Lumbar Disc Herniation Resorption: When and How Does It Occur?

Abstract

Low back pain is a leading cause of disability worldwide, with intervertebral disc herniation contributing substantially to its burden. Most patients improve with conservative care, often associated with disc resorption. Although increasingly recognized as a major determinant of recovery, the mechanisms underlying resorption remain poorly understood. Herniated disc tissue induces immune cell infiltration and release of cytokines and proteolytic enzymes, yet standard anti-inflammatory treatments may paradoxically impede this process. Outcomes are also influenced by physical therapy, lifestyle, herniation characteristics, and immunological background, but predictive biomarkers are lacking. This review summarizes the current knowledge gap and explores strategies to harness intrinsic healing for personalized management.

INTRODUCTION

The intervertebral disc (IVD) is the largest avascular and immune-privileged organ in the human body [1]. It consists of a jelly-like nucleus pulposus (NP) enclosed within concentric layers of collagenous annulus fibrosus (AF), which connect to adjacent vertebrae through cartilaginous endplates. Degenerative changes or mechanical stress may compromise the integrity of the AF, allowing NP tissue to herniate out and be exposed to circulation. This herniation may compress spinal nerve roots and cauda equina, initiating a complex immune response with diverse clinical outcomes ranging from spontaneous disc resorption and symptom resolution to chronic inflammation, neurological symptoms, and persistent pain. While IVD herniation may occur in the cervical, thoracic, and lumbar regions, most of the evidence for spontaneous resorption is derived from lumbar disc herniation (LDH).

Given its strong association with low back pain (LBP), LDH poses a significant socioeconomic burden to patients and the healthcare systems globally. To address this unmet medical need, considerable progress has been made in understanding the pathophysiology and management of LDH over the past few decades. A crucial aspect of the current exploration focuses on the phenomenon of disc resorption following herniation. However, the exact etiology behind disc resorption remains unclear, despite multiple proposed hypotheses. This review aims to summarize current knowledge of disc resorption across epidemiology, impacting factors, management strategies, molecular mechanisms, and future directions, evaluating its potential as both a biological healing process and a novel therapeutic target.

1. Epidemiology of LDH and Resorption

LDH affects approximately 30% of individuals over their lifetime, although only 1%–3% present with persistent symptoms [2]. True prevalence is likely undervalued due to asymptomatic cases and unrecognized resorption. LDH occurs most frequently in the male workforce aged 30–50 and accounts for nearly one-third of all LBP cases [3,4]. Among those affected, over 40% develop chronic LBP, contributing substantially to global disability—with over 64 million years lived with disability recorded in 2017 [5,6].

IVD resorption refers to the process by which a herniated IVD shrinks or is resorbed by the body, often leading to improved outcomes and pain relief. The phenomenon of IVD resorption was first reported by Guinto et al. [7] in 1984, and subsequently, numerous studies have validated the potential for partial or complete regression of herniated disc tissue (Fig. 1). Notably, reported resorption rates vary among studies ranging from 57% to almost 100% [8]. Mechanistically, the exposure of NP tissue into circulation initiates inflammatory cascades, which could promote either healing or tissue damage. Current understanding of mechanisms involved in resorption includes dehydration of disc content, mechanical retraction, and immunological activities such as macrophage infiltration, neovascularization, and matrix metalloproteinase (MMP) activation [9-14]. All these findings support IVD resorption as a dynamic and biologically active process with therapeutic relevance.

Fig. 1.

T2 magnetic resonance imaging showing a large herniated intervertebral disc (IVD) at L4–5 left paracentral of a female patient in 2020. At the follow-up visit in 2022, the herniated IVD was resorbed completely after conservative treatments. Red arrows point to the herniated disc in both sagittal and axial views. Asterisks indicate the previous location of the herniated disc in both sagittal and axial views.

2. A New Perspective: Inflammation, a Double-Edged Sword

Emerging evidence highlights the role of macrophages in disease progression [15-18]. Notably, Ribeiro-Machado et al. [19] presented the first proof-of-concept preclinical study demonstrating macrophage-mediated regression of herniated IVD tissue. This emerging perspective challenges the current paradigm, wherein anti-inflammatory therapies, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids, remain the primary treatment for LDH [20]. In preclinical studies, corticosteroids have inhibited resorption, while lipopolysaccharides enhanced disc matrix fragmentation and accelerated regression [21]. Furthermore, a clinical study involving avoidance of anti-inflammatory medications showed IVD resorption in all patients over 1 year [22]. However, earlier studies reported notable resorption in both methylprednisolone and tumor necrosis factor α (TNF-α) antagonist Infliximab and placebo groups [23]. These conflicting results underscore the complexity of the inflammatory response and its dual role in healing and tissue damage. As such, clinical decision-making remains challenging, constrained by an incomplete understanding of the biological drivers behind IVD resorption.

CELLULAR AND MOLECULAR MECHANISMS OF LDH RESORPTION

Multiple mechanisms may act in combination to support spontaneous LDH regression [9], however, inflammatory pathways are most consistently implicated. The proposed theory is that the gradual hernia resorption occurs through enzymatic degradation and efferocytosis induced by an inflammatory reaction that is triggered when the disc content extrudes into the epidural space, being recognized as foreign. This biological process is orchestrated through a multifactorial interplay of vascular and neural ingrowth, immune cell infiltration, cytokine signaling, matrix remodeling, and cell death [24].

1. Monocyte Recruitment and Macrophage Activity

The IVD is an immune-privileged site, so that the extrusion of the IVD tissue to the epidural space evokes an autoimmune reaction that leads to the recruitment of monocytes [23,25]. The disc cells can produce monocyte chemoattractant protein (MCP)-1, a CC chemokine that contributes to the activation and recruitment of monocytes [23,25,26]. The infiltrating monocytes also produce MCP-1, increasing the monocyte recruitment to the IVD [27]. Monocyte-derived macrophages are indicated as the most important immune players in the resorption process of herniated IVD. Numerous studies have found by immunohistochemistry the presence of macrophages in herniated IVD tissue specimens [15-18,28,29]. Macrophages serve as the primary mediators of IVD tissue resorption, they are able to phagocytose the herniated tissue, produce inflammatory cytokines that promote further immune cell recruitment and produce MMPs that promote extracellular matrix (ECM) tissue components breakdown such as proteoglycans and collagens [30]. MMPs (e.g., MMP-1, MMP-3, and MMP-7) are particularly important in degrading the ECM, facilitating hernia resorption. Interestingly, in LDH histological samples, macrophage phagocytosis was observed more often in sequestration subtype LDH than subligamentous ones [31], in accordance with the clinical evidence showing that sequestered hernias are more likely to regress.

2. Neovascularization and Neoinnervation

Neovascularization has been demonstrated at the margins of the herniated tissue and it is thought to be a major determinant of hernia regression [23,32]. Proliferation of new blood vessels provides a conduit for effective immune cell infiltration (macrophages, T cells, neutrophils) into herniated IVD tissue. The presence of capillaries invading the hernia and monocyte-derived macrophages migrating out of these capillaries has been demonstrated by light and transmission electron microscopy [33]. Normally avascular, the IVD becomes vascularized due to the action of proangiogenic factors such as vascular endothelial growth factor (VEGF), TNF-α, and basic fibroblast growth factor (bFGF), which are released in response to hypoxia and inflammation. Alongside neovascularization, neoinnervation also occurs, which can contribute to discogenic pain but may also have a role in regulating tissue remodeling through neuroimmune signaling [34].

3. Apoptosis and Efferocytosis

Apoptosis of resident disc cells, especially notochordal and chondrocyte-like cells, is observed in hernia regression [35]. Apoptotic cells release ‘find-me’ signals, such as membrane lipids, nucleotides, and chemokines, and display specific ‘eat-me’ signals on the cell surface that promote clearance by phagocytic cells, especially macrophages, a process known as efferocytosis. This process is vital for maintaining tissue homeostasis and resolving inflammation [36]. Together with the degradation of the ECM components, proteoglycans and collagens [37], efferocytosis contributes to significant disc volume reduction and hernia resorption.

4. Role of Cytokines and Chemokines

Cytokines and chemokines orchestrate the immune and remodeling responses. These signaling molecules create a chemotactic gradient that facilitates immune cell infiltration and modulates cellular behavior within the herniated disc environment [38]. TNF-α is a potent proinflammatory cytokine secreted by macrophages and disc cells that increases vascular permeability, promotes pain sensitization, and stimulates MMP production [39]. Interleukin (IL)-1β similarly contributes to catabolic activity by enhancing ECM degradation and inflammation, and it further stimulates the release of MMPs, nitric oxide (NO), IL-6, and prostaglandin E2 (PGE2) from herniated disc tissue, showing that IVD cells are responsive to inflammatory stimuli [40]. Chemokines such as MCP-1 (CCL2) and IL-8, which are produced by IVD tissue, facilitate macrophage recruitment and angiogenesis at the herniation site, while IL-6 and IL-8 promote neutrophil infiltration and amplify the inflammatory response. Studies have also shown that coculturing IVD cells with macrophages significantly upregulates IL-6, IL-8, COX-2, and PGE2, with TNF-α being necessary for IL-6 and PGE2 induction but not IL-8, highlighting its central regulatory role [41]. MMP-3 and MMP-7, key mediators in disc matrix degradation, are upregulated in IVD/macrophage cocultures, with MMP-3 produced by both disc cells and macrophages and MMP-7 mainly by macrophages. These enzymes not only mediate tissue breakdown but also enable macrophage infiltration, facilitating herniated disc resorption. Additionally, MMP-7 can promote resorption by releasing soluble TNF-α, which further induces MMPs and VEGF, contributing to neovascularization of the herniated disc tissue [42]. For a detailed review of inflammation in the process, please see [43].

5. Infiltration of Other Immune Cells

Beyond macrophages, other immune cells participate in the immune response associated to hernia formation and regression. Neutrophils are typically early responders, releasing enzymes and reactive oxygen species that further digest disc tissue. B lymphocytes and T lymphocytes (especially CD4+ T helper cells) can modulate macrophage polarization through cytokine secretion (e.g., interferon-γ promotes M1, IL-4 promotes M2) [44]. Natural killer cells and plasmacytoid dendritic cells may also be involved in LDH resorption, through antigen presentation and immune surveillance [45].

Regression of LDH is a complex, immune-regulated process involving initial inflammation followed by tissue remodeling and resolution. Key contributors include macrophage infiltration and polarization, cytokine and chemokine signaling, angiogenesis, apoptosis, and efferocytosis. The immune response behind hernia resorption is nevertheless far more complex than the sum of mechanisms described. Understanding these mechanisms provides insight into potential therapeutic approaches that could mimic or enhance natural disc regression without the need for surgical intervention.

CLINICAL AND ANATOMICAL FACTORS INFLUENCING LDH RESORPTION

Multiple factors may influence IVD resorption, summarized in Fig. 2 and discussed further in the sections below.

Fig. 2.

Potential factors determining the pathogenesis progression of disc herniation. These factors include disc herniation type, tissue composition, lifestyle, age, disease duration, therapies, and local inflammatory cues.

1. What Type of Herniation Is More Likely to be Resorbed?

LDH is classified into 3 types: protrusion, extrusion, and sequestration [46]. Protrusion occurs when the NP presses against the AF without breaking through. In extrusion, the NP breaches the annular barrier but remains partially connected to the disc. Extrusions are the most common herniation type [47]. Sequestration occurs when disc material completely separates and loses any continuity with parental discs [46].

Extrusions and sequestrations, particularly sequestrations, are more likely to undergo resorption, largely due to the body’s immune response to the herniated disc material [48]. Larger extrusions, especially sequestrated ones, typically have a greater surface area in contact with adjacent tissues and neovascularization, which can lead to a more robust inflammatory reaction and, consequently, increased resorption [49]. In a meta-analysis by Rashed et al. [48], MRI follow-up of LDH has shown that a more significant herniation is associated with a higher likelihood of spontaneous resorption and complete regression. The probabilities of tissue regression were 52.5% for protrusion, 70.4% for extrusion, and 93.0% for sequestration. Additionally, the disease duration may impact the rate of IVD tissue resorption. Significant resorption (≥50%) was observed in one-third of patients within 1 year of symptom onset, compared to 6.43% in those with a disease duration exceeding 1 year [50].

2. What Type of Tissues Are More Likely to be Regressed?

Herniated disc material can comprise the AF, cartilage endplate, and NP (Fig. 3), with a higher likelihood of resorption when the NP is predominant [14]. Iwabuchi et al. [51] utilized conventional MRI to assess the relationship between disc composition and resorption potential. Based on T1- and T2-weighted signal intensities, herniated discs were categorized into 5 types, each characterized by distinct tissue components: NP, AF, mucinous tissue, granulation tissue hyperplasia, and partial AF [12]. Their findings indicated that disc herniations with highly hydrated, minimally degenerated NP were more likely to undergo resorption. Histologically, patients older than 50 years tend to have more fibrous tissue composition than younger patients, thus less resorption [49].

Fig. 3.

Alcian blue/Picrosirius red staining of human intervertebral disc herniation tissue from a single patient surgical specimen, highlighting key anatomical regions including the annulus fibrosus, nucleus pulposus, and cartilage endplate.

Conversely, the presence of cartilage tissue in herniated protrusions may hinder resorption. Schmid et al. [52] suggested that altered bone marrow signal intensity in endplates was indicative of cartilage fragments within extruded LDH tissue. Some of these protrusions showed Modic changes. The rate of disc tissue resorption was found to be lower in patients with Modic changes than in those without [53]. These changes are strongly associated with hyaline cartilage content, which exhibits reduced capillary growth and macrophage infiltration, thereby impeding resorption. In vivo studies revealed significant angiogenesis and inflammatory infiltration in corneas implanted with AF compared to endplate tissue, whereas cartilaginous endplates suppressed neovascularization [54]. Lama et al. [55] demonstrated that hyaline cartilage fragments exhibit minimal swelling, proteoglycan loss, and inflammatory response in saline. In contrast, NP and AF swell rapidly, increasing pore size and facilitating proteoglycan release, factors that encourage vascular development. Altogether, the potential for resorption is closely linked to the component’s capacity to support vascularization; while NP-rich herniations may resorb readily, those with a high cartilage content may be resistant, limiting the effectiveness of conservative treatment.

3. Smoking

Smoking has been identified as a risk factor for degenerative disc disease [56-58]. Given tobacco’s vasoconstrictive and proinflammatory properties, it may influence disc resorption by reducing blood flow to the spine and potentially suppressing disc resorption [12]. However, a prospective LDH study by Hornung et al. [59] suggested that smoking status did not significantly affect the rate of disc resorption (early ≤3 months versus late >3 months). Many studies have shown that exposure to cigarette smoke modulates inflammation, macrophage phenotype, and alters many macrophage functions such as phagocytosis of microbes [60-62]. Smoking was found to inhibit macrophage response to infection [63]. In a transcriptional profiling study, alveolar macrophages were isolated from healthy nonsmokers, healthy smokers, and chronic obstructive pulmonary disease smokers, where it was found that smoking induced macrophage reprogramming toward M1-deactivated and partially M2-polarized macrophages that contribute to the pathogenesis of COPD [64]. All these findings suggest that smoking is not only an independent risk factor for disc herniation but may also delay resorption, although further studies are needed.

4. Heavy Physical Workload

Heavy physical workload and occupational lifting have been proposed as risk factors for LDH [65,66]. A dose-response relationship between cumulative lumbar loading and LDH was demonstrated in a case-control study [67], and biomechanical cadaveric experiments further support this link. Unsafe lifting techniques simulating high compressive forces were associated with increased risk of endplate failure, whereas safer techniques involving lower compressive loads endured more loading cycles before failure and tended to fail via LDH or disc protrusion [68]. Conversely, a Danish study found that greater aerobic capacity in men was not associated with hospitalization for LDH [69], suggesting that general physical fitness may not confer protection. While a direct relationship between heavy lifting and disc resorption has not been established, mechanical loading may influence the postherniation environment by modulating disc fluid flow, ECM composition, and cellular activity [70].

5. Obesity

Obesity is a widespread public health problem and is associated with various negative outcomes, including IVD pathology. Excess body weight places increased mechanical stress on the spine, especially the lumbar region. Epidemiological evidence supports this association: Shiri et al. [71] identified both overweight and obesity as risk factors for lumbar radicular pain and sciatica in men and women, demonstrating a dose-response relationship. In the European Genodisc Study, Segar et al. [72] further reported that elevated body mass index (BMI) correlates with greater odds of LDH. Similarly, a prospective cohort study of 2,727 nurses with confirmed LDH revealed a linear increase in risk corresponding to BMI [73]. Although direct evidence linking obesity to disc resorption is lacking, it is plausible that obesity influences the resorptive process through its effects on neovascularization. Future studies are warranted to explore how obesity-driven vascular changes may affect post-herniation disc remodeling.

TREATMENTS THAT MAY PROMOTE OR IMPEDE HERNIATED TISSUE RESORPTION

1. Physical Therapy and Exercise

Physical therapy is a cornerstone of conservative management for LDH and is widely appreciated by patients [74]. Early introduction of physiotherapy or isometric exercises has been shown to effectively improve pain following LDH [74]. Noninvasive spinal decompression therapy (NSDT) has been studied, although Demirel et al. [75] reported no significant benefits from adding NSDT to standard physiotherapy. While current data do not support a direct link between physical therapy and resorption rates, low-impact exercise is associated with evidence of healthier IVDs. Long-term running is correlated with increased disc height and reduced degeneration [76,77] and enhanced IVD hydration and glycosaminoglycan content have also been observed in running younger adults [76]. A meta-analysis by Du et al. [78] demonstrated that Tai Chi and Yoga significantly improved the visual analogue scale pain score and the Oswestry Disability Index compared to the control group. Given the known association between disc resorption and symptom improvement, it is possible that exercise may promote resorption [79].

2. Chiropractic or Spinal Manipulation

Chiropractic and spinal manipulation are frequently sought by patients experiencing LBP [80,81]. In a prospective randomized controlled trial, patients with unilateral lumbar radiculopathy who failed 3 months of nonoperative management showed comparable improvements after spinal manipulation or microdiscectomy at 1-year follow-up [82]. A recent network meta-analysis also suggested a favorable impact of manipulation for treating sciatica compared to inactive or generalized care [83]. However, it remains unclear whether observed disc resorption reflects the natural healing process or the management. Case reports have described improvements when chiropractic manipulation was included in conservative regimens [84-86]. Mechanical traction has been proposed to facilitate disc resorption by increasing intervertebral space and reducing pressure on the disc [87]. Yet, experimental data indicate that disc pressures during high-velocity low-amplitude manipulation remain within physiological levels, offering little support for claims that manipulation directly induces or reduces herniation [88]. While manipulation and traction may contribute to symptom relief and potentially create a more favorable environment for disc resorption, the evidence remains limited and causality is unclear.

3. Complementary Medicine

Complementary approaches such as acupuncture and herbal medicine have been explored in the management of LDH, though the overall evidence remains limited. Acupuncture is often incorporated as an adjunct to conservative care and has shown potential for improving sciatica symptoms compared with inactive controls or conventional care [83]. Meta-analyses suggest benefits for postoperative pain and high reported cure rates [89]. Mechanistically, acupuncture may modulate inflammatory mediators and enhance local blood flow, which support disc resorption [90]. Small clinical studies and case reports have described radiographic regression of herniated discs following acupuncture or electroacupuncture [22,91,92], but these findings require cautious interpretation given methodological limitations. Herbal medicine has also been reported, often in combination with acupuncture or spinal manipulation. Large prospective cohorts have reported high rates of disc resorption and symptomatic improvement with multimodal traditional therapies, though the specific contribution of herbal formulations remains unclear [50,83,93]. Overall, while traditional medicine appears safe, the evidence base is weak, and further large, well-controlled studies are needed to clarify its role in disc resorption.

4. Anti-inflammatory Medications

Anti-inflammatory medications, particularly NSAIDs and steroids, are often used to reduce pain and inflammation in patients with LDH. However, their analgesic efficacy in cases of acute radicular pain remains contentious. Multiple randomized trials have demonstrated statistically significant reductions in pain versus placebo [94-96]. Yet, the magnitude of improvement consistently falls below clinically meaningful thresholds. Trials involving piroxicam, etodolac, diclofenac, and lornoxicam similarly report small or inconsistent benefits, and a Cochrane review highlighted the low-to-very-low quality of evidence and high risk of bias across existing trials [97]. A recent Norwegian multicenter study of naproxen found only minimal improvements in moderate-to-severe sciatica [98].

In a retrospective study of 9 patients treated with NSAIDs, complete disc resorption occurred at a mean of 8.7 months, accompanied by clinical improvement at a mean of 5.7 weeks. Of the treated patients, a 37-year-old female patient experienced complete regression of disc herniation on MRI 2 months after treatment with bed rest, analgesics, and anti-inflammatory drugs [99]. In contrast, a prospective study by Albert et al. [22] recruited 90 patients with LDH who received gabapentin and 12 sessions of acupuncture while avoiding any anti-inflammatory medications. Nineteen patients demonstrated disc regression on follow-up MRI after 3 months, 44 after 6 months, 21 after 9 months, and 6 after 12 months, with a resorption of at least 40%. All participants achieved disc resorption within 1 year without requiring surgical intervention. Although the study lacked no-treatment or anti-inflammatory controls, its findings support the hypothesis that anti-inflammatory medications may delay resorption, although results are inconsistent across studies.

Epidural steroid injections (ESIs) demonstrate mixed efficacy in relieving radicular and discogenic pain. Meta-analyses by Oliveira et al. [100] suggest modest short-term improvements in leg pain and functional outcomes. However, other investigations, such as Cervera-Irimia and Tomé-Bermejo [101], report no significant advantage over NSAIDs. Compared to surgical discectomy, ESIs are generally less effective in reducing pain and disability, with outcomes constrained by moderate-quality evidence and methodological inconsistencies [102].

An animal study raised questions about the impact of antiinflammatory agents on disc resorption [21]. In a rabbit study, high-dose epidural steroid administration was shown to inhibit disc resorption. This aligns with the study showing glucocorticoids exert their anti-inflammatory effect on macrophages by inhibiting their differentiation to an M1 phenotype, essential for disc tissue resorption [103]. Conversely, in a randomized trial, patients with sciatica found significant resorption over 1 year in both methylprednisolone and saline groups [23]. Although the steroid group exhibited a trend toward greater resorption in contained and extruded discs, differences did not reach statistical significance (p=0.13 vs. p=0.16). Another retrospective study of 28 patients with massive LDH treated with transforaminal ESIs reported radiographic reduction in 24 patients, with a mean reduction of 59% in size on follow-up MRI [104].

Notably, the timing and duration of anti-inflammatory drug administration were not clearly documented across these studies. Early suppression of inflammation may inhibit or delay disc resorption, whereas later-stage anti-inflammatory intervention may help restore tissue homeostasis without impeding resolution.

CONCLUSION AND FUTURE DIRECTIONS

LDH and subsequent resorption represent a dynamic biological process, where mechanical injury, immune activation, and tissue repair intersect. Despite the high prevalence and burden of disc herniation worldwide, current treatment strategies remain largely symptomatic and nonspecific. Conservative management leads to symptomatic improvement in most patients, but a subset experiences persistent pain and neurological deficits requiring surgical intervention. The inability to predict which patients will recover versus those who progress to chronic pain remains a major clinical challenge, reflecting an incomplete understanding of the cellular and molecular programs that govern disc resorption.

Emerging evidence highlights the paradoxical role of inflammation: excessive or dysregulated responses drive pain and degeneration, yet controlled inflammatory responses are necessary for disc resorption and tissue remodeling. Macrophages and monocytes infiltrating herniated disc tissues are increasingly recognized as critical regulators of this balance, but their phenotypes, temporal dynamics, and interactions with disc cells and neurons remain poorly characterized. Similarly, the contribution of genetic background, lifestyle, and anatomical or mechanical factors to resorption outcomes are incompletely understood.

Future research should prioritize conceptual integration across scales, linking molecular signaling pathways with clinical phenotypes. Dissecting mechanisms that distinguish “pro-resorptive” from “pro-degenerative” inflammation will be essential for the development of immunomodulatory therapies. Selectively reprogramming macrophages to promote resolution and tissue clearance, while minimizing pain signaling, represents a promising approach. Precision medicine approaches, tailoring treatments to herniation type, immune profile, and genetic predisposition, will be essential to address clinical heterogeneity. Large longitudinal cohort studies are needed to identify potential predictive biomarkers and stratify patients according to risk and therapeutic response.

Methodological innovations will accelerate this progress. Patient- derived disc tissues, single-cell and spatial transcriptomics, and organ-on-chip platforms [105-108] offer powerful tools to interrogate human-specific mechanisms in physiologically relevant contexts. These platforms may enable the testing of candidate drugs that modulate immune-disc crosstalk, paving the way for disease-modifying therapies. Beyond pharmacological interventions, multimodal strategies, including physical therapy, exercise, nutrition, acupuncture, and lifestyle modification should be evaluated in defined patient subgroups, recognizing the multifactorial nature of disc disease. Advancing our understanding of disc resorption biology requires a conceptual framework that integrates mechanical injury, immune activation and tissue repair in a unified model. By harnessing the body’s innate capacity for repair, guiding immune responses, and predicting patient trajectories, future therapies may reduce unnecessary surgeries, improve long-term outcomes, and significantly lessen the global burden of radiculopathy and back pain.