By Helmtrud I. Roach, Simon Tilley (auth.), Felix Bronner PhD, Mary C. Farach-Carson PhD (eds.)
Bone and Osteoarthritis locations emphasis at the molecular and mobile occasions that result in osteoarthritis, stressing the function of subchondral bone, which distinguishes this from different books at the sickness.
A novel point is the eye given to the potential epigenetic foundation, including a dialogue of the genetics predisposing to osteoarthritis.
Detailed analyses are given of the position of the synovium, of the molecular mechanisms that result in degradation of the cartilage matrix, of the hypertrophy of the cartilage cellphone, of the anabolic and catabolic roles of cytokines, could lead to novel methods to scientific remedy, using anabolic mediators or molecules that concentrate on steps within the ailment approach. additionally mentioned are animal versions and the way mechano-responsiveness is compromised through mechanical injury.
Orthopedics and rheumatology became shut conceptually, as advances in bone and joint biology have enabled bench and translational scientists, in addition to practitioners, to procedure scientific difficulties comprehensively. simply because bone performs a task in beginning osteoarthritis, healing techniques concentrating on bone tissue are integrated within the dialogue of novel remedies. the final subject of osteoarthritis is for that reason a well timed topic for a sequence on bone biology.
This ebook, meant for clinicians, researchers and scholars, presents details that would orient the beginner and replace the expert. No different booklet treats the connection of bone to osteoarthritis in comparable type or presents a related underpinning of joint pathophysiology.
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Additional info for Bone and Osteoarthritis
13 Conclusion It is well established that changes in subchondral bone and modifications of osteoblast metabolism are key in the initiation and progression of OA. Both animal and clinical studies support the emerging concept that changes in bone may precede changes in a cartilage. Hence, bone tissue rather than cartilage may be the initiating site of the events that bring about OA. Acknowledgement Daniel Lajeunesse is a Chercheur-National Scholar from the Fonds de la Recherche en Santé du Québec (FRSQ).
Arthritis Rheum 44:585–594. 93. Tetlow LC, Woolley DE (2001) Expression of vitamin D receptors and matrix metalloproteinases in osteoarthritic cartilage and human articular chondrocytes in vitro. Osteoarthritis Cartilage 9:423–431. 94. Tortorella MD, Malfait AM, Deccico C, Arner E (2001) The role of ADAM-TS4 (aggrecanase-1) and ADAM-TS5 (aggrecanase-2) in a model of cartilage degradation. Osteoarthritis Cartilage 9:539–552. 95. Tsuchiya K, Maloney WJ, Vu T, Hoffman AR, Schurman DJ, Smith RL (1996) RT-PCR analysis of MMP-9 expression in human articular cartilage chondrocytes and synovial fluid cells.
The etiology is multifactorial, but common features can be observed. The end point of OA is cartilage destruction that impairs joint movement and causes pain. In knee joints, the cartilage destruction is associated with or preceded by subchondral bone sclerosis. Joint destruction is also associated with joint inflammation, with the synovial membrane playing a key role. The chronologic events of these phenomena are still debated in the literature. However, because of the complexity of the disease, it may be initiated via each of these tissues, although inflammation of the synovial membrane is less likely to be a primary cause.
Bone and Osteoarthritis by Helmtrud I. Roach, Simon Tilley (auth.), Felix Bronner PhD, Mary C. Farach-Carson PhD (eds.)