ABSTRACT
Purpose
Traditionally, the epidural fat (EF) is known as a physical buffer for the dural sac against the force and a lubricant facilitating the relative motion of the latter on the osseous spine. Along with the development of the studies on EF, controversies still exist on vital questions, such as the underlying mechanism of the spinal epidural lipomatosis. Meanwhile, the scattered and fragmented researches hinder the global insight into the seemingly dispensable tissue.
Methods
Herein, we reviewed literature on the EF and its derivatives to elucidate the dynamic change and complex function of EF in the local milieu, especially at the pathophysiological conditions. We start with an introduction to EF and the current pathogenic landscape, emphasizing the interlink between the EF and adjacent structures. We generally categorize the major pathological changes of the EF into hypertrophy, atrophy, and inflammation.
Results and conclusions
It is acknowledged that not only the EF (or its cellular components) may be influenced by various endogenic/exogenic and focal/systematic stimuli, but the adjacent structures can also in turn be affected by the EF, which may be a hidden pathogenic clue for specific spinal disease. Meanwhile, the unrevealed sections, which are also the directions the future research, are proposed according to the objective result and rational inference. Further effort should be taken to reveal the underlying mechanism and develop novel therapeutic pathways for the relevant diseases.
Abbreviations
ASCs | = | adipose-derived stem cells |
CES | = | cauda equina syndrome |
CT | = | computed tomography |
EF | = | epidural fat |
EF-MSCs | = | EF-derived mesenchymal stem cells |
ECM | = | extra-cellular matrix |
ERG4 | = | expression of proteoglycan 4 |
ERK1/2 | = | extracellular regulated protein kinases1/2 |
FBSS | = | failed back surgery syndrome |
GM-CSF | = | granulocyte-macrophage colony-stimulating factor |
GRO | = | growth-related oncogene |
HA | = | hyaluronic acid |
IL-5 | = | interleukin 5 |
JNK | = | c-Jun N-terminal kinase |
LSS | = | lumbar spinal stenosis |
LBP | = | low back pain |
LPS | = | lipopolysaccharide |
MRI | = | Magnetic Resonance Imaging |
MPCs | = | mesenchymal progenitor cells |
MIP-1α | = | macrophage Inflammatory Protein-1 Alpha |
MMP-9 | = | matrix metalloproteinase-9 |
NOS2 | = | nitroxide synthase 2 |
OLF | = | ossification of ligamentum flavum |
PLGA | = | poly lactic-co-glycolic acid |
Runx2 | = | Runt-related transcription factor 2 |
SEL | = | spinal epidural lipomatosis |
SF | = | subcutaneous fat |
SF-MSCs | = | SF-derived mesenchymal stem cells |
SCI | = | spinal cord injury |
SRC-1 | = | steroid receptor coactivator-1 |
STAT3 | = | signal transducer and activator of transcription 3 |
TNF-α | = | tumor necrosis factor alpha |
VEGF | = | vascular endothelial growth factor |
Disclosure statement
No potential conflict of interest was reported by the author(s).
Author contributions
ZML and CW had the idea for the article, ZML and YDW performed the literature search, data analysis, and drafted the work, and XXM, LZ, and CW critically revised the work. All authors read and approved the final manuscript.
Availability of data and materials
All relevant data are contained within the article.