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* Mercy Hospital and Medical Center, Chicago, IL.
Department of Anatomy, Rush-Presbyterian-St. Lukes Medical Center, Chicago, IL.
Department of Orthopedic Surgery, Rush-Presbyterian-St. Lukes Medical Center, Chicago, IL.
Illinois Institute of Technology, Chicago, IL.
|| Department of Biochemistry, Rush Medical College, Chicago, IL.
Corresponding author: Carol Muehleman, PhD, Department of Anatomy, Rush-Presbyterian-St. Lukes Medical Center, 600 S Paulina St, Chicago, IL 60612.
Abstract
Osteoarthritis is a disease of synovial joints that involves articular cartilage breakdown with accompanying bone changes, including subchondral sclerosis and osteophytosis. However, conflicting data have been reported concerning the cause-and-effect relationship, if any, between these changes. The authors studied the subchondral plate (subchondral bone plus calcified cartilage) in relation to the degree of articular cartilage degeneration on the distal articular surface of the first metatarsal, a region prone to osteoarthritis. No correlation was found between subchondral plate thickness or porosity and the degree of cartilage degeneration in the study sample of 96 metatarsals. Owing to the suggestion that initiation of cartilage fibrillation may be a result of steep stiffness gradients in the subchondral bone, the ratios of subchondral plate thickness in adjacent regions of the metatarsal head were examined in detail, but no correlation was found with subchondral degeneration. Thus increases in subchondral bone thickness are not associated with increases in cartilage degeneration on the first metatarsal, which may imply that subchondral bone changes do not cause osteoarthritis in this joint. (J Am Podiatr Med Assoc 93(2): 104-110, 2003)
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