Defects of the joint cartilage are of enormous medical and socio-economic impact. Meanwhile is widely acknowledged that untreated cartilage defects lead to an early onset of osteoarthritis. Intrinsic factors for the genesis of osteoarthritis are unknown. It is wellknown however that joint cartilage has only a limited capacity of regeneration. The conservative treatment of early osteoarthritis should focus on the following principles: Limit the pain. Various drugs are available for the symptomatic treatment of osteoarthritis (e.g. NSAIR, cortison, herbal preparations). Intrarticular injections with antiinflammatory agents (e.g. hyaluronan, cortison, IL-1 antagonists) have been proven to reduce pain and dysfunction. Orthetic devices are able to unload joint compartments destroyed by osteoarthritic cartilage lesions. Arthroscopic lavage and debridement eliminate inflammation mediating substances and balance the synovial environment. Maintain the function. Physiotherapy and massage fight the stiffness of the joint and enhance the periarticular circulation. Daily activity should be encouraged and supported e.g. by walking aids and custom-made shoewear. Reduce factors for progression. A successful dietary program can minimize overload of osteoarthritic joints. Surgical procedures to restore and maintain meniscal function, joint stability and physiological loading are beneficial to prevent further cartilage deterioration. Regeneration of cartilaginous surfaces e.g. by marrow stimulation techniques or autologous chondrocyte transplantation will ease joint function and inhibit enzymatic degradation of healthy cartilage. In the last 10 years modern biochemical and cell biological techniques opened new horizons for the treatment of cartilage defects and osteoarthritis Future will teach us the value of cartilage regeneration to treat osteoarthritis.

The biologic approach of cell based therapies and the arthroscopic application of resorbable implants widen the indications for the conservative surgical treatment of osteoarthritis.

New cellular-based operation techniques like autologous chondrocyte transplantation (ACT) are performed more frequently for the treatment of full thickness cartilage defects. Non-steroid antiinflammatory drugs (NSIAD) are used universally after joint operations. Adverse effects of NSIAD on hyaline cartilage are discussed. Possible alterations regarding proliferation and vitality of transplanted chondrocytes after administration of NSAID are studied.

Twenty two specimen of human cartilage were harvested during joint operations (trauma, arthroplasty). The chondrocytes were encymatically (collagenase 0.2%/Biochrom) isolated After cryoconservation as used for ACT the cells were cultivated using standard medium (HAM’s F12, FCS 10%, Pen/Strep 1%, MEM-Vit 1%). Ibuprofen (Imbun/Merckle Germany) was added to the cultures analogous to the therapeutical synovial concentration (10μg/ml). Corresponding cultures in standard medium served as controls.

After 5 and 10 days the cells were trypsinized, counted in a Neubauer chamber and the vitality was tested with trypan blue staining. After 5 and 10 days the cultures showed an significant (p< 0.005) increase of cells from 0.25x106 to 0.51x106 resp.0.83x106 with Ibuprofen and 0.42x106 resp 0.67x106 in the controls. The vitality changed minorly from 96.0% after 5 days to 96.6% after 10 days in the Ibuprofen group and 94.1% to 96.3% in the controls. Age and gender of the donors as well as location of the harvesting site had no significant impact on proliferation rate and vitality of the chondrocytes.

The proliferation rate of human chondrocytes in monolayer culture increased significantly under the influence of Ibuprofen. The vitality of the cells was not affected by Ibuprofen. The results of various studies indicating an adverse effect of NSAID on hyaline cartilage and chondrocytes might be based on different substances in higher concentrations or animal models with unknown comparability to humans. Ongoing studies will focus on the influence of NSIAD on matrix synthesis of human chondrocytes.