title: Herniated intervertebral disc-associated periradicular fibrosis and vascular abnormalities occur without inflammatory cell infiltration.
abstract: METHODS
  Prospective histologic comparison of perineural tissues from patients requiring decompression surgery for herniated intervertebral disc with those from cadaveric controls.
  
  
  OBJECTIVE
  To examine the significance of herniated intervertebral-disc-associated perineural vascular and fibrotic abnormalities with respect to back pain symptom generation.
  
  
  BACKGROUND
  Previous cadaveric studies have demonstrated perineural vascular congestion, dilatation, and thrombosis and perineural and intraneural fibrosis occurring in association with herniated intervertebral disc. It was suggested that these neural abnormalities were the result of ischemia, due to venous outflow obstruction, and also represented a possible cause of ongoing back pain symptoms. Criticisms of such a conclusion arose, however, because the possibility could not be excluded that these abnormalities were the result of postmortem artifact.
  
  
  METHODS
  Histologic and immunohistochemical comparison of discal and peridiscal tissues removed from 11 patients with radiographically proven herniated intervertebral disc requiring decompressive surgery and from 6 fresh cadavers without history of back pain in life.
  
  
  RESULTS
  Histology and immunohistochemistry of perineural and extraneural tissues from patients revealed vascular congestion, neovascularization, and endothelial abnormalities including luminal platelet adhesion, in association with reductions in von Willebrand factor levels, together with perivascular and perineural fibrosis. Elevated fibrogenic cytokine concentrations were also detected in patients' tissues. These changes occurred without evidence of inflammation and were absent in cadaveric control tissues.
  
  
  CONCLUSIONS
  The vascular abnormalities detected in patients may represent an important etiopathologic factor predisposing to intraneural and perineural fibrosis, and hence to chronic pain symptoms, after disc herniation. It seems important to preserve the perineural microcirculation following disc herniation.
authors.affiliation: Department of Rheumatology, University of Manchester, United Kingdom.
authors.forename: R G
authors.initials: RG
authors.lastname: Cooper
authors.forename: A J
authors.initials: AJ
authors.lastname: Freemont
authors.forename: J A
authors.initials: JA
authors.lastname: Hoyland
authors.forename: J P
authors.initials: JP
authors.lastname: Jenkins
authors.forename: C G
authors.initials: CG
authors.lastname: West
authors.forename: K J
authors.initials: KJ
authors.lastname: Illingworth
authors.forename: M I
authors.initials: MI
authors.lastname: Jayson
mesh_terms: D000328:Adult; D005260:Female; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000032:analysis; D007403:Intervertebral Disc / Q000098:blood supply*; D007405:Intervertebral Disc Displacement / Q000150:complications / Q000473:pathology*; D017116:Low Back Pain / Q000209:etiology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013116:Spinal Cord / Q000098:blood supply; D013127:Spinal Nerves / Q000473:pathology*; D014057:Tomography, X-Ray Computed; D016211:Transforming Growth Factor alpha / Q000032:analysis; D016212:Transforming Growth Factor beta / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D007375:Interleukin-1; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D014841:von Willebrand Factor