Division of Pain Medicine, Department of Anesthesiology and Pain Medicine, Clinical Learning, Evidence And Research (CLEAR) Center for Musculoskeletal Research, University of Washington School of Medicine, Seattle, WA, USA.
Center for Neuroplasticity and Pain (CNAP), SMI, Aalborg University, School of Medicine, Aalborg, Denmark.
Minerva Anestesiol. 2024 Apr;90(4):330-338. doi: 10.23736/S0375-9393.24.17843-1.
Intervertebral disc degeneration is characterized by deterioration in structural support that is potentially followed by stimulated neuronal ingrowth, and dysfunction of cellular physiology in the disc. Discogenic low back pain originates from nociceptors within the intervertebral disc or the cartilage endplate. This narrative review examines the mechanisms of disc degeneration, the association between degeneration and pain, and the current diagnosis and treatment of discogenic low back pain. Mechanisms of disc degeneration include dysregulated homeostasis of the extracellular matrix of the disc, altered spine mechanics, DNA damage, oxidative stress, perturbed cell signaling pathways, and cellular senescence. Although disc degeneration is more common in individuals with low back pain than in asymptomatic ones, degeneration occurs in a large proportion of asymptomatic individuals. Therefore, degeneration itself is not sufficient to trigger low back pain. Imaging and discography are common diagnostic tools of discogenic low back pain but have limited validity to diagnose discogenic pain. Most of current treatments options are not specific to discogenic pain but are unspecific treatments of low back pain of any origin. There is an urgent need to clarify and distinguish the molecular mechanisms of discogenic pain from mechanisms of disc degeneration that are not involved in nociception. Future research should make use of current methods to study molecular mechanisms of human pain in comprehensively and quantitatively phenotyped patients with low back pain, with the objective to identify molecular triggers of discogenic pain and determine the relationship between molecular mechanisms, pain, and patient-relevant outcomes.
椎间盘退变的特征是结构支撑恶化，随后可能会刺激神经元向内生长，并导致椎间盘细胞生理功能障碍。椎间盘源性腰痛源于椎间盘内的伤害感受器或软骨终板。本综述探讨了椎间盘退变的机制、退变与疼痛的关系，以及椎间盘源性腰痛的现行诊断和治疗方法。椎间盘退变的机制包括椎间盘细胞外基质的稳态失调、脊柱力学改变、DNA 损伤、氧化应激、细胞信号通路紊乱和细胞衰老。虽然椎间盘退变在腰痛患者中比在无症状者中更为常见，但在很大一部分无症状者中也会发生退变。因此，退变本身不足以引发腰痛。影像学和椎间盘造影术是椎间盘源性腰痛的常见诊断工具，但对诊断椎间盘源性疼痛的有效性有限。目前大多数治疗选择并非针对椎间盘源性疼痛，而是针对任何来源的腰痛的非特异性治疗。目前迫切需要明确和区分椎间盘源性疼痛的分子机制与不涉及伤害感受的椎间盘退变机制。未来的研究应利用现有方法，在全面和定量表型的腰痛患者中研究人类疼痛的分子机制，以确定椎间盘源性疼痛的分子触发因素，并确定分子机制、疼痛与患者相关结果之间的关系。
