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Originally published online as doi:10.2353/ajpath.2009.080705 on October 15, 2009

Published online before print October 15, 2009
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(American Journal of Pathology. 2009;175:1905-1914.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.080705

Matrix Metalloproteinase-3 Accelerates Wound Healing following Dental Pulp Injury

Li Zheng*, Kazuharu Amano{dagger}, Koichiro Iohara*, Masataka Ito{ddagger}, Kiyomi Imabayashi*, Takeshi Into*, Kenji Matsushita*, Hiroshi Nakamura{dagger} and Misako Nakashima*

From the Department of Oral Disease Research,* National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Aichi; the Department of Endodontics,{dagger} School of Dentistry, Aichi-Gakuin University, Nagoya, and the Department of Developmental Anatomy and Regenerative Medicine,{ddagger} National Defense Medical College, Saitama, Japan

Matrix metalloproteinases (MMPs) are implicated in a wide range of physiological and pathological processes, including morphogenesis, wound healing, angiogenesis, inflammation, and cancer. Angiogenesis is essential for reparative dentin formation during pulp wound healing. The mechanism of angiogenesis, however, still remains unclear. We hypothesized that certain MMPs expressed during pulp wound healing may support recovery processes. To address this issue, a rat pulp injury model was established to investigate expression of MMPs during wound healing. Real-time RT-PCR analysis showed that expression MMP-3 and MMP-9 (albeit lower extent) was up-regulated at 24 and 12 hours after pulp injury, respectively, whereas expression of MMP-2 and MMP-14 was not changed. MMP-3 mRNA and protein were localized in endothelial cells and/or endothelial progenitor cells in injured pulp in vivo. In addition, MMP-3 enhanced proliferation, migration, and survival of human umbilical vein endothelial cells in vitro. Furthermore, the topical application of MMP-3 protein on the rat-injured pulp tissue in vivo induced angiogenesis and reparative dentin formation at significantly higher levels compared with controls at 24 and 72 hours after treatment, respectively. Inhibition of endogenous MMP-3 by N-Isobutyl-N-(4-methoxyphenylsulfonyl)-glycylhydroxamic acid resulted in untoward wound healing. These results provide suggestive evidence that MMP-3 released from endothelial cells and/or endothelial progenitor cells in injured pulp plays critical roles in angiogenesis and pulp wound healing.






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