ArticleFrontiers in genetics2024
Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers.
Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Integrated metabolomic and gut microbiota analyses reveal TCA cycle dysfunction in broiler skeletal disorders and the protective effect of L‑malic acid.Journal of animal science and biotechnology · 2026Article
- Bone growth and metabolism in broilers exposed to dietary PUFA or cyclical heat stress under two levels of dietary vitamins and minerals.Frontiers in physiology · 2026Article
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Authors and funding
7 authors.
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Abstract
Tibial dyschondroplasia (TD) is a severe bone disease that affects fast-growing broiler chickens and causes economic loss. Despite previous studies, the regulatory mechanism of TD remains unclear and is thought to be primarily based on thiram induction, which may differ from that of naturally occurring diseases. To better understand TD, a digital X-ray machine was used in the present study to determine its incidence in four hundred yellow-feathered broiler chickens. The results showed that the incidence of TD was 22% after 6 weeks and gradually decreased after 8 and 10 weeks. The body weight of broilers with TD decreased significantly compared to that of NTD broilers. In addition, the length and density of the tibia were reduced after eight and 10 weeks, and the density of the tibia was reduced after 6 weeks compared with the NTD chickens. This study also examined tibial quality parameters from TD (n = 12) and NTD broilers (n = 12) and found that bone mineral content, bone mineral density, bone ash content, calcium content, and phosphorus content were significantly reduced in TD broilers. Transcriptome analysis revealed 849 differentially expressed genes (DEGs) in the growth plate between TD (n = 6) and NTD groups (n = 6). These genes were enriched in ECM-receptor interaction, cytokine-cytokine receptor interaction, calcium signaling pathway, and TGF-β signaling. Genes encoding the alpha chain of type XII collagen, that is,
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