Does Periodontal Inflammation Affect Type 1 Diabetes in Childhood and Adolescence? A Meta-Analysis

Abstract

The emergence of link between periodontal disease and diabetes has created conditions for analyzing new interdisciplinary approach making toward tackling oral health and systemic issues. As periodontal disease is a readily modifiable risk factor this association has potential clinical implications. The aim of this paper was systematically review the extant literature related to analytics data in order to identify the association between type 1 diabetes (T1DM) in childhood and adolescence with periodontal inflammation. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we conducted a database search between 2004 and 2019. A manual search of the literature was conducted as an additional phase of the search process, with the aim of identifying studies that were missed in the primary search. One hundred and thirty-nine records were screened and 10 fulfilled the inclusion criteria. Most studies were of moderate methodological quality. Outcomes included assessments of diabetes and periodontal status. In diabetic populations, compared to healthy subjects, interindividual differences in periodontal status are reflected in higher severity of periodontal inflammation. The most reported barriers to evidence uptake were the intrinsic limits of cross-sectional report data and relevant research, and lack of timely research output. Based on the evidence presented within the literature, the aforementioned biomarkers correlate with poor periodontal status in type 1 diabetic patients. Whilst the corpus of the evidence suggests that there may be an association between periodontal status and type 1 diabetes, study designs and methodological limitations hinder interpretation of the current research.

Gingival Crevicular Blood as a Potential Screening Tool: A Cross Sectional Comparative Study

“…Our data extend previous findings using the same study design that have documented successful blood glucose evaluation in undiagnosed diabetic patients and diabetic population. Interest in the detection of diabetes using GCB has been heightened by the results of several trials for the treatment of periodontal patients [ 7 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. Of course, the optimal condition for GCB measurement occurs when the bleeding is abundant.…”

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

“…The exposure to these hormonal changes is postulated to trigger the oral microbial community shift, resulting in the manifestation of more disruptive periodontitis [18], [19], [20], [21], [53], [54], [55], [56]. This transition may provide an explanation of understanding the relationship between periodontal pathogens and PTB [56], [57], [58], [59].…”

“…The oral cavity encompasses a number of bacteria that share many virulence characteristics and that may be capable of causing a low-grade systemic inflammation [16], [17], [18], [19], [31], [45], [48], [59]. However, instead of contributing on systemic alterations, some periodontal pathogens seem to disseminate overcoming the placental barrier leading to localized placental inflammation, triggering preterm membrane rupture [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [45], [51].…”

“…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.…”