Abstract
Epidural fibrosis is an inevitable aspect of the postoperative healing process which is one of the causes of failed back surgery syndrome following spinal surgery. The aim of the present study was to examine the inhibitory effect of 1,4-butanediol diglycidyl ether-crosslinked hyaluronan (cHA) on spinal epidural fibrosis in a swine model. Epidural fibrosis was induced through conduction of hemi-laminotomy (L2 and L3) or laminectomy (L4 and L5), while L1 was assigned as the control group in six pigs. The cHA was applied to L3 and L5 surgical sites. MRI evaluation, histologic examination, expressions of matrix metalloproteinases (MMPs), and cytokines in scar tissue were assessed four months after surgery. cHA treatment significantly decreased the scar formation in both hemi-laminotomy and laminectomy sites. cHA also significantly increased MMP-3 and MMP-9 expression in scar tissue. Further, the epithelial-mesenchymal transition -related factors (transforming growth factor-β and vimentin) were suppressed and the anti-inflammatory cytokines (CD44 and interleukin-6) were increasingly expressed in cHA-treated sites. The current study demonstrated that cHA may attenuate spinal epidural fibrosis formation after laminectomy surgery by enhancing the expression of MMPs and anti-inflammatory pathways.
Highlights
Polymer with minimal cytotoxicity and adverse effects in regards to electrophysiology and neurobehavior[8,10]
CHA attenuated the formation of epidural fibrosis after surgical intervention
It was hypothesized that 1,4-butanediol diglycidyl ether-crosslinked hyaluronan would demonstrate inhibitory effects on EF through the effects of matrix metalloproteinases (MMPs)-mediated extracellular matrix (ECM) remodeling and anti- inflammatory pathways
Summary
Polymer with minimal cytotoxicity and adverse effects in regards to electrophysiology and neurobehavior[8,10]. The matrix metalloproteinases (MMPs) are responsible for the remodeling of connective tissues under normal physiologic and pathologic conditions. The MMPs play important roles in regulating extracellular matrix (ECM) turnover in fibrotic tissues[11,12]. Degradation of normal ECM components in the early stages of fibrosis during repair and scar formation promotes the deposition of newly synthesized collagen through cell migration mediation, leukocyte activation, antimicrobial defense mechanisms, and inflammatory reactions[13,14,15,16,17]. In addition to histological assessments, this study will attempt to describe the mechanism of cHA hydrogels’ anti-fibrosis effects. It was hypothesized that the 1,4-butanediol diglycidyl ether-crosslinked hyaluronan would have inhibitory effects on EF through the effects of MMPs-mediated ECM remodeling and anti- inflammatory pathways
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