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- (TNF-), interleukin (IL)-1, 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. 25.2kg/m(2), 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. 1699.0m(2), P=0.017). Furthermore, the expression levels of the transcripts for TNF- and IL-1 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.Level of Evidence: 3