Abstract
Tibial dyschondroplasia (TD) is an intractable avian bone disease that causes severe poultry economic losses. The pathogenicity of TD is unknown. Therefore, TD disease has not been evacuated yet. Based on continuous research findings, we have gone through the molecular and cellular insight into the TD and proposed possible pathogenicity for future studies. Immunity and angiogenesis-related genes expressed in the erythrocytes of chicken, influenced the apoptosis of chicken chondrocytes to cause TD. TD could be defined as the irregular, unmineralized and un-vascularized mass of cartilage, which is caused by apoptosis, degeneration and insufficient blood supply at the site of the chicken growth plate. The failure of angiogenesis attributed improper nutrients supply to the chondrocytes; ultimately, bone development stopped, poor calcification of cartilage matrix, and apoptosis of chondrocytes occurred. Recent studies explore potential signaling pathways that regulated TD in broiler chickens, including parathyroid hormone-related peptide (PTHrP), transforming growth factor β (TGF- β)/bone morphogenic proteins (BMPs), and hypoxia-inducible factor (HIF). Several studies have reported many medicines to treat TD. However, recently, rGSTA3 protein (50 μg·kg−1) is considered the most proper TD treatment. The present review has summarized the molecular and cellular insight into the TD, which will help researchers in medicine development to evacuate TD completely.
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