CLDN16 and Hypercalciuria: We also evaluated the expression of Cldn16 and Cldn19, since their crucial role in ameloblast tight-junction formation has been recently indicated; their mutation causing familial hypomagnesaemia with hypercalciuria and nephrocalcinosis and amelogenesis imperfecta (Bardet et al., 2016; Yamaguti et al., 2017).