Tibial dyschondroplasia (TD) is an intractable tibiotarsal bone disorder of rapid growing avian species, which leads to huge economic losses and compromised poultry welfare. However, the exact pathogenesis and treatment of TD remain largely unknown. Based on continuous research findings, we propose the TD pathogenesis hypothesis: during skeletal development of TD chickens, due to the absence of vasculature of proximal tibial growth plates (TGP), hypertrophic chondrocytes of the TGP are unable to complete calcification in normal bone development and less dead chondrocytes in the corresponding area can be timely transported through the blood vessels. Moreover, recent studies demonstrate that the TD formation mechanism gradually tends to a large number of dead chondrocytes in the TGP region or apoptosis occur due to various factors (such as, reduction of vascular invasion and blood cells, and increased weight or mechanical force of the tibia), while the reduction of blood vessels is insufficient to remove these chondrocytes and eventually leads to the TD formation. Recognizing the possible role of the blood vessels in the incidence of TD and can propose that the improvement in vasculature might be a novel therapeutic approach for ending TD in chickens.
Keywords: blood vessels; bone development; chondrocyte; mechanical force; tibial dyschondroplasia.
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