title: Nerve regeneration after radiofrequency application.
abstract: BACKGROUND
  Many patients with chronic tendinosis have experienced early pain relief after application of bipolar radiofrequency treatment. It is hypothesized that the mechanism of action may be the acute degeneration and/or ablation of sensory nerve fibers.
  
  
  OBJECTIVE
  After ablation or degeneration by bipolar radiofrequency, nerve fibers will have the ability to regenerate with time.
  
  
  METHODS
  Controlled laboratory study.
  
  
  METHODS
  Eighteen Sprague-Dawley rats were used in this study. These rats were divided into 3 groups (30, 60, and 90 days after bipolar radiofrequency). These rats were treated with 2 points of bipolar radiofrequency applications to the left hindpaws with the Topaz microdebrider device. Right hindpaws were used as the contralateral control. Tissues were processed for neural class III beta-tubulin or calcitonin gene-related peptide immunohistochemistry by using the free-floating avidin biotin complex technique. The numbers of neural class III beta-tubulin-immunoreactive and calcitonin gene-related peptide-immunoreactive nerve fibers in the epidermis were counted and compared with those in the contralateral control.
  
  
  RESULTS
  Although the numbers of nerve fibers demonstrated by both the antibodies of neural class III beta-tubulin and calcitonin gene-related peptide were significantly decreased (P <.0001) until 60 days after bipolar radiofrequency treatment, regeneration of the epidermal nerve fibers occurred 90 days after treatment.
  
  
  CONCLUSIONS
  Bipolar radiofrequency treatment induced degeneration of sensory nerve fibers immediately after treatment, but by 90 days posttreatment, there was evidence of complete regeneration.
  
  
  CONCLUSIONS
  Early degeneration followed by later regeneration of nerve fibers after bipolar radiofrequency treatment may explain long-term postoperative pain relief after microtenotomy for tendinosis.
authors.affiliation: Department of Orthopedic Surgery, University of California San Diego, La Jolla, California, USA.
authors.forename: Nobuyasu
authors.initials: N
authors.lastname: Ochiai
authors.forename: James P
authors.initials: JP
authors.lastname: Tasto
authors.forename: Seiji
authors.initials: S
authors.lastname: Ohtori
authors.forename: Norimasa
authors.initials: N
authors.lastname: Takahashi
authors.forename: Hideshige
authors.initials: H
authors.lastname: Moriya
authors.forename: David
authors.initials: D
authors.lastname: Amiel
mesh_terms: D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D017115:Catheter Ablation; D006614:Hindlimb / Q000294:innervation*; D007150:Immunohistochemistry; D008297:Male; D009412:Nerve Fibers / Q000378:metabolism / Q000528:radiation effects*; D009416:Nerve Regeneration; D010147:Pain Measurement; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014404:Tubulin / Q000378:metabolism
chemical_list: D014404:Tubulin; D015740:Calcitonin Gene-Related Peptide