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.

胫骨软骨发育不良（TD）是一种难治性禽骨疾病，会导致严重的家禽经济损失。TD的致病性未知。因此，TD疾病尚未被疏散。基于持续的研究发现，我们对TD进行了分子和细胞研究，并提出了可能的致病性，以备将来研究之用。鸡红细胞中表达的与免疫和血管生成相关的基因影响了鸡软骨细胞的凋亡，从而引起TD。TD可定义为软骨的不规则，未矿化和未血管化的肿块，这是由鸡生长板部位的细胞凋亡，变性和血液供应不足引起的。血管生成的失败归因于软骨细胞营养供应不当。最终，骨骼发育停止了，软骨基质钙化不良，发生软骨细胞凋亡。最近的研究探索了调节肉鸡TD的潜在信号通路，包括甲状旁腺激素相关肽（PTHrP），转化生长因子β（TGF-β）/骨形态发生蛋白（BMP）和缺氧诱导因子（HIF）。几项研究报告了许多治疗TD的药物。然而，最近，rGSTA3蛋白（50μg·kg^-1）被认为是最合适的TD治疗。本综述总结了对TD的分子和细胞见解，这将有助于医学研究的研究人员完全撤离TD。