# Membrane Fluidity and Oxidative Stress in Patients with Periodontitis
###### Abstract  
Periodontitis leads to the destruction of dental tissue through polymicrobial interactions, inflammation, and increased oxidative stress. The aim of this study was to measure the levels of nitrates (NO3 ), malondialdehydedehyde (MDA), and membranal fluidity (MF) in the gingival tissue of subjects with or without periodontitis. A total of 120 participants from the Dentistry School of the University of Guadalajara were investigated. The study was approved by the ethics committee of our institution, with the registration number of CI-01221. The clinical parameters measured were probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BoP). NO3  was measured using the Greiss reaction, while MDA was determined colorimetrically with the FR12 Kit (Oxford Biomedical Research). Membrane fluidity (MF) was measured using the quotient \(le/lm\) according to the method of [PERSON] and collaborators. The Student \(t\)-test, Spearman correlation, and chi-square are used to calculate the results. The results showed higher levels of PD, CAL, and BoP in patients. There was a positive correlation between MF and PD. Moreover, MDA was positively correlated with PD and CAL. Increases in PD resulted in higher levels of NO3, MDA, and MF. Similarly, increases in CAL resulted in higher levels of MDA and MF in patients. We conclude that PD and CAL facilitated the progression of periodontitis through increases in MDA and MF.  
periodontitis; oxidative stress; nitrates; lipoperoxide; membrane fluidity; dentistry; periodontology +
Footnote †: journal: Applied Sciences  
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Footnote 13: email: _  
inflammatory cytokines stimulates the production of nitric oxide (NO), and its interaction with O\({}_{2}\)\({}^{-}\) releases the peroxinitrite radical (ONOO\({}^{-}\)). This chemical reaction releases NO\({}_{3}\)\({}^{-}\), nitrites (NO\({}_{2}\)\({}^{-}\)), and OH\({}^{-}\). Previous studies have shown that high concentrations of NO and NO\({}_{3}\)\({}^{-}\) were associated with the development of severe periodontitis [7, 8]. Recent data indicate that periodontal damage disrupts the oxidative/antioxidant equilibrium [9, 10, 11, 12], affecting the increase in lipoperoxide levels [9, 11]. [PERSON] and collaborators (2022) report high levels of MDA in patients with gingival inflammation [10]; this increase is also reported in the clinical trial by [PERSON] (2022), which included patients with stage II periodontitis [12]. Peroxidation stimulates a greater activity of lipoxygenases (type 5), which are responsible for oxidizing membrane phospholipids. This leads to a rearrangement of the periodontal membrane. This phenomenon decreases the thickness of the membrane, and generates changes in membrane fluidity and permeability, leading to tissue damage which may result in apoptosis [9, 13]. It has been suggested that excess ROS indirectly promote the degeneration of hard tissue through osteoclastogenesis, as well as the destruction of soft tissue, thereby favoring the progression of periodontitis [1, 6]. Previous studies have reported changes in some parameters of oxidative stress in saliva [14, 15, 16], serum [14], and gingival reticular fluid [17]. Several studies are looking at biomarkers of oxidative stress in order to find a periodontal diagnostic [7, 18, 19, 20]. However, the published data in this area are not conclusive, due to a high degree of heterogeneity in the methodology and results, in addition to the absence of MF evaluations in the gingival tissue of patients with periodontitis [7, 14, 15, 16, 19, 21, 22]. The objective of this study was to determine the levels of NO\({}_{3}\)\({}^{-}\), MDA, and MF in the gingival tissues of patients with periodontitis, in relation to the corresponding levels in healthy subjects. This is the first trial to evaluate membrane fluidity levels in periodontal patients.