Root canal microbiota as an augmented reservoir of antimicrobial resistance genes in type 2 diabetes mellitus patients

Abstract

Root canal microbiota as an augmented reservoir of antimicrobial resistance genes in type 2 diabetes mellitus patients Antimicrobial resistance is a global public health problem. Root canal microbiota associated with apical periodontitis represents a well-known reservoir of antimicrobial resistance genes (ARGs). However, the effect of type 2 diabetes mellitus (T2DM) in this reservoir is unknown. This study aimed to establish if root canal microbiota associated with apical periodontitis in T2DM patients is an augmented reservoir by identifying the prevalence of nine common ARGs and comparing it with the prevalence in nondiabetic patients.Methodology: This cross-sectional study included two groups: A T2DM group conformed of 20 patients with at least ten years of living with T2DM and a control group of 30 nondiabetic participants. Premolar or molar teeth with pulp necrosis and apical periodontitis were included. A sample was collected from each root canal before endodontic treatment. DNA was extracted, and ARGs were identified by polymerase chain reaction. Results: tetW and tetM genes were the most frequent (93.3 and 91.6%, respectively), while ermA was the least frequent (8.3%) in the total population. The distribution of the ARGs was similar in both groups, but a significant difference (p<0.005) was present in ermB, ermC, cfxA, and tetQ genes, being more frequent in the T2DM group. A total of eighty percent of the T2DM patients presented a minimum of four ARGs, while 76.6% of the control group presented a maximum of three. Conclusions: Root canal microbiota associated with apical periodontitis in T2DM patients carries more ARGs. Therefore, this pathological niche could be considered an augmented reservoir.

The Distribution of Eight Antimicrobial Resistance Genes in Streptococcus oralis, Streptococcus sanguinis, and Streptococcus gordonii Strains Isolated from Dental Plaque as Oral Commensals

“…Otherwise, only nine patients (11.2%) tested negative for all the tested ARGs, while 26 patients (32.5%) carried five to six of the ARGs. This fact is striking because in a similar group of patients [26] taken from the same university clinic but in a well-established pathological niche (necrotic root canals with apical periodontitis), only 3.3% carried five to six of these same ARGs. This clearly shows that DP should be considered as an extensive reservoir of ARGs, even more than the microbiota of a well-established pathological niche.…”

“…Historically, the antimicrobial resistance of specific pathogenic oral bacteria [24,25] or from pathologic niches (necrotic root canal or periodontal pocket) has been widely studied [26][27][28]. However, in the last decade, there has been increased attention on studying commensal bacteria from the oral cavity as potential silent reservoirs of a wide variety of ARGs [29,30].…”

Inferring diet, disease and antibiotic resistance from ancient human oral microbiomes

“…ARGs are plentiful in the modern human oral cavity, increasing the likelihood of resistant bacterial infections [71]. One of the most common ARGs found in the oral cavity today are those that confer tetracycline resistance [75][76][77][78][79][80]. A high proportion of resistance genes probably originate from streptococci, which are abundant in the oral cavity [81].…”

Relationship between Diabetes Mellitus and Root Canal Infections

“…Periradikuler semptomu olan vakalarda artan lezyon varlığı veya ara seanslardaki flare-up sıklığı Diyabethastalarının pulpa ve kök kanallarındaki daha virulan mikroorganizmaların varlığıyla ilişkili olabileceği bildirilmiştir (4). Güncel bir çalışmada ise antimikrobiyal direnç genlerinin Tip 2 diyabet hastalarının apikal periododontitisli kök kanallarında diyabet olmayan hastalara oranla daha fazla olduğu bildirilmiştir (33). Apikal periododontitise neden olan anaerobik grambakterilerin lipopolisakkaritleri bağışıklık hücrelerindeki özel reseptörlere (TLRs) bağlanır ve hücre içi yolları özellikle makrofajların üzerindeki NF-Kβ aktive ederek, IL-1,IL-6, IL-8, TNF-α gibi proinflamatuar sitokinlerin salınımına neden olarak diyabet hastalarında görülen proenflamatuvar sistemik durumu etkiler (34) (37,38).…”