Literature DB >> 10602084

Use of recombinant human osteogenic protein-1 for the repair of subchondral defects in articular cartilage in goats.

R T Louwerse1, I C Heyligers, J Klein-Nulend, S Sugihara, G P van Kampen, C M Semeins, S W Goei, M H de Koning, P I Wuisman, E H Burger.   

Abstract

The objective of this pilot study was to examine in vivo the potential of recombinant human osteogenic protein-1 (rhOP-1, also called bone morphogenetic protein-7, BMP-7) for treatment of subchondral lesions by induction of new hyaline cartilage formation. Subchondral left knee defects in 17 mature goats were treated with fresh coagulated blood mixed with (1) rhOP-1 combined with collagen (OP-1 device, 400 microgram/mL); (2) rhOP-1 alone (OP-1 peptide, 200 microgram/mL); (3) OP-1 device with small particles of autologous ear perichondrium; (4) OP-1 peptide with small particles of autologous ear perichondrium; or (5) autologous ear perichondrium alone (controls). rhOP-1 was combined with either collagen (OP-1 device) or not (OP-1 peptide). The defects were closed with a periosteal flap. The formation of cartilage tissue was studied by histologic and biochemical evaluation at 1, 2, and 4 months after implantation. One and 2 months after implantation there were no obvious differences between control and rhOP-1-treated defects. Four months after implantation, only one out of three controls (without rhOP-1) showed beginning signs of cartilage formation while all four rhOP-1-treated defects were completely or partly filled with cartilage. A significant linear relationship was found between rhOP-1 concentration and the total amount of aggrecan in the defects. These results suggest that implantation of rhOP-1 promotes cartilage formation in subchondral defects in goats at 4 months after implantation. Therefore, rhOP-1 could be a novel factor for regeneration of cartilage in articular cartilage defects. Copyright 2000 John Wiley & Sons, Inc.

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Year:  2000        PMID: 10602084     DOI: 10.1002/(sici)1097-4636(20000315)49:4<506::aid-jbm9>3.0.co;2-a

Source DB:  PubMed          Journal:  J Biomed Mater Res        ISSN: 0021-9304


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