Cyclooxygenase (COX)-2 has been identified as an important mediator elaborated during ischemia/reperfusion, with pro- and anti-inflammatory properties having been reported. As the role of COX-2 in the small intestine remains unclear, we hypothesized that COX-2 expression would mediate mesenteric ischemia/reperfusion-induced gut injury, inflammation, and impaired transit and that these deleterious effects could be reversed by the selective COX-2 inhibitor, N-[2-(cyclohexyloxy)-4-nitrophenyl] methanesulphanamide (NS-398). Additionally, we sought to determine the role of peroxisome proliferator-activated receptor gamma (PPARgamma) in mediating protection by NS-398 in this model. Rats underwent sham surgery or were pretreated with NS-398 (3, 10, or 30 mg/kg) intraperitoneally 1 h before 60 min of superior mesenteric artery occlusion and 30 min to 6 h of reperfusion. In some experiments, NS-398 (30 mg/kg) was administered postischemia. Ileum was harvested for COX-2 mRNA and protein, PGE2, myeloperoxidase (inflammation), histology (injury), intestinal transit and PPARgamma protein expression, and DNA-binding activity. COX-2 expression and PGE2 production increased after mesenteric ischemia/reperfusion and were associated with gut inflammation, injury, and impaired transit. Inhibition of COX-2 by NS-398 (30 mg/kg, but not 3 or 10 mg/kg) not only reversed the deleterious effects of COX-2, but additionally induced expression and nuclear translocation of PPARgamma. NS-398 given postischemia was equally protective. In conclusion, COX-2 may function as a proinflammatory mediator in a rodent model of mesenteric ischemia/reperfusion. Reversal of gut inflammation, injury, and impaired transit by high-dose NS-398 is associated with PPAR activation, suggesting a potential role for PPAR-gamma in shock-induced gut protection.

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Level IV, retrospective case series.

Osteomyelitis following arthroscopically assisted anterior cruciate ligament (ACL) reconstruction has rarely been reported in the literature. We report a case of a 20-year-old female who had delayed tibial osteomyelitis and a pretibial cyst with culture-positive, oxacillin sensitive Staphylococcus epidermidis 15 months after an ACL reconstruction with hamstring autograft. Soft tissue fixation within the tibial tunnel was with a poly-L-D-lactic acid (PLDLA) bioabsorbable interference screw. The patient underwent surgical treatment with curettage, debridement, hardware removal, and bone grafting of the tibial tunnel followed by a course of intravenous antibiotics. Arthroscopic evaluation demonstrated an intact ACL graft without any evidence of intra-articular infection. The patient returned to collegiate athletics without any complications. While the most common biologic complications include pretibial cysts, granuloma formation, tunnel widening, and inflammatory reactions, infection is exceedingly rare. Late infection and osteomyelitis are also rare but can occur and should be considered in the differential diagnosis.

No abstract