Maternal methylmercury exposure during early-life periods adversely affects mature enamel structure of offspring rats at human exposure levels: a concern for oral health.

Although there are many studies on the health effects of methylmercury (MeHg) toxicity during in utero and early development, little is known about its effects on mineralized tissues present in the oral cavity, such as enamel structure. Therefore, this study evaluated the effects of MeHg exposure on the physico-chemical, ultrastructural and functional properties of mature tooth enamel. Specifically, we studied offspring of mothers exposed to MeHg during the prenatal and postnatal periods which are the developmental stages associated with tooth enamel formation. Female rats were exposed to MeHg at a dose of 40 µg/kg/day for 42 days of pregnancy and lactation. The enamel of offspring was analyzed by (1) Fourier Transform Infrared Spectroscopy and Raman to assess physicochemical composition, (2) Scanning Electron Microscopy for ultrastructural evaluation, (3) Transmitted Polarizing Light Microscopy for analysis of the enamel extracellular matrix, and (4) resistance and hardness were evaluated by microhardness. The results showed that MeHg exposure during this sensitive enamel formation period induced changes in inorganic and organic content and enamel prisms ultrastructure alterations and disturbed the organic extracellular matrix due to a decreased enamel strength. These novel findings establish for the first time that maternal exposure to MeHg pre and postnatal promoted relevant changes in mature enamel of their offspring rats.

In utero and lactational exposure to methylmercury elicits physical-chemical and morphological damages in the alveolar bone of offspring rats: The first toxicological findings.

Methylmercury (MeHg) is the most common organic form of mercury (Hg) that humans are exposed and is considered an environmental pollutant. Several populations that live in endemic regions of MeHg exposure are subject to the toxicant for long periods, including pregnant women and children, causing damage to several organs during early periods of development. Alveolar bone is an essential structure for the oral cavity, responsible for supporting teeth and masticatory forces. However, evidence on the effects of MeHg on alveolar bone and the intrauterine and lactation period is lacking. Thus, this study aimed to investigate the effects of MeHg exposure during gestation and lactation on the developing alveolar bone of offspring rats after maternal exposure. Dams were exposed during 41 days of pregnancy and lactation, and the mandibles of the offspring were collected. The alveolar bone was analyzed by Fourier Transform Infrared Spectroscopy to evaluate the physicochemical composition; by Scanning Electron Microscopy for ultrastructural evaluation; by histopathological, histochemical, and morphometric for tissue analyses. In addition, bone quality was assessed by X-ray microtomography. MeHg exposure altered the mineral composition and caused histological damage associated with a lower quantity and thickness of bone trabeculae, as well as reduced osteocyte density and collagen fiber content. A reduction in trabecular thickness and bone volume and an increase in trabecular spaces were observed and were associated with anatomical compromise of the vertical bone dimensions. Thus, the results suggest that the developing alveolar bone is susceptible to the toxic effects of MeHg when organisms are exposed during intrauterine and lactation periods. From a translational perspective, these changes in the alveolar bone can help us understand possible abnormalities induced by toxic metals and highlight the need for care for structures other than those already seen as targets for damage triggered by environmental MeHg exposure.

Effects of inorganic mercury exposure in the alveolar bone of rats: an approach of qualitative and morphological aspects.

BACKGROUND: In comparison to organic mercury (MeHg), the environmental inorganic mercury (IHg) can be found in some skin-lightening cosmestics were considered "harmless" for a long time. However, recent studies have shown that long-term exposure to low doses of IHg may affect biological systems. Therefore, this study investigated the effects of IHg long-term exposure to the alveolar bone of adult rats. METHODS: Adult Wistar rats were distributed in control and HgCl2 exposed (0.375 mg/kg/day). After 45 days, the rats were euthanized and both blood and hemimandibles were collected. Total blood Hg levels were measured and both inorganic and organic components of the alveolar bone were determined through XRD and ATR-FTIR. The microstructure of the alveolar bone was assessed by using micro-CT and the morphometric analysis was performed by using stereomicroscopy. RESULTS: Alterations in the physicochemical components of the alveolar bone of exposed animals were observed. The bone changes represented a tissue reaction at the microstructural level, such as bone volume increase. However, no significant dimensional changes (bone height) were observed. CONCLUSION: Exposure to IHg at this dose can promote microstructural changes and alteration in the organic and inorganic components in the alveolar bone.

Chronic exposure to lead acetate promotes changes in the alveolar bone of rats: microstructural and physical-chemical characterization.

There are a few data relating to the effects of lead (Pb) exposure on the alveolar bone, which has very distinct morphophysiological characteristics and is of great importance in the oral cavity. In this context, the aim of this study was to investigate the changes promoted after long-term exposure to Pb in the microstructure of the alveolar bone of rats. Twenty adult Wistar rats were exposed to 50 mg/kg/day of lead acetate for 55 days. These animals were euthanized and had their mandible removed. Each mandible was divided into hemimandibles, and the alveolar bone was used for bone lead quantification, crystallinity analysis, microstructure evaluation by the percentage of bone volume (BV/TV), number of trabeculae (Tb.N), thickness of the trabecular (Tb.Th), and trabecular space (Tb.Sp). Morphometric analysis of the exposed root area was also performed. Long-term exposure to Pb resulted in high levels of Pb in the alveolar bone but showed no changes in the organization of crystallinity. The microstructural analyses showed a reduction of BV/TV, Tb.Th, and Tb.N and increase of Tb.Sp parameters, resulting in an increase in the exposed root area and an alveolar bone loss in height. The findings of this study reveal the ability of Pb to alter the alveolar bone microstructure after long-term exposure to the metal, possibly due to changes in tissue homeostasis, contributing to the reduction of bone quality.

Long-term exposure to low doses of aluminum affects mineral content and microarchitecture of rats alveolar bone.

Aluminum (Al) is one of the most found elements in nature in many forms, and human exposure can be quite common. Therefore, it is important to investigate the effects of exposure to Al mainly at low doses and for a prolonged period, in order to simulate human exposure in the periodontium, an important structure for support and protection of the teeth. This investigation aimed to study the aluminum chloride (AlCl3) toxicological effects in the mineral composition and micromorphology of the alveolar bone of rats. Two groups of eight male Wistar rats were used for the experiment. AlCl3 group was exposed to AlCl3 orally at a dose of 8.3 mg/kg/day for 60 days, while the control group received only distilled water. After that, the mandibles were collected and submitted to the following analyses: Fourier transform infrared spectroscopy, Raman spectroscopy, and X-ray microtomography analysis; blood was also collected for determination of Al circulating levels. Our data showed that AlCl3 was capable of increasing Al circulating levels in blood. It was able to promote changes in the mineral content and triggers significant changes in the mineralized bone microstructure, such as number and thickness of trabeculae, being associated with alveolar bone-loss.