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Ongoing monitoring

Ongoing monitoring

It is important to distinguish ongoing BMD monitoring for patients on, and not on, treatment.

Recommendation 33


Regularly reassess fracture risk and the requirement for anti-osteoporotic therapy in patients not receiving therapy, but who remain at increased fracture risk.



The frequency of reassessment should be determined by the individual’s overall fracture risk or circumstances that may worsen bone loss. Vigilance should be exercised for height loss and new episodes of back pain, which may indicate a new vertebral fracture.

Recommendation 34


Clinically review all patients 3–6 months after initiating pharmacological therapy for osteoporosis, and 6–12 monthly thereafter for medication side effects and therapy adherence.


Recommendation 35


Measurement of bone turnover markers should be confined to specialist practice. Measurement of bone turnover markers may be useful for monitoring medication adherence and efficacy and for evaluation of secondary causes of bone loss.


At present, there are no validated criteria for failure of medical therapy. However, therapeutic failure should be considered if:

  • minimal trauma fractures occur (usually more than one fracture event), in which case other non-pharmacological measures need to be or reinforced, as required (refer to Section 2)
  • there is a documented decrease in height ≥3 cm since the last examination or acute back pain, which may be symptomatic of a new fracture; in these cases, a radiological examination is recommended.

Osteoporosis treatment is required for many years. Monitoring patients with BMD assessment by DXA must be at practical intervals to check gradual improvement while avoiding unnecessary imaging. A meta-regression of published trials has shown that greater improvements in BMD were strongly associated with greater reductions in vertebral and hip fracture, but not non-vertebral fractures.1 It also found that improvement in total hip BMD accounted for 56% of the fracture risk reduction seen with osteoporosis treatment.1

For those ON bone protective pharmacotherapy:

  • In patients with confirmed osteoporosis, a repeat BMD test is generally not required, but may be conducted before initiating a change in, or cessation of, anti-osteoporotic therapy.
  • The occurrence of a new minimal trauma fracture while on bone-protective pharmacotherapy may warrant a repeat DXA sooner than two years to detect ongoing BMD loss. This may prompt a treatment switch (e.g., to parenteral antiresorptive therapy [denosumab or zoledronate] or an osteoanabolic agent).

For those NOT on bone protective pharmacotherapy:

  • A decrease in BMD greater than measurement error is generally not seen before two years; hence, follow-up bone densitometry is not generally recommended at intervals of less than two years.2,3 Specific exceptions are patients at high risk of bone loss (e.g., those on corticosteroids, ADT or aromatase inhibitors), in whom yearly monitoring may be warranted.
  • It may be appropriate to repeat DXA assessment after two years in patients at risk of developing osteoporosis, to assist in re-evaluation of fracture risk (refer also to Sections 1.2 and 1.3).
  • Consider timing of subsequent BMD measurement based on the current absolute risk and likelihood of change in BMD to an extent that would change management.
  • Wherever possible, perform repeat BMD testing on the same instrument, or at least the same type (manufacturer and model type) of instrument, to improve the comparability of results in interpreting change in BMD. The lumbar spine and total proximal femur are the optimal sites to monitor BMD. Dual-hip DXA should also be considered to improve diagnosis and precision of monitoring at the hip.4
  • Changes of <5% or 0.05 g/cm2 at the lumbar spine or hip are within the precision error of most DXA machines and should therefore be regarded as representing no significant change.
  • A radiographic assessment should be initiated if new fractures are suspected (eg height loss ≥3 cm, new or acute pain).
  • Refer to Appendix C, which provides a list of current Medicare Benefit Schedule (MBS) item numbers for bone density testing using DXA.

Biochemical markers of bone turnover decrease rapidly (within three months) after initiation of antiresorptive drugs such as oral or IV bisphosphonates, denosumab or raloxifene, and increase with commencement of osteoanabolic therapies.5–8 They have also been shown to provide information on the antifracture efficacy of these agents.8,9 For these reasons, bone turnover markers may be used to assess the effect of therapy on bone metabolism.

Measuring a bone resorption marker (e.g., serum C-telopeptide) after three months of antiresorptive treatment and finding a level in the lower half of the premenopausal range generally indicates adherence with antiresorptive therapy. However, in the absence of clear evidence of improved patient outcomes from the use of bone resorption markers, as well as cost-effectiveness data, their routine use in patient monitoring in general practice is not recommended.

Evidence Statement

Failure to observe an increase in BMD during therapy with bisphosphonates, denosumab, or raloxifene does not indicate decreased antifracture efficacy of the drug and is no indication to change treatment.10–15 A stable or increasing BMD during treatment should be considered as adequate therapy response.10,12–16 In contrast, detectable loss of BMD while on antiresorptive treatment may be associated with negative clinical outcomes (increased fracture risk) and should prompt review of diagnosis, treatment regimen, and patient medication adherence.2,17

A decision to change treatment based solely on a new fracture occurring during treatment is not supported by RCT data. Because fractures will occur in some individuals even on effective therapy, fracture per se is not an indication to change. However, patient tolerance, treatment adherence, and side effect profile may suggest changing the type or route of administration of therapy on an individual basis. Evidence of lack of response (e.g., falling BMD or failure to achieve expected changes in bone turnover markers) could justify a change. However, adherence with, and the correct mode of taking medications should be evaluated first, because problems with these aspects are the most likely explanation. Although long-term adherence with non-pharmacological and pharmacological interventions is crucial, it is often low, even in patients with fractures.18,19

Follow-up visits, close contact between patient and health professionals, and repeat BMD and/or bone turnover marker measurements, may be used to improve medication adherence. In a British study, review of results of serial BMD and/or bone turnover marker measurements between nurse and patient, or doctor and patient, resulted in improved adherence to, and persistence with, medication.20 However, there is no current consensus on the use of surrogate parameters to increase patient treatment adherence. Three major international guidelines recommend follow-up to ensure that treatment is effective. Regular monitoring is an important component of any osteoporosis treatment plan.21–23 This applies to at-risk patients whether or not they are on bone-protective drug treatment. Follow-up BMD testing and physician check-ups are also recommended.21–23

Patients with an increased risk of fracture at initial examination should be re-evaluated at regular intervals for implementation of non-pharmacological measures, risk factors, and fracture risk. Because a decrease in BMD below measurement error before two years is unlikely, follow-up BMD examinations are usually not recommended at intervals of less than two years.24 Repeat DXA scans at intervals of two years or longer are appropriate when the efficacy of treatment, risk assessment, or decision to change or interrupt treatment is being considered.24 Repeat scans may also be useful for addressing patient concerns in relation to treatment adherence. Change in BMD may be difficult to interpret if less than the precision error (2.8×precision measured as the standard deviation or coefficient of variation of repeat measurements). Pretest probability, as well as concordance of change at different skeletal sites, assists in determining a significant change.

After initiating a specific pharmacological intervention, clinical examinations are recommended after 3–6 months and after 6–12 months. This may include documenting pain, functionality, weight, and height.22 Ongoing monitoring of patients taking medication, particularly those taking oral bisphosphonates, should be conducted to ensure adherence with administration instructions. Laboratory tests may be used to identify drug-induced side effects or potentially treatable conditions contributing to the patient’s bone health (e.g., low vitamin D or thyroid disease).

  1. 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.
  2. Melton LJ 3rd, Atkinson EJ, O’Connor MK, O’Fallon WM, Riggs BL. Determinants of bone loss from the femoral neck in women of different ages. J Bone Miner Res 2000;15(1):24–31.
  3. Abrahamsen B, Nissen N, Hermann AP, et al. When should densitometry be repeated in healthy peri- and postmenopausal women: The Danish osteoporosis prevention study. J Bone Miner Res 2002;17(11):2061–67.
  4. Chen W, Khan Z, Freund J, Pocock N. Dual hip DXA. Is it time to change standard protocol? J Clin Densitom 2022;25(1):20–23.
  5. Naylor KE, Jacques RM, Paggiosi M, et al. Response of bone turnover markers to three oral bisphosphonate therapies in postmenopausal osteoporosis: The TRIO study. Osteoporos Int 2016;27(1):21–31.
  6. Brown JP, Roux C, Ho PR, et al. Denosumab significantly increases bone mineral density and reduces bone turnover compared with monthly oral ibandronate and risedronate in postmenopausal women who remained at higher risk for fracture despite previous suboptimal treatment with an oral bisphosphonate. Osteoporos Int 2014;25(7):1953–61.
  7. Majima T, Shimatsu A, Satoh N, et al. Three-month changes in bone turnover markers and bone mineral density response to raloxifene in Japanese postmenopausal women with osteoporosis. J Bone Miner Metab 2008;26(2):178–84.
  8. Farahmand P, Marin F, Hawkins F, et al. Early changes in biochemical markers of bone formation during teriparatide therapy correlate with improvements in vertebral strength in men with glucocorticoid-induced osteoporosis. Osteoporos Int 2013;24(12):2971–81.
  9. Reginster JY, Sarkar S, Zegels B, et al. Reduction in PINP, a marker of bone metabolism, with raloxifene treatment and its relationship with vertebral fracture risk. Bone 2004;34(2):344–51.
  10. Watts NB, Cooper C, Lindsay R, et al. Relationship between changes in bone mineral density and vertebral fracture risk associated with risedronate: Greater increases in bone mineral density do not relate to greater decreases in fracture risk. J Clin Densitom 2004;7(3):255–61.
  11. Cummings SR, Palermo L, Browner W, et al. Monitoring osteoporosis therapy with bone densitometry: Misleading changes and regression to the mean. JAMA 2000;283(10):1318–21.
  12. Caro JJ, Ishak KJ, Huybrechts KF, Raggio G, Naujoks C. The impact of compliance with osteoporosis therapy on fracture rates in actual practice. Osteoporos Int 2004;15(12):1003–08.
  13. Cummings SR, Karpf DB, Harris F, et al. Improvement in spine bone density and reduction in risk of vertebral fractures during treatment with antiresorptive drugs. Am J Med 2002;112(4):281–89.
  14. Delmas PD, Seeman E. Changes in bone mineral density explain little of the reduction in vertebral or nonvertebral fracture risk with anti-resorptive therapy. Bone 2004;34(4):599–604.
  15. Sarkar S, Reginster JY, Crans GG, Diez-Perez A, Pinette KV, Delmas PD. Relationship between changes in biochemical markers of bone turnover and BMD to predict vertebral fracture risk. J Bone Miner Res 2004;19(3):394–401.
  16. Sarkar S, Mitlak BH, Wong M, Stock JL, Black DM, Harper KD. Relationships between bone mineral density and incident vertebral fracture risk with raloxifene therapy. J Bone Miner Res 2002;17(1):1–10.
  17. Leslie WD, Majumdar SR, Morin SN, Lix LM. Change in bone mineral density is an indicator of treatment-related antifracture effect in routine clinical practice: A registry-based cohort study. Ann Intern Med 2016;165(7):465–72.
  18. Mayoux-Benhamou MA, Roux C, Perraud A, Fermanian J, Rahali-Kachlouf H, Revel M. Predictors of compliance with a home-based exercise program added to usual medical care in preventing postmenopausal osteoporosis: An 18-month prospective study. Osteoporos Int 2005;16(3):325–31.
  19. McCombs JS, Thiebaud P, McLaughlin-Miley C, Shi J. Compliance with drug therapies for the treatment and prevention of osteoporosis. Maturitas 2004;48(3):271–87.
  20. Clowes JA, Peel NF, Eastell R. The impact of monitoring on adherence and persistence with antiresorptive treatment for postmenopausal osteoporosis: A randomized controlled trial. J Clin Endocrinol Metab 2004;89(3):1117–23.
  21. Pfeilschifter J; German Specialist Organisation for Osteology. 2006 DVO-guideline for prevention, diagnosis, and therapy of osteoporosis for women after menopause, for men after age 60 executive summary guidelines. Exp Clin Endocrinol Diabetes 2006;114(10):611–22.
  22. Scottish Intercollegiate Guidelines Network (SIGN). Management of osteoporosis and the prevention of fragility fractures. SIGN, 2021 [Accessed 30 October 2023].
  23. American Association of Clinical Endocrinologists Osteoporosis Task Force. American Association of Clinical Endocrinologists 2001 medical guidelines for clinical practice for the prevention and management of postmenopausal osteoporosis. Endocr Pract 2001;7(4):293–312.
  24. 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.
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