Osteoporosis is the most prevalent metabolic bone disease, characterized by low bone mass and microarchitectural deterioration. Here, we show that warmth exposure (34°C) protects against ovariectomy-induced bone loss by increasing trabecular bone volume, connectivity density, and thickness, leading to improved biomechanical bone strength in adult female, as well as in young male mice. Transplantation of the warm-adapted microbiota phenocopies the warmth-induced bone effects. Both warmth and warm microbiota transplantation revert the ovariectomy-induced transcriptomics changes of the tibia and increase periosteal bone formation. Combinatorial metagenomics/metabolomics analysis shows that warmth enhances bacterial polyamine biosynthesis, resulting in higher total polyamine levels in vivo. Spermine and spermidine supplementation increases bone strength, while inhibiting polyamine biosynthesis in vivo limits the beneficial warmth effects on the bone. Our data suggest warmth exposure as a potential treatment option for osteoporosis while providing a mechanistic framework for its benefits in bone disease.

骨质疏松症是最普遍的代谢性骨病，其特征是低骨量和微结构退化。在这里，我们表明，温暖暴露 (34°C) 通过增加小梁骨体积、连接密度和厚度来防止卵巢切除术引起的骨质流失，从而改善成年雌性和年轻雄性小鼠的生物力学骨强度。温适应微生物群的移植表型复制了温暖引起的骨骼效应。温暖和温暖的微生物群移植都可以逆转卵巢切除引起的胫骨转录组学变化并增加骨膜骨形成。组合宏基因组学/代谢组学分析表明，温暖可增强细菌多胺的生物合成，从而导致体内多胺总水平升高. 补充精胺和亚精胺可增加骨骼强度，同时抑制体内多胺生物合成限制了对骨骼有益的保暖作用。我们的数据表明，温暖暴露作为骨质疏松症的潜在治疗选择，同时为其在骨病中的益处提供了一个机制框架。