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Research Article Free access | 10.1172/JCI116912

Platelet-derived growth factor inhibits bone regeneration induced by osteogenin, a bone morphogenetic protein, in rat craniotomy defects.

L J Marden, R S Fan, G F Pierce, A H Reddi, and J O Hollinger

Department of Physiology, U.S. Army Institute of Dental Research, Walter Reed Army Medical Center, Washington, DC 20307-5300.

Find articles by Marden, L. in: PubMed | Google Scholar

Department of Physiology, U.S. Army Institute of Dental Research, Walter Reed Army Medical Center, Washington, DC 20307-5300.

Find articles by Fan, R. in: PubMed | Google Scholar

Department of Physiology, U.S. Army Institute of Dental Research, Walter Reed Army Medical Center, Washington, DC 20307-5300.

Find articles by Pierce, G. in: PubMed | Google Scholar

Department of Physiology, U.S. Army Institute of Dental Research, Walter Reed Army Medical Center, Washington, DC 20307-5300.

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Department of Physiology, U.S. Army Institute of Dental Research, Walter Reed Army Medical Center, Washington, DC 20307-5300.

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Published December 1, 1993 - More info

Published in Volume 92, Issue 6 on December 1, 1993
J Clin Invest. 1993;92(6):2897–2905. https://doi.org/10.1172/JCI116912.
© 1993 The American Society for Clinical Investigation
Published December 1, 1993 - Version history
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Abstract

Platelet-derived growth factor (PDGF) is a potent moderator of soft tissue repair through induction of the inflammatory phase of repair and subsequent enhanced collagen deposition. We examined the effect of recombinant BB homodimer PDGF (rPDGF-BB) applied to rat craniotomy defects, treated with and without bovine osteogenin (OG), to see if bone regeneration would be stimulated. Implants containing 0, 20, 60, or 200 micrograms rPDGF-BB, reconstituted with insoluble rat collagenous bone matrix containing 0, 30, or 150 micrograms OG, were placed into 8-mm craniotomies. After 11 d, 21 of the 144 rats presented subcutaneous masses superior to the defect sites. The masses, comprised of serosanguinous fluid encapsulated by fibrous connective tissue, were larger and occurred more frequently in rats treated with 200 micrograms rPDGF-BB, and were absent in rats not treated with rPDGF-BB. The masses underwent resorption within 28 d after surgery. OG (2-256 micrograms) caused a dose-dependent increase in radiopacity and a marked regeneration of calcified tissue in a dose-dependent fashion within defect sites. However, OG-induced bone regeneration was inhibited 17-53% in the presence of rPDGF-BB. These results suggest that rPDGF-BB inhibited OG-induced bone regeneration and stimulated a soft tissue repair wound phenotype and response.

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