BMP/WNT-Dependent Mechanisms of Junctional Epithelium Turnover

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Abstract
As a first line of defense against periodontal diseases, the junctional epithelium must establish a firm attachment to the tooth surface while allowing new cells arising from the stem cell niche to migrate through the tissue. How these static and dynamic cell behaviors are coordinated in the junctional epithelium is not clear; we hypothesize it involves the epithelial-to-mesenchymal transition (EMT). An intact junctional epithelium was interrogated via quantitative immunohistochemistry for molecular markers of EMT; since EMT is also critical for tissue repair, the junctional epithelium was also interrogated at multiple time points after ligature-induced periodontitis. These analyses revealed that junctional epithelial cells transition from a polarized, cell-adherent phenotype to one in which cytoskeletal remodeling and increased motility occur. To gain insights into molecular mechanisms regulating EMT, we used a genetic system to delete the BMP type I receptor (BMPR1a) in postnatal mice. Within 7 d of BMPR1a inactivation, multiple EMT signaling pathways including Wnt/β-catenin, transforming growth factor–β, and Notch signaling were upregulated in the junctional epithelium. The mutant junctional epithelium exhibited extensive EMT accompanied by downregulation of the hemidesmosomal proteins Laminin5, plectin, and β4 integrin. Together, these findings demonstrate that normal junctional epithelium turnover used EMT and that this physiological process is controlled in part by WNT/BMP signaling.

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