Successful orthopaedic management of displaced intra-articular fractures, to forestall post-traumatic osteoarthritis (OA), depends on avoidance of a mechanical environment that is deleterious to articular cartilage. Clinically, there are many reports of cases or series where patients have done surprisingly well in the presence of substantial incongruency, provided that joint stability is maintained, whereas minimally displaced or congruously repaired intra-articular fractures often fare poorly in the presence of joint instability. To date, almost no attention has been directed to the causative mechanisms by which instability induces post-traumatic OA. Many confounding factors, especially heterogeneity of injury, preclude systematic human clinical study of the relative importance of instability versus incongruency as causes of osteoarthritis secondary to intra-articular fractures. We propose laboratory studies, to investigate mechanisms of how global joint instability manifests itself in terms of mechanical anomaly at the tissue and cellular level, where osteoarthritis metabolically originates. And, we propose to study how local incongruity and global instability interact in that regard.
Three specific aims will be pursued. First, in an established cadaver model of stepoff tibial plafond fracture, we will measure transient intra-articular contact stresses under quasi-physiologic loading throughout plantar-dorsiflexion cycles, for meta(stable) versus unstable articulations. Second, using a contact finite element model of a tibial plafond fracture stepoff incongruity that incorporates a (rate-dependent) poroelastic constitutive formulation for cartilage, we will compute internal cartilage stresses for loading and motion inputs spanning the instant of transition of transition from (meta)stable to unstable articulation. Third, in an established rabbit knee defect model, we modulate instability by means of partial sectionings of the anterior cruciate ligament, and document the speed/severity of the resulting secondary degenerative changes. If dynamic instability can be shown to be a more potent determinant of post-traumatic OA following intra-articular fractures than is chronically elevated contract, this would strongly argue that orthopaedic management of these difficult injuries ought to prioritize attaining suitable thresholds of joint stability, rather than the presently dominant strategy of aggressive interventions to attain precise congruency in order to minimize contact stress elevations.
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