Biological action of bleaching agents on tooth structure: A review.

The use of bleaching agents to remove stains is one of the main dental procedures to improve the aesthetics of teeth. This review presents the main agents used for tooth whitening, existing clinical protocols, and the structural changes that may occur through their use. The main bleaching agents consist of hydrogen peroxide and carbamide peroxide, which are used in bleaching techniques for vital teeth. These techniques can be performed in the office by a professional or by the individual in a home en-vironment under professional guidance. Bleaching agents come in a variety of concentrations and there are over-the-counter products available on the market with lower concentrations of hydrogen peroxide. Due to the chemical characteristics of the agents, changes in the organic and inorganic content of the tooth structure can be observed. These changes are related to morphological changes characterized by in-creased permeability and surface roughness, such changes compromise the mechanical resistance of the tooth. Furthermore, bleaching agents can promote molecular changes after reaching the dental pulp, resulting in oxidative stress of pulp cells and the release of pro-inflammatory mediators. Despite the bleaching effectiveness, tooth sensitivity is considered the main side effect of use. Therefore, among the heterogeneity of protocols, those that used the bleaching agent for a prolonged time and in lower con-centrations presented more harmful effects on the tooth structure.

Prolonged exposure to high fluoride levels during adolescence to adulthood elicits molecular, morphological, and functional impairments in the hippocampus.

Fluoride is added to water due to its anticariogenic activity. However, due to its natural presence in soils and reservoirs at high levels, it could be a potential environmental toxicant. This study investigated whether prolonged exposure to fluoride from adolescence to adulthood-at concentrations commonly found in artificially fluoridated water and in fluorosis endemic areas-is associated with memory and learning impairments in mice, and assessed the molecular and morphological aspects involved. For this endeavor, 21-days-old mice received 10 or 50 mg/L of fluoride in drinking water for 60 days and the results indicated that the increased plasma fluoride bioavailability was associated with the triggering of short- and long-term memory impairments after high F concentration levels. These changes were associated with modulation of the hippocampal proteomic profile, especially of proteins related to synaptic communication, and a neurodegenerative pattern in the CA3 and DG. From a translational perspective, our data provide evidence of potential molecular targets of fluoride neurotoxicity in the hippocampus at levels much higher than that in artificially fluoridated water and reinforce the safety of exposure to low concentrations of fluoride. In conclusion, prolonged exposure to the optimum fluoride level of artificially fluoridated water was not associated with cognitive impairments, while a higher concentration associated with fluorosis triggered memory and learning deficits, associated with a neuronal density reduction in the hippocampus.

Physical Exercise Mitigates Salivary Gland and Saliva Damages in Rats Exposed to Binge-like Ethanol Pattern.

Heavy episodic ethanol (EtOH) consumption is a typical pattern, especially among younger people. The therapeutic effect of exercise on EtOH damage has not yet been fully elucidated. Therefore, this study aims to investigate whether moderate exercise can reduce the damage generated by ethanol consumption in salivary glands and saliva. Thus, 32 male Wistar rats were divided into four groups: control (sedentary animals treated with water); training (trained animals treated with EtOH); EtOH (sedentary animals treated with EtOH); and EtOH + training (trained animals treated with ethanol). EtOH was administered to the animals at a dose of 3 g/kg/day at a concentration of 20% w/v for three consecutive days per week via intragastric gavage. The training was performed on a treadmill for five successive days. At the end of the 4-week experimental protocol, the animals were euthanized, and salivary glands and saliva were collected for oxidative biochemistry analysis. Our results showed that EtOH consumption generated changes in the oxidative biochemistry of the salivary glands and saliva. Thus, it was possible to conclude that moderate physical exercise can significantly recover antioxidant activity, reducing the damage generated by EtOH.

One binge-type cycle of alcohol plus ketamine exposure induces emotional-like disorders associated with oxidative damage in adolescent female rats.

Drug abuse is a global public health problem among adolescents, with alcohol often used in association with other psychotropic drugs, such as ketamine. Considering the scarcity of evidence, this study aimed to investigate emotional behavioral effects induced by ethanol plus ketamine co-abuse, as well as oxidative biochemistry, and neurotrophic mediator in the prefrontal cortex and hippocampus in the early withdrawal of adolescent female rats. Animals were divided into control, ethanol, ketamine, and ethanol plus ketamine groups. The protocol administration was performed for 3 consecutive days (binge-like pattern). Behavioral assays of open field, elevated plus maze, and forced swim test were performed. After that, the prefrontal cortex and hippocampus were collected to evaluate oxidative biochemistry (reactive oxygen species-ROS; Antioxidant capacity against peroxyl radicals-ACAP; and lipid peroxidation). We found that isolated or combined ethanol and ketamine exposure displayed anxiety- and depressive-like profile, in a non-synergistically manner during early withdrawal. However, oxidative damage was aggravated in the co-administered animals than in isolated exposed subjects. We concluded that ethanol plus ketamine co-abuse may intensify oxidative damage in the hippocampus and prefrontal cortex in the early withdrawal of adolescent female rats, which was not reflected in the emotional behavioral phenotype. DATA AVAILABILITY STATEMENT: The datasets used and/or analyzed during the current investigation are available upon reasonable request from the corresponding author.

Exposure to tolerable concentrations of aluminum triggers systemic and local oxidative stress and global proteomic modulation in the spinal cord of rats.

The tolerable aluminum (Al) intake levels for humans are constantly under review by regulatory agencies due to novel pre-clinical evidence on the neurotoxicity of prolonged Al exposure; however, little is known about the effects of Al on the spinal cord. This study aimed to investigate potential adverse effects on both spinal cord and systemic biochemical balance after prolonged exposure to a low dose of Al. Twenty adult rats were distributed in the control (distilled water) and exposed group (8.3 mg of AlCl3/kg/day). After 60 days, both blood and spinal cord samples were collected for oxidative stress and proteomic analyses. In plasma and erythrocytes, glutathione level was not different between groups; however, exposure to AlCl3 significantly decreased glutathione level in the spinal cord. Thiobarbituric acid reactive substances levels in the plasma and spinal cord of animals from the control group were significantly lower than those animals exposed to AlCl3. Exposure to AlCl3 significantly modulated the expression of proteins associated with the cell cycle, stimulus-response, cytoskeleton, nervous system regulation, protein activity, and synaptic signaling. Therefore, prolonged exposure to a low dose of Al triggered oxidative stress and proteomic changes that may affect spinal cord homeostasis.

Global Scientific Research Landscape on Aluminum Toxicology.

This study aimed to identify the landscape of current aluminum toxicity based on knowledge mapping of the 100 most-cited articles on toxicological aspects of aluminum in biological organisms. The research was searched in the Web of Science Core Collection (WoS-CC) with publications between 1945 and 2022. Data regarding authorship, title, journal, year of publication, citation count, country, keywords, study design, and research hotspots were extracted and all elected articles were analyzed. Our results showed that among the articles selected, literature review and in vivo studies were the most common study designs. The USA and England were found as the countries with most publications. Alzheimer's disease (AD), aluminum, and neurotoxicity were found as the most frequent keywords. The articles most cited in world literature suggested that aluminum exposure is associated with Alzheimer's disease, Parkinson's disease (PD), dialysis encephalopathy, amyotrophic lateral sclerosis, neurodegeneration changes, cognitive impairment, such as bone damage, oxidative alterations, and cytotoxicity.

Effects of Photobiomodulation on Oral Mucositis: Visualization and Analysis of Knowledge.

This review article mapped and analyzed the most cited articles on the association of photobiomodulation (PBM) with oral mucositis (OM) and the evolution of clinical protocols in the area. A comprehensive search was performed on the Web of Science Core Collection (WoS-CC) database, leading to the extraction of information such as title, authors, abstract, journal name, number, average of citations, study design, year of publication, institutions, continents, countries, type of laser used, irradiated anatomical points, primary anti-cancer therapy, and laser parameters. Among those, clinical trials and literature reviews were the most common study designs. The main type of laser used was the InGaAlP diode, with a wavelength ranging from 630-660 nm, power going in 40-100 mW, and energy density ranging from 0.375-22 J/cm2. As for the anatomical sites irradiated by PBM, the cheek mucosa, upper and lower lips, lateral tongue, and bottom of the mouth stood out. This analysis highlights an increasing interest in PBM as a supportive treatment in cases of OM, as well as the evolution of the technique, types of laser devices, and protocols used.

Treatment for dental erosion: a systematic review of in vitro studies.

Background: Dental erosion is a chemical loss of the mineralized dental tissue caused by exposure to nonbacterial acids. Different treatment protocols have been adopted with the use of fluoride compounds to promote the formation of a layer of mineral precipitation in eroded lesions. Aim: This systematic review aimed to evaluate the main treatments for dental erosion. Methodology: This study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and recorded in the Open Science Framework database (OSF) under DOI 10.17605/OSF.IO/XMFNZ. The searches were conducted in six electronic databases (Pubmed, Embase, Web of Science, Cochrane, Scopus, Lilacs) and two grey literature sources (Google Scholar and OpenGrey). The eligibility criteria included in vitro studies that evaluated eroded teeth under treatment with some topical agent. Risk of bias assessment and qualitative synthesis were performed using the Cochrane collaboration's tool for assessing risk of bias modified for in vitro studies. Results: A total of 522 studies were identified, and only four studies that fulfilled our eligibility criteria were included in this review. Among these studies, three were considered to have a low risk of bias, and one to have a high risk of bias. Two studies evaluated the anti-erosion effect of fluoride toothpaste, and the other two assessed the action of casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) on the surface of human teeth. Among the products analyzed, CPP-ACP was the only one that promoted a significant increase in enamel microhardness and reduced tooth wear. Conclusion: Based on the in vitro studies included in this review, there was no anti-erosion effect after using different fluoride toothpaste. However, it should be considered that one of these studies presented a high risk of bias. On the other hand, studies with CPP-ACP showed anti-erosion efficacy when applied before or after erosive wear.

Global Proteomic Profile of Aluminum-Induced Hippocampal Impairments in Rats: Are Low Doses of Aluminum Really Safe?

Hippocampus is the brain area where aluminum (Al) accumulates in abundance and is widely associated with learning and memory. In the present study, we evaluate behavioral, tissue, and proteomic changes in the hippocampus of Wistar rats caused by exposure to doses that mimic human consumption of aluminum chloride (AlCl3) in urban areas. For this, male Wistar rats were divided into two groups: Control (distilled water) and AlCl3 (8.3 mg/kg/day), both groups were exposed orally for 60 days. After the Al exposure protocol, cognitive functions were assessed by the Water maze test, followed by a collection for analysis of the global proteomic profile of the hippocampus by mass spectrometry. Aside from proteomic analysis, we performed a histological analysis of the hippocampus, to the determination of cell body density by cresyl violet staining in Cornu Ammonis fields (CA) 1 and 3, and hilus regions. Our results indicated that exposure to low doses of aluminum chloride triggered a decreased cognitive performance in learning and memory, being associated with the deregulation of proteins expression, mainly those related to the regulation of the cytoskeleton, cellular metabolism, mitochondrial activity, redox regulation, nervous system regulation, and synaptic signaling, reduced cell body density in CA1, CA3, and hilus.

Deciphering the Global Proteomic Profile Involved in Methylmercury-Induced Cerebellar Neurodegeneration and Motor Dysfunction in Adult Rats.

Mercury is a ubiquitous pollutant in the environment with potential neurotoxic effects. Several populations are susceptible to mercurial exposure, especially methylmercury (MeHg) at low doses for long periods through food consumption. Given this, the present work aimed to assess the effects of long-term MeHg exposure on the cerebellum of rats from a translational perspective using a representative dose, assessing molecular, biochemical, morphological, and behavioral parameters. The model was produced by administering 40 µg/kg of MeHg for 60 days to adult male Wistar rats by oral gavage. As a result of this exposure, the animals presented motor deficits in open field and rotarod tests which were associated with an increase in total mercury content in cerebellar parenchyma, a reduction in antioxidant competence against peroxyl radicals, and increased nitrite and lipid peroxidation levels. The proteomic approach showed 317 modulated proteins. Such findings were associated with reductions in mature neuron and Purkinje cell densities and glial fibrillary acidic protein immunostained areas and increased microglial density. In addition, decreases in myelin basic protein and synaptophysin immunostaining were also observed. The results thus provided new evidence of the mechanisms underlying complex MeHg-induced neurodegeneration, especially the proteins underlying the biochemical and morphological features associated with motor dysfunction.

Intrauterine and Postnatal Exposure to High Levels of Fluoride Is Associated with Motor Impairments, Oxidative Stress, and Morphological Damage in the Cerebellum of Offspring Rats.

Fluoride (F) is abundantly present on Earth and plays a beneficial role in human health. However, exposure to high doses of F can be a risk, mainly in endemic fluorosis regions. In light of this, we investigated the effects of F exposure during the intrauterine and postnatal periods of rats, in doses similar to those recommended in drinking water and the levels of F in regions with endemic fluorosis, on the offspring rats' cerebellum. Pregnant rats were divided into three groups: control (received ultrapure water only), 10 mg F/L, and 50 mg F/L for a period of 42 days (21 days gestation and 21 days lactation). At the end of the lactation period, the male pups were evaluated by behavioral tests, morphological markers, and biochemistry assays. The results pointed out that 50 mg F/L exposure during the intrauterine and lactational period of rats is capable of promoting oxidative stress in the cerebellum with a decrease in Purkinje cell density and myelin basic protein compromise, which could be associated with functional motor impairments. In addition, although 10 mg F/L exposure promoted redox alterations, it did not affect other parameters evaluated, highlighting the safe use of F in low doses.

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study.

The environmental contamination by methylmercury (MeHg) is a major concern for public health. The effects of MeHg in the central nervous system (CNS) of adult animals have been extensively investigated; however, little is known about the effects of MeHg exposure during intrauterine and lactation periods on motor and cognitive functions of adolescent rats. Therefore, this study aimed to investigate the effect of MeHg exposure during intrauterine life and lactation on both motor and cognitive functions of offspring rats. Ten female Wistar rats were exposed to 40 µg/kg/day of MeHg through cookie treats from the first day of pregnancy until the last day of breastfeeding. Both motor and cognitive functions of offspring male rats were assessed by open field, rotarod, and step-down inhibitory avoidance tests. Forty-one days after birth, the hippocampus and cerebellum were collected to determine total Hg content, antioxidant capacity against peroxyl radicals (ACAP), reduced glutathione (GSH) levels, lipid peroxidation (LPO), and nitrite levels. MeHg exposure during CNS development increased Hg levels in both hippocampal and cerebellar parenchymas, triggered oxidative stress throughout ACAP and GSH decrease, increased LPO and nitrite levels. These alterations resulted in reduced spontaneous and stimulated locomotion and short- and long-term memory deficits. Therefore, damages triggered by MeHg exposure during intrauterine life and lactation had detrimental effects on oxidative biochemistry and motor and cognitive functions of offspring rats.

Salivary Glands after Prolonged Aluminum Exposure: Proteomic Approach Underlying Biochemical and Morphological Impairments in Rats.

Aluminum (Al) is one of the most abundant elements on Earth, and its high extraction rate and industrial use make human exposure very common. As Al may be a human toxicant, it is important to investigate the effects of Al exposure, mainly at low doses and for prolonged periods, by simulating human exposure. This work aimed to study the effects of low-dose exposure to chloride aluminum (AlCl3) on the oxidative biochemistry, proteomic profile, and morphology of the major salivary glands. Wistar male rats were exposed to 8.3 mg/kg/day of AlCl3 via intragastric gavage for 60 days. Then, the parotid and submandibular glands were subjected to biochemical assays, proteomic evaluation, and histological analysis. Al caused oxidative imbalance in both salivary glands. Dysregulation of protein expression, mainly of those related to cytoarchitecture, energy metabolism and glandular function, was detected in both salivary glands. Al also promoted histological alterations, such as acinar atrophy and an increase in parenchymal tissue. Prolonged exposure to Al, even at low doses, was able to modulate molecular alterations associated with morphological impairments in the salivary glands of rats. From this perspective, prolonged Al exposure may be a risk to exposed populations and their oral health.

DNA Damage and Proteomic Profile Changes in Rat Salivary Glands After Chronic Exposure to Inorganic Mercury.

Mercury (Hg) is a toxic metal that became a public health problem due to environmental contamination caused by anthropogenic activity. In this sense, oral homeostasis can undergo changes due to the toxic effects of metal on the salivary glands. Therefore, our objective was to investigate the proteomic and genotoxic changes in salivary glands after exposure to inorganic mercury (IHg). Forty Wistar rats that were divided into a control group, which received distilled water, and an exposed group, which received 0.375 mg/kg of mercury chloride for 45 days via orogastric gavage. After that, the animals were euthanized, and the parotid and submandibular glands were collected for analysis of the genotoxic effects, using the comet assay and proteome global profile assessment. The results showed that IHg promoted damage to cellular DNA associated with proteomic changes that showed events such as oxidative stress, mitochondrial dysfunction, changes in the cytoskeleton, and apoptosis. Therefore, these findings show a profile of molecular changes due to the interactions of IHg with several proteins and mechanisms inherent to the cell, which consequently may result in dysfunction of the salivary glands and impaired homeostasis of the oral cavity.

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.

Effects of Fluoride on Submandibular Glands of Mice: Changes in Oxidative Biochemistry, Proteomic Profile, and Genotoxicity.

Although fluoride (F) is well-known to prevent dental caries, changes in cell processes in different tissues have been associated with its excessive exposure. Thus, this study aimed to evaluate the effects of F exposure on biochemical, proteomic, and genotoxic parameters of submandibular glands. Twenty one old rats (n = 30) were allocated into three groups: 60 days administration of drinking water containing 10 mgF/L, 50 mgF/L, or only deionized water (control). The submandibular glands were collected for oxidative biochemistry, protein expression profile, and genotoxic potential analyses. The results showed that both F concentrations increased the levels of thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH) and changed the proteomic profile, mainly regarding the cytoskeleton and cellular activity. Only the exposure to 50 mgF/L induced significant changes in DNA integrity. These findings reinforce the importance of continuous monitoring of F concentration in drinking water and the need for strategies to minimize F intake from other sources to obtain maximum preventive/therapeutic effects and avoid potential adverse effects.

Is There Any Association Between Chronic Periodontitis and Anxiety in Adults? A Systematic Review.

Periodontitis is a multifactorial disease triggered by dysbiotic biofilms, involving the host's immune response, systemic and behavioral factors, including psychosocial conditions. This systematic review aimed to investigate the possible association between periodontitis and anxiety in adults. Searches were performed in PubMed, Scopus, Web of Science, Lilacs, Cochrane, and OpenGrey databases, without language restrictions, considering studies in adults (P-Participants), with (E-Exposure) and without periodontitis (C- Comparison) in an outcome of association with anxiety (O-outcome). Methodological quality assessment was carried out using the Newcastle-Ottawa protocol for case-control and cross-sectional studies, followed by an analysis of the level of evidence using the GRADE tool. Metanalysis was not performed due to several differences in methods applied by authors in primary studies. Eleven observational studies were selected according to the inclusion criteria from the total of 6,380 studies retrieved from databases. Eight studies demonstrated higher anxiety levels in subjects with periodontitis, among which only one study presented a high risk of bias. The GRADE tool revealed a low level of evidence for the anxiety outcome measured by the State-Trait Anxiety Inventory (STAI), both for case-control and cross-sectional studies. However, since anxiety may affect the quality of life of many subjects, it reinforces the need for further studies that evaluate this association for more extended periods. Clinical Trial Registration:PROSPERO-CRD42020190445.

Salivary parameters alterations after early exposure to environmental methylmercury: A preclinical study in offspring rats.

BACKGROUND: Methylmercury (MeHg) is still considered a global pollutant of major concern; thus, it becomes relevant to investigate and validate alternative diagnostic methods to track early-life human exposure. This study aimed to evaluate the salivary parameters and to characterize potential mechanisms of oxidative damage on the salivary glands (SG) of offspring rats after pre- and postnatal environmental-experimental MeHg exposure. METHODS: Pregnant Wistar rats were daily exposed to 40 µg/kg MeHg during both gestational and lactation periods. Then, the saliva of offspring rats was analyzed in terms of flow rate, amylase activity, and total protein concentration. The SG of the offspring rats were dissected to perform the oxidative biochemistry analyses of antioxidant capacity against peroxyl radicals (ACAP), lipid peroxidation (LPO), and nitrite levels. RESULTS: Exposure to MeHg significantly decreased the ACAP, increased LPO and nitrite levels, decreased salivary flow rate, amylase activity, and total protein concentration. CONCLUSION: Saliva analyses can predict damages induced by early-life MeHg exposure and may be used as an auxiliary diagnostic method.

Lead exposure and its association with neurological damage: systematic review and meta-analysis.

Lead (Pb) is one of the most toxic and abundant elements in the earth's crust, which is pointed out that the intoxication caused by it may damage biological systems. This systematic review with meta-analysis aimed to evaluate the association between Pb exposure and neurological damage. This work was executed according to PRISMA guidelines, and seven online databases were consulted. Based on the PECO strategy, studies presenting humans as participants (populations) exposed to Pb (exposure) compared to non-exposed to Pb (control) evaluating the neurological impairment (outcome) were included. The quality and risk of bias were verified by Fowkes and Fulton checklist. Two meta-analyses were conducted considering Digit Symbol and Profile Mood tests. The certainty of the evidence was evaluated with the GRADE tool. This review identified 2019 studies, of which 12 were eligible according to the inclusion criteria. Eight were considered with a low risk of bias. All the studies elected showed that exposure to Pb is associated with neurological damage, but the meta-analysis did not show any difference for the evaluated tests, and the certainty of the evidence was considered very low. Nevertheless, the included studies showed that Pb occupational exposure is associated with neurological damage, and the main parameters evaluated for possible neurological damage were related to mnemonic aspects, reaction time, intelligence, attention disorders, and mood changes. Thus, our results revealed that a definitive demonstration of an association of Pb and neurological changes in humans is still a pending issue. Future studies should take into consideration more confident methods to answer this question.

Imaging Microstructural Damage and Alveolar Bone Loss in Rats Systemically Exposed to Methylmercury: First Experimental Evidence.

The alveolar bone is an important mineralized structure of the periodontal support apparatus, and information about the methylmercury (MeHg) effects on the structural integrity is scarce. Therefore, this study aimed to investigate whether systemic, chronic, and low-dose exposure to MeHg can change the alveolar bone microstructure of rats. Adult Wistar rats (n = 30) were exposed to 0.04 mg/kg/day of MeHg or vehicle through intragastric gavage. The animals were euthanized after 60 days, and blood samples were collected for trolox equivalent antioxidant capacity (TEAC), glutathione (GSH), lipid peroxidation (LPO), and comet assays. The mandible of each animal was collected and separated into hemimandibles that were used to determine the total Hg level in the bone and to analyze microstructural damage and alveolar bone loss in terms of trabecular number (Tb.N), trabecular thickness (Tb.Th), bone volume fraction (BV/TV), and exposed root area of the second molars. MeHg exposure triggered oxidative stress in blood represented by lower levels of GSH and TEAC and the increase in LPO and DNA damage of the blood cells. High total Hg levels were found in the alveolar bone, and the microstructural analyses showed a reduction in Tb.N, Tb.Th, and BV/TV, which resulted in an increase in the exposed root area and a decrease in bone height. Long-term MeHg exposure promotes a systemic redox imbalance associated with microstructural changes and alveolar bone loss and may indicate a potential risk indicator for periodontal diseases.