density"). Quantitative computerised tomography (QCT) directly measures trabecular bone density, but with greater radiation dose, imprecision and expense, and is therefore not the preferred approach. However, QCT is useful when DXA is not readily available (e.g., in some rural areas).

Due to differences in both hardware and software, bone density values obtained from instruments produced by different manufacturers cannot be compared directly. Therefore, for the diagnosis of low bone density, the individual's absolute value derived from any given instrument must be related to the sex-specific reference range derived from the same model instrument. Similarly, for meaningful detection of change over time, serial measurements in the same individual should be performed on the same instrument.

Regional bone mass measurements can be readily performed on skeletal sites commonly involved in osteoporotic fracture (e.g., lumbar spine, forearm, proximal femur). In older individuals, caution is required in assessing bone mass in the lumbar spine, where there may be a partial or complete compression fracture, vascular calcification or degenerative spinal disease. Greater diagnostic accuracy may result from bone mass measurements at more than one skeletal site.

At present ultrasound measurement of bone strength lacks acceptable measurement precision and long-term stability to be recommended for use in diagnosis of osteoporosis. The results of further prospective studies are awaited.

Pathology testing

The extent to which investigations are necessary is determined by the clinical picture, but the index of suspicion for secondary causes of osteoporosis should increase in patients with severe bone loss for age (e.g., bone density lower than 2.0 standard deviations below the age-related mean).

Extensive pathology testing is not required. However, specific pathology tests should be considered in a range of conditions. Relevant initial tests include adjusted total calcium, total alkaline phosphatase, creatinine, full blood count and erythrocyte sedimentation rate.

Further testing (guided by clinical indicators) includes:

  • 25-hydroxyvitamin D (vitamin D deficiency);
  • thyroid function tests (hyperthyroidism or long term thyroid hormone therapy);
  • sex steroids (e.g., testosterone in hypogonadal men);
  • intact parathyroid hormone (hyperparathyroidism);
  • liver function tests (in people possibly consuming excessive amounts of alcohol); and
  • protein electrophoresis (multiple myeloma).  
Is screening of the general population or high risk groups for osteoporosis effective or cost-effective?

  Mass screening

Mass screening for low bone density by densitometry or ultrasound is not advocated for a variety of reasons.

The likelihood of poor attendance at screening programs, poor uptake and compliance with therapy, and a relatively low efficacy of available treatments (30%-50%) suggest that the cost of a mass screening program would not be justified by the resulting change in the incidence of fractures in the whole community.

Individual assessment

Bone density measurement is necessary when it is likely to affect treatments offered to or accepted by an individual. It would appear to be unnecessary to test bone density in a woman who has decided to take oestrogens for other reasons. By contrast, when there is indecision, bone density measurement will allow the postmenopausal woman at low risk to avoid costly long-term interventions. Some of the clinical indications for bone density measurement are the predictors of risk listed in

Genetics

Inherited factors appear to play a major role in determining peak bone mass. Although the mechanism of such effects remains unclear, these factors form an important component of risk assessment. In particular, careful questioning about fractures and/or kyphosis in older family members (male and female) should be a routine part of any review of osteoporosis risk.  

What interventions are effective in preventing osteoporosis and osteoporotic fractures?  

Childhood and early adulthood

Achieving a higher peak bone mass is likely to reduce the risk of osteoporotic fracture in later life. Since peak bone mass is achieved by late adolescence or early adulthood, intervention in childhood and adolescence may be important.

Exercise

Several studies suggest that exercise in prepubertal children has positive effects on bone density. Whether benefits achieved before puberty are sustained into adulthood is uncertain, although cross-sectional studies of retired athletes suggest this may occur.

Calcium

Dietary calcium supplementation has a small positive effect on bone. Intakes substantially below the current recommended dietary intake (about 900 mg/day) should be avoided. Extremely low intakes of calcium may have irreversible effects on bone mass.

If nutrition is not adequate to maintain normal body weight in childhood and early adulthood, bone density may be lost due to gonadal dysfunction.

Summary

A healthy lifestyle can be advocated in adolescence and early adulthood, including regular exercise, adequate calcium intake and avoidance of tobacco smoking or excessive alcohol intake. There are insufficient data to prove that such interventions will lead to reduction in osteoporosis in later life. The extent to which lifestyle factors in adolescence and early adulthood affect peak bone mass is unknown.

Older adults

General advice

In adults trials using weight training or increasing calcium intake by about 1000 mg/day have achieved differences of 1%-3% in bone mass over about two years. These effects are small in relation to the 5%-10% differential in mass theoretically needed to alter fracture rates by 25%-50%. Whether these results are due to changes in bone mass homeostasis or whether they reflect a continuing effect on loss of bone is unclear.

The effect of exercise on fall reduction may be more important than any effects on bone density.

Specific therapies

Decisions about management depend on the absolute risk of fracture and the potential benefits and adverse effects of alternative treatment options. For those at moderate risk, prophylaxis or intervention should have minimal adverse effects. For those at high risk (e.g., previous fracture, very low bone density) more aggressive therapy is indicated.

Although most fracture studies have been performed in women, the relationship between bone density and fracture is similar in men. Therefore, treatments which increase bone density in women are likely to have equivalent efficacy in men. With all therapies for osteoporosis, it is likely that the beneficial effects on fracture risk are maintained for only a limited period after the treatment is stopped.

Hormone replacement therapy

Hormone replacement therapy has been shown to prevent early postmenopausal bone loss. Long-term therapy (for more than five to ten years) after menopause probably reduces fracture risk, although it may need to be continued indefinitely to show any benefit. In late postmenopausal women, hormone replacement therapy may increase bone density by about 5% above baseline in the lumbar spine over two years. Observational studies have shown its use to be associated with reduced fracture rates throughout the skeleton, and vertebral fractures have been shown to be reduced in randomised controlled trials. There are no data from randomised controlled trials on the effect of hormone replacement therapy on hip fractures.

Hormone replacement therapy has other benefits in postmenopausal women. It relieves urogenital symptoms and may be associated with a reduction in the incidence of cardiovascular disease. It is clear that any effect on the risk of breast cancer is small; evidence on the risk from long-term use (more than five to ten years) is awaited from current prospective randomised studies. The effects on bone density of oestrogen with supplemental calcium may be additive or more than additive.

The extensive documentation on its efficacy and safety make hormone replacement therapy the treatment of choice in postmenopausal osteoporosis.

Bisphosphonates

The early bisphosphonate, etidronate, increases bone density in the lumbar spine by 3%-5% above baseline after two years of therapy in late postmenopausal women, with a reduction in fracture risk. Newer, more potent bisphosphonates may have a better therapeutic profile. Two large randomised three-year studies of one of these, alendronate, found increases in bone density comparable to those seen with hormone replacement therapy, and a reduction in relative fracture risk of about 50%. There is little experience with bisphosphonate use beyond three years of continuous therapy. Their safety and efficacy make the newer, more potent bisphosphonates first line therapy in older individuals unable or unwilling to take hormone replacement therapy.

Vitamin D (calciferol)

Recent studies from a number of countries have demonstrated that vitamin D deficiency is common in the institutionalised elderly due to poor sunlight exposure. Correction of this deficiency reduces hip and other non-vertebral fractures. This intervention involves the use of replacement doses of calciferol (500-1000 units/day or 50 000 units/month). Avoiding vitamin D deficiency in this at-risk group is an important part of providing care for the elderly. The continuing availability of oral formulations of vitamin D is a priority (supplies of vitamin D were difficult to obtain last year, despite being listed on the PBS).

Active vitamin D metabolites (calcitriol)

Calcitriol has a therapeutic profile distinct from vitamin D and should not be used in the treatment of vitamin D deficiency. Calcium supplements should be stopped while using calcitriol.

There is disagreement about the place of active vitamin D metabolites in the management of postmenopausal osteoporosis. One study showed a reduced fracture rate with calcitriol, while other, smaller, studies with limited power did not. Calcitriol may be more effective in people with reduced efficiency of calcium absorption. These uncertainties should be resolved by further large randomised controlled trials. However, calcitriol may have a major role in the management of glucocorticoid-induced osteoporosis. In patients commencing glucocorticoids, calcitriol has been shown to prevent spinal bone loss.

Calcium

Long-term high calcium intake in postmenopausal women appears to prevent or reduce loss of bone, resulting in a 1%-3% difference in bone density compared with untreated individuals over two years. Several small studies in the elderly have suggested there may also be a reduction in the number of fractures after taking calcium supplementation. Although calcium intake by itself is less effective than hormone replacement therapy or other therapies, adequate calcium intake should be part of routine management. The target total intake should be about 1500 mg/day in those not using more effective treatments. Dietary and supplemental forms of calcium appear to be equally well absorbed, with no need for additional components for effective absorption other than normal vitamin D status.

Other agents

Anabolic steroids (e.g., nandrolone decanoate) are testosterone analogues. A number of randomised controlled trials have shown moderate increases in spinal bone mineral density. However, data regarding their antifracture efficacy are inconclusive. Their long-term use in effective doses is accompanied by a high incidence of side effects.

The use of fluoride should be restricted to research and specialist centres.

Calcitonin is an antiresorptive agent used in some parts of the world for treating osteoporosis. Its expense, side effects and difficulties with administration mean that it is not widely used in most countries.

Hip protectors have been shown in one randomised controlled study to halve the rate of fractures in the institutionalised elderly, although compliance may be poor.

Alternative therapies

In the community, a variety of alternative therapies, such as phytoestrogens, herbal medicines and nutritional additives, are used for osteoporosis. Their cost and potential side effects must be considered.

Effectiveness of interventions in reducing osteoporotic fractures

Strategies that reduce the risk of fractures overall do not guarantee that osteoporotic fractures will not occur. This is not surprising, as even the most effective interventions for improving bone density, if applied late in the osteoporotic process, do not return bone mass to young normal levels. Rather, they slow down the loss or effect a modest increase in bone density. Since some untreated individuals at risk will not sustain a fracture anyway and therefore will not benefit from treatment, any interventions (drug or non-drug) requiring long-term application must be safe, efficacious and free of serious side effects. The total cost of all such interventions, including diagnostic testing, monitoring and costs for the community or the individual, must be included as part of any cost-benefit evaluation.

The availability of safe and effective therapies for osteoporosis raises questions about whom they should be offered to. The cost-benefit analysis of a decision to treat is heavily influenced by the likelihood of fracture. If an intervention halves fracture risk, a large number of fractures will be prevented if it is used in a population with a high baseline risk of fracture

What are the goals of treatment and how do you choose an appropriate management strategy for individual patients?

THE KEY OBJECTIVES in managing osteoporosis are to:

  • restore and maintain bone strength to prevent fractures; and
  • reduce the overall morbidity and mortality associated with the condition.

Encouraging adequate calcium and vitamin D intakes and modification of other lifestyle factors such as smoking, excessive alcohol intake, inactive lifestyle or excessive exercise is appropriate in all individuals, from childhood to old age.

Younger hypogonadal females

Hypogonadism in young women needs to be appropriately investigated and treated. This condition often results from excessive exercise or anorexia and may benefit from appropriate sex hormone replacement, if modification of contributing lifestyle factors is unsuccessful.

Early postmenopausal women

In women within 15 years of menopause, hormone replacement therapy has been shown to prevent bone loss and should be offered to symptomatic menopausal women and those at increased risk based on bone density measurement and other factors. In women without oestrogen deficiency symptoms, there is debate about the level of bone density reduction at which treatment with hormone therapy is required. However, as up to 60% of women experience osteoporotic fractures during their lifetime, any postmenopausal woman with a T score for bone density less than -1 and/or with risk factors for bone loss should be considered for hormone replacement therapy.

Older postmenopausal women

In women who are more than 15 years past menopause, clinical risk factors may provide additional information about the risk of fracture (e.g., those related to falling). Bone density measurement remains the best method of assessing fracture risk. The proximal femur may be the most reliable site for measurement because of the greater incidence of osteoarthritis of the lumbar spine in older patients. Hormone replacement therapy is first line treatment in older postmenopausal women. To improve compliance, continuous combined regimens should be used, starting with a low dose and increasing slowly over several months to the full replacement dose. In women for whom hormone replacement therapy is unsuitable, the available evidence suggests the order of choice is alendronate, followed by etidronate or calcitriol.

Housebound or institutionalised patients

In these patients vitamin D deficiency should be considered and treated when present, in addition to the strategies outlined above.

Men

In men, causes of secondary osteoporosis, including hypogonadism, need to be excluded or treated. If no such causes are found, treatments (other than oestrogen) which have been shown to increase bone mineral density in women are likely to be effective in men. Calcitriol is available for the treatment of male osteoporosis in Australia. Excessive use of alcohol and multiple myeloma are important risk factors for osteoporosis in men.

Glucocorticoid-treated patients

Glucocorticoid treatment represents a major iatrogenic cause of osteoporosis and fractures, especially vertebral and rib fractures. In patients starting glucocorticoid therapy, bone loss is most rapid in the first one to two years, and randomised controlled trials have shown it is possible to prevent spinal bone loss with calcitriol or etidronate. Some restoration of bone mass has also been reported with these agents and other bisphosphonates in patients undergoing long-term glucocorticoid therapy. Therefore, these agents are appropriate to consider in patients starting glucocorticoid therapy or treated with long-term high dose therapy. Patients should be given the lowest dose of glucocorticoids possible, local administration (e.g., inhalation) is preferred, and sex hormones should be replaced where deficient (in both men and women).

What is the optimal approach to follow-up and monitoring of treatment of the patient with osteoporosis?

THE GOAL in treating osteoporosis is to prevent fracture, however, fracture is not a sufficiently frequent event in individuals to meaningfully reflect the adequacy of therapy, so bone density is an important surrogate endpoint.

Side effects and safety

These are important considerations for patient benefit.

All women receiving hormone replacement therapy should have mammography every two years. There should also be monitoring of side effects and appropriate dose adjustment. In older postmenopausal women, a "low and slow" policy when initiating therapy is advised, to avoid unacceptable side effects and allow appropriate dose adjustment.

When bisphosphonates are used there should be monitoring of gastrointestinal tract symptoms.

In patients taking more than 0.25g of calcitriol per day, total calcium intake should not exceed 1000 mg/day, including supplementary calcium from other sources, and plasma calcium and urinary calcium excretion should be monitored.

What strategy should be employed when response to initial therapy is inadequate?

THE EXPECTED RESPONSE to specific drug therapy is an increase in bone mass over one to two years, followed by stabilisation.

If significant bone loss ( > 5%-6% of lumbar spine per year) continues despite the institution of a standard therapy for osteoporosis, several steps should be followed:

  1. Scrutinise serial bone density scans to ensure that they are technically comparable, that the same vertebrae have been assessed and that there have not been changes in vertebral dimensions, scan outlines, software or the instrument used for analysis.
  2. If the bone loss is thought to be real, then assess patient compliance. Is the patient actually taking the medication? How often are tablets being missed? Oral bisphosphonate therapy must be taken fasting with water and temporally separated from any form of mineral supplement or its bioavailability can be markedly reduced. Biochemical markers of bone turnover (serum levels of osteocalcin or bone-specific alkaline phosphatase, and urinary hydroxyproline or pyridinoline secretion) may be useful in the assessment of compliance, as suppressed values should be found with treatments such as bisphosphonates and oestrogens. Non-compliance may be attributable to side effects and so require changes in the dose or preparation used.
  3. In any patient not responding as expected to osteoporosis therapy, the possibility of some other underlying disease should be considered. The patient should be screened again for underlying causes of osteoporosis (e.g., multiple myeloma, coeliac disease, vitamin D deficiency). Very low calcium intake should also be excluded.
  4. If bone loss is occurring despite compliance and the lack of other causes, the dose of therapy should be reviewed. Some early postmenopausal women require doses greater than the equivalent of 625g of conjugated equine oestrogens or 50g/day of transdermal oestradiol to maintain bone mass. This may be a particular problem for women who smoke. In patients taking hormone replacement therapy who do not have oestrogenic side effects and who are losing bone density, a 50%-100% increment in dose should be considered. In those who have problems with intestinal absorption, a change in route of administration should be considered. Trial evidence with the potent bisphosphonates suggests that significant loss of bone is very uncommon in those taking tablets as instructed.
  5. In patients in whom bone loss is taking place despite optimal dosing of a single agent, specialist referral for advice is appropriate.  
How can people suffering from osteoporosis-related injury and disability best be managed and rehabilitated?

HIP FRACTURES cause significant morbidity, mortality, immobility and nearly always institutionalisation. Vertebral fractures are also associated with considerable morbidity and mortality and often occur at a younger age. Fractures of the upper limb, specifically Colles', proximal humerus and elbow, can also cause significant disability, and they consume substantial but less visible resources in emergency and outpatient facilities.

Management and rehabilitation

Early rehabilitation after initial management of all fractures is important, as is bolstering a patient's confidence, which is often lost after a fracture. Patients should be reassured that acute episodes of pain will resolve, and that exercise and movement are essential to recovery.

  • In particular, surgical management of hip fracture needs to be adequately resourced to allow early fixation and rapid mobilisation.
  • The involvement of multidisciplinary rehabilitation teams is essential to lessen morbidity and mortality, reduce length of stay and facilitate return to usual activities.
  • After initial care of any fracture, inactivity and bed rest should be kept to a minimum and physiotherapy should be considered. Adequate analgesia is an essential part of the early rehabilitation stage.
  • Graded exercise programs , including postural exercise and hydrotherapy, play a role in restoring mobility and function.
  • The pain from vertebral crush fractures may be severe, but it is usually short term (six to eight weeks) and should resolve as the fracture heals. Although anabolic steroids and calcitonin are often used in acute pain relief, there is no evidence that they are more effective than simple and less expensive forms of analgesia. Those suffering multiple crush fractures, with loss of height and deformity ("dowager's hump"), may have chronic pain. Specific pain management programs may be useful, including medications, transcutaneous electrical nerve stimulation and relaxation. There is no evidence that braces or surgical corsets are useful in these patients except in the acute situation.

Falls prevention

Falls prevention programs are worth considering in the reduction of future fractures.

Multifactorial falls prevention strategies have been shown to be effective in some studies. These include specific exercise programs, medication management (especially to reduce the use of sedatives and tranquillisers), assessment of vision and footwear, and home and environmental modifications.

Analysis of data from the Dubbo Osteoporosis Epidemiology Study found that quadriceps strength, postural sway and bone density were independent predictors of subsequent fracture. Most observational and epidemiological studies suggest that physical activity is associated with a reduced risk of falling, likely because of improved balance and coordination skills.

Hip protectors reduce the incidence of hip fracture, especially in nursing home residents. More research is needed on their effectiveness and particularly on their acceptability.

Falls prevention programs are likely to be most effective when aimed at "at risk" individuals in the community. However, they are not necessarily inexpensive and more research is required to identify the components (e.g., balance training) which are most effective and cost-effective.

What are the priorities for future research into preventing and managing osteoporosis in Australia, and how can such research be promoted?

THERE have been relatively few trials investigating the efficacy of possible treatments or preventive interventions for osteoporosis and osteoporotic fractures, and most of the existing studies have had small numbers of subjects. Large studies are required before clear recommendations about the prevention and management of osteoporosis, and comparisons between treatments, can be made.

There are several levels at which research into osteoporosis should be carried out in Australia, with a focus on groups that have expertise in the areas of osteoporosis, bone biology, epidemiology, rehabilitation or large scale trials. Much of the basic research can and should be supported through expansion of existing peer reviewed funding. However, there is room for targeted interactions between basic scientific research and industry.

Research issues identified as being crucial to better and more cost-effective prevention and treatment of osteoporosis include:

Defining the magnitude of the problem

  • Better understanding of the epidemiology of osteoporosis in general and in various ethnic groups in particular.
  • Better understanding of costs, morbidity and mortality in non-hip fractures.

Pathophysiology color=#008080>

  • Basic bone biology, including identification of effective bone anabolic agents and understanding of genetic mechanisms.

Detectioncolor=#008080>

  • More efficient and cost-effective identification of individuals at high risk before fracture.
  • New methods to measure bone fragility, to supplement or replace the measurement of density.
  • Analysis of the role of genetic markers in diagnosis and selection of therapy.

A major focus in clinical application is the targeting of interventions to those at greatest risk and those most likely to respond to particular therapies. The roles of ultrasound, bone turnover markers, genetic factors and other clinical and biochemical indices need to be evaluated, to assess whether they assist in the selection of optimal therapy and could improve cost-effectiveness.

Prevention

  • Clarification of factors in attainment of peak bone mass, including genetic and lifestyle factors.
  • Clarification of the role and costs of lifestyle changes in preventing bone loss.
  • Identification of the components of fall prevention programs which contribute most to reducing falls and fractures.

The role of genetics and lifestyle factors in attainment of peak bone mass, including their action in prepubertal children, needs to be addressed. The relative effects of genetics and lifestyle factors may vary at different points during life. Some studies indicate that the effects of exercise or calcium are greater before than during adolescence. However, these studies have not followed children through to adulthood to determine whether peak bone mass is actually altered. Clarification of these points would allow recommendations about whether osteoporosis-related health promotion activities should be directed towards children or adolescents. Evaluation should be built in to all such health promotion programs. Community-based intervention studies are needed to determine the uptake of messages about lifestyle changes and whether these lead to changes in important indicators of osteoporosis in the population.

Treatment

  • Large scale comparative studies, including studies of combination therapies.
  • Investigation of whether targeting therapies to those most likely to benefit from them is useful.
  • Better understanding of optimal treatment (and prevention) of osteoporosis in men.

There is a major need for the definition and testing of "anabolic" therapies that will restore bone to a younger, healthier condition. Such agents are currently being investigated around the world and Australian osteoporosis scientists should be part of this effort.

There is also a clear need for direct testing of possible drug combinations, when positive or negative interaction cannot be predicted reliably from current data. These should be in large scale, long-term controlled studies. There is room for partnerships between clinical science, pharmaceutical companies and government health bodies for the exploration of comparative drug studies, with appropriate evaluation of non-drug interventions as well. Identification of those most likely to benefit from any pharmaceutical or lifestyle intervention is a critical issue.

It is vital that the Australian community, including the public, health professionals, public health authorities and governments, recognise the scope and magnitude of the osteoporosis problem, both in human and economic terms. With this recognition, research can be targeted towards the prevention and optimal management of osteoporosis and associated fractures.

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