The Effect of Gaseous Ozone Therapy in Conjunction with Periodontal Treatment on Glycated Hemoglobin Level in Subjects with Type 2 Diabetes Mellitus: An Unmasked Randomized Controlled Trial

Abstract

Background: It is established that inflammation is involved in the pathogenesis of Type 2 Diabetes Mellitus (T2DM) by promoting insulin resistance and impaired beta cell function in the pancreas. Among the hypothesized independent risk factors implicated in the pathogenetic basis of disease, periodontal infection has been proposed to promote an amplification of the magnitude of the advanced glycation end product (AGE)-mediated upregulation of cytokine synthesis and secretion. These findings suggest an interrelationship between periodontal disease and type 2 diabetes, describing poor metabolic control in subjects with periodontitis as compared to nondiabetic subjects and more severe periodontitis in subjects with T2DM as compared to a healthy population, with a significant positive correlation between periodontal inflammatory parameters and glycated hemoglobin level. Results from clinical trials show that periodontal treatment is able to improve glycemic control in subjects with diabetes. Many therapeutic strategies have been developed to improve periodontal conditions in conjunction with conventional treatment, among which ozone (O3) is of specific concern. The principal aim of this trial was to compare the clinical effectiveness of an intensive periodontal intervention consisting of conventional periodontal treatment in conjunction with ozone gas therapy in reducing glycated hemoglobin level in type 2 diabetic patients and standard periodontal treatment. Methods: This study was a 12-month unmasked randomized trial and included 100 patients aged 40–74 years older, with type 2 diabetes mellitus diagnosed. All the patients received conventional periodontal treatment, or periodontal treatment in conjunction with ozone gas therapy in a randomly assigned order (1:1). The primary outcome was a clinical measure of glycated hemoglobin level at 3, 6, 9 and 12 months from randomization. Secondary outcomes were changes in periodontal inflammatory parameters. Results: At 12 months, the periodontal treatment in conjunction with ozone gas therapy did not show significant differences than standard therapy in decreasing glycated hemoglobin (HbA1C) level and the lack of significant differences in balance is evident. Conclusions: Although the change was not significant, periodontal treatment in conjunction with the gaseous ozone therapy tended to reduce the levels of glycated hemoglobin. The study shows a benefit with ozone therapy as compared to traditional periodontal treatment.

Exploring the Role of Fusobacterium nucleatum in Preterm Birth: A Narrative Review

“…In this study, the mechanisms by which EAEC 042 triggers this inflammatory event were assessed. The immunofluorescent staining analysis of expression of FadA on the FN 12230 USF81 strain, fad-A-complementing clone, confirmed that FadA is equally exposed on the bacterial cell surface, promoting adherence and invasion of host cells [59], [60], [61]. This study provided the first evidence that the expression of FadA was correlated to placental colonization in vivo [60].…”

“…The immunofluorescent staining analysis of expression of FadA on the FN 12230 USF81 strain, fad-A-complementing clone, confirmed that FadA is equally exposed on the bacterial cell surface, promoting adherence and invasion of host cells [59], [60], [61]. This study provided the first evidence that the expression of FadA was correlated to placental colonization in vivo [60]. Studies aimed at elucidating the process of FN translocation into host cells, include genetic analysis defining components that are required for FadA activity [32].…”

“…Through analyzing the dynamic character of the oral microbial communities and their interactions with the organism, we sought to reveal through which way the association between periodontal disease and general health is understand and interpreted, focus on the relationship between oral microbiome and pregnancy [11]. There has been considerable debate as to whether the oral microbiome should be seen [13] as a risk factor for PTB and whether this induced [26] development of new care strategies in response to the changed scientific discoveries [60]. However, it seems clear that the new conceptualization has critical function through the idea of overlapping microbial community specificity and proinflammatory response [13], [15].…”

“…Specifically, it has been investigated the role of the Gram-negative periodontal pathogen FN, an opportunistic pathogen agent having a specific role in the pathogenesis of different periodontal conditions, and it is increasingly recognized as an important agent of PTB [42], [50]. FN is credited with the distinction of being the most crucial pathogen implicated in the pathogenesis of periodontitis [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41], [42], [43], counting its systemic effects on immune system [59], [60]. The localized infection and inflammation of the mouse placenta mediated by oral FN colonization have been described previously by several researchers who suggested that the hematogenous transmission of this bacterium had a detrimental effect on pregnancy, producing intrauterine inflammatory response [51].…”

“…It has been demonstrated that FadA adhesion gene (fadA) may be a microbial determinant contributing to placental invasion, causing a localized inflammatory response, responsible for fetal demise prematurely [29], [30], [31], [32]. The role of Fusobacterium adhesion A in PTB was first reported in pregnant mice infected with FN [37], [38], [39], [40], [41], [54], [59], [60], [61]. It was the first genetic complementation study which confirmed that the promotion of cellular invasion and placental colonization mediated by the exposure of FadA, through construction of FN 12230 USF81, a fadAcomplementing clone.…”