THE ROLE OF PLASTICIZERS ON TOOTH DEVELOPMENTAL DEFECTS: A SCOPING REVIEW
Resumo
This review evaluated the role of plasticizers on tooth developmental defects (TDD). Six electronic databases were searched without language or date restrictions. Studies with humans and animals that evaluated the effect of any plasticizer on dental structures were considered eligible. From 1,716 studies, nine were included: eight experimental studies with rats and one case-control in humans. All studies observed TDD clinically that verified enamel opacities (n=8) and shorter incisors with blunted tips (n=1). Bisphenol A (BPA) and di-(2-ethylhexyl) phthalate (DEHP) were associated to TDD. Children of pregnant women exposed to BPA are 2.9 times more likely to have Molar Incisor Hypomineralisation (MIH); and rats exposed to BPA + fluoride presented more severe enamel defects. One article states that male rats exposed to BPA had more enamel defects during amelogenesis due to disruption of estrogen receptors; other three observed lower amounts of calcium and phosphorus from teeth of rats treated with BPA. Two papers reported that rat molar surfaces were opaque and rough in the BPA group, while another showed besides opacities, scratches, and enamel breakdown in incisors of rats exposed to DEHP. Almost of all investigated proteins and genes affected by BPA (n=7) and DEHP (n=1), and detected alterations in levels of the Enamelin, Amelogenin, Ameloblastin, and polymorphisms in H3K27me3, Klk4 and Mmp12 genes. BPA and DEHP exposure leads to enamel defects and changes in length and shape of the incisors of rats. BPA transmutes preferentially amelogenesis in male rats and may be a causative agent of MIH in humans.
Keywords: Plasticizers; Bisphenol A; Phthalic Acids; Tooth Abnormalities; Dental Enamel Hypoplasia
Resumo
Avaliou-se o papel dos plastificantes nos defeitos de desenvolvimento dentário (DDD). Estudos em humanos e animais que avaliaram o efeito de qualquer plastificante nos dentes foram elegíveis. De 1.716 estudos, nove foram incluído: oito experimentais em ratos e um caso-controle em humanos. Todos observaram DDD clinicamente (em oito, opacidades de esmalte e, em um, incisivos mais curtos com bordas rombas). Entre os plastificantes, Bisfenol A (BFA) e di(2-etilhexil)ftalato (DEHP) estavam associados com DDD. Crianças de mães expostas, na gestação, ao BFA são 2.9 vezes mais sujeitas a hipomineralização molar incisivo (HMI); já em ratos, se expostos ao BPA+fluoreto, apresentaram defeitos de esmalte (DE) mais severos. Um artigo afirmou que ratos machos expostos ao BFA têm mais DE durante a amelogênese devido à ruptura dos receptores de estrogênio; outros 3 observaram níveis menores de cálcio e fósforo nos dentes de ratos tratados com BFA. Dois manuscritos reportaram que as superfícies de molares de ratos eram opacas e rugosas no grupo BFA, enquanto outro, mostrou, além das opacidades, arranhões e quebra do esmalte em incisivos de ratos expostos ao DEHP. Quase todos investigaram proteínas e genes afetados pelo BFA (n=7) e DEHP (n=1), e detectaram alterações nos níveis de enamelina, amelogenina, ameloblastina, além de polimorfismos nos genes H3K27me3, Klk4 e Mmp12. Exposição a BFA e DEHP leva a DE e mudanças no comprimento e forma de incisivos em ratos. Além disso, o BFA altera preferencialmente a amelogênese em ratos machos e pode ser um agente etiológico de HMI em humanos.
Palavras chave: Plastificantes; Ácidos Ftálicos; Anormalidades Dentárias; Hipoplasia do Esmalte Dentário
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