Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis

Study Design. Multicenter case-control study. Objective. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). Summary of Background Data. SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Methods. Sixteen patients who underwent lumbar decompression surgery due to severe idiopathic SEL were included in the study (L group, 15 men and 1 woman; mean age, 71.5 yrs). Fifteen patients without SEL, who underwent decompression surgery for lumbar canal stenosis, were selected as controls (C group, 14 men and 1 woman; mean age, 70.3 yrs). The following parameters were analyzed in these two groups: body mass index (BMI), medical history, histology, the size of adipocytes in the epidural fat (EF) tissues, and the expression level of the transcripts for adiponectin, leptin, tumor necrosis factor-a (TNF-a), interleukin (IL)-1b, IL-6, and IL-8. Results. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m2, P= 0.006), and there was a significant correlation between BMI and the width of EF in both groups. The average adipocyte size in the EF was significantly larger in the L group than in the C group (2846.8 vs. 1699.0 mm2, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-a and IL-1b in the L group were significantly higher than those in the C group [2.59-fold increase (P = 0.023) and 2.60-fold increase (P = 0.015), respectively]. Conclusion. Our data suggest that the pathogenesis of idiopathic SEL is associated with obesity. In addition, the increased expression of two major inflammatory cytokines in the EF in the L group may indicate that SEL is causally related to chronic inflammation.