Matching osteochondritis dissecans lesions in identical twin brothers.

Osteochondritis dissecans is a disorder of unknown etiology that can result in fragmentation of osteochondral surfaces, most commonly of the knee, shoulder, elbow, and ankle. This may lead to sequelae of pain and an inability to participate in desired activities. Multiple theories exist as to the true cause of the disorder, but none have been fully proven. One such proposed etiology is genetic causation. Familial cases of osteochondritis dissecans are rare, yet these cases offer support to growing evidence that may support a genetic link. This article describes osteochondritis dissecans lesions of the femoral trochlea in monozygotic (identical) twins. Both twins presented with similar symptoms 1 year apart. Neither twin had any clear inciting trauma. Magnetic resonance imaging revealed osteochondral lesions in similar positions of the lateral trochlear of the same knee in both brothers. Osteochondral autograft transfer and tibial tubercle anteromedialization were performed on both patients. An identical postoperative protocol was followed, and recovery with full return to sport was comparable for the brothers. To the authors' knowledge, only 1 other case report exists of osteochondritis dissecans lesions in monozygotic twins. Although debate continues regarding the true etiology of this disorder, cases of identical twins presenting with a similar disease process are highly suggestive of a genetic component and may lead to early identification and treatment of these lesions. Continued research in the area of osteochondritis dissecans and its genetic basis is needed to completely understand this disorder.

Macrophage exposure to particulate titanium induces phosphorylation of the protein tyrosine kinase lyn and the phospholipases Cgamma-1 and Cgamma-2.

A frequent long-term complication of total joint arthroplasty is aseptic loosening, the end result of wear debris production, synovial macrophage activation, inflammatory mediator release, and osteolysis about the implant-bone or cement-bone interface. To elucidate the mechanisms of particle-induced macrophage activation and mediator production, we studied early signal transduction events using J774A.1 macrophages and 3 microm titanium particles. Treating macrophages with herbimycin A or genistein, two inhibitors of protein tyrosine kinases (PTKs), inhibited titanium phagocytosis as well as secretion of tumor necrosis factor-alpha (TNF-alpha) and prostaglandin-E2 (PGE2) in a dose-dependent manner. Both processes therefore depend on a PTK signaling cascade. Specifically, macrophage exposure to titanium-induced phosphorylation of multiple proteins including the Src kinase Lyn and phospholipase Cgamma-1 and Cgamma-2. Phosphorylation peaked within 2 min and returned to baseline within 45 min. Similar but not identical phosphorylation patterns were obtained when cells were stimulated with titanium preincubated with serum or albumin, suggesting distinct signal transduction pathways dependent on particle coating.