Effects Of Manganese Deficiency On The Morphology Of Tibia And OPG/RANKL Signal Transduction Pathways In Broiler

The aim of this study was to investigate the effect of manganese deficiency on themorphology of tibia and the OPG/RANKL signal transduction pathways. Tibia anatomy,morphology and relative expression of OPG/RANKLmRNA were tested in the study forproviding the foundation for pathogenesis of perosis caused by manganese deficiency.Manganese (Mn) deficiency can result in perosis in chicks, but the mechanisms of Mndeficiency on tibia development remain poorly understood. Ninety one-day-old Arbor Acresmale broiler chickens received control diet (60mg Mn/Kg. diet) and low-manganese diet (40mg Mn/Kg. diet,8.7mg Mn/Kg. diet) to investigate the effects of Mn deficiency onmorphology of tibia and related signal transduction pathways in broiler chickens. At the ageof42days, the full-length of tibia and tibial diameters were detected. Simultaneously, thebone trabecula, damaged osteoblasts and OPG/RANKL mRNA expression levels wereinvestigated by histological assessment, electron microscopic examination and real-timequantitative PCR analyses, respectively. Compared with the control group, Mn deficiencyinduced the shorter tibia and the narrower growth plate. Histological observations involvedthe decreased percentage of the trabecular bone area, decreased trabecular thickness, reducedtrabecular number and increased trabecular bone separation. The most striking ultrastructuralmodifications involved disruption of nuclear membrane and mitochondria outer membrane,loss of mitochondrion cristae and alternation in endoplasmic reticulum in osteoblasts of theMn-deficient groups. Likewise, Mn deficiency decreased the OPG/RANKL mRNAexpression levels with the increased RANKL/OPG mRNA ratio. In conclusion, Mn deficiencycan affect the development of tibia in broiler chickens, leading to metaphyseal osteoporosisby decreasing OPG/RANKL mRNA expression levels.