Nobuyuki Fujita1,2, Naobumi Hosogane2,3, Tomohiro Hikata1,2, Akio Iwanami1,2, Kota Watanabe1,2, Yuta Shiono2,4, Eijiro Okada2,5, Masayuki Ishikawa2,6, Takashi Tsuji2,7, Masayuki Shimoda8, Keisuke Horiuchi1, Masaya Nakamura1,2, Morio Matsumoto1,2, Ken Ishii1,2. 1. Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan. 2. Keio Spine Research Group, Tokyo, Japan. 3. Department of Orthopaedic Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan. 4. Department of Orthopaedic Surgery, Nerima General Hospital, Tokyo, Japan. 5. Department of Orthopaedic Surgery, Saiseikai Central Hospital, Tokyo, Japan. 6. Spine and Spinal Cord Center, Mita Hospital, International University of Health and Welfare, Tokyo, Japan. 7. Department of Orthopaedic Surgery, Kitasato University Kitasato Institute Hospital, Tokyo, Japan. 8. Department of Pathology, Keio University School of Medicine, Tokyo, Japan.
Abstract
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-α (TNF-α), interleukin (IL)-1β, 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/m, 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 μm, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-α and IL-1β 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.
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-α (TNF-α), interleukin (IL)-1β, 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/m, 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 μm, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-α and IL-1β 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.