Elevated TGF-β2 signaling in dentin results in sex related enamel defects

Initiation of enamel formation requires reciprocal signaling between epithelially and mesenchymally derived cells. ive s study, we used a transgenic mouse model which drives overexpression of an activated form of TGF-β2 under control of the osteocalcin promoter, to investigate the role of TGF-β2 in the dental mesenchyme, on enamel formation. and enamel were imaged by scanning electron microscopy (SEM) and atomic force microscopy (AFM). Dentin mechanical properties were characterized for hardness and elasticity, following nanoindentation with a modified AFM. Pores found in enamel were quantified and compared using image analysis software (Scion Image™). s astic modulus of dentin was significantly reduced in the male TGF-β2 overexpressor mice as compared to male wildtype mice, with no significant differences between female mice. Similarly, there were significantly more pores in enamel of the male transgenic mice as compared to male wildtype mice, with no significant differences between female mice. In situ hybridization of the continuously erupting incisor confirmed that osteocalcin expression was limited to the odontoblast cell layer at all stages of tooth formation. sion overexpression in the dentin matrix, results in sex-linked differences in dentin and enamel formation.