Pathophysiology, diagnosis, and management of discogenic low back pain: a phenotype-driven precision framework for surgical and interventional decision-making.

Background: Discogenic Low Back Pain (DLBP) remains a major diagnostic and therapeutic challenge due to its heterogeneous pathophysiology and overlapping clinical presentation. Current management frequently relies on empirical stepwise strategies with limited mechanistic specificity. The distinct mechanisms of disc degeneration have drawn significant attention, highlighting the need for a phenotype-driven precision framework to support rational surgical and interventional decision-making. Methods: This narrative review evaluates literature from PubMed, Embase, and Web of Science up to April 2026, focusing on the pathophysiology and phenotype-based management of DLBP. Key terms included "discogenic low back pain," "phenotype," "basivertebral nerve ablation," "thoracolumbar fascia," "myofascial trigger point," and "ultrasound-guided dry needling." The review highlights the "triad" of disc degeneration-structural damage, functional impairment, and metabolic dysregulation-and integrates myofascial and thoracolumbar fascial dysfunction as functional modifiers that may coexist with structural disc phenotypes and influence diagnostic interpretation and therapeutic escalation. Results: Existing evidence supports the conceptual stratification of DLBP into four clinical phenotypes based on dominant pain-generating mechanisms. Vertebrogenic DLBP is characterized by endplate inflammation and Modic changes, for which basivertebral nerve (BVN) ablation is the primary supported intervention in appropriately selected patients. Annulogenic DLBP involves annular fissures associated with high-intensity zones (HIZ), where bipolar cooled radiofrequency ablation (biacuplasty) provides a targeted option. Mixed DLBP features concurrent endplate and annular pathology, potentially necessitating combined denervation strategies, whereas neuro-sensitized DLBP is dominated by central and peripheral sensitization, for which neuromodulation may serve as a salvage option. Across these phenotypes, functional myofascial or fascial involvement may be assessed using clinical examination and, when available, ultrasound-based dynamic evaluation. A staged therapeutic pathway places rehabilitation and manual therapy as early global strategies, ultrasound-guided dry needling as a potential intermediate functional intervention, and ablative, neuromodulatory, or surgical procedures as options for refractory or structurally dominant cases. Conclusion: DLBP management should move from generalized algorithms toward mechanism-informed precision care. Integrating structural imaging, functional soft-tissue assessment, and phenotype-specific interventions may improve individualized treatment selection while reducing unnecessary procedural escalation.