Abstract

Epidural fibrosis is a challenging topic in spinal surgery. This phenomenon constitutes one of the main reasons behind postlaminectomy syndrome or failed back surgery syndrome, which leads to persistent back and leg pain in association with compression and/or stretching the nerve root or the dura. The exact mechanism of action in epidural fibrosis is complex and remains uncertain. Excessive deposition of collagen, fibronectin, and dermatan sulfate, known as the "extracellular matrix," and decrease of tissue cellularity results in epidural fibrosis. The most investigated and important actor in epidural fibrosis as well as in other forms of aberrant wound healing is presumed to be transforming growth factor-1β formation. Tamoxifen (TAM), a synthetic nonsteroidal antiestrogen used in breast cancer, is also effective in inhibiting fibroblast proliferation via downregulation of transforming growth factor-1β. Twenty-four adult male rats were randomly divided into 3 groups. Laminectomy was the sole intervention in the control group. Spongostan was placed in the operation lodge after laminectomy in the second group. In the treatment group, TAM was administrated orally after laminectomy. Epidural fibrosis, dural thickness, inflammatory response, and arachnoidal involvement were evaluated and graded histopathologically. Epidural fibrosis, dural thickness, and inflammatory response in the subjects treated with TAM were significantly less than in the control and Spongostan group and the differences were statistically significant. Although arachnoidal involvement was observed in a subject in the TAM group, the differences between all groups weren't statistically significant. Tamoxifen reduced epidural fibrosis, dural thickness, and inflammatory response after laminectomy in rats.

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