Abstract
FOR MANY YEARS NOW the Consensus Development Conference definition of osteoporosis has attributed the cause of the enhanced bone fragility to both ‘‘low bone mass and microarchitectural deterioration of bone tissue.’’(1) Although the changes in trabecular architecture that occur in women after menopause have been recognized as a major contributory factor to the higher fracture incidence in this population, the role of trabecular architecture in men with osteoporosis has received relatively little attention. In this issue of the Journal, Legrand et al. provide convincing evidence that compromised trabecular architecture is an important, and independent, causal factor in the pathogenesis of vertebral fractures.(2) The authors studied 108 men with osteoporosis as defined by the World Health Organization criterion of a bone mineral density (BMD) T score of # 22.5. Subjects were divided into two groups: those with at least one vertebral deformity in their spinal radiographs and those without such deformities (controls). These deformities were defined as a .20% reduction in anterior, middle, or posterior vertebral height, as determined independently by two observers. Transiliac crest biopsy specimens from the same subjects were analyzed for a number of measured and derived variables related to bone mass and structure. After adjusting for age, body mass index and BMD, the authors found that the interconnectivity index (ICI), free end–to– free end strut length (a measure of trabecular discontinuity), and trabecular spacing were all higher in the fracture cases versus the controls. Note that the variable that they refer to as the ICI measures the level of connectivity of the marrow cavities, not that of the trabecular lattice. An increase in ICI, therefore, implies a reduction in trabecular connectivity. Conversely, the fracture cases displayed lower values for trabecular number and node-to-node strut length, an index of trabecular connectivity. Furthermore, in a logistic regression analysis, only the architectural variables were significant predictors of the presence of a single vertebral fracture. Several factors should be borne in mind when reading the paper by Legrand et al. First, fractures and microarchitecture were assessed at different skeletal sites. While there are significant correlations between structural variables measured at the iliac crest and in the lumbar vertebrae, the correlation coefficients are only ,0.7 at best.(3) Second, there are functional differences between the two sites; the vertebrae are weight-bearing, whereas the iliac crest is not. Third, as a consequence of the functional difference, the structure of cancellous bone differs between the two sites.(4) In normal subjects, cancellous bone in the iliac crest is anisotropic, whereas in the spine the trabeculae are oriented in vertical and horizontal planes. If microarchitecture and fractures could both have been assessed in the spine, or even better in the same vertebra, perhaps the relationship between the two would have been even stronger in the study by Legrand et al.(2)
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