A Proposed Mechanism for Congenitally Missing Teeth: Basic and Clinical Evidence

Abstract

Introduction: Although the development of normal dentition has been explored extensively, the mechanisms underlying congenitally missing teeth are far less understood.

The hypothesis: Congenital absence of teeth occurs due to arrested development of a tooth primordium followed by involution, only at a stages preceding mineralized tissue formation.

Evaluation of the hypothesis: We compared H & E stained serial sagittal sections of wild-type and EL mice that are congenitally missing 3rd molars (3M). 3M development was followed longitudinally in both types of mice. Occurrence of apoptosis was examined using a fluorescent TUNEL assay. To determine if a similar process might account for congenital absence of human teeth, we examined serial radiographs of developing dentitions. In EL mice, congenital absence of 3M is caused, not by a failure of initiation of tooth development rather; tooth development is initiated and subsequently arrested during early cap stage. This arrested tooth primordium is subsequently removed physiologically by apoptosis.  Examination of serial radiographs where missing teeth were identified lent further evidence to support this hypothesis. Follicle spaces, with no calcified tissue within them, were noted at early stages which were seen to remodel and eventually blend with adjacent bone. Permanent teeth failed to develop in those locations. Based on the animal and human data, we propose a new model for congenital absence of teeth. Validation of this model could have profound clinical implications. If the genetic mechanisms involved in this proposed mechanism can be elucidated, it might lead to non-surgical management of supernumerary teeth.

Key words: Tooth development; Congenital absence; Apoptosis; Tooth primordium; Mice; Human; Dental radiographs.

doi:10.5436/j.dehy.2011.2.00029