Overdiagnosis of osteoporosis: fact or fallacy?

Abstract

In their paper in the British Medical Journal, BOverdiagnosis of bone fragility in the quest to prevent hip fracture^, Jarvinen et al. claim that there is inadequate evidence to support current pharmacological approaches to the prevention of hip fracture [1]. They state, correctly, that the vast majority of hip fractures follow a fall but fail to recognize the obvious connection between the consequence of a fall and bone strength. With the use of selective and misleading presentation of published evidence, they provide a biased critique of current strategies for risk assessment and prevention of hip fracture. Most surprisingly, they fail even to mention Fracture Liaison Services, a model of care that has been shown to be both effective and cost-effective in the secondary prevention of fracture and has been successfully adopted in many parts of the world [2–7]. No one would deny that, as in many fields of medicine, there are gaps in the evidence or that current practice can be improved. Indeed, we know that themajority of elderly people who suffer a hip fracture are not assessed for osteoporosis or offered treatment in the form of lifestyle advice, falls counselling or bone protective therapy [8, 9]. These individuals are at high risk of further fractures and the proven anti-fracture efficacy of pharmacological interventions in this situation provides a strong rationale for their use in secondary prevention. Prevention of the first fracture is another important but more difficult goal, and the efficacy of pharmacotherapy for the primary prevention of fracture has been less well studied. In much of their analysis, Jarvinen et al. fail to make the critical distinction between primary and secondary prevention and by combining figures from studies of both in their meta-analysis, they arrive at a NNT for hip fracture that is too high and meaningless in the context of secondary prevention. Jarvinen et al. acknowledge the large body of published literature demonstrating that the majority of older people whose fracture do not have osteoporosis as defined by the WHO, i.e. a bone mineral density (BMD) T-score ≤−2.5, but appear to miss the point that this provides the rationale for fracture risk algorithms which include clinical risk factors that act independently of bone density. In particular, the strong effect of age has been recognized for decades and its inclusion in risk algorithms greatly improves prediction of fracture risk when compared to BMD alone [10, 11]. Furthermore, both in the title and body of their manuscript, the authors use the terms bone fragility and osteoporosis interchangeably. This is incorrect, since factors other than BMD contribute to bone strength and there is not a single BMD T-score threshold that defines bone fragility. The authors claim that estimations of absolute fracture risk are Bfundamentally flawed^ because fewer than one in three hip fractures is attributable to bone fragility; this statement is based on BMDmeasurements in a single study in postmenopausal women with a mean age of 71 years [12]. This is misleading, first, because BMD-defined osteoporosis, not bone fragility, was assessed and secondly because (as repeatedly emphasized in other contexts by the authors) over 75 % of hip fractures occur in people over the age of 75 years. Another major inaccuracy in their analysis is the contention that organisations supporting the development of FRAX have advocated widespread screening for bone fragility (presumably osteoporosis). In contrast to this assertion, both organisations quoted, the National Osteoporosis Foundation and National * J. Compston jec1001@cam.ac.uk