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Mortality After Osteoporotic Fractures: What Proportion Is Caused by Fracture and Is Preventable?

Our knowledge of the association between low-trauma fractures and mortality has evolved considerably over the past half century. An early spike of mortality during the first several months after hip fracture was first established in the 1960s and was recognized as more likely for males and those with more preexisting comorbid conditions. Clinical vertebral fractures were first noted to be associated with higher than expected mortality rates in the early 1990s, and subsequently Center and colleagues demonstrated in the Dubbo observational cohort study that other major osteoporotic fractures (pelvis, proximal humerus, distal femur, proximal tibia, and multiple ribs) were also associated with higher than expected mortality rates, especially inmen. Other fractures such as those at the distal forearm were not shown in earlier studies to be associated with excess mortality. However, a subsequent analysis of the Dubbo cohort showed excess mortality associated with distal forearm and other minor low-trauma fractures among men and women aged 75 years and older, and excess mortality after distal forearm fractures has been shown among men in the Manitoba Bone Density Database cohort. The latter study also showed the risk of excess mortality after all fracture types (with the exception of distal forearm fractures among women) to be highest in the first year after fracture. However, there remains considerable debate and uncertainty as to what proportion of the excess mortality after low-trauma fractures is caused by the fracture itself (and is therefore preventable by preventing the fracture) and what proportion is caused by associated comorbid conditions and poor health status that predate the fracture. Kanis and colleagues postulated that the early spike of mortality during the first few months followed by a decreasing rate of mortality during the second 6 months after hip fracture indicated that the majority of these early deaths were caused by the fracture itself and that any excess deaths beyond this time point would likely be due to preexisting poor health status related to comorbid conditions. Two observational cohort studies reported in this issue of JBMR, by Andrich and colleagues and by Tran and colleagues, shed additional light on the association of low-trauma fractures and mortality but leave many questions unanswered.