Lumbar disc herniation (LDH) can be spontaneously absorbed without surgical treatment. However, the pathogenesis and physiological indications for predicting protrusion reabsorption are still unclear, which prevents clinicians from preferentially choosing conservative treatment options for LDH patients with reabsorption effects. The purpose of this review was to summarize previous reports on LDH reabsorption and to discuss the clinical and imaging features that favor natural absorption. We highlighted the biological mechanisms involved in the phenomenon of LDH reabsorption, including macrophage infiltration, inflammatory responses, matrix remodeling, and neovascularization. In addition, we summarized and discussed potential clinical treatments for promoting reabsorption. Current evidence suggests that macrophage regulation of inflammatory mediators, matrix metalloproteinases, and specific cytokines in intervertebral disc is essential for the spontaneous reabsorption of LDH.

Background: Lumbar disc herniation (LDH) is mainly caused by annular fiber disruption with a discrete leakage of nucleus pulposus pressing on a nerve, resulting in back pain and radiating pain. Most patients with LDH can be treated conservatively, but there are many different conservative treatments. Furthermore, most previous studies did not evaluate the long-term efficacy of these treatments and the prognosis. Therefore, an effective and safe therapeutic strategy is lacking for patients with LDH. In this study, we evaluated Xiao Sui Hua He decoction (XSHHD) in the treatment of LDH. Methods: This was a rigorous prospective observational 3-year follow-up study. We recruited 69 participants with ruptured lumbar disc herniation (RLDH) between February 2014 and February 2016. Patients took XSHHD orally twice a day for 6 months. The primary outcome measurements were visual analogue scale (VAS) pain score, Oswestry disability index (ODI) and straight leg raising test (SLRT). The secondary outcome measurements was nucleus pulposus protrusion volume on magnetic resonance imaging (MRI). Clinical outcomes were measured at baseline (Visit 1), and at 3, 6, 12, and 36 months (Visit 2, 3, 4, and 5, respectively).. Results: Sixty-three patients were followed-up for 3 years after treatment. SLRT and ODI after non-surgical treatment improved significantly compared with baseline (P < .001). There were no statistically significant differences at 6 months vs 36 months for SLRT and ODI. VAS scores (leg, back) after 3 years of treatment were statistically significantly different compared with baseline (P < .001; Z = − 6.93, − 6.637). The baseline protrusion volume was 2018.61 ± 601.16 mm³, and the volume decreased significantly to 996.51 ± 387.42 mm3 at 36 months (t = 12.863; P < .001). The volume of protrusion resorption rate (VPRR) at 36 months was 47.24 ± 23.99%, with significant resorption in 23 cases, partial resorption in 23 cases, no resorption in 15 cases, and increased volume in 2 cases. Conclusions: This study showed that non-surgical treatment with XSHHD was effective, and the study clarified the natural outcomes in LDH.

Lumbar disc herniation (LDH) is a prevalent condition driven by inflammation, which mediates both radicular pain and spontaneous resorption of herniated material. Traditional anti-inflammatory therapies alleviate pain but may impede disc regression. We propose an Inflammation Preservation Strategy (IPS) to harness inflammation’s reparative potential while managing symptoms. Molecular, clinical, and translational evidence reveals inflammation drives resorption in 60–90% of LDH cases. Key mechanisms include neovascularization, dynamic macrophage polarization (where M1 degrades matrix while M2 promotes repair), and apoptosis-autophagy synergy. Traditional anti-inflammatory therapies risk suppressing this reparative cascade, whereas IPS advocates precision modulation—avoiding pan-anti-inflammatory agents during acute phases and employing targeted interventions to balance analgesia with tissue healing. Clinical data support IPS in achieving near-complete resorption and sustained pain relief, suggesting a paradigm shift from symptomatic palliation to disease-modifying regeneration. Future directions include real-time inflammation phenotyping and smart biomaterials to advance precision IPS implementation.

Background: Excessive oxidative stress plays a critical role in the progression of various diseases, including intervertebral disk degeneration (IVDD). Recent studies have found that anemonin (ANE) possesses antioxidant and anti-inflammatory effects. However, the role of ANE in IVDD is still unclear. Therefore, this study investigated the effect and mechanism of ANE on H₂O₂ induced degeneration of nucleus pulposus cells (NPCs). Methods: NPCs were pretreated with ANE, and then treated with H₂O₂. NOX4 was upregulated by transfection of pcDNA-NOX4 into NPCs. Cytotoxicity was detected by MTT, oxidative stress-related indicators and inflammatory factors were measured by ELISA, mRNA expression was assessed by RT-PCR, and protein expression was tested by western blot. Results: ANE attenuated H₂O₂-induced inhibition of NPCs activity. H₂O₂ enhanced oxidative stress, namely, increased ROS and MDA levels and decreased SOD level. However, these were suppressed and pretreated by ANE. ANE treatment repressed the expression of inflammatory factors (IL-6, IL-1β and TNF-α) in H₂O₂-induced NPCs. ANE treatment also prevented the degradation of extracellular matrix induced by H₂O₂, showing the downregulation of MMP-3, 13 and ADAMTS-4, 5 and the upregulation of collagen II. NOX4 is a key factor regulating oxidative stress. Our study confirmed that ANE could restrain NOX4 and p-NF-κB. In addition, overexpression of NOX4 counteracted the antioxidant and anti-inflammatory activities of ANE in H₂O₂-induced NPCs, and the inhibition of the degradation of extracellular matrix induced by ANE was also reversed by overexpression of NOX4. Conclusion: ANE repressed oxidative stress, inflammation and extracellular matrix degradation in H₂O₂-induced NPCs by inhibiting NOX4/NF-κB pathway. Our study indicated that ANE might be a candidate drug for the treatment of IVDD.

Lumbar disc herniation (LDH) is a common and frequently occurring condition primarily caused by lumbar intervertebral disc degeneration (LIVDD) and protrusion of the nucleus pulposus (NP), with low back pain and lower limb pain as the main clinical manifestations. It is characterized by a prolonged disease course and a high recurrence rate, with patients often experiencing long-term suffering, significantly impairing their quality of life and mental health. Studies have found that some LDH patients, without undergoing surgery or chemonucleolysis, experience spontaneous shrinkage and resorption of the intervertebral disc (IVD) tissue, along with relief of back and leg pain-a phenomenon referred to as LDH reabsorption. Modern medical research suggests that this reabsorption process is closely related to factors such as inflammatory responses, macrophage activation, extracellular matrix enzyme balance, neovascularization, ferroptosis, mitochondrial function, oxidative stress, and cellular autophagy. However, the precise mechanisms of LDH reabsorption and commonly used clinical therapies remain unclear, leading to suboptimal treatment outcomes. This study systematically reviews the relevant literature on LDH reabsorption, focusing on clinical diagnosis, underlying mechanisms, and common therapeutic strategies, aiming to summarize recent research progress and provide theoretical references for future clinical prevention and treatment of LDH.