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Managing Degenerative Joints the Future
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Recent Progress at Healing Articular Cartilage Lesions and Resurfacing Joints
The real challenge in OA treatment is the progressive loss of articular cartilage. The failure of osteochondral defects to heal is a major limiting factor in the prognosis after the treatment of articular fractures. Arthroscopic techniques for cartilage repair have been developed and reviewed. The aim of these techniques is to enhance both the quantity and quality of cartilage repair tissue while using the well-documented advantages of arthroscopic surgery. Techniques include optimal defect debridement (complete removal of calcified cartilage [CCL]), cartilage reattachment, and subchondral microfracture (micropicking). These represent attempts to augment endogenous repair and are discussed further below. At the same time, investigations have been done in the horse using tissue engineering techniques and cellular augmentation. Not all of these techniques have been done arthroscopically, but with recognition of the optimal studies (preferably a one-stage procedure), arthroscopic techniques to support their use will be developed.
Articular Cartilage Repair
The use of the word healing implies restoration of structural integrity and function of tissue after injury or disease. Repair can be defined as replacement of damaged or lost cells and matrix with new cells and matrix but does not necessarily restore original structure or function. Repair is what is typically achieved in the repair of full-thickness articular defects. Regeneration is a special form of repair in which cells replace lost or damage tissue with a tissue identical to the original one; this is the aim of investigations in cartilage resurfacing. There are three potential means of 1 articular repair: intrinsic, extrinsic, and matrix flow. The inability of intrinsic repair is manifested best in partial-thickness lesions of the cartilage (including lacerations) that result in a non-healing phase that does not change. Although there is a reactive response, the limited mitotic ability of the chondrocyte and the ineffective increase in collagen and proteoglycan production leaves the defect unhealed but also relatively unimportant. Full-thickness cartilage lesions through the tidemark, into the subchondral bone plate, heal by extrinsic repair from mesenchymal elements from subchondral bone. [...]
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