Comparison of the effectiveness of diclofenac sodium and tenoxicam in the prevention of epidural fibrosis by topical application with an absorbable gelatin sponge on the dura in an experimental laminectomy model
Folia Neuropathologica, cilt.62, sa.4, ss.412-417, 2024 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 62 Sayı: 4
- Basım Tarihi: 2024
- Doi Numarası: 10.5114/fn.2024.141373
- Dergi Adı: Folia Neuropathologica
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.412-417
- Anahtar Kelimeler: cyclooxygenase inhibitor drugs, epidural fibrosis, laminectomy, failed back surgery
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Introduction: There has been an increasing trend in spinal surgery interventions in recent years. Low back pain is a disorder that is seen at least once in the lifetime of approximately 80% of the general population. Today, neurosurgeons perform operations including laminectomy for various reasons. Epidural fibrosis is a scar tissue that develops after posterior spinal surgery. Various synthetic and organic materials have been used in experimental studies to prevent epidural fibrosis in laminectomy defects. In this study we aimed to investigate and observe histopathologically the effectiveness of cyclooxygenase inhibitor drugs; tenoxicam and diclofenac sodium in the experimental rat laminectomy model in preventing the postoperative spinal epidural fibrosis. Material and methods: In this study, 32 Wistar-Albino female rats were used. 8 mg/kg tenoxicam and 1.5 mg/kg diclofenac sodium were applied on the dura with an absorbable gelatin sponge. After decapitation, L1-L4 laminectomy area was totally removed and histopathological examination was performed. Results and conclusions: It has been shown that the topical application of diclofenac sodium and tenoxicam, which are selective Cox inhibitor drugs, prevents fibroblast migration by forming a local barrier and Cox inhibitors are caused by the inhibition of prostanoids, which are inflammatory mediators.