Osteochondritis dissecans (OCD) is an acquired, potentially reversible idiopathic disease of subchondral bone resulting in delamination and sequestration. Although juvenile-type OCD lesions typically appear stable on superficial examination, conservative treatment results in cure in approximate 50% of patients. We hypothesized that juvenile-type OCD lesions exhibit an underlying instability despite stability at the articular surface and this underlying instability might underlie the lack of effectiveness of conservative treatment. In this study, osteochondral cylindrical tissue samples obtained from stable juvenile OCD lesions located at the medial femoral condyle (classical site) were examined. Eight patients with symptomatic juvenile-type OCD at the classical site underwent arthroscopy. Osteochondral cylindrical tissue samples were obtained from the central portion using a biopsy needle. The samples underwent macroscopic and microscopic examination. All cylindrical samples demonstrated macroscopic separation. On microscopic examination, no degenerative changes in articular cartilage and no bone necrosis were observed. Histological examination revealed two distinct patterns in the samples: (1) thick homogeneous hyaline cartilage alone with little fibrous tissue surrounding areas of separation and (2) nearly normal, thin hyaline cartilage above a mixed layer of hyaline cartilage and subchondral trabeculae and fibrous/fibro-cartilaginous tissue at the areas of separation, indicating delayed or nonunion. Pathological findings in stable juvenile OCD lesions indicate an underlying instability at deeper layers of articular cartilage and poor healing at areas of separation. Improved knowledge of the histology of juvenile-type OCD lesions may support surgical treatment. Early marrow stimulation and/or fixation may be the treatment of choice to promote healing even in macroscopically stable juvenile-type OCD lesions.

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Purpose This study aimed to identify independent predictive factors for return to sports (RTS) after anterior cruciate ligament (ACL) reconstruction in competitive‐level athletes and to determine optimal cut‐off values for these factors at 6 months after surgery. Methods A total of 124 competitive athletes (50 males and 74 females; mean age, 17.0 years; preinjury Tegner activity scale > 7) who underwent primary ACL reconstruction were enrolled. Assessments at 6 months after surgery consisted of knee functional tests [quadriceps index, hamstrings index, and single‐leg hop for distance (SLH)] and 2 self‐report questionnaires [IKDC subjective score and ACL‐Return to Sport after Injury scale (ACL‐RSI)]. At 1 year after surgery, athletes were classified into the RTS group (n = 101) or non‐RTS group (n = 23) based on self‐reported sports activities. After screening possible predictive factors of RTS, multivariate logistic regression and receiver operating characteristic curve analyses were performed to identify independent factors. Results Multivariate logistic regression analysis identified SLH (odds ratio, 2.861 per 10 unit increase; P < 0.001) and ACL‐RSI (odds ratio, 1.810 per 10 unit increase; P = 0.001) at 6 months as independent predictors of RTS at 1 year after surgery. Optimal cut‐off values of SLH and ACL‐RSI were 81.3% (sensitivity = 0.891; specificity = 0.609) and 55 points (sensitivity = 0.693; specificity = 0.826), respectively. Conclusion In competitive athletes, SLH < 81% and ACL‐RSI < 55 points at 6 months after surgery were associated with a greater risk of unsuccessful RTS at 1 year after surgery. SLH and ACL‐RSI at 6 months could serve as screening tools to identify athletes who have difficulties with returning to sports after ACL reconstruction. Level of evidence III.

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We investigated the in vivo introduction of a reporter gene into healing rat patellar ligaments using the hemagglutinating virus of Japan (HVJ)-liposome-mediated gene transfer method. The mid-portion of the medial half of the patellar ligament was cut transversely with a scalpel in 14-wk-old male Wistar rats. A HVJ-liposome suspension containing ␤ -galactosidase ( ␤ -gal) cDNA was injected directly into the injured site and pooled in the fascial pocket covering the injured site 3 d postoperatively. Thereafter, ␤ -gal-labeled cells were observed in the wound site accounting for 3% of the wound cells on the first day, 2% on the third, 7% on the seventh, 6% on the 14th, 2% on the 28th, and 0.2% on the 56th day after injection. The ␤ -gal-labeled cells were initially localized in and adjacent to the wound site, but they were observed spreading into the ligament substance away from the wound on the seventh day after injection. On day 28, ␤ -gal-labeled cells were observed throughout the length of the ligament substance. With double-labeling for marker antigens for monocyte/macrophage (ED-1) and for collagen I aminopropeptide (pN collagen I), it was revealed that fibroblastic (pN collagen I-positive) cells accounted for 63% and monocyte/macrophage lineage cells for 32% of the ␤ -gal-labeled cells in the day 7 wound. On day 28, they formed 58 and 35% of the ␤ -gal-labeled cells in the wound, respectively.Thus, we succeeded in introducing the ␤ -gal gene into healing rat patellar ligament. Moreover, labeling of the transfected cells made it possible to identify a biological event, namely that the cells in and around the wound site infiltrate into the uninjured ligament substance and come to populate the whole length of the ligament substance as repair progresses. These results suggest that ligament healing may involve not only the repair of the wound site itself but also extensive cellular infiltration of ligament substance adjacent to the wound. ( J. Clin. Invest. 1996. 97:226-231.)