Intra-articular fractures frequently lead rapidly to functional deficit and patient symptoms from progressive post-traumatic OA, although the mechanisms responsible are not established. In particular, the relative role of acute cartilage injury vs. chronic contact stress elevation from residual incongruity after treatment are unknown, because there have been no means of objectively measuring these mechanical insults to cartilage. We have developed two enabling technologies which overcome previous obstacles to assessing acute and chronic cartilage injury, by providing objective biomechanical indices. We have also developed and demonstrated the efficacy of articulated external fixation, combined with indirect reduction from the articular surface, for high-energy tibial plafond fractures. Our strategy is to prospectively follow patients treated with this technique and studied with these new indices of acute and chronic cartilage injury and assess the development of OA and their clinical outcome. The ankle is an ideal joint to study the pathogenesis of post-traumatic OA since it often develops OA following fractures, but it rarely develops OA without traumatic injury. We hypothesize that the independent variables: 1) quantifiable mechanical insult to the joint during the original injury, 2) and the duration and amount of contact stress elevation after healing, correlate with patient symptoms and function and the development of post-traumatic OA. These hypotheses will be tested through five interrelated specific aims: 1) Apply hinged external fixators to the ankle joints of 80 patients with fractures of the tibial plafond; 2) From CT scans, index the severity of injury on the basis of the energy released, estimated from fragment surface area, and the degree of displacement, estimated from volumetric fragment displacement, estimated from volumetric fragment displacement; 3) From post-reduction CT scans, index the severity of injury on the basis of the energy released, estimated from fragment surface area, and the degree of displacement, estimated from volumetric fragment displacement; 3) From post-reduction CT scans, index the cartilage stress elevation from three-dimensional maps of the subchondral plate and articular surface and by performing finite element analyses; 4) By comparing 4 month and 2 year CT scans determine the capacity for subchondral remodeling; and 5) At one year and two years post-injury, assess the results bu measuring the degree of osteoarthritis and by determining the clinical outcome and test whether these outcomes are more influenced by the acute or chronic cartilage injury. This study will enhance our understanding of the pathogenesis of post traumatic OA and form the basis for improved ability to prevent OA, decreased patient symptoms and improve function following intra-articular fractures.
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