Abstract
Osteoporotic bone is structurally insufficient and predisposed to low-energy fracture [1]. Fractures are deemed osteoporotic when they result from generalized skeletal demineralization and low-energy trauma rather than from focal pathologic destruction of bone or high-energy trauma. Osteoporotic fractures are accompanied by substantial morbidity and signify increased mortality [2]. Vertebral fractures, the most prevalent osteoporotic fracture, is a powerful harbinger of future vertebral and non-vertebral fracture. Since vertebrae generally fail by compression in axial loading, these fractures are often called vertebral compression fractures. Since fracture morphology is often more complex then this name suggests, the more inclusive term, vertebral fracture (VF), is preferred. In clinical practice, osteoporotic VFs are usually identified by characteristic changes in vertebral shape on a lateral spine radiograph. For research consensus, VFs are defined by a reduction in anterior, middle, or posterior vertebral height although the minimum required reduction (e.g., 15% or 20% of vertebral height) varies among definition schemes [3]. Alterations in vertebral shape consistent with osteoporotic VF are further classified based on the presence or absence of fracture symptoms. Those associated with fracture pain are termed “clinical” while all others “morphometric” VFs (Fig. 1). This dichotomous view teaches that the majority of osteoporotic VFs are morphometric (75%), that is, clinically silent, rather than clinical (25%) [4]. Descriptive fracture morphology further characterizes VFs by shape (e.g., compression, wedge, concave, plana), severity (mild, moderate, severe), number and location within the spine. In this discussion, the term “vertebral deformity” will refer to other non-osteoporotic, non-fracture alterations of vertebral shape. These binary fracture definition schemes have served as the basis for the epidemiology of osteoporosis, defining the economic burden of osteoporotic fractures and as therapeutic endpoints in pivotal pharmaceutical osteoporosis trials [5]. Prevalent VFs have been shown to increase the risk of future vertebral and non-vertebral osteoporotic fracture independent of bone mineral density (BMD). Further, a linear correlation exists between both the number and severity of prevalent VFs and future VF risk. These relationships are the underpinnings of vertebral fracture analysis (VFA) meant to enhance BMD-based fracture risk assessment by combining detected prevalent VFs with BMD T-scores [6]. Substantial clinical data indicates that osteoporotic VF, whether symptomatic or not, correlates with disability from back pain, reduced physical function, reduced quality of life, and increased mortality [2, 7–10]. While binary fracture definition schemes have served the osteoporosis community well, clinical experience, refined by recent conceptual advances in vertebral morphometry [5, 11, 12], and the emerging vertebral augmentation experience [13], suggest that the spectrum of osteoporotic VFs is broader than these definition schemes suggest. The intention of this perspective is to challenge the prevailing dichotomous view of osteoporotic VF. Some of what follows is speculation based upon published clinical and bench research of varying rigor. All of what follows is intended to stimulate a multidisciplinary discussion of a broader view of osteoporotic VFs. Skeletal Radiol (2009) 38:303–308 DOI 10.1007/s00256-008-0632-3
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