Potential Involvement of Obesity-Associated Chronic Inflammation in the Pathogenesis of Idiopathic Spinal Epidural Lipomatosis.
METHODS
Multicenter case-control study.


OBJECTIVE
To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL).


BACKGROUND
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].


CONCLUSIONS
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.


METHODS
3.
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Nobuyuki
N
Fujita
Keio Spine Research Group, Tokyo, Japan.|Department of Orthopaedic Surgery, National Defense Medical College, Tokorozawa, Saitama, Japan.
Naobumi
N
Hosogane
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Tomohiro
T
Hikata
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Akio
A
Iwanami
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Kota
K
Watanabe
Keio Spine Research Group, Tokyo, Japan.|Department of Orthopaedic Surgery, Nerima General Hospital, Tokyo, Japan.
Yuta
Y
Shiono
Keio Spine Research Group, Tokyo, Japan.|Department of Orthopaedic Surgery, Saiseikai Central Hospital, Tokyo, Japan.
Eijiro
E
Okada
Keio Spine Research Group, Tokyo, Japan.|Spine and Spinal Cord Center, Mita Hospital, International University of Health and Welfare, Tokyo, Japan.
Masayuki
M
Ishikawa
Keio Spine Research Group, Tokyo, Japan.|Department of Orthopaedic Surgery, Kitasato University Kitasato Institute Hospital, Tokyo, Japan.
Takashi
T
Tsuji
Department of Pathology, Keio University School of Medicine, Tokyo, Japan.
Masayuki
M
Shimoda
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.
Keisuke
K
Horiuchi
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Masaya
M
Nakamura
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Morio
M
Matsumoto
Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan.|Keio Spine Research Group, Tokyo, Japan.
Ken
K
Ishii
D000273:Adipose Tissue / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D019299:Decompression, Surgical / Q000379:methods; D004824:Epidural Space / Q000473:pathology / Q000601:surgery*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008068:Lipomatosis / Q000209:etiology / Q000473:pathology* / Q000601:surgery*; D008297:Male; D009765:Obesity / Q000150:complications* / Q000601:surgery; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D014409:Tumor Necrosis Factor-alpha