Evaluation of Oxidative Damage and Inflammation in Periodontal Tissues of Rats with Paclitaxel-Induced Neuropathic Pain


Toraman E., Toraman A., Özkaraca M., Budak H.

Eurasia Biochemical Approaches & Technologies Congress (3. EBAT), Antalya, Türkiye, 4 - 07 Kasım 2021, ss.91

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Antalya
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.91
  • Atatürk Üniversitesi Adresli: Evet

Özet

Over one-third of the world's population suffers from persistent or recurrent pain. Chronic pain is associated with conditions such as migraine, arthritis, herpes zoster, diabetic neuropathy, temporomandibular joint disorders, orofacial pain, rheumatoid arthritis, and cancer. 1, 2 Cancer-related pain is very difficult to treat, and the emotional burden of being cancer increases this situation. This is particularly common in certain types of cancer, such as head and neck carcinomas. Periodontal disease is a chronic bacterial inflammatory process that causes periodontal tissue destruction. Periodontal disease is a very common public health problem in the world. It has been reported that some diseases such as migraine, which can cause chronic pain, increase periodontal inflammation. Although the underlying mechanism should be well known to treat chronic pain, this mechanism is still unclear today. The aim of this study is to evaluate the effect of oxidative stress and inflammation on the periodontal tissue of rats in the paclitaxel-induced neuropathic pain model. For this purpose, 16 male albino Wistar rats (220-295 g body weight) were divided into 2 groups as Control (C) and Neuropathic pain model (NP) groups. Neuropathic pain was induced by intraperitoneal administration of 2 mg/kg paclitaxel (PTX) (4 doses) to the NA group. After the treatment of PTX, all rats were sacrificed by decapitation and all gingival tissue samples of the right mandible first and second molar teeth were collected. Then, the gene expression changes of Hcn2, Scn9a which are painrelated genes, were examined by Real-Time PCR. The left mandible was taken together with the surrounding gingiva, and the number of 8-hydroxy-2-deoxyguanosine (8-OHdG) immune positive cells was examined in histological sections of the first and second molar teeth to evaluate the oxidative stress. The results showed that there was a significant increase in Hcn2 and Scn9a gene expression of the NA group compared to the C group. The number of 8-OHdG positive cells in the NA group was significantly higher than in C group. In the histopathological examination, clinical attachment loss was observed to be significantly higher in the NA group compared to the C group.