Architecture and vertebral fracture

Summary

Bone strength is determined by mass density, structural arrangement, and the presence of microdamage. This presentation focuses on trabecular microstructure as an element of bone strength, particularly in the syndrome of vertebral compression fracture. The base material comes from transilial biopsies from 90 patients with the crush fracture syndrome and from 34 normal volunteers who underwent transilial biopsy. Trabecular connectivity was compared in these two groups. Patients and normals were then matched for trabecular bone volume (BV/TV). To highlight measures of trabecular connectivity, three general methods for examining trabecular connectivity were applied to the 23 patient-control pairs matched for BV/TV. The conventional method of Parfitt [1] showed that trabecular number was decreased by 11%, trabecular separation was increased by 9%, and trabecular thickness was increased by 9% in patients compared with controls. The method of counting trabecular nodes and trabecular free ends showed that in the patients, free ends were decreased by 37% and nodes were decreased by 37%. The marrow space star volume (the average volume of marrow measured from radii placed at random points within the marrow and extending to trabecular surface) was 36% greater in the patients. All three methods are measures of trabecular connectivity (the density of connections between trabeculae). All three demonstrated less trabecular connectivity in the patients versus controls for identical BV/TV. Patients with vertebral fractures had fewer trabecular elements rather than global thinning of trabeculae. Differences in measures of connectivity were not accompanied by significant differences in any of the measures of bone remodeling dynamics, as examined by tetracycline labels. Loss of trabecular elements would result in increased mechanical loads during ordinary activity for the trabecular elements remaining. Such increased loads would produce increased strain in these elements. This could shorten the fatigue life of the remaining elements by an order of magnitude, and thus outstrip the rate of fatigue damage repair by the bone remodeling system. This could result in accumulation of trabecular fractures such as those observed by J. S. Arnold in the 1960s [2]. Osteoporotic bone fragility due to loss of trabecular connectivity can be demonstrated by independent methods. This feature of the bone loss in osteoporosis may be at least partly responsible for the observation that skeletal fragility seems to be excessive in proportion to the amount of bone lost. Finally, the loss of trabecular elements is not accompanied by demonstrable defects in bone remodeling dynamics.