Risk factors, fracture risk assessment and case-finding

Measurement of Bone Mineral Density

Measurement of BMD

Recommendation 4


Measure BMD by DXA scanning on at least two skeletal sites, including the lumbar spine and hip, unless these sites are unsuitable (eg hip prosthesis).


The WHO international reference standard for osteoporosis diagnosis is a T-score of –2.5 or less at the femoral neck (FN).1 The reference standard from which the T-score is calculated is the female, White, age 20–29 years, Third National Health and Nutrition Examination Survey (NHANES III) database, or equivalent. Osteoporosis may be diagnosed in postmenopausal women and men aged >50 years if the T-score of the lumbar spine, total hip or FN is –2.5 or less. In certain circumstances, the 33% radius (also called the ‘one-third radius’; i.e., distal forearm) may be used.2 The WHO BMD diagnostic osteopenia and osteoporosis classifications should not be used in premenopausal women and in men <50 years of age, or in children. In these patient groups, the diagnosis of osteoporosis should not be made using DXA criteria alone.2

As a reference for fracture risk calculation in women in Australia, T-scores calculated from the Geelong Osteoporosis Study database are used for the lumbar spine and proximal femur. Normative data in Australian men are not currently available. Most BMD assessments currently report hip T-scores for men based on the US NHANES III normative data. There are no standardised reference ranges for spine BMD in men and the only option is the use of reference ranges provided by densitometer manufacturers. In some cases, this may change the diagnostic classification.3

DXA is the current gold standard for the diagnosis of osteoporosis. The best sites at which to measure BMD for prediction of future fracture risk are the lumbar spine and the proximal femur.2,4 Both sites should be measured with consideration to dual hip scanning. DXA is reliable, with a reported precision of approximately 1%, although in routine clinical practice this is closer to 2%.2 At this level of precision, the least significant change at the lumbar spine would be 5.6% between measurements, with 95% confidence that the change is real.

Each SD reduction in FN BMD increases the age-adjusted risk of hip fracture by a factor of approximately 2.5 (range 2.0–3.5), whereas the risk attributable to any minimal trauma fracture is almost the same (range 1.7–2.4). Similarly, each SD reduction in lumbar spine BMD increases the risk of spinal fracture by a factor of approximately 2.3 (range 1.9–2.8). FN and total hip BMD appear the best overall predictors of fracture risk. Total hip is the better site for monitoring BMD because it has good precision (less affected by positioning) and is relatively unaffected by osteoarthritis, which can spuriously elevate spinal BMD values, as can vertebral fractures and arterial calcification.2,5

The initial assessment of BMD by DXA has the following aims:

  • to determine the patient’s BMD: Fracture risk is multifactorial and may be significantly elevated in individuals outside the osteoporotic range. However, the use of the osteoporotic T-score threshold is the criterion by which healthcare funders define osteoporosis, as well as being consistent with studies in which antifracture effects of anti-osteoporotic drugs have been demonstrated.
  • to determine the precise extent of BMD reduction: This is important for refining assessment of individual fracture risk and the extent of recommended therapeutic measures. Absolute fracture risk algorithms (e.g., FRAX® [available at] or the Garvan Fracture Risk Calculator [available at]) may be useful in more accurately determining individual fracture risk and assisting the patient in making a treatment decision (refer to Section 1.3).

Repeat DXA scans at intervals of two years or longer can be considered to assist risk assessment or when a change or interruption in treatment is being considered (also refer to Section 4).6–8 The treatment-related change in BMD correlates with the proportion of fracture risk reduction.7–9 In addition, repeat BMD measurement can identify people with ongoing bone loss, which is an independent predictor of fracture risk.6 Repeat DXA scans may improve adherence to therapy in some people.10 However, a minimum of two years may be needed to reliably measure a change in BMD due to limitations in DXA precision. If BMD is stable and/or the individual is at low risk of fracture (normal or mild osteopenia; T-score >–1.5), less frequent monitoring, up to an interval of 5–15 years, can be considered. Shorter intervals between repeat DXA scans at intervals of one year may be appropriate in high-risk individuals (e.g., patients on corticosteroid therapy or ADT for prostate cancer). In all cases, the expected rate of change in BMD and fracture risk should guide repeat measurement.6

Quantitative computed tomography (QCT) BMD measurement can provide equivalent hip BMD to DXA scans and may be interpreted using the WHO T-score criteria.1 Spinal QCT also provides information on fracture risk, but it is important to note the WHO T-score osteoporotic criteria cannot be applied in this situation.11

Fracture risk using QCT of the spine is mostly interpreted using American College of Radiology criteria.12 There are no data demonstrating a reduction in fracture risk by specific anti-osteoporotic treatment chosen based on QCT measurements. However, given the equivalency of hip QCT to hip DXA, there is no reason to doubt the utility of hip QCT in guiding therapy.13 The disadvantage of QCT remains the significantly higher radiation exposure compared with DXA,13 particularly at the hip. DXA of the spine and hip remains the recommended measurement for the diagnosis of osteoporosis and baseline BMD assessment. In some patients with moderate-to-severe osteoarthritic changes, spine QCT may have a particular advantage because it is less affected by osteoarthritic changes than DXA.

Quantitative ultrasound

Quantitative ultrasound of the heel and other sites can provide information on fracture risk.2 However, quantitative ultrasound has not been demonstrated to provide information on absolute fracture risk and reduction of fracture risk by anti-osteoporotic treatment. DXA measurements at the spine and proximal femur are preferred for making therapeutic decisions and should be used, if possible. Quantitative ultrasound is not recommended as a routine diagnostic test for osteoporosis.

Biochemical markers of bone turnover

Increased biochemical markers of bone turnover in the blood and/or urine (e.g., serum C-terminal telopeptide or serum alkaline phosphatase) have been shown in trials to be independent risk factors for fractures in women and men.14 Bone turnover markers are useful markers of medication adherence and response to treatment, and may help guide choice of treatment. Short-term treatment-related changes in bone turnover markers account for a large proportion of the treatment effect of vertebral fracture.15 However, variability in analysis and lack of standardisation may reduce the utility of these assessments on an individual basis in routine clinical practice.

  • For patients with ready access to DXA, a BMD measurement before commencing therapy is recommended. A normal or near-normal BMD despite existing fractures should prompt a more extensive work-up to exclude other causes of fracture.
  • A normal BMD despite typical vertebral fractures also poses a problem regarding the usefulness of anti-osteoporotic treatments that have not been tested in such a population. Such discrepant findings should be resolved on an individual basis and may require specialist (e.g., endocrinologist, rheumatologist) referral.
  • A history of high-trauma falls resulting in vertebral fracture can leave evidence of vertebral deformities that may not indicate underlying osteoporosis. In such situations, consultation with a specialist may be warranted.
  • Conventional radiographs should not be used for the diagnosis or exclusion of osteoporosis.
  • Evaluation of osteoporosis is based on the lower T-score of either the lumbar spine, FN or total hip.1
  • The BMD at the forearm may be measured by DXA, but caution is advised because there are limited data on its use in guiding therapy.
  • Repeat BMD measurements may be performed to assess the efficacy of treatment and residual fracture risk or to assist in improving patient medication adherence.
  • If possible, it is recommended repeat BMD tests are performed using the same instrument or at least the same make of instrument (manufacturer and model type) to improve the comparability of results in interpreting BMD change.6
  • Relevant blood and urine studies should be obtained prior to initiating therapy if the medical history and/or clinical examination is suggestive of secondary osteoporosis, or the DXA Z-score is ≤–2.0 (i.e., two or more SDs different from age- and sex-matched controls).16
  • If radiographs reveal one or more vertebral fractures typical of osteoporosis, BMD measurement may not be essential before starting medical therapy, if clinically appropriate. There are a limited number of scenarios in which meaningful evaluation of BMD is not possible (e.g., bilateral hip replacements and osteoporotic fractures in the lumbar spine region of BMD measurement [L2–4]). In such cases, it should be assumed that BMD measurement would have been low and that therapy is likely to be beneficial. Forearm BMD may be useful; however, its precise value has not been as well characterised as spine and hip BMD.
  1. World Health Organization (WHO). Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO study group [meeting held in Rome from 22 to 25 June 1992]. WHO, 1994 [Accessed 16 January 2024]
  2. International Society for Clinical Densitometry (ISCD). Official positions adult of the ISCD. ISCD, 2019 [Accessed 30 October 2023]
  3. McMahon K, Nightingale J, Pocock N. Discordance in DXA male reference ranges. J Clin Densitom 2004;7(2):121–26.
  4. Johansson H, Kanis JA, Oden A, Johnell O, McCloskey E. BMD, clinical risk factors and their combination for hip fracture prevention. Osteoporos Int 2009;20(10):1675–82.
  5. Kanis JA, Glüer CC. An update on the diagnosis and assessment of osteoporosis with densitometry. Committee of Scientific Advisors, International Osteoporosis Foundation. Osteoporos Int 2000;11(3):192–202.
  6. Kendler DL, Compston J, Carey JJ, Wu CH, Ibrahim A, Lewiecki EM. Repeating measurement of bone mineral density when monitoring with dual-energy X-ray absorptiometry: 2019 ISCD official position. J Clin Densitom 2019;22(4):489–500.
  7. Leslie WD, Majumdar SR, Morin SN, Lix LM. Change in bone mineral density is an indicator of treatment-related antifracture effect. Ann Intern Med 2017;166(2):152–53.
  8. Black DM, Bauer DC, Vittinghoff E, et al. Treatment-related changes in bone mineral density as a surrogate biomarker for fracture risk reduction: Meta-regression analyses of individual patient data from multiple randomised controlled trials. Lancet Diabetes Endocrinol 2020;8(8):672–82.
  9. Bouxsein ML, Eastell R, Lui LY, et al. Change in bone density and reduction in fracture risk: A meta-regression of published trials. J Bone Miner Res 2019;34(4):632–42.
  10. Kline GA, Lix LM, Leslie WD. Patient outcomes in the years after a DXA-BMD treatment monitoring test: Improved medication adherence in some, but too little too late. J Bone Miner Res 2021;36(8):1425–31.
  11. Faulkner KG, von Stetten E, Miller P. Discordance in patient classification using T-scores. J Clin Densitom 1999;2(3):343–50.
  12. American College of Radiology (ACR). ACR practice guideline for the performance of quantitative computed tomography (QCT) bone densitometry (Resolution 33). ACR, 2008 [Accessed 30 October 2023]
  13. Brett AD, Brown JK. Quantitative computed tomography and opportunistic bone density screening by dual use of computed tomography scans. J Orthop Translat 2015;3(4):178–84.
  14. Vasikaran S, Eastell R, Bruyère O, et al. Markers of bone turnover for the prediction of fracture risk and monitoring of osteoporosis treatment: A need for international reference standards. Osteoporos Int 2011;22(2):391–420.
  15. Eastell R, Black DM, Lui LY, et al. Treatment-related changes in bone turnover and fracture risk reduction in clinical trials of antiresorptive drugs: Proportion of treatment effect explained. J Bone Miner Res 2021;36(2):236–43.
  16. Cosman F, de Beur SJ, LeBoff MS, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int 2014;25(10):2359–81.
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