成人退行性脊柱侧凸(adult degenerative scoliosis, ADS)是伴随脊柱结构退变出现的进行性三维畸形,其发病率随着老龄化的加剧显著上升,已成为中老年人群慢性腰背痛、神经功能障碍及生活质量下降的重要病因。近年来,ADS的病因学研究逐...成人退行性脊柱侧凸(adult degenerative scoliosis, ADS)是伴随脊柱结构退变出现的进行性三维畸形,其发病率随着老龄化的加剧显著上升,已成为中老年人群慢性腰背痛、神经功能障碍及生活质量下降的重要病因。近年来,ADS的病因学研究逐步从单一退变机制转向多维度交互作用模型的探索,但退变与侧凸的因果关系、遗传–环境因素的权重及研究方法学的局限性等问题仍存争议。本文系统综述ADS的病因学研究进展,重点剖析:1) 脊柱退变的核心病理机制,包括椎间盘蛋白多糖流失、关节突关节退变及骨质疏松的协同作用;2) 多维度病因学证据,如遗传易感基因及代谢综合征的独立影响;3) 病因学假说的核心争议,包括“退变先行”与“侧凸导致退变”的循证分歧。现有研究表明,ADS的发生发展是遗传易感性、局部退变、生物力学失衡及全身代谢异常共同作用的动态过程,其中椎间盘非对称退变可能通过“应力集中–炎症激活–骨重塑异常”反馈环路驱动畸形进展。然而,现有研究多局限于横断面分析或低仿真模型,难以揭示病因的时序性与空间特异性。未来需依托纵向队列、多组学整合及人工智能辅助分析,构建“分子–影像–力学”跨尺度病因网络,以明确关键靶点并指导早期干预。本文强调多学科交叉研究的重要性,为ADS的精准分型与个体化防治提供理论依据。Adult degenerative scoliosis (ADS) is a progressive three-dimensional malformation accompanied by the degeneration of spinal structure. Its incidence rate has increased significantly with aging and has become an important cause of chronic low back pain, neurological dysfunction and declining quality of life in middle-aged and elderly people. In recent years, the etiology research of ADS has gradually shifted from a single degeneration mechanism to exploring multidimensional interaction models. However, there is still controversy over the causal relationship between degeneration and scoliosis, the weight of genetic-environmental factors, and the limitations of research methodology. This article provides a systematic review of the etiology research progress of ADS, with a focus on analyzing: 1) The core pathological mechanisms of spinal degeneration, including the synergistic effects of intervertebral disc proteoglycan loss, facet joint degeneration, and osteoporosis;2) Multidimensional etiological evidence, such as the independent effects of genetic susceptibility genes and metabolic syndrome;3) The core controversy of the etiological hypothesis includes the evidence-based divergence between “degeneration first” and “scoliosis leading to degeneration”. Existing research indicates that the occurrence and development of ADS is a dynamic process of genetic susceptibility, local degeneration, biomechanical imbalance, and systemic metabolic abnormalities. Among them, asymmetric degeneration of intervertebral discs may be driven by a feedback loop of “stress concentration-inflammation activation-bone remodeling abnormalities” to promote the progression of deformities. However, existing research is mostly limited to cross-sectional analysis or low simulation models, making it difficult to reveal the temporal and spatial specificity of the etiology. In the future, it is necessary to rely on longitudinal queues, multi-omics integration, and artificial intelligence-assisted analysis to construct a “molecular-imaging-mechanics” cross-scale etiological network, in order to identify key targets and guide early intervention. This article emphasizes the importance of interdisciplinary research, providing a theoretical basis for the precise classification and individualized prevention and treatment of ADS.展开更多
文摘成人退行性脊柱侧凸(adult degenerative scoliosis, ADS)是伴随脊柱结构退变出现的进行性三维畸形,其发病率随着老龄化的加剧显著上升,已成为中老年人群慢性腰背痛、神经功能障碍及生活质量下降的重要病因。近年来,ADS的病因学研究逐步从单一退变机制转向多维度交互作用模型的探索,但退变与侧凸的因果关系、遗传–环境因素的权重及研究方法学的局限性等问题仍存争议。本文系统综述ADS的病因学研究进展,重点剖析:1) 脊柱退变的核心病理机制,包括椎间盘蛋白多糖流失、关节突关节退变及骨质疏松的协同作用;2) 多维度病因学证据,如遗传易感基因及代谢综合征的独立影响;3) 病因学假说的核心争议,包括“退变先行”与“侧凸导致退变”的循证分歧。现有研究表明,ADS的发生发展是遗传易感性、局部退变、生物力学失衡及全身代谢异常共同作用的动态过程,其中椎间盘非对称退变可能通过“应力集中–炎症激活–骨重塑异常”反馈环路驱动畸形进展。然而,现有研究多局限于横断面分析或低仿真模型,难以揭示病因的时序性与空间特异性。未来需依托纵向队列、多组学整合及人工智能辅助分析,构建“分子–影像–力学”跨尺度病因网络,以明确关键靶点并指导早期干预。本文强调多学科交叉研究的重要性,为ADS的精准分型与个体化防治提供理论依据。Adult degenerative scoliosis (ADS) is a progressive three-dimensional malformation accompanied by the degeneration of spinal structure. Its incidence rate has increased significantly with aging and has become an important cause of chronic low back pain, neurological dysfunction and declining quality of life in middle-aged and elderly people. In recent years, the etiology research of ADS has gradually shifted from a single degeneration mechanism to exploring multidimensional interaction models. However, there is still controversy over the causal relationship between degeneration and scoliosis, the weight of genetic-environmental factors, and the limitations of research methodology. This article provides a systematic review of the etiology research progress of ADS, with a focus on analyzing: 1) The core pathological mechanisms of spinal degeneration, including the synergistic effects of intervertebral disc proteoglycan loss, facet joint degeneration, and osteoporosis;2) Multidimensional etiological evidence, such as the independent effects of genetic susceptibility genes and metabolic syndrome;3) The core controversy of the etiological hypothesis includes the evidence-based divergence between “degeneration first” and “scoliosis leading to degeneration”. Existing research indicates that the occurrence and development of ADS is a dynamic process of genetic susceptibility, local degeneration, biomechanical imbalance, and systemic metabolic abnormalities. Among them, asymmetric degeneration of intervertebral discs may be driven by a feedback loop of “stress concentration-inflammation activation-bone remodeling abnormalities” to promote the progression of deformities. However, existing research is mostly limited to cross-sectional analysis or low simulation models, making it difficult to reveal the temporal and spatial specificity of the etiology. In the future, it is necessary to rely on longitudinal queues, multi-omics integration, and artificial intelligence-assisted analysis to construct a “molecular-imaging-mechanics” cross-scale etiological network, in order to identify key targets and guide early intervention. This article emphasizes the importance of interdisciplinary research, providing a theoretical basis for the precise classification and individualized prevention and treatment of ADS.
