Frequently Asked Questions (FAQs)

Updated September 2021

Any postmenopausal woman, or man over the age of 50 years, who has a clinical risk factor for osteoporosis, or where knowledge of fracture risk will impact clinical decision-making. The first step is to use FRAX (the first step is not to perform a DXA scan). With the results from FRAX, clicking the link to the NOGG website will give guidance on management (lifestyle advice, DXA scanning, necessity of pharmacological treatment).

Clinical risk factors for osteoporosis and/or fragility fracture, and therefore a trigger for a FRAX assessment include: a prior fragility fracture, a fall, use of glucocorticoids, parental history of hip fracture, rheumatoid arthritis, alcohol ≥3U/day, smoking, diabetes (either type), frailty, thoracic kyphosis, height loss >4cm, chronic malabsorption and bariatric surgery, chronic lung, liver, muscle, renal, neurological or inflammatory disease, HIV, malignancy, primary hyperthyroidism, hyperparathyroidism, hypogonadism, premature menopause, use of aromatase inhibitors and androgen deprivation therapy.

NOGG recommends the use of FRAX, which can be used with or without DXA results and calculates the 10-year probability of hip and major osteoporotic fracture (hip, spine, humerus or wrist). The results of FRAX are linked to NOGG treatment thresholds which guide management.

Use FRAX online to calculate the fracture probability entering the BMD result, then click to forward to the NOGG website where a treatment recommendation is provided.

This is quite common. You can adjust the probability of MOF. Deduct the femoral neck T-Score from the lumbar spine T-Score, and multiply this number by 10% of the original MOF probability. Add this number to the original MOF probability.

Worked example:
Original MOF = 15%
Femoral Neck T-Score = -1.0
Lumbar Spine T-Score = -3.5
Difference in T-Scores = (-3.5) – (-1.0) = -2.5

Calculate the MOF inflation (%) = difference in T-Scores x 10% x original MOF
= -2.5 x 0.1 x 15 = 3.75
Adjust the original MOF probability for low lumbar spine BMD = original MOF (15%) + inflation (3.75) = 18.75%

Where the lumbar spine is affected by artefact, it is best to use the mean of the two lowest T-Scores, least affected by artefact.

When doing a FRAX assessment, for patients with type II diabetes tick ‘rheumatoid arthritis’ (because type II diabetes increases fracture risk to a similar amount as does RA). For patients with type I diabetes, you can also tick ‘rheumatoid arthritis’.

Vitamin D deficiency leads to undermineralised bone and fractures due to osteomalacia. This results in low BMD which can mimic (or co-exist with) osteoporosis. Therefore, in patients with low BMD and/or fragility fractures, it is important to test for and treat vitamin D deficiency.

No. T-scores from local databases or ethnic-specific reference ranges can give misleading results. T-scores should be based on international reference data. For femoral neck BMD, the T-score should be derived from the reference standard, the NHANES III database for female Caucasians aged 20-29 years as widely recommended. Note that the same reference range is used for men (e.g., the NHANES III database for female Caucasians aged 20-29 years).

You should input a T-score for the femoral neck derived from the reference standard (the NHANES III database for female Caucasians aged 20-29 years as widely recommended). If you are uncertain about the T-score, input the manufacturer of the DXA device and the BMD result. The T (WHO)-score will be calculated for you.

Yes. It may not always be possible to obtain a DXA scan if a patient is particularly frail, unable to lie flat on a DXA table, or DXA is unavailable. But where possible patients at high or very high fracture risk should have a DXA when a baseline measurement is needed against which to compare future BMD measurements. Antiresorptive treatment should be considered:

  • When FRAX (calculated without BMD) indicates the risk of MOF and/or risk of hip fracture exceeds the intervention threshold,
  • In postmenopausal women, and men age ≥50 years, who have had a fragility fracture (FRAX is also recommended to aid risk-stratification and decisions when to measure BMD), drug treatment is particularly important in older people who have had a fragility fracture given their higher risk of re-fracture.

Because bone loss and increased fracture risk occur early after starting glucocorticoids, bone-protective treatment should be started at the same time as glucocorticoids are started, without waiting for bone density assessment (which can follow later), if you anticipate treating with glucocorticoids for 3 months of more, in the following circumstances:

Postmenopausal women, and men age ≥50 years:

  • With a prior fragility fracture,
  • Prescribed high doses of glucocorticoids, e.g., ≥7.5 mg/day of prednisolone or equivalent over 3 months,
  • With a FRAX probability of MOF or of hip fracture exceeding the intervention threshold.

The evidence is currently inconclusive. In patients with COPD, a large meta-analysis of RCTs did confirm an association between exposure to inhaled glucocorticoids and an approximately 1.3 x increased risk of fractures. In other meta-analyses the relationship was not seen at all or was only present (also at approximately 1.3 x increased risk) in those on high doses of inhaled glucocorticoids. Pragmatically, higher doses and continuous use of inhaled glucocorticoids should be borne in mind when deciding on investigations and management of bone health in such patients.

A person’s risk of sustaining another fracture is highest immediately after their first fracture; this increase in risk (known as imminent risk) remains particularly high for up to 2 years. This is the reason behind wanting to get patients onto treatment as soon as possible after a fracture.

The strongest evidence supporting fracture risk reduction of vertebral, non-vertebral and hip fractures is seen for alendronate, risedronate, zoledronate, denosumab, HRT and teriparatide. There is insufficient evidence to show that ibandronate, calcitriol or raloxifene reduce the risk of hip fracture, whilst the evidence for strontium is limited to post-hoc analyses. All the osteoporosis drug treatments recommended by NOGG reduce the risk of vertebral fractures, with the greatest reductions seen with the anabolic treatments teriparatide and romosozumab (which are prescribed in secondary care). Romosozumab followed by alendronate also substantially reduces the risk of non-vertebral, clinical and hip fractures.

Of the antiresorptive drugs denosumab and zoledronate induce the greater gains in BMD, whilst of the oral bisphosphonates, alendronate (if adherence is good) is the most effective at increasing BMD. Alendronate (if adherence is good) can lead to BMD gains close to those seen with zoledronate.

There is evidence that in postmenopausal women with severe osteoporosis who are at very high fracture risk, anabolic therapy, with teriparatide or romosozumab, has greater anti-fracture efficacy than an oral bisphosphonate. In men with osteoporosis, teriparatide is also effective at reducing fracture risk. Furthermore, anabolic treatments perform better when given to treatment naïve patients than as a second line treatment. Thus, certain high-risk patients should be considered for referral to an osteoporosis specialist in secondary care, for further evaluation.

  • a recent vertebral fracture [within the last 2 years]
  • ≥2 vertebral fractures [whenever these have occurred]
  • BMD T-Score ≤-3.5
  • treatment with high dose glucocorticoids [≥7.5 mg/day of prednisolone or equivalent over 3 months] (refer urgently given rapid loss in bone post initiation of glucocorticoids; if any delay is anticipated, start an oral bisphosphonate in the meantime)
  • the presence of multiple clinical risk factors, particularly with a recent fragility fracture indicating high imminent risk of re-fracture.

The guideline states that in these cases consideration to the need to referral should be made, not that it is mandated. A referral decision will depend upon the clinical judgement of the physician taking into consideration the wider clinical picture.

Patients with a recent hip fracture are generally considered to be at very high fracture risk. As part of their post-operative recovery, they should be reviewed by an orthogeriatrician who can advise on osteoporosis treatment. Post-hip fracture, use of zoledronate has a strong evidence base to support use in those at very high fracture risk, although anabolic therapy may also be considered.

Good communication between healthcare professionals and patients is needed to involve patients in decisions about medicines and to support adherence. When osteoporosis treatments are first recommended:

  • Explain why the treatment is recommended (explain osteoporosis and potential consequences)
  • Discuss potential benefits. Ensure patients have realistic treatment expectations, it can be helpful to explain the treatment works ‘silently in the background’ to strengthen bones and lower risk of future fractures.
  • Discuss practical issues about taking medicine. Explain why there are special instructions for taking bisphosphonates (to increase efficacy and lower risk of side effects), and that denosumab has to be given every 6 months (to avoid rebound vertebral fracture risk).
  • Address any concerns. When discussing risks (of benefit and harm) use simple frequencies e.g., positive, and negative framing (e.g., 1 in 100 will, meaning 99 in 100 will not) and avoid words such as ‘common’ or ‘rare’ which have variable interpretations.
  • Reassure patients that there are other potential treatment options if required.
  • Ensure patients are asked about adherence at medicine reviews and restate the need for medicine and offer opportunities to address any concerns.

The approach set out here is a guide and communication needs to be adapted to each individual patient. The approach is applicable to professionals in both primary and secondary care and their co-working.

Schedule a review of tolerance and adherence 12-16 weeks after starting bisphosphonates. Also ask about adherence and tolerance at routine medicine reviews. Ask if patients are remaining upright for at least 30 minutes and taking plenty of water with medicines, which is important in preventing upper gastro-intestinal symptoms. If available, measurement of the bone resorption marker, serum CTX (after an overnight fast) or bone formation marker serum P1NP, may be helpful in showing adherence and response to treatment.

If patients are unable to tolerate alendronate and risedronate, consider referral to secondary care services for consideration of a parenteral form of treatment. These include IV zoledronate, SC denosumab or anabolic drug treatments (teriparatide and romosozumab). Other options to consider are second-line treatment choices of hormone replacement therapy, raloxifene (or strontium ranelate if all other treatments are not tolerated or contraindicated). Alternatively, in some areas denosumab may be initiated in primary care, although use in younger people is now advised against, due to the risk of rebound increase in bone turnover and increased fracture risk when the drug is stopped – see also FAQ 23: ‘What should you consider when choosing between use of denosumab or zoledronate?’

  • Very high-risk patients for further assessment of causes of osteoporosis, and evaluation for parenteral therapies. A sub-group may potentially benefit from anabolic therapy, particularly those with multiple vertebral fractures.
  • Referral indications include those with a recent vertebral fracture [within the last 2 years], ≥2 vertebral fractures [whenever these have occurred], BMD T-Score ≤-3.5, treatment with high dose glucocorticoids (≥7.5 mg/day of prednisolone or equivalent over a period of 3 months), or other indicators of very high fracture risk as defined by FRAX.
  • Consider carefully patients at very high risk of fracture who are then starting high dose glucocorticoids (≥7.5 mg/day of prednisolone or equivalent over a period of 3 months) as they are at particularly high risk of fracture, they often need to be referred urgently to secondary care, as bone loss is seen early in this situation. Some may benefit from first-line anabolic treatment; however, if any delay is anticipated then start an anti-resorptive whilst waiting for secondary care review.
  • Denosumab is a parenteral therapy – if there is access to initiate this in primary care it is advisable to do this in liaison with a secondary care specialist and in high risk patients to seek advice and guidance about whether this is the most appropriate treatment option.
  • Patients who fracture despite adherence to first-line therapy for 2 years or more (remember it is worth checking for secondary causes of osteoporosis in this situation, see next question).
  • Patients who are intolerant of oral bisphosphonates who you wish to treat with IV zoledronate or SC denosumab, if access to these treatments is not available through local community or primary care-based services.
  • Patients with CKD4 or 5 who sustain a fragility fracture.
  • Women treated with aromatase inhibitors and men treated with androgen deprivation who are at high risk of fracture may benefit from secondary care assessment, as may patients with severe malabsorption.
  • Younger men and women with osteoporosis who may need specialist investigation and guidance over management.

  • Check blood tests: FBC, CRP (or ESR), Calcium, Phosphate, ALP, LFTs, 25-hydroxyvitamin D, TFTs,
  • Measure PTH if albumin-adjusted serum calcium ≥2.6mmol/l twice, or if ≥2.5mmol/l twice if primary hyperparathyroidism is suspected
  • Consider testing for myeloma: Serum electrophoresis and serum free light chains.
  • Consider measuring PSA in men.
  • TTG as a screen for coeliac disease- if there is anaemia, weight loss or bowel disturbance.
  • Less routine tests to consider include:
    • Serum testosterone, sex hormone binding globulin, FSH, LH, Serum prolactin
    • 24-hour urinary free cortisol/overnight dexamethasone suppression test
    • Urinary calcium excretion

No. Routine pre-treatment checks by a dentist are not necessary. You should do these simple things:

  1. Ask the patient if they need any teeth extractions or implants (in which case these should be done before starting parenteral therapies),
  2. Advise the patient to take good care of their teeth and attend their routine dental check-ups.
  3. Provide additional resources as needed, e.g., the Scottish Medicines Consortium leaflet ‘Dental advice for patients prescribed anti-resorptive drugs for the treatment of osteoporosis’

The choice of drug treatment should be informed by the level of fracture risk, patient suitability and patient preference. HRT can be considered in younger post-menopausal women (age ≤ 60 years) who have low risk of malignancy and of thromboembolic events. Generally, at this age, treatment with oral HRT could be offered for 5 years, after which fracture risk should be re-assessed (sooner in the case of an incident fracture).

After a patient has received two doses, if denosumab is then missed or delayed by more than 7 months since the last injection (e.g., by more than 1 month from the due dose), there is a risk of rebound high bone turnover and bone loss which can lead to multiple vertebral fractures in some cases. This risk is greater in patients who have received longer durations of treatment. It is challenging to stop denosumab, therefore, it is important that both clinicians and patients are made aware of this before treatment is started. Denosumab should not be stopped suddenly before a further treatment plan is made.

Denosumab and zoledronate have similar clinical efficacy in terms of fracture risk reduction. Their use is associated with similarly low rates of rare AFFs and ONJ. The logistical considerations of drug administration and patient preference are important to consider. Zoledronate must be given IV annually, whist denosumab is given subcutaneously biannually. Delays in zoledronate administration are not associated with the risk of rebound high bone turnover and fracture risk that is seen when denosumab dosing is delayed. When denosumab is started consideration must be given to how and when treatment might be stopped; this is not an issue with zoledronate. An additional consideration is the duration of treatment as zoledronate can frequently be paused for several years (after 3 annual infusions) whereas denosumab treatment needs to be continued long-term. Zoledronate requires a creatine clearance >35 mL/min; whilst denosumab can be used with a creatinine clearance <35 mL/min, the risk of hypocalcaemia is increased, and monitoring is warranted in liaison with secondary care. If denosumab therapy is stopped, intravenous infusion of zoledronate is recommended 6 months after the last injection of denosumab.

Vitamin D deficiency (< 25 nmol/L) and insufficiency (25-50 nmol/L) should be treated before parenteral treatments are started, and alongside initiation of oral treatments. Where rapid correction of vitamin D deficiency is required, such as in patients about to start zoledronate, denosumab, teriparatide or romosozumab, the recommended treatment regimen is based on fixed loading doses followed by regular maintenance therapy. In the case of vitamin D deficiency a loading regimen should provide a total of 300,000 IU vitamin D, in divided doses, given weekly (or daily) over 6 to 10 weeks. Where correction of vitamin D deficiency is less urgent and when co-prescribing vitamin D supplements with an oral antiresorptive agent (e.g., when starting alendronate, risedronate, ibandronate, HRT, raloxifene), maintenance therapy may be started without the use of loading doses (maintenance usually 800 IU daily, sometimes up to 2,000 IU daily). Either way, adjusted plasma calcium should be checked one month after completing the loading regimen or after starting lower dose vitamin D supplementation in case, albeit rarely, primary hyperparathyroidism has been unmasked.

Lifestyle advice for people with osteoporosis and/or high fracture risk should include advice on optimisation of CRP, smoking cessation and reducing alcohol intake to ≤2 units/day.A healthy, nutrient-rich balanced diet should be recommended to people with osteoporosis, with specific focus on protein intake and calcium (minimum 700mg daily). If dietary intake is suboptimal calcium supplements should be considered, and people with osteoporosis or high fracture risk who are likely to have vitamin D insufficiency (e.g., individuals who are housebound or living in residential or nursing care) should receive 800IU vitamin D supplements. Dietary calcium calculators are available from the University of Edinburgh and the IOF, and the ROS provides information on calcium-rich foods). A combination of weight-bearing and muscle strengthening exercise to promote bone strength is recommended, tailored according to the individual patient’s needs and ability; the ROS website includes detailed exercise advice, leaflets and videos.

There is no clear evidence that calcium supplementation increases cardiovascular risk.

FRAX can be helpful when assessing fracture risk, with CKD added as a secondary cause of osteoporosis. DXA ESR T-Score is helpful at predicting fracture risk in those with CKD. The osteoporosis drug treatments have different kidney function thresholds for use. Most stringent is that for zoledronate (a Cockroft Gault creatinine clearance >35 ml/min). Alendronate requires an eGFR >35 ml/min, whilst risedronate and ibandronate require an eGFR >30 ml/min. Although denosumab can be used in patients with impaired renal function, specialist advice is advised for those with an Cockroft Gault creatine clearance <30 ml/min given the increased risk of hypocalcaemia. Teriparatide, raloxifene and strontium are not licensed for use in severe renal impairment. Patients with CKD 4 or 5 often need referral to secondary care to guide management of increased fracture risk.

If a patient sustains a fragility fracture whilst on treatment (this excludes fractures of the skull, nose, feet and hands), review treatment adherence and investigate for secondary causes of osteoporosis, such as vitamin D deficiency. If a patient has been adherent to an established treatment for 2 or more years and has fractured, consider changing the treatment, in consultation with the patient. Re-assess their fracture risk using FRAX, consider repeating a DXA scan and consider specialist referral.

Any patient who is age >70 years, has previously fractured a hip or a vertebra, or is exposed to oral glucocorticoids (≥7.5 mg/day of prednisolone or equivalent over 3 months) should be counselled for at least 10 years of treatment when the bisphosphonate is started.

In those who are at lower risk, treat for 5 years in the first instance with a plan to re-assess. If a patient experiences a fracture during treatment, they should receive at least 10 years of treatment (although the drug of choice may change).

All patients should be reviewed at 12-16 weeks post oral treatment initiation to check they are able to tolerate the drug, and then at 1 year to check they are still taking the drug. After 5 years of treatment all patients should be reviewed again to re-assess adherence, the emergence of new secondary causes of osteoporosis and whether the drug is still the right choice for them.

Because bisphosphonates are retained long term in bone (unlike other osteoporosis treatments), the beneficial effects can persist for some months or years after treatment is paused. However, this effect wanes with time. A temporary treatment pause of 18 to 36 months may be considered in lower risk patients, after 5 years’ oral bisphosphonate or 3 years’ intravenous bisphosphonate (see clinical flowchart in the main guideline). However, it is important to reassess risk after 2 years, and sooner if a patient sustains a fracture, or their clinical risk factors change. If bisphosphonate treatment is discontinued and no new fracture occurs, it is recommended to reassess using FRAX after 18 months for risedronate and ibandronate, 2 years for alendronate, and 3 years for zoledronate.

At a minimum, patients receiving osteoporosis treatment usually need a rescan at 5 years to guide treatment decisions. More frequent scans might be appropriate if patients are very high risk or if they fracture on treatment, but not usually at intervals of less than 2 years.

There is no evidence one way or the other for efficacy and safety beyond 10 years. Patients should be reviewed, fracture risk reassessed, and a clinical judgement made. You may need to seek advice from an osteoporosis specialist.

When glucocorticoids are stopped it is important to re-assess fracture risk using FRAX as the patient may have other clinical risk factors (besides glucocorticoids) that justify ongoing bisphosphonate treatment. If on re-assessment the probabilities of both MOF and of hip fracture lie below the intervention threshold then bisphosphonate treatment can be stopped with a plan to re-assess fracture risk using FRAX after e.g., 2 years.

ONJ and AFFs are rarely associated with long-term use of bisphosphonates, each with a risk of between 1 in 1000 and 1 in 10,000. Unexplained thigh pain can be investigated initially by plain X-ray. The ROS provides free patient information leaflets for AFF and ONJ.

If the vitamin D level is below 25 nmol/L, treat with high dose vitamin D (50,000 units weekly for 6 weeks or equivalent) and delay the denosumab by 4 weeks.

Creatinine clearance should be calculated using the patient’s weight. If calculated creatinine clearance is ≤ 30ml/min, seek guidance from secondary care specialists before giving denosumab.

Patients on denosumab should be reviewed every 5 years, or sooner if they fracture or their clinical risk factors worsen. Denosumab should not be stopped suddenly before a further treatment plan is made. If clinically indicated, denosumab can be continued safely over a 10-year period.

There is no evidence one way or the other for efficacy and safety beyond 10 years. Patients should be reviewed, and a clinical judgement made. Often a specialist opinion is needed before stopping denosumab.

ONJ and AFFs are rarely associated with long-term use of antiresorptives, each with a risk of between 1 in 1,000 and 1 in 10,000. Unexplained thigh pain should therefore be investigated, initially by plain X-ray. These rare risks need to be balanced against the risk of MOF, quantified by FRAX, for example a MOF of 20% equates to a 1 in 5 risk of a major fracture over 10 years, and the potential fracture risk reduction with treatment (e.g., halving fracture risk). The ROS provides free patient information leaflets for AFF and ONJ.

While access to BTMs from primary care remains limited, there is some evidence to support their use in the monitoring of response to treatment, and they have a particular role to play in patients starting treatment with oral bisphosphonates. They show large and rapid changes in response to osteoporosis treatment allowing detection of a significant treatment response within a few months. Those who do not show a response tend to have smaller gains (if any) in BMD and smaller reductions in fracture risk; detection of a non-response can direct consideration of other treatment options (e.g., parenteral therapies). BTM should not be measured within 12 months of a fracture as bone turnover increases during fracture healing and therefore interpretation is difficult. Some centres have translated their extensive experience with BTMs into routine clinical management and more detail can be found at the following links:

Pain from a vertebral fracture can be felt anywhere in the lower back or thoracic region. It may radiate round to the waist. It is usually constant but exacerbated by standing and relieved by lying down. The pain is usually described as a dull toothache but can also be sharp and stinging, and often builds to a crescendo. Other features that suggest back pain may be related to vertebral fractures are reported height loss of more than 4cm, known osteoporosis or risk factors for osteoporosis, such as glucocorticoid use.

  1. If confirming a vertebral fracture will cause you to treat and/or refer to secondary care a person who would otherwise go untreated (e.g., vertebral fractures may identify someone at very high fracture risk); and/or
  2. If a patient has back pain, particularly crescendo pain when leaning forward such as when washing up, as interventions including physiotherapy and back strengthening exercises are likely to improve health-related quality of life.
  3. If a patient loses ≥4cm in height and DXA VFA is unavailable

Vertebral fractures are often one of the first types of osteoporotic fracture a patient may experience, and they signal an increased risk of further fractures to come (e.g., of the hip) if no action is taken. Vertebral fractures cause pain, disability, and impact long-term quality of life. Of all the fracture types, the treatments we have available are best at reducing vertebral fracture risk, so overlooking vertebral fractures means patients don’t access effective and necessary medications. Patients should be established on treatment as soon as possible after a vertebral fracture has been identified. If a patient has had ≥2 vertebral fractures they may be eligible for anabolic treatment so specialist referral should be considered.

Yes. FRAX, unlike other risk tools, calculates a fracture probability which is dependent both on the risk of fracture and on the risk of death. Thus, FRAX takes account of the competing effects of mortality and can be used in individuals at advanced age up to 90-years of age.

Two reasons. The first is that the cohort data used to create the FRAX model reported falls in very different ways, so that it was not possible to derive a standardised metric. Second, uncertainties remain as to whether patients identified through falls risk would benefit from osteoporosis drug intervention. Studies are underway to enlarge the international database on falls risk. NB. FRAX is based on the inclusion of individuals who are at all levels of falls risk so, though not an input variable, falls are partly accounted for in the calculation of FRAX.

It is important to remember to perform a FRAX assessment on any postmenopausal woman, or man age ≥ 50, who reports a fall or a near fall.

No. Physiological age is more important that chronological age. FRAX assessment indicates when a DXA scan would aid fracture risk assessment. A DXA scan should also be considered where a baseline measurement is expected to be needed in 5 and/or 10 years’ time when a DXA is repeated to assess treatment response, life-expectancy may challenge this requirement.

Patients who are frail are often at very high fracture risk, so assessment and treatment are important. Use FRAX to calculate the probability of fracture. When a patient is aged ≥ 70 years you should consider antiresorptive treatment when the probability of MOF is ≥ 20.3% or hip fracture is ≥ 5.4% (these figures are those of the fixed intervention thresholds for those age ≥ 70). In this case, if you are starting oral anti-resorptive treatment, you should counsel the patient for at least 10 years of treatment (e.g., the rest of their life).

This is a balance as towards the end-of-life fracture risk is highest. It is also often difficult to judge when someone is in the last year of life. When bisphosphonates are stopped, they continue to have a protective effect on the skeleton for many months, so stopping a bisphosphonate for someone in the last year of life is reasonable. When denosumab is stopped, within a month of missing the due dose, vertebral fracture risk increases. When they occur, vertebral fractures are painful and debilitating. So, whilst stopping denosumab in the last months of life may be reasonable, doing so routinely in the last year of life is less advisable. It remains important to discuss the pros and cons of treatment carefully with the patient and/or their family/carer, to enable shared decision-making.

Fractures can still occur in those who are bedbound, so this decision depends on the reason for being bedbound and the patient’s prognosis. If the reason stems from frailty at the end-of-life, then see the response above. If the reason stems from a chronic disability that precludes weight-bearing then the reasoning is very different (e.g., stable disability post-stroke, spinal cord injury). Those who are unable to weight-bear are at very high risk of fracture, as loading of the skeleton is so important in maintaining bone density and strength. Patients may need to live with this disability for many years and hence may benefit greatly from bone protective medication.

DXA measurement may be appropriately undertaken in younger individuals where there has been a prior fragility fracture or there is a strong clinical risk factor for low bone density, such as malnutrition or malabsorption, particular medications, e.g., glucocorticoids, or a disease associated with bone loss. FRAX can be used to assess fracture risk and guide BMD measurement and treatment in those age ≥ 40 years, but not below this age.

Fragility fractures and osteoporosis are uncommon in younger individuals and therefore when these occur patients need thorough investigation for secondary causes of osteoporosis, and careful consideration of treatment options. Specialist referral is usually required.

Treatment decisions in younger patients should usually be made via referral to, or in discussion with, specialist osteoporosis care. Baseline absolute fracture probability is usually low, even when bone mineral density is in the osteoporosis range, and in the majority, intervention with antiosteoporosis treatments may be most appropriately targeted to those who have experienced a fragility fracture.

If you have a question that is not addressed by these FAQs, please email,
and if frequently asked, we will look at adding additional FAQs in the future.
Thank you