Roy K Aaron1, Jennifer Racine2, Jonathan P Dyke3. 1. Department of Orthopedics, Warren Alpert Medical School of Brown University, 100 Butler Drive, Providence, RI, 02906, USA. Roy_Aaron@brown.edu. 2. Department of Orthopedics, Warren Alpert Medical School of Brown University, 100 Butler Drive, Providence, RI, 02906, USA. 3. Department of Radiology, Weill Cornell Medicine Citigroup Biomedical Imaging Center , 516 E 72nd Street, New York, NY, 10021, USA.
Abstract
PURPOSE OF REVIEW: This review describes the contributions of abnormal bone circulation to the pathophysiology of osteoarthritis. Combining dynamic imaging with MRI and PET with previous observations reveals that venous stasis and a venous outlet syndrome is most likely the key circulatory pathology associated with the initiation or progression of osteoarthritis. RECENT FINDINGS: MRI and PET have revealed that venous outflow obstruction results in physicochemical changes in subchondral bone to which osteoblasts are responsive. The osteoblasts express an altered pattern of cytokines, many of which can serve as structural or signaling molecules contributing to both bone remodeling and cartilage degeneration. The patterns of circulatory changes are associated with alterations in the physicochemical environment of subchondral bone, including hypoxia. Osteoblast cytokines can transit the subchondral bone plate and calcified cartilage and communicate with chondrocytes.
PURPOSE OF REVIEW: This review describes the contributions of abnormal bone circulation to the pathophysiology of osteoarthritis. Combining dynamic imaging with MRI and PET with previous observations reveals that venous stasis and a venous outlet syndrome is most likely the key circulatory pathology associated with the initiation or progression of osteoarthritis. RECENT FINDINGS: MRI and PET have revealed that venous outflow obstruction results in physicochemical changes in subchondral bone to which osteoblasts are responsive. The osteoblasts express an altered pattern of cytokines, many of which can serve as structural or signaling molecules contributing to both bone remodeling and cartilage degeneration. The patterns of circulatory changes are associated with alterations in the physicochemical environment of subchondral bone, including hypoxia. Osteoblast cytokines can transit the subchondral bone plate and calcified cartilage and communicate with chondrocytes.
Entities:
Keywords:
Bone circulation; Crosstalk; Dynamic imaging; Hypoxia; Osteoarthritis; Venous stasis
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