Xue Yuan1, Jinlong Chen1,2, Lauren A Van Brunt1, Joseph Grauer1,3, Quanchen Xu1,4, Xibo Pei1,2, Liao Wang1,2, Yuan Zhao1,5, Jill A Helms1. 1. Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine, Palo Alto, CA, USA. 2. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. 3. Dr Gerald Niznick College of Dentistry, University of Manitoba, Winnipeg, MB, Canada. 4. The Affiliated Hospital of Qingdao University, Qingdao, China. 5. Department of Cariology and Endodontology, School of Dentistry, Lanzhou University, Lanzhou, China.
Abstract
AIM: To identify the molecular mechanisms mediating the persistent defensive functions of the self-renewing junctional epithelium (JE). MATERIALS AND METHODS: Two strains of Wnt reporter mice, Axin2CreErt2 /+ ;R26RmTmG /+ and Axin2LacZ /+ , were employed, along with three clinically relevant experimental scenarios where the function of the JE is disrupted: after tooth extraction, after a partial gingivectomy, and after a complete circumferential gingivectomy. RESULTS: Using transgenic Wnt reporter strains of mice, we established the JE is a Wnt-responsive epithelium beginning at the time of its formation and that it maintains this status into adulthood. After tooth extraction, progeny of the initial Wnt-responsive JE population directly contributed to healing and ultimately adopted an oral epithelium (OE) phenotype. In the traditional partial gingivectomy model, the JE completely regenerated and did so via progeny of the original Wnt-responsive population. However, following circumferential gingivectomy, the OE was incapable of re-establishing a functional JE. CONCLUSIONS: A Wnt-responsive niche at the interface between tooth and oral epithelia is required for a functional JE.
AIM: To identify the molecular mechanisms mediating the persistent defensive functions of the self-renewing junctional epithelium (JE). MATERIALS AND METHODS: Two strains of Wnt reporter mice, Axin2CreErt2 /+ ;R26RmTmG /+ and Axin2LacZ /+ , were employed, along with three clinically relevant experimental scenarios where the function of the JE is disrupted: after tooth extraction, after a partial gingivectomy, and after a complete circumferential gingivectomy. RESULTS: Using transgenic Wnt reporter strains of mice, we established the JE is a Wnt-responsive epithelium beginning at the time of its formation and that it maintains this status into adulthood. After tooth extraction, progeny of the initial Wnt-responsive JE population directly contributed to healing and ultimately adopted an oral epithelium (OE) phenotype. In the traditional partial gingivectomy model, the JE completely regenerated and did so via progeny of the original Wnt-responsive population. However, following circumferential gingivectomy, the OE was incapable of re-establishing a functional JE. CONCLUSIONS: A Wnt-responsive niche at the interface between tooth and oral epithelia is required for a functional JE.
Authors: Barbara Lustig; Boris Jerchow; Martin Sachs; Sigrid Weiler; Torsten Pietsch; Uwe Karsten; Marc van de Wetering; Hans Clevers; Peter M Schlag; Walter Birchmeier; Jürgen Behrens Journal: Mol Cell Biol Date: 2002-02 Impact factor: 4.272