title: Nucleus pulposus-induced nerve root injury: effects of diclofenac and ketoprofen.
abstract: OBJECTIVE
  Nucleus pulposus and/or chronic compression can induce spinal nerve root injury. Inflammation has been proposed as having major importance in the pathophysiologic mechanisms involved in the induction of such injuries. Corticosteroids, potent anti-inflammatory drugs, have been demonstrated to reduce nucleus pulposus-induced spinal nerve root injury. The aim of the present study was to assess the effects of two potent non-steroidal anti-inflammatory drugs (NSAIDs), diclofenac and ketoprofen, in experimental nucleus pulposus-induced spinal nerve root injury in a pig model.
  
  
  METHODS
  Eighteen pigs were included in the study. Autologous nucleus pulposus was harvested from a lumbar disc and applied locally around the first sacral nerve root after a partial laminectomy of the first and second sacral vertebrae. Six pigs were treated with daily intramuscular injections of diclofenac, 3 mg/kg body weight, for 7 days. Six other pigs were treated with daily intramuscular injections of ketoprofen, 4 mg/kg body weight, for 7 days. As controls, six pigs received injections with physiologic saline. After 7 days, the pigs were reanesthetized and the nerve conduction velocity over the exposed nerve root area was determined.
  
  
  RESULTS
  The nerve conduction velocity was significantly higher in pigs treated with diclofenac than in the saline-treated controls, (57 +/- 6 m/s vs 38 +/- 18 m/s, P<0.05, Student's t-test). The velocity in pigs treated with ketoprofen, 42 +/- 24 m/s, did not differ significantly from that of controls.
  
  
  CONCLUSIONS
  This study of two potent NSAIDs indicates that nucleus pulposus-induced nerve root dysfunction may be reduced by diclofenac but not by ketoprofen. The reason for this difference is not known, but it might be related to the fact that ketoprofen and diclofenac belong to different NSAID subgroups and have a different selectivity for the two cyclo-oxygenases COX-1 and COX-2.
authors.affiliation: Department of Orthopaedics, Gothenburg University, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Cornefjord
authors.forename: K
authors.initials: K
authors.lastname: Olmarker
authors.forename: K
authors.initials: K
authors.lastname: Otani
authors.forename: B
authors.initials: B
authors.lastname: Rydevik
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D004008:Diclofenac / Q000494:pharmacology*; D004195:Disease Models, Animal; D007403:Intervertebral Disc / Q000473:pathology*; D007660:Ketoprofen / Q000494:pharmacology*; D009431:Neural Conduction / Q000187:drug effects; D011843:Radiculopathy / Q000188:drug therapy* / Q000473:pathology; D013552:Swine
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D004008:Diclofenac; D007660:Ketoprofen