Biomechanical Study of Osteochondral Lesions of the Talus and Autologous Osteochondral Transplantation. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Osteochondral lesions of the talus (OLT) frequently result in limited ankle joint functionality, necessitating prompt intervention. For large-area OLT, autologous osteochondral transplantation (AOT) is a prevalent treatment; however, standardized criteria for its implementation are lacking. OBJECTIVE: This study aims to examine the influence of OLT on stress transmission within the talus, assess how OLT of varying sizes and depths affects the peak stress of talar cartilage, and identify the optimal timing for AOT to effectively restore the peak stress of talar cartilage, thereby offering guidance for AOT procedures. METHODS: Initially, a finite element model of a healthy human ankle joint was developed, and OLT defect models of different sizes and depths were created in designated areas of the talar cartilage. The impact of OLT on talus stress transmission was analyzed through gait simulation. Subsequently, biomechanical experiments were performed to evaluate the variations in peak stress of the talar cartilage across OLT models with differing sizes and depths, as well as in the AOT repair model. RESULTS: Finite element analysis indicated that OLT alters the distribution of stress within the talus. Biomechanical experiments demonstrated that OLT initially reduces the peak stress of the talar cartilage, which subsequently increases after reaching a critical threshold, with this variation remaining unaffected by the position of the ankle joint. The stress changes of talar cartilage mainly depend on the defect area rather than the depth. When the area reaches 120 mm2, AOT can effectively restore the stress level of talar cartilage. CONCLUSION: OLT affects the biomechanical properties of the ankle joint. When the defect area reaches 120 mm2, AOT can effectively restore the stress levels of the talar cartilage to normal.

publication date

  • October 10, 2025

Identity

Digital Object Identifier (DOI)

  • 10.1097/JS9.0000000000003605

PubMed ID

  • 41085654