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<p>Discogenic low back pain (DLBP) is one of the main causes of chronic low back pain, and its core pathological mechanism is due to various molecular changes caused by intervertebral disc degeneration. The normal intervertebral disc is composed of the nucleus pulposus, annulus fibrosus, and cartilaginous endplate, and has structural characteristics without blood vessels or nerves, relying on dispersed support to maintain homeostasis. During the process of degeneration, nucleus pulposus cells undergo apoptosis and cell senescence, its synthesis ability decreases, and the balance of extracellular matrix (ECM) is disrupted. Meanwhile, inflammatory factors such as IL-1β and TNF-α are continuously upregulated, activating pathways such as NF-κB and MAPK, inducing the expression of MMPs and ADAMTS, and accelerating ECM degradation. Matrix disruption further promotes the release of neurotrophic factors (such as NGF, VEGF), induces angiogenesis and nerve fiber invasion into the nucleus pulposus area, destroys the immune barrier, and leads to peripheral nerve sensitization. The central system mediates central remodeling through factors such as BDNF and CGRP, maintaining and amplifying pain signals. This article systematically summarizes the molecular mechanism of DLBP and summarizes relevant treatment strategies based on it, including conservative treatments such as NSAIDs, interventional methods such as radiofrequency ablation and fusion, as well as emerging therapies such as targeted anti-inflammatory, anti-neurogenic, matrix protection, and stem cell regeneration. The aim is to provide theoretical support and research directions for personalized treatment and mechanism interventions of DLBP.</p>

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Molecular mechanisms and treatment strategies for discogenic lumbar pain

  • 期刊论文

  • 发表日期：

    2025年7月26日

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  • Sumin Yan,
  • Bingqiu Han,
  • Chao Song,
  • Limin Yan

摘要

Discogenic low back pain (DLBP) is one of the main causes of chronic low back pain, and its core pathological mechanism is due to various molecular changes caused by intervertebral disc degeneration. The normal intervertebral disc is composed of the nucleus pulposus, annulus fibrosus, and cartilaginous endplate, and has structural characteristics without blood vessels or nerves, relying on dispersed support to maintain homeostasis. During the process of degeneration, nucleus pulposus cells undergo apoptosis and cell senescence, its synthesis ability decreases, and the balance of extracellular matrix (ECM) is disrupted. Meanwhile, inflammatory factors such as IL-1β and TNF-α are continuously upregulated, activating pathways such as NF-κB and MAPK, inducing the expression of MMPs and ADAMTS, and accelerating ECM degradation. Matrix disruption further promotes the release of neurotrophic factors (such as NGF, VEGF), induces angiogenesis and nerve fiber invasion into the nucleus pulposus area, destroys the immune barrier, and leads to peripheral nerve sensitization. The central system mediates central remodeling through factors such as BDNF and CGRP, maintaining and amplifying pain signals. This article systematically summarizes the molecular mechanism of DLBP and summarizes relevant treatment strategies based on it, including conservative treatments such as NSAIDs, interventional methods such as radiofrequency ablation and fusion, as well as emerging therapies such as targeted anti-inflammatory, anti-neurogenic, matrix protection, and stem cell regeneration. The aim is to provide theoretical support and research directions for personalized treatment and mechanism interventions of DLBP.