Tibial dyschondroplasia (TD) is a common and economically significant skeletal disorder in broilers, characterized by unmineralized, avascular cartilage plugs protruding into the metaphyseal region. Despite some evidence connecting the gut microbiota to skeletal disorders, the specific microbial drivers of TD pathogenesis remain unclear. In this study, we performed fecal microbiota transplantation in both healthy and TD model broilers to assess the influence and contribution of gut microbiota dysbiosis to TD pathogenesis. The broilers were allocated into 4 groups: CON (normal control group broilers), TD (TD model broilers), TDRN (TD model broilers that received FMT from normal broilers) and NRTD (normal broilers that received FMT from TD model broilers). Results demonstrated that FMT successfully transferred the TD phenotype from diseased to healthy broilers (NRTD group), whereas transplantation from healthy donors did not reverse the TD phenotype in TD broilers (TDRN group). This to some extent indicates that gut microbiota as a critical pathogenic driver. Microbiome analysis revealed significant depletion of Lactobacillus and enrichment of Streptococcus and Escherichia-Shigella in all TD-affected groups (TD, TDRN, NRTD) compared to controls ( P < 0.05). Metabolomic profiling identified seven stably dysregulated metabolites. Among them, chenodeoxycholic acid showed a strong positive correlation with Lactobacillus abundance and tibial mineral content, while 2-methoxyestradiol (an estrogen metabolite) exhibited inverse associations. Collectively, these findings provide evidence that gut microbiota dysbiosis causally contributes to TD and define the Lactobacillus -chenodeoxycholic acid axis and estrogen metabolism as promising targets for preventive and management strategies against TD in broilers. Graphical abstract representing the experimental design.
Song et al. (Wed,) studied this question.