Oral Presentation 50th International Society for the Study of the Lumbar Spine Annual Meeting 2024

INTRODUCTION: Chronic alcohol consumption is known to cause a variety of health defects and is implicated in health conditions that cause back pain. Intervertebral disc (IVD) degeneration is a major contributor to back pain. Despite various non-scientific studies reporting a correlation between IVD degeneration and alcohol consumption, to our knowledge, there are no scientific publications studying the effect of alcohol use on IVD health. The aim of our study was to investigate if chronic alcohol consumption is associated with IVD and vertebral pathology.

METHODS: Mouse experiments were performed with IACUC approval. Male and female C57BL/6J mice (8-10 weeks old, n=4-5 sex/group) were randomly divided into two groups: control (CTR) and ethanol (EtOH). EtOH mice were acclimated to ethanol (added to their drinking water) over a two-week period until reaching a constant concentration of 20% w/v (blood alcohol volume of 0.12%), which was maintained for 10 weeks. Mice were euthanized, and lumbar motion segments (L3-6) were collected. L3-5 underwent mCT for trabecular analysis (L4) and histology, and L5-6 IVDs were used for nanoindentation. For histological analysis, motion segments were stained with Safranin O/Fast Green and two IVDs/mouse were evaluated for IVD degeneration (modified Tam grading) and notochordal band area (using ImageJ). AF stiffness was measured by Nanoindentation on 10 mm-thick cryosections. Data were analyzed using GraphPad Prism 10. Mann-Whitney U tests were used for female and male mice. A p<0.05 was considered statistically significant. Data is displayed as median with interquartile range. 

RESULTS: Micro-CT analysis of male vertebral structures demonstrated that chronic EtOH consumption significantly increased trabecular bone mineral density (BMD), number, bone surface, and bone volume, and decreased trabecular spacing (Figure 1A-C), supporting findings from the literature that report increased BMD with moderate alcohol consumption. Increased BMD is known to be positively correlated with IVD degeneration and our preliminary data on IVD stiffness suggests that chronic EtOH consumption increases AF stiffness as determined by nanoindentation (Figure 1D+E). Nanoindentation experiments and mCT analysis of female vertebrae is ongoing. Histological assessment of morphological IVD changes revealed that the nucleus pulposus (NP) of EtOH treated mice often contained granulated structures and fissures in female and male mice, suggesting early degenerative changes after chronic alcohol consumption (Figure 2A-B). Additionally, the notochordal band of female EtOH mice was significantly more compressed compared to their controls (Figure 2C). No changes were observed in the notochordal bands of male mice.

CONCLUSION: While chronic alcohol consumption is known to have a deleterious effect on bone and cartilage composition and function, little is known about its effect on spinal health. Our results in mice suggest that chronic alcohol consumption is detrimental to IVD health, as indicated by degenerative changes in the NP morphology, with increased structural defects, compressed notochordal bands, and increased AF stiffness. Additionally, significant trabecular changes in lumbar vertebra suggest that EtOH has a harmful effect on larger spinal structures. Further examination will include additional vertebrae analysis, nanoindentation, immunohistochemical analysis for inflammation, as well as an ex vivo study to investigate matrix metabolism and biomechanical effects.