Abstract

Purpose: Clear links have been made between both lateral ankle sprains and chronic ankle instability (CAI) and the development of ankle post-traumatic osteoarthritis (PTOA). Current visualization techniques such as arthroscopy and standard MRI are ineffective at quantifying early degenerative changes to the talar articular cartilage. The most promising approaches for slowing ankle PTOA progression include early conservative interventions to restore appropriate joint biomechanics. Thus, identifying visualization techniques sensitive to early degenerative changes of the talar articular cartilage is needed. Therefore, the purpose of this investigation is to determine if CAI patients have lower proteoglycan density in their talar cartilage compared to uninjured controls as measured by T1ρ MRI. Methods: Fifteen CAI (age: 21.2 ± 1.8 years, height: 1.7 ± .8 m, mass: 67.0 ± 7.7 kg) and fifteen controls (age: 21.0 ± 2.5 years, height: 1.7 ± .8 m, weight: 69.6 ± 13.2 kg) volunteered to participate. CAI inclusion criteria were in accordance with the International Ankle Consortium guidelines. Relative to the controls, CAI participants had a history of multiple lateral ankle sprains (4.0 ± 2.1 vs. 0.0 ± 0.0 sprains), multiple giving way episodes within the past 6 months (6.6 ± 5.1 vs. 0.0 ± 0.0 episodes), higher Identification of Functional Ankle Instability scores (22.9 ± 2.8 vs. 0.1 ± 0.5), and greater limitations in self-reported function based on the Foot and Ankle Ability Measure (85.9 ± 9.7% vs. 100.0 ± 0.0%) and Foot and Ankle Ability Measure Sport (68.4 ± 20.6% vs. 100.0 ± 0.0%). Proteoglycan density was assessed using T1ρ MRI with greater T1ρ relaxation times interpreted as reduced proteoglycan density. A Siemens Magnetom TIM Trio 3T scanner and an 8-channel flex coil in conjunction with three-dimensional Fast Low Angle Shot (FLASH) with a spin lock power at 500 Hz, five different spin lock durations (40, 30, 20,10, 0 ms) was used to acquire the T1ρ MRI. Participants were non-weight bearing for 30 minutes prior to the scan to unload the cartilage. Voxel by voxel T1rho relaxation times were calculated from a five image sequence created with a MatLab program. Segmentation of the T1ρ talar cartilage was performed manually using ITK-SNAP software. Four regions of interest: anteromeidal, anterolateral, posteromedial, and posterolateral were identified during segmentation. Mean T1ρ relaxation times in each region of interest were compared between CAI patients and healthy controls using independent sample t-tests and an a priori alpha level of 0.05. Results: The CAI and controls groups were similar in terms of their age, height, and mass (P ≥ 0.433). Measures of injury history and self-reported function differed between the groups (P < 0.001) as expected. CAI patients had significantly higher T1ρ relaxation times in three of the four regions of interest including the anterolateral region (CAI: 66.57 ± 11.42 ms, Control: 57.73 ± 5.91 ms, P = 0.013), posteromedial region (CAI: 63.48 ± 12.43 ms, Control: 54.71 ± 10.84 ms, P = 0.049), and posterolateral region (CAI: 65.97 ± 11.75 ms, Control: 54.20 ± 10.03 ms, P = 0.006). No differences were noted in the anteromedial region (CAI: 67.61 ± 13.30 ms, Control: 60.91 ± 13.65 ms, P = 0.184). Conclusions: CAI patients showed higher T1ρ relaxation times compared to controls in three of the four regions of interest suggesting reduced proteoglycan density in the talar cartilage. This finding supports the existing arthroscopic literature that illustrates early degenerative changes in CAI patients. Further research is needed to determine the underlying mechanisms of these degenerative changes and to identify therapeutic interventions capable of slowing the progression of these degenerative changes following lateral ankle sprains and CAI.

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