The pathomechanical etiology of post-traumatic osteoarthritis following intraarticular fractures.

Many intra-articular fracture patients eventually experience significant functional deficits, pain, and stiffness from post-traumatic osteoarthritis (PTOA). Over the last several decades, continued refinement of surgical reconstruction techniques has failed to markedly improve patient outcomes. New treatment paradigms are needed - ideally, bio/pharmaceutical. Progress in that direction has been impeded because the pathomechanical etiology of PTOA development is poorly understood. In particular, the relative roles and pathomechanisms of acute joint injury (from the initial trauma) versus chronic contact stress elevation (from residual incongruity) are unknown, primarily because there have been no objective methods for reliably quantifying either of these insult entities. Over the past decade, novel enabling technologies have been developed that provide objective biomechanical indices of injury severity and of chronic contact stress challenge to fractured joint surfaces. The severity of the initial joint injury is indexed primarily on the basis of the energy released in fracture, obtained from validated digital image analysis of CT scans. Chronic contact stress elevations are indexed by patient-specific finite element stress analysis, using models derived from post-reduction CT scans. These new measures, conceived in the laboratory, have been taken through the stage of validation, and then have been applied in studies of intra-articular fracture patients, to relate these biomechanical indices of cartilage insult to the incidence and severity of PTOA This body of work has provided a novel framework for developing and testing new approaches to forestall PTOA following intra-articular fractures.