Joints are functional units that transmit mechanical loads between contacting bones during normal daily or specialized activities, e.g., sports. All components of the joint, i.e. articular cartilage, bone, muscles, ligaments/tendons and nerves, participate in load transmission. Failure in any of these components can cause joint malfunction, which, in turn, may lead to accumulation of damage in other joint components. Mechanical forces have great influence on the synthesis and rate of turnover of articular cartilage molecules, such as proteoglycans (PGs). Regular cyclic loading of the joint enhances PG synthesis and makes cartilage stiff. On the other hand, loading appears to have less evident effects on the articular cartilage collagen fibril network. Continuous compression of the cartilage diminishes PG synthesis and causes damage of the tissue through necrosis. The prevailing view is that osteoarthrosis (OA) starts from the cartilage surface through PG depletion and fibrillation of the superficial collagen network. It has also been suggested that the initial structural changes take place in the subchondral bone, especially when the joint is exposed to an impact type of loading. This in turn would create an altered stress pattern on joint surfaces, which leads to structural damage and mechanical failure of articular cartilage. The importance of the neuromuscular system to the initiation and progression of OA is still poorly understood. Many surgical extra- and intra-articular procedures have been used for the treatment of OA. Although some of the new methods, such as autologous chondrocyte transplantation and mosaicplasty, have given good clinical results, it is reasonable to emphasize that the methods still are experimental and more controlled studies are needed.

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Previous laboratory measurements showed topographical variation in the properties of articular cartilage in several animal species and in humans. In this study we characterize for the first time the topographical variation of the stiffness of the human knee articular cartilage in vivo using a novel arthroscopic indentation instrument. The instrument indicates the stiffness in the form of force (Newtons) by which the tissue resists the constant deformation (300 microm) produced by the small (1-mm diameter) cylindrical indenter. Measurements were carried out at eight sites in the knee joint of 20 persons who had intact cartilage in the arthroscopic examination. The stiffest cartilage (5.6 +/- 1.2 N, mean +/- SD) was located in the lateral condyle of the femur, whereas the softest cartilage (2.4 +/- 0.8 N) was in the medial plateau of the tibia. In general, the cartilage stiffness was higher in the femur than in the tibia (p < 0. 01) or in the patella (p < 0.01). In the femur, the condyles were stiffer than the patellar surface (p < 0.01). The stiffness variation was consistent with earlier biphasic indentation analyses of laboratory measurements with the knee joint cartilage of cadavers. This study provides baseline data for characterization of cartilage stiffness in pathological situations or follow-up of the cartilage quality after surgical interventions.

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Background:The optimal treatment of acute, complete dislocation of the acromioclavicular joint (ACJ) is still unresolved.Purpose:To determine the difference between operative and nonoperative treatment in acute Rockwood types III and V ACJ dislocation.Study Design:Randomized controlled trial; Level of evidence, 2.Methods:In the operative treatment group, the ACJ was reduced and fixed with 2 transarticular Kirschner wires and ACJ ligament suturing. The Kirschner wires were extracted after 6 weeks. Nonoperatively treated patients received a reduction splint for 4 weeks. At the 18- to 20-year follow-up, the Constant, University of California at Los Angeles Shoulder Rating Scale (UCLA), Larsen, and Simple Shoulder Test (SST) scores were obtained, and clinical and radiographic examinations of both shoulders were performed.Results:Twenty-five of 35 potential patients were examined at the 18- to 20-year follow-up. There were 11 patients with Rockwood type III and 14 with type V dislocations. Delayed surgical treatment for ACJ was used in 2 patients during follow-up: 1 in the operatively treated group and 1 in the nonoperatively treated group. Clinically, ACJs were statistically significantly less prominent or unstable in the operative group than in the nonoperative group (normal/prominent/unstable: 9/4/3 and 0/6/3, respectively; P = .02) and in the operative type III (P = .03) but not type V dislocation groups. In operatively and nonoperatively treated patients, the mean Constant scores were 83 and 85, UCLA scores 25 and 27, Larsen scores 11 and 11, and SST scores 11 and 12 at follow-up, respectively. There were no statistically significant differences in type III and type V dislocations. In the radiographic analysis, the ACJ was wider in the nonoperative than the operative group (8.3 vs 3.4 mm; P = .004), and in the type V dislocations (nonoperative vs operative: 8.5 vs 2.4 mm; P = .007). There was no statistically significant difference between study groups in the elevation of the lateral end of the clavicle. Both groups showed equal levels of radiologic signs of ACJ osteoarthritis and calcification of the coracoclavicular ligaments.Conclusion:Nonoperative treatment was shown to produce more prominent or unstable and radiographically wider ACJs than was operative treatment, but clinical results were equally good in the study groups at 18- to 20-year follow-up. Both treatment methods showed statistically significant radiographic elevations of the lateral clavicle when compared with a noninjured ACJ.