Peridural scar prevention

see Epidural free fat graft.

Other measures include the placement of barrier films or gels. There are numerous products available, none has been shown to have reproducible benefit.

The prevention of scar formation has become a hotspot in spinal surgery. A series of biological, pharmaceutical and synthetic materials are used to study the prevention of scar formation after laminectomy. Silicone rubber, polyester materials, fat transplantation, cholesterol, mitomycin C, recombinant tissue plasminogen activator and anti-inflammatory drugs were used to study, but the results were not consistent ^{1) 2) 3) 4) 5) 6) 7)}.

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 ^{8) 9) 10) 11) 12)}.

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 ¹³⁾.

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 ¹⁴⁾.