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    Osteochondral alterations in osteoarthritis

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    Author
    Walsh, David A
    Keyword
    Osteochondral junction
    Bone
    Cartilage
    Osteoarthritis
    Vessels
    Pain
    Date
    2012-08
    
    Metadata
    Show full item record
    Publisher's URL
    https://www.sciencedirect.com/science/article/abs/pii/S8756328211012907?via%3Dihub
    Abstract
    Osteoarthritis (OA) is a major cause of pain and disability in the aging population, but its pathogenesis remains incompletely understood. Alterations beneath the articular cartilage at the osteochondral junction are attracting interest as possible mediators of pain and structural progression in OA. Osteochondral changes occur early during the development of OA and may aggravate pathology elsewhere in the joint. Loss of osteochondral integrity removes the barrier between intra-articular and subchondral compartments, exposing subchondral bone and its nerves to abnormal chemical and biomechanical influence. Osteochondral plasticity results in a merging of tissue compartments across the junction. Loss of the clearly differentiated demarcation between bone and articular cartilage is associated with invasion of articular cartilage by blood vessels and sensory nerves, and advancing endochondral ossification. Increased subchondral bone turnover is intimately associated with these alterations at the osteochondral junction. Cells signal across the osteochondral junction, and this cross-talk may be both a consequence of, and contribute to these pathological changes. Bone turnover, angiogenesis and nerve growth are also features of other diseases such as osteoporosis and cancers, for which therapeutic interventions are already advanced in their development. Here we review pathological changes at the osteochondral junction and explore their potential therapeutic implications for OA. This article is part of a Special Issue entitled "Osteoarthritis".
    Citation
    Suri, S. and Walsh, D. A. (2012) ‘Osteochondral alterations in osteoarthritis’, Bone, 51(2), pp. 204–211
    Publisher
    Bone
    Type
    Article
    URI
    http://hdl.handle.net/20.500.12904/15566
    Collections
    Rheumatology

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