Postoperative epidural fibrosis (PEF) localized around the exposed dura and nerve roots is a known radiologic entity seen after lumbar spine surgery. Although excessive PEF is associated with residual and new lumbar pain and radiculopathy, its role as the generator of the pain is still discussed. Various materials acting as an adhesion barrier have been tested. There is no undebated class I evidence that any one of them is suitable to reduce or avoid PEF and provide a better clinical outcome.
Dural fibrosis and epidural adhesion after laminectomy are developed from adjacent dense scar tissue, which is a natural wound healing process 1) 2) 3) 4). , and ranked as the major contributor for postoperative pain recurrence after laminectomy or discectomy, and has been implicated as an important cause of failed back surgery syndrome.
At the same time, dural fibrosis made the risk of nerve root injury, dural laceration and Iatrogenic injury greatly improved, which challenging doctors for exploring the operation technology 10) 11) 12).
Researchers tried to reduce scar formation through various operation techniques such as minimally invasive discectomy, application of local anti-inflammatory drugs, but the effects of these methods were not uniform 18) 19) 20) 21) 22).
A study has clearly demonstrated the fact that the use of suction drainage alone or combined with only fat grafts, fats grafts and local steroids application, or only local steroids application significantly improved patient outcome with respect to pain relief and functional outcome and significantly reduced EF as measured by an MRI 23).
Recently, CCN5 exhibited an inhibitory effect on connective tissue growth factor (CTGF)/CCN2 (a critical regulator for fibrotic disease)‑mediated fibrogenesis. However, its function in epidural fibrosis and the underlying mechanisms involved remain to be determined. In this study, an obvious downregulation of CCN5 was observed in scar tissues from laminectomized rats, concomitant with a marked upregulation of CCN2, suggesting a potential negative regulatory role of CCN5 in fibrogenesis. Furthermore, CCN5 overexpression notably mitigated transforming growth factor‑β1-enhanced fibroblast viability and proliferation. Of note, CCN5 upregulation inhibited the switch of fibroblasts into myofibroblasts as its overexpression abrogated the expression of the myoﬁbroblast marker, α-smooth muscle actin (α-SMA). CCN5 upregulation also reduced an increase in collagen type I, α1 (COL1A1) and total collagen concentrations. Additionally, CCN5 over-expression decreased CCN2 expression and increased Smad6 phosphorylation. Mechanism analysis revealed that blocking Smad6 signaling significantly ameliorated the inhibitory effect of CCN5 on the CCN2 levels, accompanied by the reduction in cell proliferation and collagen production. These results confirm that CCN5 exerts an anti-fibrotic function by regulating the Smad6-CCN2 pathway, thereby indicating a potential approach for ameliorating epidural ﬁbrosis after laminectomy 24).