Luo Zhenhua, Liu Yao, Liu Yitong, Chen Hui, Shi Songtao, Liu Yi
Laboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Tian Tan Xi Li No. 4, Beijing, 100050, People's Republic of China.
Liaoning Province Key Laboratory of Oral Disease, 117 Nanjing North Street, Shenyang, 110002, People's Republic of China.
Cell Mol Life Sci. 2017 Dec;74(24):4443-4453. doi: 10.1007/s00018-017-2585-y. Epub 2017 Jul 3.
Alcoholic beverages are widely consumed, resulting in a staggering economic cost in different social and cultural settings. Types of alcohol consumption vary from light occasional to heavy, binge drinking, and chronic alcohol abuse at all ages. In general, heavy alcohol consumption is widely recognized as a major epidemiological risk factor for chronic diseases and is detrimental to many organs and tissues, including bones. Indeed, recent findings demonstrate that alcohol has a dose-dependent toxic effect in promoting imbalanced bone remodeling. This imbalance eventually results in osteopenia, an established risk factor for osteoporosis. Decreased bone mass and strength are major hallmarks of osteopenia, which is predominantly attributed not only to inhibition of bone synthesis but also to increased bone resorption through direct and indirect pathways. In this review, we present knowledge to elucidate the epidemiology, potential pathogenesis, and major molecular mechanisms and cellular effects that underlie alcoholism-induced bone loss in osteopenia. Novel therapeutic targets for correcting alcohol-induced osteopenia are also reviewed, such as modulation of proinflammatory cytokines and Wnt and mTOR signaling and the application of new drugs.
酒精饮料的消费十分广泛，在不同的社会和文化环境中造成了惊人的经济成本。各个年龄段的饮酒类型各不相同，从轻量偶尔饮酒到重度、暴饮以及慢性酒精滥用。一般来说，大量饮酒被广泛认为是慢性疾病的主要流行病学风险因素，对包括骨骼在内的许多器官和组织都有害。事实上，最近的研究结果表明，酒精在促进骨重塑失衡方面具有剂量依赖性毒性作用。这种失衡最终会导致骨质减少，而骨质减少是骨质疏松症的既定风险因素。骨量和骨强度的降低是骨质减少的主要特征，这主要不仅归因于骨合成的抑制，还归因于通过直接和间接途径导致的骨吸收增加。在本综述中，我们阐述了有关骨质减少中酒精成瘾性骨丢失的流行病学、潜在发病机制、主要分子机制和细胞效应的知识。还综述了纠正酒精性骨质减少的新治疗靶点，如调节促炎细胞因子以及Wnt和mTOR信号通路，以及新药的应用。
