The articular cartilage from the impingement lesion in patients with FAI showed biologically higher inflammation and degeneration, supporting the concept that FAI may be a trigger for joint degeneration.

Level IV, therapeutic case series.

GCQ supplement was thought to be more effective than placebo in decreasing the intensity of knee OA-associated clinical symptoms.

Objective. Chondrocyte apoptosis plays an important role in cartilage degeneration in osteoarthritis (OA), and mechanical injury to cartilage induces chondrocyte apoptosis. In response to DNA damage, p53 expression is up-regulated, transcription activity is increased, and apoptosis signals are initiated. The p53-regulated apoptosis-inducing protein 1 (p53AIP-1) is one of the p53-regulated genes, and is activated in response to DNA damage. This study was undertaken to analyze p53 function after induction of apoptosis by shear strain in chondrocytes.Methods. OA cartilage samples were obtained from subjects undergoing total knee replacement surgery, and normal cartilage samples were obtained from subjects undergoing surgery for femoral neck fracture. Chondrocytes were isolated from human cartilage and cultured. Expression of p53 and p53AIP in chondrocytes was detected by reverse transcriptase-polymerase chain reaction and Western blotting. Shear strain was introduced in normal human knee chondrocytes. To explore p53 function, normal human knee chondrocytes were pretreated with pifithrin-␣ or p53 small interfering RNA (siRNA) before induction of shear strain. Chondrocyte apoptosis was detected by expression of cleaved caspase 9 with Western blotting and TUNEL staining. Expression of p53 and p53AIP-1 was analyzed by Western blotting.Results. OA and normal chondrocytes expressed p53. OA chondrocytes showed much higher expression of p53 and p53AIP-1 than did normal chondrocytes. TUNEL-positive cells and expression of p53, p53AIP-1, and cleaved caspase 9 were increased by shear strain, but chondrocyte apoptosis was suppressed after pretreatment with pifithrin-␣ or p53 siRNA.Conclusion. Our findings indicate that p53 and p53AIP-1 play important roles in human chondrocyte apoptosis. Down-regulation of p53 expression prevents cartilage from undergoing apoptosis introduced by shear strain.

Purpose Concomitant meniscus injuries in the anterior cruciate ligament (ACL) injuries have been suggested to exacerbate rotational laxity. However, the effect is supposed to be so small, if any, that some quantitative pivot-shift measurement is needed. The purpose of this prospective study was to determine the effect of meniscus tear on rotational laxity in ACL-deficient knees by an quantitative measurement. We hypothesized that a concomitant meniscus tear, especially a lateral one, would induce greater pivot-shift. Methods Fifty-seven unilateral ACL-injured patients (26 men and 31 women, mean age: 24±10 years) were included. The pivot-shift test was performed prior to ACL reconstruction while a quantitative evaluation using an electromagnetic system to determine tibial acceleration and a clinical grading according to the IKDC were performed. Meniscus injuries were diagnosed arthroscopically, and concomitant meniscus tear was confirmed in 32 knees. Chi-squared and Mann-Whitney U tests were used to assess the difference between knees with and without meniscus tear. A subgroup analysis was subsequently performed for the medial, bilateral, and lateral meniscus-torn groups compared with the meniscus-intact group, using the chi-squared test and analysis of variance. Statistical significance was defined at p<0.05.