In utero exposure to TCDD on tooth development in mice

Objectives: To evaluate the effects of 2,3,7,8- tetrachlorodibenzo -p-dioxin (TCDD) at low exposure levels in utero on tooth development, and to investigate the expression of aryl hydrocarbon receptor (AHR) on different stages during development of tooth germ in mice with or without exposure to TCDD. Methods: Confirmed pregnant mice were divided in two groups randomly, TCDD exposure and control groups with 12 mice each. Mice in TCDD group received TCDD via oral gavage at dose of 25ìg/kg on day 11 and 13 of gestation. Control animals were dosed similarly with corn oil vehicle. On 14, 18, 20 of gestational day (GD14, GD18, GD20) and post-natal 1 (PD1), pregnant mice were sacrificed respectively and the embryos were collected. The jaws of pups with tooth germs were fixed and sectioned for histological examination. The expressions of AHR of the tooth germs were observed by a standard indirect immunoperoxidase localization technique. Results: The growth bodyweight of the pregnant mice in TCDD exposure group was lower than the control group. In TCDD exposure group, the sizes of tooth germs were smaller, the tooth germ development delayed, the number of cells decreased, and the differentiation degrees were weaker than in the control group. The temporal and spatial patterns of AHR expression in TCDD exposure group were similar to control group. The expression intension of AHR in TCDD group was higher than in the control (GD18:125.28 ±10.22vs136.94±9.44, P<0.01; GD20: 154.47±9.34vs175.75±6.98, P<0.01; PD1: 142.36±7.15vs159.57±9.27, P<0.01). Conclusions: Prenatally TCDD exposure may interrupt normal development of tooth germ. The toxic effect of TCDD exposure in utero to development of tooth germ may be mediated by AHR.