By Helmtrud I. Roach, Simon Tilley (auth.), Felix Bronner PhD, Mary C. Farach-Carson PhD (eds.)
Bone and Osteoarthritis areas emphasis at the molecular and mobile occasions that result in osteoarthritis, stressing the position of subchondral bone, which distinguishes this from different books at the illness.
A novel element is the eye given to the prospective epigenetic foundation, including a dialogue of the genetics predisposing to osteoarthritis.
Detailed analyses are given of the function of the synovium, of the molecular mechanisms that result in degradation of the cartilage matrix, of the hypertrophy of the cartilage phone, of the anabolic and catabolic roles of cytokines, could lead to novel ways to medical therapy, using anabolic mediators or molecules that concentrate on steps within the ailment strategy. additionally mentioned are animal types and the way mechano-responsiveness is compromised by way of 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 technique medical difficulties comprehensively. simply because bone performs a task in starting up osteoarthritis, healing ways concentrating on bone tissue are incorporated within the dialogue of novel remedies. the overall subject of osteoarthritis is for this reason a well timed topic for a sequence on bone biology.
This ebook, meant for clinicians, researchers and scholars, presents details that might orient the amateur and replace the professional. No different ebook treats the connection of bone to osteoarthritis in comparable model or presents a similar underpinning of joint pathophysiology.
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Additional info for Bone and Osteoarthritis
Effects of 1,25(OH)2 D3 , 24,25(OH)2 D3 , parathyroid hormone, and glucocorticoids. Metab Bone Dis Relat Res 5:229–234. 13. Bettica P, Cline G, Hart DJ, Meyer J, Spector TD (2002) Evidence for increased bone resorption in patients with progressive knee osteoarthritis: longitudinal results from the Chingford study. Arthritis Rheum 46:3178–3184. 14. Beuf O, Ghosh S, Newitt DC, Link TM, Steinbach L, Ries M, Lane N, Majumdar S (2002) Magnetic resonance imaging of normal and osteoarthritic trabecular bone structure in the human knee.
The articular vasculature, therefore, derives its nutritional supply partly from the vascular bed of subchondral bone, as well as from the synovial fluid. Therefore, any loss of vascular tone in the subchondral bone could affect the cartilage. Early microvascular damages that affect the venous circulation in the bony tissue, therefore, may be considered a plausible cause of altered chondrocyte function . Whether these vascular changes are secondary to bony changes or their primary cause remains unexplored.
91. Tehranzadeh J, Booya F, Root J (2005) Cartilage metabolism in osteoarthritis and the influence of viscosupplementation and steroid: a review. Acta Radiol 46:288–296. 92. Tetlow LC, Adlam DJ, Woolley DE (2001) Matrix metalloproteinase and proinflammatory cytokine production by chondrocytes of human osteoarthritic cartilage: associations with degenerative changes. 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.