Experimental And Clinical Study Of Repairing Articular Cartilage Defects And Blood-induced Damage To Articular Cartilage

During the course of Osteoarthritis(OA), structural lesion typically develop within the articular cartilage layer. The process is initiated by the loss of proteoglycans from the extracellular matrix and a disruption of the collagenous fibrillar network therein, these events being followed by cell metaplasia and loss. The initially small local lesion gradually increase not only in girth but also in length, such that ultimately the entire thickness of the articular cartilage layer may be destroyed. Albert that the metabolic activity of the surviving resident population of chondrocytes is augmented, this is altered in such a way that degradative processes predominate over anabolic ones.The numerous experimental and clinical attempts that have been made to induce the healing of histologic and macroscopic lesion within mature articular cartilage aim at re-establishing a structurally and functionally competent repair tissue of an enduring nature. Such lesion are generated during the course of many joint diseases, notably OA. In conjunction with a large number of genetic or metabolic conditions. Such as acromegaly, Paget's diseases, the Stickler-Syndrome and hemophilia,or as a result of trauma. Articular cartilage lesions generally do not heal, or heal only partially under certain biological conditions. They are frequently associated within disability and within symptoms such as joint pain, locking phenomena and reduced or disturbed function. Moreover, such lesions are generally believed to progresss to severe forms of OA. Attempts to heal articular cartilage lesions have obviously involved symptomatic measures, which are usefull only if patients gain relief, if joint functionality can be significantly restored and if the progression to severe joint destruction can be prevented or at least materially slowed down. Thereby the experiment was divided into three parts to study of repairing articular cartilage defects and blood-induced damage to articular...