Novel metallic implantation technique for osteochondral defects of the medial talar dome: A cadaver study

BACKGROUND AND PURPOSE: A metallic inlay implant (HemiCAP) with 15 offset sizes has been developed for the treatment of localized osteochondral defects of the medial talar dome. The aim of this study was to test the following hypotheses: (1) a matching offset size is available for each talus, (2) the prosthetic device can be reproducibly implanted slightly recessed in relation to the talar cartilage level, and (3) with this implantation level, excessive contact pressures on the opposite tibial cartilage are avoided. METHODS: The prosthetic device was implanted in 11 intact fresh-frozen human cadaver ankles, aiming its surface 0.5 mm below cartilage level. The implantation level was measured at 4 margins of each implant. Intraarticular contact pressures were measured before and after implantation, with compressive forces of 1,000-2,000 N and the ankle joint in plantigrade position, 10 dorsiflexion, and 14 plantar flexion. RESULTS: There was a matching offset size available for each specimen. The mean implantation level was 0.45 (SD 0.18) mm below the cartilage surface. The defect area accounted for a median of 3% (0.02-18) of the total ankle contact pressure before implantation. This was reduced to 0.1% (0.02-13) after prosthetic implantation. INTERPRETATION: These results suggest that the implant can be applied clinically in a safe way, with appropriate offset sizes for various talar domes and without excessive pressure on the opposite cartilag

Osteochondral defects in the ankle: why painful?

Osteochondral defects of the ankle can either heal and remain asymptomatic or progress to deep ankle pain on weight bearing and formation of subchondral bone cysts. The development of a symptomatic OD depends on various factors, including the damage and insufficient repair of the subchondral bone plate. The ankle joint has a high congruency. During loading, compressed cartilage forces its water into the microfractured subchondral bone, leading to a localized high increased flow and pressure of fluid in the subchondral bone. This will result in local osteolysis and can explain the slow development of a subchondral cyst. The pain does not arise from the cartilage lesion, but is most probably caused by repetitive high fluid pressure during walking, which results in stimulation of the highly innervated subchondral bone underneath the cartilage defect. Understanding the natural history of osteochondral defects could lead to the development of strategies for preventing progressive joint damage

In vivo measures of cartilage deformation: patterns in healthy and osteoarthritic female knees using 3T MR imaging

ObjectiveTo explore and to compare the magnitude and spatial pattern of in vivo femorotibial cartilage deformation in healthy and in osteoarthritic (OA) knees.MethodsOne knee each in 30 women (age: 55 ± 6 years; BMI: 28 ± 2.4 kg/m(2); 11 healthy and 19 with radiographic femorotibial OA) was examined at 3Tesla using a coronal fat-suppressed gradient echo SPGR sequence. Regional and subregional femorotibial cartilage thickness was determined under unloaded and loaded conditions, with 50% body weight being applied to the knee in 20° knee flexion during imaging.ResultsCartilage became significantly (p < 0.05) thinner during loading in the medial tibia (-2.7%), the weight-bearing medial femur (-4.1%) and in the lateral tibia (-1.8%), but not in the lateral femur (+0.1%). The magnitude of deformation in the medial tibia and femur tended to be greater in osteoarthritic knees than in healthy knees. The subregional pattern of cartilage deformation was similar for the different stages of radiographic OA.ConclusionOsteoarthritic cartilage tended to display greater deformation upon loading than healthy cartilage, suggesting that knee OA affects the mechanical properties of cartilage. The pattern of in vivo deformation indicated that cartilage loss in OA progression is mechanically driven