Ochiai Nobuyasu, Tasto James P, Ohtori Seiji, Takahashi Norimasa, Moriya Hideshige, Amiel David
Department of Orthopedic Surgery, University of California San Diego, La Jolla, California, USA.
Am J Sports Med. 2007 Nov;35(11):1940-4. doi: 10.1177/0363546507304175. Epub 2007 Jul 16.
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.
After ablation or degeneration by bipolar radiofrequency, nerve fibers will have the ability to regenerate with time.
Controlled laboratory study.
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.
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.
Bipolar radiofrequency treatment induced degeneration of sensory nerve fibers immediately after treatment, but by 90 days posttreatment, there was evidence of complete regeneration.
Early degeneration followed by later regeneration of nerve fibers after bipolar radiofrequency treatment may explain long-term postoperative pain relief after microtenotomy for tendinosis.
许多慢性肌腱病患者在接受双极射频治疗后早期疼痛得到缓解。据推测,其作用机制可能是感觉神经纤维的急性变性和/或消融。
双极射频消融或变性后,神经纤维会随时间再生。
对照实验室研究。
本研究使用了18只Sprague-Dawley大鼠。这些大鼠被分为3组(双极射频治疗后30、60和90天)。使用Topaz微型清创器对这些大鼠的左后爪进行2点双极射频治疗。右后爪用作对侧对照。采用游离漂浮抗生物素蛋白生物素复合物技术对组织进行神经Ⅲ类β-微管蛋白或降钙素基因相关肽免疫组织化学处理。计数表皮中神经Ⅲ类β-微管蛋白免疫反应性和降钙素基因相关肽免疫反应性神经纤维的数量,并与对侧对照进行比较。
尽管直到双极射频治疗后60天,神经Ⅲ类β-微管蛋白和降钙素基因相关肽抗体所显示的神经纤维数量均显著减少(P<.0001),但治疗后90天表皮神经纤维出现再生。
双极射频治疗后立即导致感觉神经纤维变性,但治疗后90天有完全再生的证据。
双极射频治疗后神经纤维早期变性随后再生可能解释了肌腱病微切开术后长期的疼痛缓解。