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1.
PLoS One ; 17(1): e0261252, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35085268

RESUMO

BACKGROUND: Fluoride has become widely used in dentistry because of its effectiveness in caries control. However, evidence indicates that excessive intake interferes with the metabolic processes of different tissues. Thus, this study aimed to investigate the effects of long-term exposure to F on the parotid salivary gland of mice, from the analysis of oxidative, proteomic and genotoxic parameters. MATERIALS AND METHODS: The animals received deionized water containing 0, 10 or 50 mg/L of F, as sodium fluoride, for 60 days. After, parotid glands were collected for analysis of oxidative biochemistry, global proteomic profile, genotoxicity assessment and histopathological analyses. RESULTS: The results revealed that exposure to fluoride interfered in the biochemical homeostasis of the parotid gland, with increased levels of thiobarbituric acid reactive species and reduced glutathione in the exposed groups; as well as promoted alteration of the glandular proteomic profile in these groups, especially in structural proteins and proteins related to oxidative stress. However, genotoxic assessment demonstrated that exposure to fluoride did not interfere with DNA integrity in these concentrations and durations of exposure. Also, it was not observed histopathological alterations in parotid gland. CONCLUSIONS: Thus, our results suggest that long-term exposure to fluoride promoted modulation of the proteomic and biochemical profile in the parotid glands, without inducing damage to the genetic component. These findings reinforce the importance of rationalizing the use of fluorides to maximize their preventative effects while minimizing the environmental risks.


Assuntos
Glândula Parótida/metabolismo , Proteoma/efeitos dos fármacos , Proteômica/métodos , Fluoreto de Sódio/efeitos adversos , Animais , Regulação da Expressão Gênica/efeitos dos fármacos , Glutationa/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Camundongos , Oxirredução , Glândula Parótida/efeitos dos fármacos , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Fatores de Tempo
2.
Sleep Breath ; 26(3): 1447-1458, 2022 09.
Artigo em Inglês | MEDLINE | ID: mdl-34482502

RESUMO

PURPOSE: This review aimed to evaluate the effects of oral appliance (OA) therapy on serum inflammatory cytokines in adults diagnosed with obstructive sleep apnea (OSA). METHODS: Seven electronic databases and partial gray literature were searched without restrictions through March 2021. Articles evaluating the levels of serum inflammatory cytokines in patients with OSA after OA treatment were included. The risk of bias (RoB) was assessed using the before-and-after tool or RoB 2.0. The level of certainty was assessed using the GRADE tool. RESULTS: Five studies met the eligibility criteria. One was a randomized clinical trial (RCT), while four were non-randomized clinical trials (NRCTs). Among the studies, C-reactive protein (CRP), IL-6, IL-10, IL-1ß, and tumor necrosis factor α (TNF-α) were investigated. The RCT reported no significant differences in marker levels after 2 months of OA therapy, while the NRCTs showed improvement on CRP, TNF-α, and IL-1ß levels after longer follow-up periods. The RoB was evaluated as showing some concern in the RCT. Three NRCTs presented good RoB, and one showed a fair RoB. The level of certainty was graded as moderate quality for inflammatory marker levels assessed in the RCT The levels of certainty evaluated in NRCTs were classified as very low. CONCLUSIONS: Although limited, existing scientific evidence showed that OA therapy may improve serum cytokine levels in adults with OSA. However, short treatment periods are not effective in reducing markers of systemic inflammation which may require extended time and a decrease of in apneic events to improve.


Assuntos
Avanço Mandibular , Apneia Obstrutiva do Sono , Adulto , Biomarcadores , Proteína C-Reativa , Citocinas , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Fator de Necrose Tumoral alfa
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