ISAKOS: 2019 Congress in Cancun, Mexico

2019 ISAKOS Biennial Congress ePoster #113


Osteochondral Lesions of the Talus: Alterations in Ankle Joint Contact Mechanics with Increasing Size of OLT Shoulder Lesion

Peter J. Lawson, BA, Denver, CO UNITED STATES
Pam Kumparatana, MSW, MPH, Aurora, CO UNITED STATES
Todd H. Baldini, MS, Denver, CO UNITED STATES
Shanthan C. Challa, BS, Denver, CO UNITED STATES
Daniel K. Moon, MD, MS, MBA, Aurora, CO UNITED STATES
Kenneth J. Hunt, MD, Aurora, CO UNITED STATES

University of Colorado, Dept. of Orthopaedics, Aurora, CO, UNITED STATES

FDA Status Not Applicable


As OLT shoulder lesions increase in size, peak pressure also increases and the location of maximal pressure relative to the defect rim shifts, suggesting a biomechanical explanation for symptoms and treatment thresholds. Loaded inversion, simulating ankle injury position, significantly increases pressure magnitudes on the talar dome, with a consistent peak pressure 8mm from the defect.



Osteochondral lesions of the talus (OLT) are a common ankle injury that can result in pain, disability, and secondary injury, with poor outcomes often even after surgery. Unconstrained shoulder lesions on the medial edge of the talar dome can present a particular challenge. The purpose of this study was to assess the effect of increasing size of a medial OLT shoulder lesion on ankle joint contact mechanics. Our objective was to determine a threshold size that would warrant bulk grafting of the defect.


Nine cadaver ankle joints were dissected without disrupting the medial and lateral stabilizing ligaments. A Tekscan pressure sensor was inserted into the ankle joint. Intact specimens were axially compressed up to 800N with the foot in neutral and again at 20° inversion, simulating ankle position during inversion injury. The specimens were then tested with progressively larger semicircular osteochondral lesions at diameters of 8, 10, 12, 14, and 16mm that were centered on the edge of the medial talar dome, followed by a final ovoid lesion of 16x20mm. After each lesion was created the specimens were retested. Linear mixed models adjusted for donor characteristics and assessed changes in peak pressure (MPa), contact area (mm2), peak pressure location (mm), and distance from peak pressure location to the lateral rim of the defect (mm) by defect size and ankle position.


For all defect sizes, mean peak pressures were significantly higher in inversion compared to neutral. Mean peak pressure magnitude progressively increased with defect size in both ankle positions. Donor characteristics did not significantly affect mean peak pressure. Contact area decreased in both positions as defect size increased, but inversion led to significantly lower contact areas than in neutral. Mean contact area was 225.18 mm2 higher in male specimens than in female specimens. For every one-year increase in age, mean contact area increased 8.87 mm2. In neutral positions, the location of peak pressure moved laterally on the talar dome but also moved closer to the defect rim as the size of the defect increased. The rim-peak pressure distance stabilized at about 8 mm at defect sizes of 10mm and above. In inversion, however, the rim-peak pressure distance remained at about 8mm for all defect sizes.


As OLT defect sizes increased, we observed an increase in peak pressure, a decrease in contact surface area, and a lateral translation of peak pressure location relative to the defect rim. The distance between location of peak pressure and defect rim decreased with neutral loading until a 10 mm defect, but remained consistent in inversion loading. These findings may support a biomechanical explanation for mechanism of secondary injuries and treatment failures in larger OLT shoulder lesions due to increased magnitudes of peak pressure and location shifts of pressure applied across damaged or maladaptive cartilage tissue on the dome of the talus. Larger defects (=10mm) remain a critical point of interest that may suggest predictive clinical value for OLT treatment.