Experiment shows that thyroid dysfunction alters gut microbiota and alveolar bone in female mice, indicating a gut-thyroid-bone connection.
Thyroid hormone dysfunction has been implicated in both bone metabolism and gut microbial composition, yet the interplay between thyroid status, gut microbiota, and alveolar bone homeostasis remains unclear. In this study, female C57BL/6J mice were treated with triiodothyronine (T3) and thyroxine (T4) to induce hyperthyroidism or with methimazole (MMI) to induce hypothyroidism. Hyperthyroid mice exhibited decreased alveolar bone levels, measured as greater root exposure between the cementoenamel junction (CEJ) and alveolar bone crest (ABC) (buccal: 41% increase, p = 1.566e-07, 1-β = 1.0; lingual: 8% increase, p = 0.011, 1-β = 0.71) relative to controls, whereas hypothyroid mice exhibited reduced root exposure (buccal: 23% decrease, p = 0.020, 1-β = 0.65; lingual: 11% decrease, p = 0.011, 1-β = 0.74) relative to controls. 16S rDNA sequencing revealed that both hyper- and hypothyroid treatments reduced gut microbial diversity and altered community composition. These findings indicate that thyroid dysfunction can influence both gut microbiota and alveolar bone homeostasis, suggesting a potential gut-thyroid-bone axis. Further investigation is needed to elucidate the mechanistic links between endocrine status, microbial metabolites, and bone remodeling.
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Thompson et al. (2026) studied this question.
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