title: The presence of pleiotrophin in the human intervertebral disc is associated with increased vascularization: an immunohistologic study.
abstract: METHODS
  An immunohistological study of surgical specimens of human intervertebral disc.
  
  
  OBJECTIVE
  To examine the presence of pleiotrophin in diseased or damaged intervertebral disc tissue and the association between its presence and the extent of tissue vascularization and innervation.
  
  
  BACKGROUND
  Increased levels of pleiotrophin, a growth and differentiation factor that is active in various pathophysiologic processes, including angiogenesis, has been associated with osteoarthritic changes of human articular cartilage. The association between pleiotrophin expression and pathologic conditions of the human intervertebral disc is unknown.
  
  
  METHODS
  Specimens of human lumbar intervertebral discs, obtained following surgical discectomy, were divided into 3 groups: non-degenerated discs (n = 7), degenerated discs (n = 6), and prolapsed discs (n = 11). Serial tissue sections of each specimen were immunostained to determine the presence of pleiotrophin, blood vessels (CD34-positive endothelial cells), and nerves (neurofilament 200 kDa [NF200]-positive nerve fibers).
  
  
  RESULTS
  Pleiotrophin immunoreactivity was seen in disc cells, endothelial cells, and in the extracellular matrix in most specimens of intervertebral disc but was most prevalent in vascularized tissue in prolapsed discs. There was a significant correlation between the presence of pleiotrophin-positive disc cells and that of CD34-positive blood vessels. NF200-positive nerves were seen in vascularized areas of more degenerated discs, but nerves did not appear to codistribute with blood vessels or pleiotrophin positivity in prolapsed discs.
  
  
  CONCLUSIONS
  Pleiotrophin is present in pathologic human intervertebral discs, and its prevalence and distribution suggest that it may play a role in neovascularization of diseased or damaged disc tissue.
authors.affiliation: Centre for Spinal Studies, Institute for Science & Technology in Medicine of Keele University, Robert Jones and Agnes Hunt Orthopaedic Hospital, Oswestry, United Kingdom. Eustace.Johnson@rjah.nhs.uk
authors.forename: William E B
authors.initials: WE
authors.lastname: Johnson
authors.forename: Angela M
authors.initials: AM
authors.lastname: Patterson
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Eisenstein
authors.forename: Sally
authors.initials: S
authors.lastname: Roberts
mesh_terms: D000328:Adult; D002352:Carrier Proteins / Q000378:metabolism*; D002648:Child; D016207:Cytokines / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007403:Intervertebral Disc / Q000098:blood supply* / Q000294:innervation / Q000378:metabolism* / Q000473:pathology; D007405:Intervertebral Disc Displacement / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000378:metabolism* / Q000473:pathology; D009412:Nerve Fibers / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D016900:Neurofilament Proteins; C051774:neurofilament protein H; C066845:pleiotrophin