rhBMP-2 (ACS and CRM formulations) overcomes pseudarthrosis in a New Zealand white rabbit posterolateral fusion model. Academic Article uri icon

Overview

abstract

  • STUDY DESIGN: The study design consisted of a New Zealand white rabbit model of pseudarthrosis repair. Study groups consisting of no graft, autograft, or recombinant human bone morphogenetic protein-2 (rhBMP-2) with absorbable collagen sponge (ACS) or compression resistant matrix (CRM) were evaluated. OBJECTIVE: To evaluate the relative efficacy of bone graft materials (autograft, ACS, and CRM). SUMMARY OF BACKGROUND DATA: rhBMP-2 has been shown to have a 100% fusion rate in a primary rabbit fusion model, even in the presence of nicotine, which is known to inhibit fusion. METHODS: Seventy-two New Zealand white rabbits underwent posterolateral lumbar fusion with iliac crest autograft. To establish pseudarthroses, nicotine was administered to all animals. At 5 weeks, the spines were explored and all pseudarthroses were redecorticated and implanted with no graft, autograft, rhBMP-2/ACS, or rhBMP-2/CRM. At 10 weeks, fusions were assessed by manual palpation and histology. RESULTS: Eight rabbits (11%) were lost to complications. At 5 weeks, 66 (97%) had pseudarthroses. At 10 weeks, attempted pseudarthrosis repairs were fused in 1 of 16 of no graft rabbits (6%), 5 of 17 autograft rabbits (29%), and 31 of 31 rhBMP-2 rabbits (with ACS or CRM) (100%). Histologic analysis demonstrated more mature bone formation in the rhBMP-2 groups. CONCLUSIONS: The 2 rhBMP-2 formulations led to significantly higher fusion rates and histologic bone formation than no graft and autograft controls in this pseudarthrosis repair model.

publication date

  • May 15, 2007

Research

keywords

  • Bone Morphogenetic Proteins
  • Lumbar Vertebrae
  • Osseointegration
  • Pseudarthrosis
  • Recombinant Proteins
  • Spinal Fusion
  • Transforming Growth Factor beta

Identity

Scopus Document Identifier

  • 34248390955

Digital Object Identifier (DOI)

  • 10.1097/BRS.0b013e318054721e

PubMed ID

  • 17495777

Additional Document Info

volume

  • 32

issue

  • 11