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Journal of Dental Research
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BIOLOGICAL

Acceleration of Palatal Wound Healing in Smad3-deficient Mice

K. Jinno1,*, T. Takahashi1, K. Tsuchida2, E. Tanaka1 and K. Moriyama3

1 Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Oral Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8504, Japan;
2 Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 470-1192, Japan; and
3 Department of Maxillofacial Orthognathics, Tokyo Medical and Dental University Graduate School, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan

Correspondence: * k.jinno{at}h7.dion.ne.jp

Wound healing is a well-orchestrated complex process leading to the repair of injured tissues. It is suggested that transforming growth factor (TGF)-β/Smad3 signaling is involved in wound healing. The purpose of this study was to investigate the role of TGF-β/Smad3 signaling in palatal wound healing in Smad3-deficient (Smad3–/–) mice. Histological examination showed that wound closure was accelerated by the proliferation of epithelium and dermal cells in Smad3–/– mice compared with wild-type (WT) mice. Macrophage/monocyte infiltration at wounded regions in Smad3–/– mice was decreased in parallel with the diminished production of TGF-β1, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1{alpha} compared with WT mice. Fibrocytes, expressing hematopoietic surface marker and fibroblast products, were recruited and produced {alpha}-smooth-muscle actin in WT mice, but were not observed in Smad3–/– mice. These results suggest that TGF-β/Smad3 signaling may play an important role in the regulation of palatal wound healing.

Key Words: Smad3 • TGF-β • palatal wound healing • myofibroblast • fibrocyte

Journal of Dental Research, Vol. 88, No. 8, 757-761 (2009)
DOI: 10.1177/0022034509341798
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