Bone and Osteoarthritis by Helmtrud I. Roach, Simon Tilley (auth.), Felix Bronner PhD,

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 bring about osteoarthritis, stressing the position of subchondral bone, which distinguishes this from different books at the disorder.

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 mobilephone, of the anabolic and catabolic roles of cytokines, could lead on to novel ways to scientific remedy, using anabolic mediators or molecules that concentrate on steps within the illness 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 procedure medical difficulties comprehensively. simply because bone performs a job in starting up osteoarthritis, healing techniques concentrating on bone tissue are incorporated within the dialogue of novel remedies. the final subject of osteoarthritis is consequently a well timed topic for a sequence on bone biology.

This ebook, meant for clinicians, researchers and scholars, presents info that might orient the amateur and replace the expert. No different e-book treats the connection of bone to osteoarthritis in related model or offers a related underpinning of joint pathophysiology.

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Extra resources for Bone and Osteoarthritis

Example text

Indeed leptin may be a key factor in the etiology of OA [60,124,138]. The potential role of bone tissue in OA initiation or progression may also be due to its capacity to serve as a reservoir for MSCs and to provide nutrition for the hyaline cartilage. The role of mesenchymal cells in the appearance or progression of OA is a key issue that has received recent attention. Because there is increasing evidence of the abnormal behavior and phenotypic features of osteoblasts, chondrocytes, myoblasts, and tenocytes in OA joints, MSC development and differentiation are likely to be altered in affected individuals.

Similarly, Gevers and Dequeker [80] have reported elevated serum osteocalcin levels in women with OA of the hand, and elevated osteocalcin in cortical bone explants. The levels of IGF-1, IGF-2, and TGF- , were also found elevated in samples of iliac crest bone of patients with OA [53]. This is a site distant from weight-bearing joints. High TGFand IGF-1 activity in OA bone tissue would promote bone remodeling [101] by altering the balance between bone matrix synthesis [175] and degradation via activation or inhibition of MMPs [206].

Other studies have indicated that subchondral bone changes proceed simultaneously or even follow changes in cartilage. Subchondral bone changes, therefore, would be only secondary to cartilage degradation [20,29,38]. Although the pathways involved in crosstalk between subchondral bone and cartilage remain largely unknown, several factors synthesized by subchondral bone cells are capable of inducing metabolic changes in the cartilage. Subchondral bone tissue may, by the production of cytokines and growth factors, induce OA [29,32,112].

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