RESUMO
The molar-incisor permineralização (MIH) is a qualitative enamel developing abnormality involving the occlusal and/or incisal third of one or more molars or permanent incisors, caused by systemic factors. Several systemic disorders and environmental factors, such as respiratory diseases, have been reported as probable causes of MIH. Thus, this work aimed to evaluate whether respiratory diseases and MIH are associated. The searches were carried out in electronic databases, including PubMed, Scopus, Web of Science, the Cochrane Library, LILACS, OpenGrey, and Google Scholar. The acronym PECO was used, in which the P (population) was humans in permanent dentition stage; (E-exposure) molar-incisor hypomineralization; (C-comparison) reference population and (O - outcome) respiratory diseases. After the search retrieval, the duplicates were removed, and the articles were evaluated by title and abstract; then, the papers were read and thoroughly assessed. After selection, the risk of bias assessment was performed using the Newcastle-Ottawa Scale (NOS) for observational studies. The Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) tool was used to assess the level of evidence. Three thousand six hundred and sixty six were found through the searches. After exclusion by duplicates, title, abstract, and full-reading, 13 articles remained. The articles included in this review evaluated the association of MIH with asthma, tonsilitis, pneumonia, and bronchitis. Most reports showed a low risk of bias. When exploring through GRADE, a very low level of evidence was found. We observed that the included studies showed that children with MIH had more respiratory diseases than the group that did not have MIH. Systematic review registration: https://osf.io/un76d.
RESUMO
This study aimed to investigate the effects of lead (Pb) exposure on parotid and submandibular glands through morphological aspects as well as the systemic and salivary gland redox state. Male Wistar rats were exposed to 50 mg/kg/day of Pb-acetate or distilled water by intragastric gavage for 55 days (n = 40). Blood samples were used for lipid peroxidation (LPO), glutathione (GSH), and trolox equivalent antioxidant capacity (TEAC) assays. Samples of salivary glands were analyzed by LPO, nitrites (NO), and antioxidant capacity against peroxyl radicals (ACAP) levels. Morphometric analyses (total stromal area [TSA], total parenchyma area [TPA], total ductal area [TDA], and total acinar area [TAA]) and immunohistochemistry for cytokeratin-19 (CK-19), metallothionein I/II (MT I/II), and anti-smooth muscle actin (α-SMA) were performed. The results revealed that exposure to Pb triggered systemic oxidative stress represented by lower GSH levels and increased TBARS/TEAC ratio in blood plasma. ACAP was reduced, while NO and LPO were increased in both parotid and submandibular. The morphological analyses showed increase on MT I/II expression, reduced CK-19 expression in both glands, and α-SMA reduced the immunostaining only in the parotid glands. The morphometric analyses revealed an increase in TPA in both glands, while TAA was reduced only in submandibular glands and TDA was increased only in parotid glands. Our findings are pioneer in showing that long-term exposure to Pb is able to promote blood and glandular oxidative stress associated with cellular, morphological, and biochemical damage in both parotid and submandibular glands.