Mosaicplasty resulted in satisfactory clinical outcomes and smooth cartilage surface integrity in teenage athletes with OCD on their return to competition-level sports activities irrespective of lesion location.

The information obtained from the CT images can useful for early detection of overstress conditions of the elbow joint.

To analyze the genetic and biomolecular mechanisms underlying cartilage repair, an optimized mouse model of osteochondral repair is required. Although several models of articular cartilage injury in mice have recently been established, the articular surface in adult C57Bl/6 mice heals poorly. Since C57Bl/6 mice are the most popular strain of genetically manipulated mice, an articular cartilage repair model using C57Bl/6 mice would be helpful for analysis of the mechanisms of cartilage repair. The purpose of this study was to establish a cartilage repair model in C57Bl/6 mice using immature animals. To achieve this goal, fullthickness injuries were generated in 3-week-old (young), 4-week-old (juvenile), and 8-week-old (adult) C57Bl/6 mice. To investigate the reproducibility and consistency of full-thickness injuries, mice were sacrificed immediately after operation, and cartilage thickness at the patellar groove, depth of the cartilage injury, cross-sectional width, and cross-sectional area were compared among the three age groups. The depth of cartilage injury/cartilage thickness ratio (%depth) and the coefficient of variation (CV) for each parameter were also calculated. At 8 weeks postoperatively, articular cartilage repair was assessed using a histological scoring system. With respect to the reproducibility and consistency of full-thickness injuries, cartilage thickness, depth of cartilage injury, and cross-sectional area were significantly larger in young and juvenile mice than in adult mice, whereas cross-sectional width and %depth were almost equal among the three age groups. CVs of %depths were less than 10% in all groups. With respect to articular cartilage repair, young and juvenile mice showed superior results. In conclusion, we established a novel cartilage repair model in C57Bl/6 mice. This model will be valuable in achieving mechanistic insights into the healing process of the joint surface, as it will facilitate the use of genetically modified mice, which are most commonly developed on a C57Bl/6 background.

Cartilage injuries are a common health problem resulting in the loss of daily activities. Bone marrow stimulation technique, one of the surgical techniques for the cartilage injuries, is characterized by technical simplicity and less invasiveness. However, it has been shown to result in fibrous or fibrocartilaginous repair with inferior long-term results. This study focused on using ultrapurified alginate gel (UPAL gel) as an adjuvant scaffold in combination with a bone marrow stimulation technique. The objective of this study was to assess the efficacy of a bone marrow stimulation technique augmented by UPAL gel in a rabbit osteochondral defect model. To achieve this goal, three experimental groups were prepared as follows: defects without intervention, defects treated with a bone marrow stimulation technique, and defects treated with a bone marrow stimulation technique augmented by UPAL gel. The macroscopic and histological findings of the defects augmented by UPAL gel improved significantly more than those of the others at 16 weeks postoperatively. The combination technique elicited hyaline-like cartilage repair, unlike bone marrow stimulation technique alone. This combination procedure has the potential of improving clinical outcomes after use of a bone marrow stimulation technique for articular cartilage injuries.

Juvenile tissue healing is capable of extensive scarless healing that is distinct from the scar-forming process of the adult healing response. Although many growth factors can be found in the juvenile healing process, the molecular mechanisms of juvenile tissue healing are poorly understood. Here we show that juvenile mice deficient in the chemokine receptor CCR7 exhibit diminished large-scale healing potential, whereas CCR7-depleted adult mice undergo normal scar-forming healing similar to wild type mice. In addition, the CCR7 ligand CCL21 was transiently expressed around damaged cartilage in juvenile mice, whereas it is rarely expressed in adults. Notably, exogenous CCL21 administration to adults decreased scar-forming healing and enhanced hyaline-cartilage repair in rabbit osteochondral defects. Our data indicate that the CCL21/CCR7 axis may play a role in the molecular control mechanism of juvenile cartilage repair, raising the possibility that agents modulating the production of CCL21 in vivo can improve the quality of cartilage repair in adults. Such a strategy may prevent post-traumatic arthritis by mimicking the self-repair in juvenile individuals.