The Effect of Selected Dental Materials Used in Conservative Dentistry, Endodontics, Surgery, and Orthodontics as Well as during the Periodontal Treatment on the Redox Balance in the Oral Cavity.

Oxidative stress (OS) is a redox homeostasis disorder that results in oxidation of cell components and thus disturbs cell metabolism. OS is induced by numerous internal as well as external factors. According to recent studies, dental treatment may also be one of them. The aim of our work was to assess the effect of dental treatment on the redox balance of the oral cavity. We reviewed literature available in PubMed, Medline, and Scopus databases, including the results from 2010 to 2020. Publications were searched according to the keywords: oxidative stress and dental monomers; oxidative stress and amalgam; oxidative stress and periodontitis, oxidative stress and braces, oxidative stress and titanium; oxidative stress and dental implants, oxidative stress and endodontics treatment, oxidative stress and dental treatment; and oxidative stress and dental composite. It was found that dental treatment with the use of composites, amalgams, glass-ionomers, materials for root canal filling/rinsing, orthodontic braces (made of various metal alloys), titanium implants, or whitening agents can disturb oral redox homeostasis by affecting the antioxidant barrier and increasing oxidative damage to salivary proteins, lipids, and DNA. Abnormal saliva secretion/composition was also observed in dental patients in the course of OS. It is suggested that the addition of antioxidants to dental materials or antioxidant therapy applied during dental treatment could protect the patient against harmful effects of OS in the oral cavity.

Antioxidant Defense, Oxidative Modification, and Salivary Gland Function in an Early Phase of Cerulein Pancreatitis.

Acute pancreatitis (AP) is a multifactorial disease characterized by necroinflammatory changes of the pancreas. Our study is the first study which evaluated the relationship between the free radical production, enzymatic and nonenzymatic antioxidants, oxidative damage, and secretory function of the salivary glands of AP rats. Male Wistar rats were divided equally into 2 groups: control (n = 9) and AP (n = 9). AP was induced by intraperitoneal injection with cerulein and confirmed by higher serum amylase and lipase. We have demonstrated that the superoxide dismutase and glutathione reductase activities, as well as reduced glutathione concentration, were significantly decreased in both the parotid and submandibular glands of AP rats as compared to the control rats. The production of free radicals evidenced as dichlorodihydrofluorescein assay and the activity of NADPH oxidase and xanthine oxidase and IL-1ß concentration were significantly higher in the parotid and submandibular glands of AP rats compared to the controls. In AP rats, we also showed a statistical increase in oxidation modification products (advanced glycation end products and advanced oxidation protein products), salivary amylase activity, and significant decrease in the total protein content. However, we did not show apoptosis and any morphological changes in the histological examination of the salivary glands of AP rats. To sum up, cerulein-induced AP intensifies production of oxygen free radicals, impairs the redox balance of the salivary glands, and is responsible for higher oxidative damage to these glands. Interestingly, oxidative modification of proteins and dysfunction of the antioxidant barrier are more pronounced in the submandibular glands of AP rats.

Eight-Week Consumption of High-Sucrose Diet Has a Pro-Oxidant Effect and Alters the Function of the Salivary Glands of Rats.

A high-sucrose diet (HSD) is widely known for its cariogenic effects and promotion of obesity, insulin resistance, type 2 diabetes, and cancer. However, the impact of the HSD diet on the salivary gland function as well as the level of salivary oxidative stress is still unknown and requires evaluation. Our study is the first to determine both redox balance and oxidative injury in the parotid and submandibular glands of rats fed the HSD diet compared to the control group. We have demonstrated that uric acid concentration and the activity of superoxide dismutase and peroxidase varied significantly in both the submandibular and parotid glands of HSD rats vs. the control group. However, enhanced oxidative damage to proteins, lipids, and DNA (increase in advanced glycation end products, advanced oxidation protein products, 4-hydroxynonenal, and 8-hydroxy-2'-deoxyguanosine) was observed only in the parotid glands of HSD rats. Moreover, the HSD diet also reduced the total protein content and amylase activity in both types of salivary glands and decreased the stimulated salivary flow rate. To sum up, an HSD diet reduces salivary gland function and disturbs the redox balance of the parotid as well as submandibular salivary glands. However, the parotid glands are more vulnerable to both antioxidant disturbances and oxidative damage.