The aim of this study was to quantify the effects of understuffing and overstuffing UKA on bone stresses, load distribution and ligament strains. For that purpose, a numerical knee model of a cadaveric knee was developed and was validated against experimental measurements on that same knee. Good agreement was found among the numerical and experimental results. This study showed that, even if a medial UKA is well-aligned with normal soft tissue tension and with correct thickness of the tibia component, it induces a stiffness modification in the joint that alters the load distribution between the medial and lateral compartments, the bone stress and the ligament strain potentially leading to an osteoarthritic progression.

No abstract

No abstract

To investigate the effect of modification of biological environmental conditions, one of the factors influencing the healing of anterior cruciate ligament rupture, we performed experimental anterior cruciate ligament ruptures on New Zealand rabbits. After experimental rupture, intra-articular alpha-2 macroglobulin was injected into the knees of the rabbits in the experiment group to prevent structural changes resulting from the enzymatic reactions in the ruptured anterior cruciate ligament. At the end of 10th day of the experiment, we observed that the anterior cruciate ligaments in the experiment group had retained their prerupture brightness and volume when compared with the control group in which intraarticular alpha-2 macroglobulin had not been injected. We also noted that the anterior cruciate ligaments in the experiment group had not retracted or swollen, the incision sites were regular and clean, and they did not show any signs of degeneration. In the histological examination, the anterior cruciate ligaments in the control groups showed disruption of the collagen network and a significant diminution in number of fibroblasts and fibrocytes (p <.001). At the end of this study, we concluded that the necessary conditions for the healing and repair of ruptured anterior cruciate ligament could exist if the enzymatic and biological environments were under control.

Background:Osteoarthritis (OA) is the most frequent chronic joint disease causing pain and disability. Recent reports have shown that statin may have the potential to inhibit osteoarthritis. This study of early stage OA developed in an experimental rabbit model, aimed to evaluate the chondroprotective effects of intraarticularly applied atorvastatin on cartilage tissue macroscopically and histopathologically by examining intracellular and extracellular changes by light and electron microscope.Materials and Methods:The experimental knee OA model was created by cutting the anterior cruciate ligament of the 20 mature New Zealand rabbits. The rabbits were randomly allocated into two groups of 10. Study group: The group that received intraarticular statin therapy; Control group: The group that did not receive any intraarticular statin therapy. The control group received an intraarticular administration of saline and the study group atorvastatin from the 1st week postoperatively, once a week for 3 weeks. The knee joints were removed including the femoral and tibial joint surfaces for light and electron microscopic studies of articular cartilages.Results:The mean total points obtained from the evaluation of the lesions that developed in the medial femoral condyle were 11.33 ± 0.667 for the control group and 1.5 ± 0.687 for the study group. The mean total points obtained from the evaluation of the lesions that developed in medial tibial plateau cartilage tissue were 11.56 ± 0.709 for the control group and 1.40 ± 0.618 for the study group. Electron microscopic evaluation revealed healthy cartilage tissue with appropriate chondrocyte and matrix structure in study group and impaired cartilage tissue in control group.Conclusion:Chondroprotective effect of statin on cartilage tissue was determined in this experimental OA model evaluated macroscopically and by light and electron microscope. There are some evidences to believe that the chondroprotective effect of the statin is that, by protecting the structure of the endoplasmic reticulum and the Golgi complex.