Articular cartilage tissue engineering by K A Athanasiou; Eric M Darling; Jerry C Hu

By K A Athanasiou; Eric M Darling; Jerry C Hu

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Extra resources for Articular cartilage tissue engineering

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Many in vitro studies have manipulated the molecular players highlighted above to promote the accumulation of cartilage-specific matrix, both for developmental studies and for tissue engineering. As TGF-β1, β2, and β3 have been observed during differentiation in vitro [121], their efficacy has been examined in enhancing matrix production. The same is true for the BMPs. TGF-β has been shown as effective on cells that have not yet condensed while BMP-2 achieves similar effects after the cells have condensed or differentiated [121].

The tensile stresses generated were within the range of reported tensile strength of collagen fibers, showing that failure of collagen could lead to surface fissuring. This was not the case for slowly applied loads. In another study [256], mediators of collagen damage due to mechanical injury were investigated in a fibril-reinforced poroviscoelastic model of articular cartilage. The results from investigations of surface fissuring implicate collagen as having a key role in keeping the surface intact when subjected to injurious mechanical loading.

During normal activities, like running, time to peak force is on the order of 30 ms, leading to a stress rate of 100 MPa/s. One can expect that impact injuries occur on a time scale an order of magnitude smaller, resulting in stress rates of 1000 MPa/s. Based on data such as these, Aspden and associates [179] put forth a definition for injurious impact loading as time to peak load on the order of milliseconds plus one of the following: (1) stress rate greater than 1000 MPa/s, (2) strain rate greater than 500 s−1 , or (3) loading rates in excess of 100 kN/s.

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