Fondazione Policlinico Universitario Agostino Gemelli-IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy.
Mediators Inflamm. 2020 Feb 26;2020:3686749. doi: 10.1155/2020/3686749. eCollection 2020.
Osteoporosis is a disease characterized by low bone mass and alterations of bone microarchitecture, with an increased risk of fractures. It is a multifactorial disorder that is more frequent in postmenopausal women but can be associated to other diseases (inflammatory and metabolic diseases). At present, several options are available to treat osteoporosis trying to block bone reabsorption and reduce the risk of fracture. Anyway, these drugs have safety and tolerance problems in long-term treatment. Recently, gut microbiota has been highlighted to have strong influence on bone metabolism, becoming a potential new target to modify bone mineral density. Such evidences are mainly based on mouse models, showing an involvement in modulating the interaction between the immune system and bone cells. Germ-free mice represent a basic model to understand the interaction between microbiota, immune system, and bone cells, even though data are controversial. Anyway, such models have unequivocally demonstrated a connection between such systems, even if the mechanism is unclear. Gut microbiota is a complex system that influences calcium and vitamin D absorption and modulates gut permeability, hormonal secretion, and immune response. A key role is played by the T helper 17 lymphocytes, TNF, interleukin 17, and RANK ligand system. Other important pathways include NOD1, NOD2, and Toll-like receptor 5. Prebiotics and probiotics are a wide range of substances and germs that can influence and modify microbiota. Several studies demonstrated actions by different prebiotics and probiotics in different animals, differing according to sex, age, and hormonal status. Data on the effects on humans are poor and controversial. Gut microbiota manipulation appears a possible strategy to prevent and treat osteopenia and/or osteoporosis as well as other possible bone alterations, even though further clinical studies are necessary to identify correct procedures in humans.
骨质疏松症是一种以骨量低和骨微结构改变为特征的疾病，骨折风险增加。它是一种多因素疾病，在绝经后妇女中更为常见，但也可能与其他疾病（炎症和代谢疾病）有关。目前，有多种选择可用于治疗骨质疏松症，试图阻止骨吸收并降低骨折风险。然而，这些药物在长期治疗中存在安全性和耐受性问题。最近，肠道微生物群被强调对骨代谢有很强的影响，成为改变骨矿物质密度的潜在新靶点。这些证据主要基于小鼠模型，表明其参与调节免疫系统和骨细胞之间的相互作用。无菌小鼠代表了理解微生物群、免疫系统和骨细胞之间相互作用的基本模型，尽管数据存在争议。无论如何，这些模型都明确证明了这些系统之间的联系，尽管机制尚不清楚。肠道微生物群是一个复杂的系统，它影响钙和维生素 D 的吸收，并调节肠道通透性、激素分泌和免疫反应。辅助性 T 细胞 17 淋巴细胞、TNF、白细胞介素 17 和 RANK 配体系统起着关键作用。其他重要途径包括 NOD1、NOD2 和 Toll 样受体 5。益生元和益生菌是一系列可以影响和改变微生物群的物质和细菌。几项研究表明，不同的益生元和益生菌在不同的动物中有不同的作用，这取决于性别、年龄和激素状态。关于对人类影响的数据很少且存在争议。肠道微生物群的操纵似乎是预防和治疗骨质疏松症以及其他可能的骨骼改变的一种可行策略，尽管需要进一步的临床研究来确定人类的正确程序。
