Inactivation of the Odontogenic ameloblast-associated gene affects the integrity of the junctional epithelium and gingival healing

Eur Cell Mater. 2015 Sep 28:30:187-99. doi: 10.22203/ecm.v030a13.


Odontogenic ameloblast-associated (ODAM) belongs to the secretory calcium-binding phosphoprotein (SCPP) gene cluster. It is expressed by the epithelial ameloblasts during the accrued mineralisation of enamel and by cells of the junctional epithelium (JE), a specialised portion of the gingiva that plays a critical role in periodontal health. In both cases, ODAM localises at the interface between the cells and the tooth surface. It is also present among the cells of the JE, and is distinctively highly expressed in many epithelial tumours. ODAM has been proposed to be a matricellular protein implicated in the adhesion of epithelial cells to tooth surfaces, and possibly in mediating cell status. To gain further understanding of the role of ODAM, we have created an Odam knockout (KO) mouse by deleting coding exons 2-6. Inactivation of the gene was verified by Southern blot, PCR, real-time qPCR and loss of immunostaining for the protein. Young Odam KO mice showed no readily apparent phenotype. No significant differences were observed in enamel volume and density, rod-interrod organisation, and its attrition. However, in older animals, the JE presented some detachment, an increase in inflammatory infiltrate, and apical down-growth. In addition, its regeneration was delayed following a gingivectomy challenge. Our results indicate that inactivation of Odam expression has no dramatic consequence on enamel but the phenotype in older animals replicates some JE changes seen during human periodontal disease. Altogether, our results suggest that ODAM plays a role in maintaining integrity of the JE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ameloblasts / cytology*
  • Animals
  • Epithelial Attachment / cytology*
  • Epithelial Cells / cytology*
  • Gingiva / cytology
  • Mice, Knockout
  • Odontogenesis / genetics*
  • Regeneration / genetics*
  • Regeneration / physiology
  • Wound Healing*