Meniscal tears are attributed to either trauma or degeneration processes. Clinical data suggest that meniscal degeneration (MD) is associated with knee osteoarthritis; however, the molecular events underpinning the pathogenesis of MD in humans remain elusive. Here we immunohistochemically examined the expression of p38 MAPK, its phosphorylated/activated form (p-p38), its target NF-kappaB (p50-p65 dimer), and COX-2 in ruptured menisci and investigated their involvement in MD development. Our findings demonstrate increased expression of the p38-NF-kappaB axis elements and COX-2 in disintegrated fibrocartilage, suggesting a role of these molecules in the pathobiochemistry of MD and consequential rupture.