Abstract
Research Type:
Level 3 - Retrospective cohort study, Case-control study, Meta-analysis of Level 3 studies
Introduction/Purpose:
Cavovarus foot deformity affects 8-15% of the population. Altered biomechanics place the ankle at increased risk for developing osteoarthritis (OA). Recent studies have leveraged weight bearing CT (WBCT) to better characterize joint biomechanics using computational modeling to analyze joint interactions during functional loading. The 3D models use discrete element analysis (DEA) to estimate joint contact stress. These techniques could assist in identifying patients at-risk of developing ankle OA secondary to cavovarus deformity. Various studies have indicated a link between morphologic changes of the tibiotalar joint and the development of ankle OA. We hypothesize that anatomic positioning of the ankle joint is associated with increased asymmetric loading in the setting of cavovarus hindfoot alignment. Chronic increases in contact stress would increase the risk of ankle OA.
Methods:
We studied WBCT scans of three patient cohorts: healthy controls with no underlying ankle deformity (39 feet), patients with idiopathic cavovarus (24 feet), and patients diagnosed with cavovarus deformity from Charcot-Marie-Tooth disease (22 feet). WBCT scans were segmented using DISIOR/Paragon28 to generate 3D surface models of the loaded tibia and talus. These models were aligned and smoothed using Geomagic Design X. Opposing cartilage surfaces were then imported into MATLAB for analysis using previously developed DEA code which treats subchondral bone as a rigid body and articular cartilage as an isotropic linear elastic material, idealized as a bed of springs. DEA was performed over 13 loading instances from the gait cycle with boundary conditions consistent with anatomic loading. Contact stress overexposure (CSTE) was analyzed using previously established methods (Figure 1). Statistical differences between each group were analyzed using two-tailed Wilcoxon rank-sum tests with a significance level of 0.05 (p < 0.05).
Results:
Significant differences were observed between the control group and idiopathic group for both the area over the damage threshold (0.87 mm2 vs 17mm2, p < 0.0001) and the maximum contact stress overexposure (4.17 MPa•s vs 7.08 MPa•s, p < 0.0001). Significant differences were also observed between the control group and the CMT disease group for both the area over the damage threshold (0.87 mm2 vs 7.39mm2, p = 0.01) and the maximum contact stress overexposure (4.17 MPa•s vs 5.53 MPa•s, p = 0.007).
Conclusion:
We hope that the development of this model will enable patient-specific prediction of progression to ankle arthritis, leading to subsequent identification, arthritic degeneration prevention, and management of at-risk patients.
Figure 1: Representative Patient Contact Stress Time Exposure Maps