Pathomechanism underlying the onset of scoliosis in a PNX broiler chicken model

Abstract

Results The PNX resulted in a rapid and marked loss of cancellous bone volume (8 ± 1% versus 14 ± 2%, mean ± SD, p<0.005) and profoundly disrupted trabecular structure with increases in dynamic formative parameters, such as mineralizing surface, mineralization apposition rate and adjusted appositional rate. In the chondro-osseous junction, activated osteoclasts phagocitized degenerating chondrocytes, leaving a minimal amount of cartilage matrix and activated osteoblasts, thus losing their scaffolding for bone formation directly covering the hypertrophic zone cells. The osteoid surface and thickness in the chondro-osseous junction were significantly increased in PNX chickens (43 ± 14 % versus 12 ± 6 % and 4 ± 0.2μm versus 3 ± 0.4 μm). In the subjacent cartilage regions being protected from further resorption, abundant labeled cartilage remained with higher cellularity.