According to a study published this year in the Journal of Inflammation Research – Mechanisms and Factors Influencing Resorption of Herniated Part of Lumbar Disc Herniation: Comprehensive Review – Lumbar disc herniation (LDH) is a common condition causing low back pain, radiating leg pain, and neurological symptoms.

Clinically, the phenomenon of spontaneous shrinkage or disappearance of a herniated disc without surgical intervention is called resorption. Spontaneous resorption of herniated disc material without surgical intervention is a well-documented phenomenon, occurring in approximately 70% of cases, offering a basis for conservative treatment.

Here are some of the mechanisms that play a role in resorption:

– – Inflammation and Macrophage Infiltration: The herniated nucleus pulposus (NP) is recognized as a foreign antigen, triggering an autoimmune response. Macrophages, particularly M1-type (pro-inflammatory) and M2-type (anti-inflammatory), infiltrate the herniated tissue. M1 macrophages produce pro-inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6), which stimulate matrix metalloproteinases (MMPs) like MMP-3 and MMP-7. These enzymes degrade collagen and proteoglycans, facilitating resorption. M2 macrophages support tissue repair and resolution of inflammation in later stages.
– – Neovascularization: New blood vessel formation around the herniated disc enhances macrophage access and nutrient supply, aiding resorption. Cytokines such as vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (bFGF) drive angiogenesis.
– – Apoptosis and Autophagy: Programmed cell death (apoptosis) and autophagy (cellular self-degradation) in the herniated tissue contribute to its breakdown. The Fas-FasL pathway mediates apoptosis, reducing disc volume.
– – Dehydration and Retraction: Dehydration of the NP reduces disc volume, while mechanical retraction of the herniated material back into the annulus fibrosus may occur, particularly in cases with intact fibrous rings.
– – Matrix Degradation: MMPs, activated by inflammatory mediators, break down the extracellular matrix of the herniated disc, accelerating resorption.

And there are several factors that influence resorption:

– – Herniation Type and Size: Extruded and sequestered discs are more likely to resorb (87.77% and 66.91% incidence, respectively) compared to protruded (37.53%) or bulging discs (13.33%). Larger herniations, particularly those exceeding 50% of the spinal canal diameter (“giant” herniations), show higher resorption rates due to greater exposure to epidural vessels
– – Posterior Longitudinal Ligament (PLL) Integrity: Rupture of the PLL allows the NP to contact epidural vessels, promoting resorption. Intact PLL may hinder this process.
– – Composition of Herniated Tissue: Discs with a higher proportion of NP (high water content) are more prone to resorption than those with cartilaginous endplate material or Modic changes, which resist vascularization and macrophage infiltration.
– – Rim Enhancement on MRI: Greater rim enhancement on gadolinium-enhanced MRI indicates increased neovascularization and inflammation, predicting higher resorption likelihood.
– – Sagittal Parameters and Posture: Studies suggest that lumbar spine alignment, such as greater L4 posterior vertebral height and sacral slope, correlates with faster resorption, possibly due to biomechanical influences.
– – Disease Duration and Age: Shorter disease duration and younger age are associated with higher resorption rates, likely due to more robust immune responses and tissue plasticity.
– – Inflammatory Mediators: The balance of pro-inflammatory (e.g., TNF-α) and anti-inflammatory mediators influences resorption speed. High levels of MMPs and chemokines enhance matrix degradation.

Spontaneous resorption of LDH is a complex process driven by inflammation, macrophage activity, neovascularization, apoptosis, autophagy, and dehydration. Predictive factors such as herniation size, type, PLL rupture, and MRI rim enhancement guide clinical decision-making. Conservative treatments show promise in promoting resorption, reducing the need for surgery. Further research is needed to refine predictive models and optimize non-surgical strategies.