title: Inflammatory responses and morphological changes of radiofrequency-induced rat sciatic nerve fibres.
abstract: BACKGROUND
  Recently, the pulsed radiofrequency (PRF, pulsed fashion) procedure was introduced for neuropathic pain management. Since PRF-induced lesions do not need high temperature compared with conventional continuous RF (CRF)-induced lesions, there is no significant loss of sensory fibres after application.
  
  
  METHODS
  The progressive changes in the expression of eight representative inflammatory cytokines - glial fibrillary acidic protein, tumour necrosis factor alpha, interleukin-6, cyclooxygenase-II, inducible nitric oxide synthase, nuclear factor-κB, monocyte chemoattractant protein-1 and macrophage inflammatory protein-1α - as well as the morphological changes in extracellular matrices by Masson's trichrome and Verhoeff-van Gieson staining and atomic force microscopy were assessed for normal (control), sham (no RF current), PRF and CRF (positive control) rats. The RF procedure used in this study was similar to the methods used in human clinical trials.
  
  
  RESULTS
  All proposed inflammatory proteins showed up-regulation after RF thermal treatments. Specifically, PRF-treated rats showed recovery of up-regulated inflammatory cytokines on day 30 after application, while CRF rats showed significant up-regulation that persisted until day 30. The control and sham groups showed normal unmyelinated axon and collagen structures. PRF-induced lesions showed less fibre destruction than CRF-induced lesions. PRF-induced lesions also showed mild axonal damage and little swelling of the mitochondria. CRF-induced lesions showed ultrastructural changes of sciatic nerve fibres that were irreversible.
  
  
  CONCLUSIONS
  PRF-induced pain relief may be due to temporary blockage of nerve signals through the nerve pathway responsible for reversible neuronal depression. However, CRF-induced pain relief may be due to permanent blockage of nerve signals through other nerve pathways. Therefore, CRF could be applied to chronic inflammatory models used to study the mechanism of neuropathic pain.
authors.affiliation: Department of Biomedical Engineering & Healthcare Industry Research Institute, Kyung Hee University, Seoul, Korea.
authors.forename: S
authors.initials: S
authors.lastname: Choi
authors.forename: H J
authors.initials: HJ
authors.lastname: Choi
authors.forename: Y
authors.initials: Y
authors.lastname: Cheong
authors.forename: S H
authors.initials: SH
authors.lastname: Chung
authors.forename: H K
authors.initials: HK
authors.lastname: Park
authors.forename: Y J
authors.initials: YJ
authors.lastname: Lim
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D008297:Male; D009437:Neuralgia / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D011846:Radio Waves; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000378:metabolism / Q000473:pathology*; D015854:Up-Regulation
chemical_list: D016207:Cytokines