Abstract
IntroductionMicrofracture does not lead to complete healing of full-thickness cartilage defects. The aim of this study was to evaluate the effect of modifying Wnt/β-catenin signaling following microfracture, on the restoration of a full-thickness cartilage defect in a rabbit model. The modification of the canonical Wnt pathway was achieved through per os administration of lithium carbonate, which is an intracellular inhibitor of glycogen synthase kinase 3-β (Gsk3-β) and therefore induces Wnt/β-catenin signaling.Materials and methodsFull-thickness cartilage defects of 4 mm in diameter were created in the patellar groove of the right femurs of 18 male New Zealand white rabbits. The rabbits were divided into three groups of six (n = 6) based on post-surgery treatment differences, as follows: microfracture only (group 1), microfracture plus lithium carbonate 7 mM in the drinking water for 1 week (group 2), microfracture plus lithium carbonate 7 mM in the drinking water for 4 weeks (group 3). All animals were sacrificed 9 weeks after surgery. The outcome was assessed histologically, by using the International Cartilage Repair Society (ICRS) visual histological scale. Immunohistochemistry for type II collagen was also conducted.ResultsStatistical analysis of the histological ICRS scores showed that group 3 was significantly superior to group 1 in four out of six ICRS categories, while group 2 was superior to 1 in only two out of six.ConclusionThe combination of microfracture and systematic administration of lithium carbonate 7 mM for 4 weeks shows statistically significant superiority in four out of six ICRS categories compared with microfracture only for the treatment of full-thickness cartilage defects in a rabbit experimental model.
Highlights
Microfracture does not lead to complete healing of full-thickness cartilage defects
In a study by Kwong et al (2009), it was shown that imbalance in the expression of bone morphogenetic proteins (BMPs) and BMP inhibitors within cartilaginous areas of developing non-unions may account for their reduced bone formation ability [11]
The histological findings for group 3 demonstrated a regular newly formed tissue surface, with a hyaline matrix mixed with fibrocartilage in some areas, but with chondrocytes distributed in a more organized pattern compared to the other groups (Fig. 3c, f)
Summary
Microfracture does not lead to complete healing of full-thickness cartilage defects. The aim of this study was to evaluate the effect of modifying Wnt/β-catenin signaling following microfracture, on the restoration of a full-thickness cartilage defect in a rabbit model. Marrow-stimulating procedures are indicated for treating small, up to 4-cm full-thickness cartilage defects. In these procedures, perforation to the subchondral bone allows blood and marrow-derived cells to fill the defect and a blood clot is formed. Cartilage formation is the desirable outcome in osteochondral lesions, but it is quite unwelcome as a final result of the fracture healing process. In several models of fracture nonunion, cartilage formation is not followed by efficient endochondral ossification, while fibrous tissue forms instead. In a study by Kwong et al (2009), it was shown that imbalance in the expression of bone morphogenetic proteins (BMPs) and BMP inhibitors within cartilaginous areas of developing non-unions may account for their reduced bone formation ability [11]
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