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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5. MOTIVATION FOR TISSUE ENGINEERING 27 not yet progressed to OA) can be four times as much as treatment of the defect itself [216], and a similar scenario can be expected for OA. 5 MOTIVATION FOR TISSUE ENGINEERING Based on over 25,000 arthroscopies surveyed, it has been shown that osteochondral and chondral lesions are the most common, accounting for 67% of the observations, while OA accounts for 29% [165]. As presented earlier, the cartilage’s inability to mount a sufficient healing response eventually results in degenerative changes, and the proportion of lesions to OA observed is expected to change in the near future due to the baby boomers, with concomitant rises in management and treatment costs.

More recently, a three-phase (collagen, matrix, and synovial fluid), transversely isotropic, unconfined half-space model of articular cartilage was created for studying surface fissures [255]. 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.

Because of the viscoelastic nature of articular cartilage, load rate affects tissue stiffness and thus failure. The rates of applied stress, strain, and load must be considered. For example, using a confined compression loading protocol, the dynamic modulus has been shown to increase from 225 to 850 MPa as the load rate was increased from 25 to 1000 MPa/s [175]. 3. 2 times body weight. For a 70 kg person, this would correspond to ∼1400 to 4900 N [177]. Taking the medial tibial plateau to have an area of 1670 mm2 [178], this corresponds to a maximum stress of ∼3 MPa.

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