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Background: Adverse long-term general and dental health effects of cancer and cancer therapy during childhood have been reported., Aim: To examine the association between chemotherapy before the age of 8 years and (1): microdontia; (2): hypodontia of premolars and permanent molars., Material and Methods: In The Danish Registry of Childhood Cancer (DBCR), we identified 203 children who met the following inclusion criteria: (1) age below 8 years at the start of treatment; (2) age between 12 to 18 years upon dental examination; (3) had received chemotherapy The exclusion criterion was radiotherapy to the head and neck. A total of 150 children fulfilled the inclusion criteria. As controls, a random sample of 193 age-matched unexposed children was included., Results: Microdontia was found in a total of 88 teeth in 29 (19.3%) of the 150 children who had been exposed to chemotherapy, while none of the controls had microdontia of premolars or permanent molars (difference: 19.3%; 95% CL: 13.5%; 26.4%). The earlier the exposure, the more frequent was microdontia. We found a total of 27 missing premolars and permanent molars in 14 (9.3%) of the exposed children and a total of 18 missing premolars and permanent molars in 8 (4.1%) of the controls (difference: 5.2%; 95% CL: -0.1%; 11.3%)., Conclusion: The present study confirms findings from previous studies that chemotherapy, especially in very young children, causes microdontia and hypodontia of premolars and permanent molars., (© 2011 The Authors. International Journal of Paediatric Dentistry © 2011 BSPD, IAPD and Blackwell Publishing Ltd.)

Objective: We evaluated the effects of different levels of the potent environmental toxicant and teratogen, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on molar development in mice in six inbred strains, all with TCDD responsive Ahr alleles., Design: Pregnant females were exposed on gestation day 13 to 4 different levels of TCDD (control, 0.01, 0.1 and 1.0 microg/kg) and their offspring were examined for the frequency of missing third molars (M3s) and for differences in first mandibular molar (M1) cuspal morphology., Results: Missing M3s were prevalent only in mice in two strains, C3H/HeJ and CBA/J, and their frequency significantly increased with increasing TCDD exposure. The frequency of the M1 variant was high in mice in only one strain, C57BL/10J, and was significantly higher in the treated compared with the control group., Conclusions: Inbred mice strains exhibited differential responses to TCDD suggesting that there is a genetic component, beyond Ahr differences, mediating the effects of TCDD on molar development.