Guideline

Background

Osteoporosis management and fracture prevention in post-menopausal women and men > 50 years of age
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Last revised: 01 Mar 2024

Background

Definition

Osteoporosis is characterised by both low bone mineral density (BMD) and microarchitectural deterioration of bone tissue, leading to decreased bone strength, increased bone fragility and a consequent increase in fracture risk. Osteoporotic fractures usually follow falls from a standing height or less in individuals with decreased bone strength. BMD can be reliably measured by scanning of the skeleton using dual energy X-ray absorptiometry (DXA).

BMD is usually reported as a T-score, the number of standard deviations (SDs) of BMD measurement above or below that of young healthy adults of the same sex. The World Health Organization (WHO) has defined osteoporosis and osteopenia based on T-score (Table 1).1 Although Australia’s Pharmaceutical Benefits Scheme (PBS) uses the WHO T-score range for osteoporosis to determine eligibility for subsidy on osteoporosis medications, it is important to note that BMD is only one of several factors that contributes to an individual’s fracture risk. Because osteopenia and normal BMD are much more common than osteoporosis, approximately 50% of first or subsequent minimal trauma fractures (trauma equivalent to a fall from standing height or less) occur in people with T-scores in the normal or osteopenic range.2–5 These people should still be considered at increased risk of subsequent fracture because fracture contributes to subsequent fracture risk independent of BMD.6

Table 1. WHO definitions of osteoporosis and osteopenia1

Normal BMD

T-score –1.0 or above

BMD not more than 1.0 SD below young adult mean

Osteopenia

T-score between –1.0 and –2.5

BMD between 1.0 and 2.5 SDs below young adult mean

Osteoporosis

T-score –2.5 or below

BMD 2.5 or more SDs below young adult mean

Osteoporosis is a ‘silent disease’ because deterioration of skeletal tissue proceeds with no symptoms until a symptomatic fracture occurs, and thus the condition is under-recognised and affected individuals are undertreated.4–9

Vertebral fractures may be asymptomatic or present with acute, usually self-limiting back pain. However, subclinical fractures are important predictors of future fracture risk, particularly for vertebral fractures.10,11

More commonly, vertebral fractures are associated with gradual height loss resulting in increasing thoracic kyphosis and back pain. Non-vertebral or peripheral fractures usually present with more obvious fracture symptoms following a fall, although stress fractures may present as acute regional musculoskeletal pain.

A 2012 burden of disease analysis report estimated that, in 2022, 6.2 million Australians aged >50 years would have osteoporosis or osteopenia, an increase of 31% from 2012.12 This modelling predicted a similar increase in the rate of fractures, from 140,882 in 2012 to 183,105 in 2022.12

In addition to significant health and social burden, poor bone health exerts considerable economic pressure on Australia’s healthcare system, with the total direct and indirect costs of osteoporosis and osteopenia predicted to reach $3.84 billion by 2022.12

Osteoporosis and osteopenia

Based on the WHO definition of osteoporosis and osteopenia, approximately 3% of men and 13% of women in Australia aged 50–69 years are osteoporotic, rising to 13% and 43% for men and women aged >70 years.12 Fifty-five per cent of men and 49% of women between 50 and 69 years of age are osteopenic, with a similar prevalence in those aged >70 years.12 By 2022, approximately 72% of women and 62% of men aged >50 years will have osteoporosis or osteopenia based on WHO criteria.12,13

Minimal trauma fractures

Approximately 70% of minimal trauma fractures occur in women, with incidence increasing with age in both sexes.12 The residual lifetime risk of minimal trauma fracture is approximately 44% for women aged >60 years, which is higher than the risk of ischaemic heart disease or some types of cancers (e.g., breast cancer).14 In men of the same age group, the lifetime fracture risk is lower (at 25%) and comparable to the lifetime risk of developing diabetes.14

Between the ages of 50 and 69 years, non-hip, non-vertebral fractures (humerus, ankle, lower limb, rib, forearm, proximal pelvis, patella, foot, and hand) are the most common minimal trauma fracture types in both men and women.12,13 Wrist fractures are also common in women in this age group.

Hip fractures

The hip fracture rate increases substantially with age, constituting only 4% of fragility fractures in women aged 50–69 years, but 26% of fractures in women aged >70 years.12 A similar trend with age is seen in men, although the overall incidence of hip fracture in men remains around one-third that in women.12 After a rise in the 1980s and stabilisation in the 1990s, the age-standardised hip fracture incidence rate declined in Australia between 1997 and 2007.15 However, the absolute number of hip fractures increased during this period due to population ageing.15 Any continued decline in incidence rate will be offset by the ageing population – the number of Australians aged >65 years is set to more than double from 4.2 million in 2020 to almost 10.2 million by 2066.14

Vertebral fractures

Vertebral fractures due to osteoporosis are associated with significant long-term disability due to pain and kyphosis. Vertebral fractures are usually defined as a 20% or greater reduction in vertebral height on X-ray and are often termed a ‘vertebral deformity’. The prevalence of radiologically identified vertebral deformities ranges from 5% in people aged 50–54 years to 50% in those aged >80 years.16 In 2012, an estimated 25,502 vertebral fractures occurred in Australia12 and by 2022 this incidence was expected to rise to over 35,000, an increase of 37%.12 Underdiagnosis of vertebral fractures is a major problem, because incident radiographic vertebral fractures are associated with a significantly higher risk of subsequent vertebral and non-vertebral fracture.12 Only around one-third of all radiographically observed vertebral deformities come to medical attention (i.e., are symptomatic with acute fracture-related pain).17 In Australia, approximately 30% of radiographically visible vertebral fractures in women with osteoporosis are not detected.18

Osteoporosis is a systemic condition. Almost all fracture types are increased in patients with low BMD. All fracture sites apart from rib fractures (in men) increase subsequent fracture risk by two- to fourfold.12,19 Moderate to high trauma fractures are also associated with increased fracture risk.20

Fracture-related morbidity can arise from pain, reduced mobility, loss of function and associated reduced quality of life.21 Many patients lose the ability to live independently following a hip fracture. Long-term morbidity is associated with almost all types of symptomatic osteoporotic fractures; only individuals with wrist, humerus or ankle fractures return to their prefracture health-related quality of life 18 months after fracture.21

Mortality in the first year after a major minimal trauma fracture in people aged >60 years is up to threefold higher than in age-matched non-fracture populations for people with hip fracture and up to twofold higher for other major fracture types (‘major fractures’ include pelvis, distal femur, proximal tibia, three or more simultaneous ribs and proximal humerus; ‘minor fractures’ include all remaining osteoporotic fractures).3,19,22 The mortality rate (per 100 person-years) is higher in men than in women following any type of minimal trauma fracture; this is most pronounced following hip fracture.19,22 The risk of death is greatest in the first year after hip fracture: approximately 20% of women die within one year of fracturing a hip, with 10% dying during hospitalisation.23 Increased mortality during the immediate post-fracture period is associated with advanced age and male sex, and has been linked both to comorbid conditions, such as congestive heart failure and liver disease,23,24 and to the fracture event itself.23,24 Acute events, such as postoperative infections and complications, are also important.

Although hip fracture is associated with the highest post-fracture mortality, followed by pelvic and vertebral fractures, one-quarter of excess mortality associated with minimal trauma fracture is attributable to non-hip, non-spine fractures due to the high prevalence of these fractures.25 Excess mortality occurs mainly in the first five years after a minimal trauma fracture, but may continue up to 10 years following fracture.26,27

Osteoporosis treatment has been shown in randomised controlled trials (RCTs) to significantly reduce mortality risk after hip fracture in older men and women,28,29 and cohort studies suggest this is also the case for other fracture types.30–32 The mechanisms behind mortality reduction remain speculative but, interestingly, a reduction in pneumonia and cardiovascular events is possible.33

Any osteoporotic fracture predisposes an individual to at least a twofold increased risk of further fractures,3,19,34–40 significant morbidity, and premature death.27,41 In a 2012 report of New South Wales (NSW) hospital admission data from the Agency for Clinical Innovation, 46% of patients with an osteoporotic fracture were readmitted to hospital due to a further fracture.42

The timely diagnosis and optimal treatment of osteoporosis prevents further fractures by up to 30%, 50%, and 70% in patients with non-vertebral, hip, and vertebral fractures, respectively.32,43,44 Safe and effective medications are available for those who have sustained a minimal trauma fracture.29,45–48 Internationally, however, 70–85% of patients presenting with a minimal trauma fracture to their general practitioner (GP) or hospital are neither assessed for osteoporosis nor appropriately managed to prevent further fractures.7,9,49–56 Two large retrospective studies of primary care practice in Australia demonstrated that less than one-third of patients presenting with a minimal trauma fracture receive specific anti-osteoporosis pharmacotherapy.7,56 A recent Australian general practice study further suggests that osteoporosis remains underdiagnosed and undertreated.9 This treatment gap is also evident in hospitals and tertiary referral centres.57

The estimated incidence rate of osteoporotic hip fracture in Australia is declining.58 Over the 10-year period from 1997–98 to 2006–07, the age-standardised rate fell by 14% in men and 20% in women.58 This reduction mainly occurred among men aged 65–84 years and women aged ≥60 years; little change was seen in those aged 40–59 years. A combination of factors may be responsible for the observed reduction, including measures to reduce risk factors and prevent falls among the ageing.58–60

Fracture liaison services (FLSs) or secondary fracture prevention (SFP) programs are the most proven methods to address the care gap in osteoporosis. These identify patients with a minimal trauma fracture, assess them for osteoporosis, initiate treatment (if appropriate) and communicate with primary care providers. Australian SFP programs have demonstrated improved osteoporosis treatment initiation and reduced refracture rates compared with standard care.66–68

The objectives of an SFP program are encapsulated by the ‘3i’s’: identify patients with osteoporosis; investigate and determine fracture and falls risk; and initiate interventions to reduce fracture risk. A systematic review divided interventions into four models of care, according to intervention intensity (see Table 2).61 A key aspect of any Type A or Type B SFP program is a coordinator who oversees the program, from initial patient contact following minimal trauma fracture to osteoporosis and falls risk assessment and to follow-up once interventions have been initiated. Once patients are ‘captured’, most programs perform a full risk factor assessment, including clinical osteoporosis risk factors, falls risk assessment and BMD testing.

Type A (3i) and Type B (2i) SFP programs have been shown in RCTs to improve outcome measures (BMD testing and treatment initiation rates) compared with less-intensive Type C (1i) and Type D (0i) programs,62,63 while also reducing refracture rates64–66 in a clinically and economically effective manner.64,67–70 A 2012 evaluation of the SFP program at Concord Hospital in Sydney, NSW, showed that it was highly cost-effective, with a cost of around $17,000 per quality-adjusted life year (QALY) gained.68

A more recent three-year costing study at Newcastle’s John Hunter Hospital in NSW also estimated annual savings of between $1.2 million and $1.8 million as a result of investing in its FLS.71 The burden of refracture on Australia’s healthcare system is demonstrated in a recently published 11-year longitudinal analysis of refracture rates in people aged >50 years and public hospital utilisation across NSW, where the annual cost of refracture to NSW Health increased from $130 million in 2009 to $194 million in 2019.72 If nothing changes, it was estimated this would increase to $2.4 billion over the next decade, providing compelling evidence for implementation of best practice statewide models of care to prevent refractures.72 However, at the time of writing, NSW remains the only Australian state with a statewide osteoporosis refracture program (ORP) built around FLSs.

Table 2. Description of models of care for secondary fracture prevention according to intervention intensity62

Model of care

Description

Type A

Identification, assessment (risk factors, bloods, BMD), treatment initiation and correspondence with GP

Type B

Identification, assessment and treatment recommendation only

Type C

Information given to GP and patient

Type D

Information given to patient only

 

FLS and SFP programs run centrally from hospital-based centres have two key limitations:

  1. They do not capture all fragility fractures managed by the hospitals in their regions.
  2. They lack capacity to manage osteoporosis long-term, as needed.

Furthermore, SFP programs will not capture all patients at high risk of fracture or refracture, such as those with vertebral fracture, frail older people, those in institutionalised care and those with hip fractures managed via orthopaedic pathways.73

General practice-led care is critical to manage this common long-term condition. Specialised services should focus on maximising the support and capacity for osteoporosis care in primary care. Almost all patients with a minimal trauma fracture will eventually see their GP (although, not necessarily for a minimal trauma fracture). Orthogeriatric services, which are now present in most Australian hospitals, have also been shown to improve osteoporosis care.74

Since the 2013 systematic review of FLS models,61 FLSs have commenced across NSW with collaboration between hospital and primary care services in many areas. Although not formally evaluated, recent experiences suggest that SFP programs that have a strong relationship with local general practices, including through codesign, may achieve better continuity of osteoporosis care without requirement for the FLS to deliver treatment initiation. HealthPathways is another widely available resource to support GP-led osteoporosis care.

A recent systematic review of orthogeriatric models of care, covering 18 (mainly retrospective cohort) studies from 1992 to 2012, demonstrated a reduction in inpatient mortality (relative risk [RR] 0.60; 95% confidence interval [CI]: 0.43–0.84) and long-term (6–12 months after fracture) mortality (RR 0.83; 95% CI: 0.74–0.94, respectively).74 Length of stay was reduced in the orthogeriatric care model.75

The treatment gap in osteoporosis care in Australia can be addressed through widespread implementation of SFP programs and orthogeriatric services in both hospital and primary care settings. Because general practice is the only extensive workforce capable of long-term care of osteoporosis, supporting GPs to manage osteoporosis is critical to ensuring all patients with a minimal trauma fracture are evaluated and managed appropriately.

In general, there is less utilisation of health services in rural and remote areas, and this is associated with poorer health outcomes.75 People living in rural and remote areas are more likely to suffer from chronic diseases than those residing in major cities. However, the diagnosis of osteoporosis is more prevalent in major cities than in other areas of Australia.75

Women living outside Australia’s major cities are slightly more likely to have an osteoporotic hip fracture than those in major cities; rates among men do not vary significantly.76 Furthermore, those living in remote Australia tend to be younger at the time of first fracture (75 years for men, 79 years for women) than those living in non-remote areas (81 and 83 years for men and women, respectively).76

Bone densitometry (DXA) Medicare claims increased by 78% in the 10 years from 2006 to 2015.76 Despite this, bone densitometry utilisation rates are significantly lower in rural and remote areas than in regional and urban areas, with those residing in capital cities around threefold more likely to undergo bone densitometry than those in remote areas.75

There is a particular need to facilitate the detection and management of osteoporosis in rural and remote areas. The fracture liaison coordinator/osteoporosis refracture prevention model of care has been shown to work well in regional NSW.77,78 Important factors are likely to be limitations in primary healthcare and bone densitometry services in rural and remote areas.

The burden of osteoporosis and fracture prevalence in Aboriginal and Torres Strait Islander people is unclear. Aboriginal and Torres Strait Islander adults may be more likely to experience a minimal trauma fracture (men 50% and women 26%) compared with non-Indigenous Australians.76 Hip fractures appear to occur, on average, at a much younger age in Aboriginal and Torres Strait Islander people than in non-Indigenous Australians (for men, 65 versus 81 years, respectively; for women, 74 versus 83 years, respectively).79 Over a 10-year period (1999–2009), there was a disproportionate increase in age-related hip fracture rates by 7.2% per year for Aboriginal and Torres Strait Islander people, whereas rates declined by 3.4% per year in non-Indigenous Australians.80 The prevalence of chronic disease, such as cardiovascular disease, type 2 diabetes and chronic kidney disease, is also higher in Aboriginal and Torres Strait Islander people. These comorbidities are associated with an increased risk of osteoporosis, falls and fracture.81

According to self-reported data from the 2018–19 National Aboriginal and Torres Strait Islander Health Survey, the prevalence of osteoporosis among Aboriginal and Torres Strait Islander peoples was 2.3%, affecting 18,900 people, with approximately 1000 living in remote areas (0.7% of the remote Aboriginal and Torres Strait Islander population).76

Different patterns of risk factors, such as smoking, poor nutrition, limited exercise, excess weight, and high alcohol consumption, are likely to be important in Aboriginal and Torres Strait Islander peoples. The interaction of these factors on lower life expectancy, higher comorbidity rates, variable access to health services, and socioeconomic factors is difficult to estimate. The promotion of good nutrition and reduction of risk factors is very important for a wide range of health issues, not only osteoporosis. It is expected that Aboriginal and Torres Strait Islander women and men experience at least the same, if not greater, limitation in accessing bone densitometry as other people living in rural and remote Australia.

  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. Schuit SC, van der Klift M, Weel AE, et al. Fracture incidence and association with bone mineral density in elderly men and women: The Rotterdam Study. Bone 2004;34(1):195–202.
  3. Bliuc D, Alarkawi D, Nguyen TV, Eisman JA, Center JR. Risk of subsequent fractures and mortality in elderly women and men with fragility fractures with and without osteoporotic bone density: The Dubbo Osteoporosis Epidemiology Study. J Bone Miner Res 2015;30(4):637–46.
  4. Mai HT, Tran TS, Ho-Le TP, Center JR, Eisman JA, Nguyen TV. Two-thirds of all fractures are not attributable to osteoporosis and advancing age: Implications for fracture prevention. J Clin Endocrinol Metab 2019;104(8):3514–20.
  5. Siris ES, Chen YT, Abbott TA, et al. Bone mineral density thresholds for pharmacological intervention to prevent fractures. Arch Intern Med 2004;164(10):1108–12.
  6. Langsetmo L, Goltzman D, Kovacs CS, et al. Repeat low-trauma fractures occur frequently among men and women who have osteopenic BMD. J Bone Miner Res 2009;24(9):1515–22.
  7. Eisman J, Clapham S, Kehoe L. Osteoporosis prevalence and levels of treatment in primary care: The Australian BoneCare Study. J Bone Miner Res 2004;19(12):1969–75.
  8. Parker D. An audit of osteoporotic patients in an Australian general practice. Aust Fam Physician 2013;42(6):423–27.
  9. Naik-Panvelkar P, Norman S, Elgebaly Z, et al. Osteoporosis management in Australian general practice: An analysis of current osteoporosis treatment patterns and gaps in practice. BMC Fam Pract 2020;21(1):32.
  10. Pongchaiyakul C, Nguyen ND, Jones G, Center JR, Eisman JA, Nguyen TV. Asymptomatic vertebral deformity as a major risk factor for subsequent fractures and mortality: A long-term prospective study. J Bone Miner Res 2005;20(8):1349–55.
  11. Johansson H, Odén A, McCloskey EV, Kanis JA. Mild morphometric vertebral fractures predict vertebral fractures but not non-vertebral fractures. Osteoporos Int 2014;25(1):235–41.
  12. Watts JJ, Abimanyi-Ochom J, Sanders KM. Osteoporosis costing all Australians: A new burden of disease analysis – 2012 to 2022. Osteoporosis Australia, 2013 [Accessed 30 October 2023]
  13. Chen W, Simpson JM, March LM, et al. Comorbidities only account for a small proportion of excess mortality after fracture: A record linkage study of individual fracture types. J Bone Miner Res 2018;33(5):795–802.
  14. Australian Institute of Health and Welfare. Older Australians. Australian Government, 2023 [Accessed 16 January 2024]
  15. Nguyen ND, Ahlborg HG, Center JR, Eisman JA, Nguyen TV. Residual lifetime risk of fractures in women and men. J Bone Miner Res 2007;22(6):781–88.
  16. Crisp A, Dixon T, Jones G, et al. Declining incidence of osteoporotic hip fracture in Australia. Arch Osteoporos 2012;7(1–2):179–85.
  17. O’Neill TW, Felsenberg D, Varlow J, Cooper C, Kanis JA, Silman AJ. The prevalence of vertebral deformity in European men and women: The European Vertebral Osteoporosis Study. J Bone Miner Res 1996;11(7):1010–18.
  18. Huang C, Ross PD, Wasnich RD. Vertebral fractures and other predictors of back pain among older women. J Bone Miner Res 1996;11(7):1026–32.
  19. Center JR, Bliuc D, Nguyen TV, Eisman JA. Risk of subsequent fracture after low-trauma fracture in men and women. JAMA 2007;297(4):387–94.
  20. Leslie WD, Schousboe JT, Morin SN, et al. Fracture risk following high-trauma versus low-trauma fracture: A registry-based cohort study. Osteoporos Int 2020;31(6):1059–67.
  21. Abimanyi-Ochom J, Watts JJ, Borgström F, et al. Changes in quality of life associated with fragility fractures: Australian arm of the International Cost and Utility Related to Osteoporotic Fractures Study (AusICUROS). Osteoporos Int 2015;26(6):1781–90.
  22. Bliuc D, Nguyen ND, Milch VE, Nguyen TV, Eisman JA, Center JR. Mortality risk associated with low-trauma osteoporotic fracture and subsequent fracture in men and women. JAMA 2009;301(5):513–21.
  23. Vestergaard P, Rejnmark L, Mosekilde L. Increased mortality in patients with a hip fracture-effect of pre-morbid conditions and post-fracture complications. Osteoporos Int 2007;18(12):1583–93.
  24. Frost SA, Nguyen ND, Black DA, Eisman JA, Nguyen TV. Risk factors for in-hospital post-hip fracture mortality. Bone 2011;49(3):553–58.
  25. Bliuc D, Nguyen TV, Eisman JA, Center JR. The impact of nonhip nonvertebral fractures in elderly women and men. J Clin Endocrinol Metab 2014;99(2):415–23.
  26. Abrahamsen B, van Staa T, Ariely R, Olson M, Cooper C. Excess mortality following hip fracture: A systematic epidemiological review. Osteoporos Int 2009;20(10):1633–50.
  27. Bliuc D, Nguyen ND, Nguyen TV, Eisman JA, Center JR. Compound risk of high mortality following osteoporotic fracture and refracture in elderly women and men. J Bone Miner Res 2013;28(11):2317–24.
  28. Reid IR, Horne AM, Mihov B, et al. Fracture prevention with zoledronate in older women with osteopenia. N Engl J Med 2018;379(25):2407–16.
  29. Lyles KW, Colón-Emeric CS, Magaziner JS, et al. Zoledronic acid and clinical fractures and mortality after hip fracture. N Engl J Med 2007;357(18):1799–809.
  30. Center JR, Bliuc D, Nguyen ND, Nguyen TV, Eisman JA. Osteoporosis medication and reduced mortality risk in elderly women and men. J Clin Endocrinol Metab 2011;96(4):1006–14.
  31. Sambrook PN, Cameron ID, Chen JS, et al. Oral bisphosphonates are associated with reduced mortality in frail older people: A prospective five-year study. Osteoporos Int 2011;22(9):2551–56.
  32. Bolland MJ, Grey AB, Gamble GD, Reid IR. Effect of osteoporosis treatment on mortality: A meta-analysis. J Clin Endocrinol Metab 2010;95(3):1174–81.
  33. Reid IR, Horne AM, Mihov B, et al. Effects of zoledronate on cancer, cardiac events, and mortality in osteopenic older women. J Bone Miner Res 2020;35(1):20–27.
  34. Ahmed LA, Center JR, Bjørnerem A, et al. Progressively increasing fracture risk with advancing age after initial incident fragility fracture: The Tromsø study. J Bone Miner Res 2013;28(10):2214–21.
  35. Johnell O, Kanis JA, Odén A, et al. Fracture risk following an osteoporotic fracture. Osteoporos Int 2004;15(3):175–79.
  36. Kanis JA, Johnell O, De Laet C, et al. A meta-analysis of previous fracture and subsequent fracture risk. Bone 2004;35(2):375–82.
  37. Klotzbuecher CM, Ross PD, Landsman PB, Abbott TA 3rd, Berger M. Patients with prior fractures have an increased risk of future fractures: A summary of the literature and statistical synthesis. J Bone Miner Res 2000;15(4):721–39.
  38. Melton LJ 3rd, Atkinson EJ, Cooper C, O’Fallon WM, Riggs BL. Vertebral fractures predict subsequent fractures. Osteoporos Int 1999;10(3):214–21.
  39. Laurs-van Geel TA, Center JR, Geusens PP, Dinant GJ, Eisman JA. Clinical fractures cluster in time after initial fracture. Maturitas 2010;67(4):339–42.
  40. van Staa TP, Leufkens HG, Cooper C. Does a fracture at one site predict later fractures at other sites? A British cohort study. Osteoporos Int 2002;13(8):624–29.
  41. Center JR, Nguyen TV, Schneider D, Sambrook PN, Eisman JA. Mortality after all major types of osteoporotic fracture in men and women: An observational study. Lancet 1999;353(9156):878–82.
  42. NSW Agency for Clinical Innovation (ACI). Model of care for osteoporotic refracture prevention model of care. 2nd edn. ACI, 2017 [Accessed 30 October 2023]
  43. Saito T, Sterbenz JM, Malay S, Zhong L, MacEachern MP, Chung KC. Effectiveness of anti-osteoporotic drugs to prevent secondary fragility fractures: Systematic review and meta-analysis. Osteoporos Int 2017;28(12):3289–300.
  44. Black DM, Delmas PD, Eastell R, et al. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med 2007;356(18):1809–22.
  45. Cranney A, Papaioannou A, Zytaruk N, et al. Parathyroid hormone for the treatment of osteoporosis: A systematic review. CMAJ 2006;175(1):52–59.
  46. Cranney A, Guyatt G, Griffith L, Wells G, Tugwell P, Rosen C, et al. Meta-analyses of therapies for postmenopausal osteoporosis. IX: Summary of meta-analyses of therapies for postmenopausal osteoporosis. Endocr Rev 2002;23(4):570–78.
  47. Stevenson M, Jones ML, De Nigris E, Brewer N, Davis S, Oakley J. A systematic review and economic evaluation of alendronate, etidronate, risedronate, raloxifene and teriparatide for the prevention and treatment of postmenopausal osteoporosis. Health Technol Assess 2005;9(22):1–160.
  48. Bone HG, Wagman RB, Brandi ML, et al. 10 years of denosumab treatment in postmenopausal women with osteoporosis: Results from the Phase 3 randomised FREEDOM trial and open-label extension. Lancet Diabetes Endocrinol 2017;5(7):513–23.
  49. Andrade SE, Majumdar SR, Chan KA, et al. Low frequency of treatment of osteoporosis among postmenopausal women following a fracture. Arch Intern Med 2003;163(17):2052–57.
  50. Elliot-Gibson V, Bogoch ER, Jamal SA, Beaton DE. Practice patterns in the diagnosis and treatment of osteoporosis after a fragility fracture: A systematic review. Osteoporos Int 2004;15(10):767–78.
  51. Follin SL, Black JN, McDermott MT. Lack of diagnosis and treatment of osteoporosis in men and women after hip fracture. Pharmacotherapy 2003;23(2):190–98.
  52. Giangregorio L, Papaioannou A, Cranney A, Zytaruk N, Adachi JD. Fragility fractures and the osteoporosis care gap: An international phenomenon. Semin Arthritis Rheum 2006;35(5):293–305.
  53. Leslie WD, Giangregorio LM, Yogendran M, et al. A population-based analysis of the post-fracture care gap 1996–2008: The situation is not improving. Osteoporos Int 2012;23(5):1623–29.
  54. Port L, Center J, Briffa NK, Nguyen T, Cumming R, Eisman J. Osteoporotic fracture: Missed opportunity for intervention. Osteoporos Int 2003;14(9):780–84.
  55. Shibli-Rahhal A, Vaughan-Sarrazin MS, Richardson K, Cram P. Testing and treatment for osteoporosis following hip fracture in an integrated U.S. healthcare delivery system. Osteoporos Int 2011;22(12):2973–80.
  56. Chen JS, Hogan C, Lyubomirsky G, Sambrook PN. Management of osteoporosis in primary care in Australia. Osteoporos Int 2009;20(3):491–96.
  57. Teede HJ, Jayasuriya IA, Gilfillan CP. Fracture prevention strategies in patients presenting to Australian hospitals with minimal-trauma fractures: A major treatment gap. Intern Med J 2007;37(10):674–79.
  58. Australian Institute of Health and Welfare. Hip fracture incidence and hospitalisations in Australia 2015–16. Australian Government, 2018 [Accessed 30 October 2023]
  59. Ballane G, Cauley JA, Luckey MM, Fuleihan GH. Secular trends in hip fractures worldwide: Opposing trends East versus West. J Bone Miner Res 2014;29(8):1745–55.
  60. Cooper C, Cole ZA, Holroyd CR, et al. Secular trends in the incidence of hip and other osteoporotic fractures. Osteoporos Int 2011;22(5):1277–88.
  61. Ganda K, Puech M, Chen JS, et al. Models of care for the secondary prevention of osteoporotic fractures: A systematic review and meta-analysis. Osteoporos Int 2013;24(2):393–406.
  62. Majumdar SR, Johnson JA, Bellerose D, et al. Nurse case-manager vs multifaceted intervention to improve quality of osteoporosis care after wrist fracture: Randomized controlled pilot study. Osteoporos Int 2011;22(1):223–30.
  63. Bliuc D, Eisman JA, Center JR. A randomized study of two different information-based interventions on the management of osteoporosis in minimal and moderate trauma fractures. Osteoporos Int 2006;17(9):1309–17.
  64. Dell R, Greene D, Schelkun SR, Williams K. Osteoporosis disease management: The role of the orthopaedic surgeon. J Bone Joint Surg Am 2008;90(Suppl 4):188–94.
  65. Lih A, Nandapalan H, Kim M, et al. Targeted intervention reduces refracture rates in patients with incident non-vertebral osteoporotic fractures: A 4-year prospective controlled study. Osteoporos Int 2011;22(3):849–58.
  66. Nakayama A, Major G, Holliday E, Attia J, Bogduk N. Evidence of effectiveness of a fracture liaison service to reduce the re-fracture rate. Osteoporos Int 2016;27(3):873–79.
  67. Sander B, Elliot-Gibson V, Beaton DE, Bogoch ER, Maetzel A. A coordinator program in post-fracture osteoporosis management improves outcomes and saves costs. J Bone Joint Surg Am 2008;90(6):1197–205.
  68. Cooper MS, Palmer AJ, Seibel MJ. Cost-effectiveness of the Concord Minimal Trauma Fracture Liaison service, a prospective, controlled fracture prevention study. Osteoporos Int 2012;23(1):97–107.
  69. Marsh D, Akesson K, Beaton DE, et al. Coordinator-based systems for secondary prevention in fragility fracture patients. Osteoporos Int 2011;22(7):2051–65.
  70. Vaile J, Sullivan L, Bennett C, Bleasel J. First Fracture Project: Addressing the osteoporosis care gap. Intern Med J 2007;37(10):717–20.
  71. Major G, Ling R, Searles A, et al. The costs of confronting osteoporosis: Cost study of an Australian fracture liaison service. JBMR Plus 2018;3(1):56–63.
  72. Williamson J, Michaleff Z, Schneuer F, et al. An 11-year longitudinal analysis of refracture rates and public hospital service utilisation in Australia’s most populous state. Arch Osteoporos 2022;17(1):76.
  73. Eekman DA, van Helden SH, Huisman AM, et al. Optimizing fracture prevention: The fracture liaison service, an observational study. Osteoporos Int 2014;25(2):701–09.
  74. Grigoryan KV, Javedan H, Rudolph JL. Orthogeriatric care models and outcomes in hip fracture patients: A systematic review and meta-analysis. J Orthop Trauma 2014;28(3):e49–55.
  75. Ewald DP, Eisman JA, Ewald BD, et al. Population rates of bone densitometry use in Australia, 2001–2005, by sex and rural versus urban location. Med J Aust 2009;190(3):126–28.
  76. Australian Institute of Health and Welfare. National hospital morbidity database 2017–18. Australian Government, 2020 [Accessed 16 January 2024]
  77. Hui N, Fraser S, Wong PKK. Patients discharged from a fracture liaison service still require follow-up and bone health advice. Arch Osteoporos 2020;15(1):118.
  78. Fraser S, Wong PK. Secondary fracture prevention needs to happen in the country too: The first two and a half years of the Coffs Fracture Prevention Clinic. Aust J Rural Health 2017;25(1):28–33.
  79. MacIntosh DJ, Pearson B. Fractures of the femoral neck in Australian Aboriginals and Torres Strait Islanders. Aust J Rural Health 2001;9(3):127–33.
  80. Wong YY, Flicker L, Draper G, Lai MM, Waldron N. Hip fractures among Indigenous Western Australians from 1999 to 2009. Intern Med J 2013;43(12):1287–92.
  81. Zengin A, Maple-Brown LJ, Brennan-Olsen S, Center JR, Eades S, Ebeling PR. Musculoskeletal health of Indigenous Australians. Arch Osteoporos 2018;13(1):77.
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