Endplate defects, not the severity of spinal stenosis, contribute to low back pain in patients with lumbar spinal stenosis

The Spine Journal 22 (2022) 370−378

It is controversial whether lumbar spinal stenosis (LSS) itself contributes to low back pain (LBP). Lower truncal skeletal muscle mass, spinopelvic malalignment, intervertebral disc degeneration, and endplate abnormalities are thought to be related to LBP. However, whether these factors cause LBP in patients with LSS is unclear.PURPOSE: To identify factors associated with LBP in patients with LSS.

STUDY DESIGN/SETTING: Cross-sectional design.

PATIENT SAMPLE: A total of 260 patients (119 men and 141 women, average age 72.8 years) with neurogenic claudication caused by LSS, as confirmed by magnetic resonance imaging (MRI).

OUTCOME MEASURES: Ratings of LBP, buttock and leg pain, and numbness on a numerical rating scale (NRS), 36-Item Short Form Survey (SF-36) scores, muscle mass measured by bioelectrical impedance analysis, and radiographic measurements including slippage and lumbopelvic alignment. The severity of LSS, endplate defects, Modic endplate changes, intervertebral disc degeneration, and facet joint osteoarthritis were assessed on MRI.

METHODS: The presence of LBP was defined as an NRS score ≥3. The demographic data, patient-reported outcomes, and radiological and MRI findings were compared between patients with and without LBP. Multivariate logistic regression analysis was used to identify the factors that were independently associated with the presence of LBP.

RESULTS: There were significant differences between patients with and without LBP for buttock and leg pain and numbness on the NRS, general health on the SF-36, presence of endplate defects, presence of Modic changes, disc degeneration grading, and disc height grading (all p < .05). Multivariate logistic regression analysis showed significant associations between LBP and diabetes (OR 2.43; 95% CI 1.07−5.53), buttock and leg numbness on the NRS (OR 1.34; 95% CI 1.17−1.52), general health on the SF-36 (OR 0.97; 95% CI 0.95−0.99), and the presence of erosive endplate defects (OR 3.04; 95% CI 1.51−6.11) (all p < .05).

CONCLUSIONS: These results suggest that LBP in patients with LSS should be carefully assessed not only for spinal stenosis but also clinical factors and endplate defects.

Lumbar disc extrusions reduce faster than bulging discs due to an active role of macrophages in sciatica

Acta Neurochirurgica (2020) 162:79–85

This retrospective observational histological study aims to associate the size and type of disc herniation with the degree of macrophage infiltration in disc material retrieved during disc surgery in patients with sciatica.

Methods Disc tissue of 119 sciatica patients was embedded in paraffin and stained with hematoxylin and CD68. Tissue samples were categorized as mild (0–10/cm2), moderate (10–100/cm2), and considerable (> 100/cm2) macrophage infiltration. All 119 patients received an MRI at baseline, and 108 received a follow-up MRI at 1-year. MRIs were reviewed for the size and type of the disc herniations, and for Modic changes in the vertebral endplates.

Results Baseline characteristics and duration of symptoms before surgery were comparable in all macrophage infiltration groups. The degree of macrophage infiltration was not associated with herniation size at baseline, but significantly associated with reduction of size of the herniated disc at 1-year post surgery. Moreover, the degree of macrophage infiltration was higher in extrusion in comparison with bulging (protrusion) of the disc. Results were comparable in patients with and without Modic changes.

Conclusion Macrophage infiltration was positively associated with an extruded type of disc herniation as well as the extent of reduction of the herniated disc during 1-year follow-up in patients with sciatica. This is an indication that the macrophages play an active role in reducing herniated discs. An extruded disc herniation has a larger surface for the macrophages to adhere to, which leads to more size reduction.

Schmorl’s nodes: current pathophysiological, diagnostic, and therapeutic paradigms

Schmorl's nodes

Neurosurg Rev (2014) 37:39–46

Schmorl’s nodes were first described by the pathologist Christian Schmorl in 1927 as a herniation of the nucleus pulposus through the cartilaginous and bony endplate into the vertebral body. Although such lesions present most commonly as incidental findings in asymptomatic patients (or in patients with back or radicular pain due to other etiology), there have been several reports emphasizing the deleterious effects of the inflammatory response and endplate changes elicited by the herniation of for such reasons, Schmorl’s nodes have been occasionally implicated in the etiology of chronic axial pain as well as in pathological osteoporotic fractures.

In this article, a thorough literature review about the most relevant historical studies on Schmorl’s nodes previously published is performed. Furthermore, the authors provide an overview about the recent advances in basic science research on the pathophysiology of such lesions, as well as on current diagnostic and therapeutic paradigms.

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