title: Effect of autologous platelet-rich plasma-releasate on intervertebral disc degeneration in the rabbit anular puncture model: a preclinical study.
abstract: BACKGROUND
  Platelet-rich plasma (PRP) is a fraction of plasma in which several growth factors are concentrated at high levels. The active soluble releasate isolated following platelet activation of PRP (PRP-releasate) has been demonstrated to stimulate the metabolism of IVD cells in vitro. The in vivo effect of PRP-releasate on degenerated IVD remains unknown. The purpose of this study was to determine the reparative effects of autologous PRP-releasate on degenerated intervertebral discs (IVDs).
  
  
  METHODS
  To induce disc degeneration, New Zealand white rabbits (n = 12) received anular puncture in two noncontiguous discs. Autologous PRP and PPP (platelet-poor plasma) were isolated from fresh blood using two centrifugation techniques. Four weeks after the initial puncture, releasate isolated from clotted PPP or PRP (PPP- or PRP-releasate), or phosphate-buffered saline (PBS; control) was injected into the punctured discs. Disc height, magnetic resonance imaging (MRI) T2-mapping and histology were assessed.
  
  
  RESULTS
  Anular puncture produced a consistent disc narrowing within four weeks. PRP-releasate induced a statistically significant restoration of disc height (PRP vs. PPP and PBS, P<0.05). In T2-quantification, the mean T2-values of the nucleus pulposus (NP) and anulus fibrosus (AF) of the discs were not significantly different among the three treatment groups. Histologically, the number of chondrocyte-like cells was significantly higher in the discs injected with PRP-releasate compared to that with PBS.
  
  
  CONCLUSIONS
  The administration of active PRP-releasate induced a reparative effect on rabbit degenerated IVDs. The results of this study suggest that the use of autologous PRP-releasate is safe and can lead to a clinical application for IVD degeneration.
authors.forename: Shuji
authors.initials: S
authors.lastname: Obata
authors.forename: Koji
authors.initials: K
authors.lastname: Akeda
authors.forename: Takao
authors.initials: T
authors.lastname: Imanishi
authors.forename: Koichi
authors.initials: K
authors.lastname: Masuda
authors.forename: Won
authors.initials: W
authors.lastname: Bae
authors.forename: Ryo
authors.initials: R
authors.lastname: Morimoto
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Asanuma
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Kasai
authors.forename: Atsumasa
authors.initials: A
authors.lastname: Uchida
authors.forename: Akihiro
authors.initials: A
authors.lastname: Sudo
mesh_terms: D000818:Animals; D019902:Chondrocytes / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D007267:Injections; D036341:Intercellular Signaling Peptides and Proteins / Q000008:administration & dosage* / Q000378:metabolism; D007403:Intervertebral Disc / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D055959:Intervertebral Disc Degeneration / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D008279:Magnetic Resonance Imaging; D053657:Platelet-Rich Plasma / Q000378:metabolism / Q000502:physiology*; D011677:Punctures / Q000009:adverse effects; D011817:Rabbits; D011859:Radiography; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D036341:Intercellular Signaling Peptides and Proteins