Association between Molecular Mechanisms and Tooth Eruption in Children with Obesity

Abstract

Different works have reported earlier permanent teething in obese/overweight children compared to control ones. In contrast, others have reported a delayed permanent teething in undernutrition/underweight children compared to control one. It has been reported that becoming overweight or suffering from obesity can increase gingival pro-inflammatory drive and can affect orthodontic treatment (among other complications). In this sense, little is known about the molecular mechanisms affecting dental eruption timing. Leptin and adiponectin are adipocytokines signaling molecules released in overweight and underweight conditions, respectively. These adipocytokines can modulate osteocyte, odontoblast, and cementoblast activity, even regulating dental lamina initiation. The present review focuses on the molecular approach wherein leptin and adiponectin act as modulators of Runt-related transcription factor 2 (Runx 2) gene regulating dental eruption timing.

Keywords: dentition; leptin; pediatric obesity; permanent; tooth eruption.

Figure 1

Under obesity/overweight conditions, early permanent teeth eruption would be explained by increased leptin levels that decrease runt-related transcription factor 2 (Runx 2) expression increasing Wnt gene expression, receptor activator of NF kappa-b (RANK-L), and TNF-α. In underweight conditions, delayed permanent tooth eruption would be explained by increased adiponectin levels or decreased adiponectin. This promotes Runx 2 expression resulting in Wnt reduced expression and decreased pro-inflammatory RANK-L and TNF-α.

Figure 2

Relationship between obesity and non-molecular factors [3,4,5,8,61,62,63,64,65,66,67,68].