Bone fragility in aging and disease is associated with increased damage at the matrix level. While often characterized as microscopic cracking, damage processes originate at the ultrastructural and molecular levels of bone structural hierarchy[1]. Thus, variations in mineral and collagen organization may influence bone mechanics and failure. This hypothesis is supported by studies which demonstrated altered collagen fibril diameter distributions in patients with osteogenesis imperfecta (OI)[2,3,4], an inherited bone disease characterized by frequent brittle fracture. Fibril diameters have been shown to change with aging in a variety of soft tissues, including skin, tendon, and ligament [5]. No systematic aging studies of diameterdistributions have been performed in bone, despite its potential significance in age-related fragility and fracture. The objective of this study was to characterize the collagen fibril diameter distribution in vertebral cancellous bone of females, afrequent fracture site among the aged.
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