To assess the prevalence and occurrence of eleven periodontopathogens in subgingival biofi lm of banded and bonded molars during the fi rst period of fi xed orthodontic treatment. Subjects were selected from patients referred to orthodontic treatment and were divided in two groups: group A comprised fi fteen patients (14.4±2.45 years of age) who received orthodontic bands on fi rst permanent molars and group B of ten patients (15.7±1.87 years of age) with directly bonded tubes on the labial surface of the same teeth. Subgingival sample collection was performed before bands and tubes application and 4-7 weeks after attachment placement. DNA-strip tehnique was used to assess the presence of eleven putative periodontopathogens at each time point. Fusobacterium nucleatum, Eikenella corrodens and Capnocytophaga spp. were found in a large number of samples, other periodontopathogens were present in a smaller rate. The 4-7 weeks after attachment placement a slight increase of putative species was observed in both groups.*Corresponding author; E-mail: lillalorinczi@yahoo.com 104 MÁRTHA et al. Acta Microbiologica et Immunologica Hungarica 63, 2016The presence of orthodontic tubes and bands infl uence the accumulation and composition of subgingival microbiota. Higher level of oral hygiene should be achieved before and during orthodontic treatment in order to prevent any side effects on periodontal tissues.

The present study aimed to investigate the link between the severity of periodontal disease (PD), coronary calcifications and unstable plaque features in patients who underwent coronary computed tomography for unstable angina (UA). Fifty-two patients with UA, included in the ATHERODENT trial (NCT03395041), underwent computed tomographic coronary angiography (CCTA) and dental examination. Based on the median value of the periodontal index (PI), patients were assigned to the low periodontal index (LPI) group (PI < 22) and a high periodontal index (HPI) group (PI > 22). Patients with HPI had higher plaque volume (p = 0.013) and noncalcified plaque volume (p = 0.0003) at CCTA. In addition, the presence of vulnerability features in the atheromatous plaques was significantly correlated with PI (p = 0.001). Among periodontal indices, loss of gingival attachment (p = 0.009) and papillary bleeding index (p = 0.002) were strongly associated with high-risk plaques. PI significantly correlated with coronary calcium score (r = 0.45, p = 0.0008), but not with traditional markers of subclinical atherosclerosis. Overall, this subgroup analysis of the ATHERODENT study indicates that patients with advanced PD and UA present a higher amount of calcium in the coronary tree and have a more vulnerable phenotype of their culprit plaques.

The study assessed whether the increased production of interleukin-1α (IL-1α) and interleukin-1β (IL-1β), as a result of chronic hepatic inflammation, could be the expression of the negative impact on periodontal disease. The study included chronic periodontitis patients who were systemically healthy, chronic periodontitis patients suffering from chronic hepatitis C, as well as control patients, being systemically and periodontally healthy. After periodontal examination and the assessment of certain periodontal parameters, gingival crevicular fluid was collected from all participating patients. By using the enzyme-linked immunosorbent assay method, a quantitative assessment of IL-1α and IL-1β levels was possible. The immunologic results were correlated to the clinical periodontal data. The gingival fluid levels of cytokines were higher for periodontitis patients with chronic hepatitis C than for the systemically healthy periodontitis patients (1.8-fold higher for IL-1α and 2.1-fold higher for IL-1β). In addition, the gingival fluid cytokine levels were significantly higher for the periodontal patients (with/without chronic hepatitis C) than for the control group. Positive correlations were found between gingival fluid IL-1α and IL-1β levels and certain clinical periodontal parameters or the age of the viral hepatitis C diagnosis, in periodontitis patients with chronic hepatitis C. The chronic hepatic inflammation may have an important additional negative impact on the periodontal status, as both inflammatory reactions seem to be promoted by common pro-inflammatory cytokines.

(1) Background: The aim of this split-mouth design study was to analyze the clinical periodontal indexes and oxidative stress markers in gingival crevicular fluid modifications after three periodontal disease treatment possibilities (scaling and root planning—SRP; SRP and diode laser—L; SRP and photodynamic therapy—PDT). (2) Methods: The study was conducted on 52 patients: systemically healthy subjects with periodontal disease—non-RA (n = 26); and test group (n = 26) subjects with rheumatoid arthritis and periodontal disease—RA. Clinical periodontal measurements (probing depth—PD; Löe and Silness gingival index—GI; papillary bleeding index—PBI; and periodontal community index of treatment needs—CPITN) and oxidative stress markers (8-hydroxy-2’-deoxyguanosine (8-OHdG) and 4 hydroxynonenal (4-HNE)) were analyzed at baseline (T0), after three sessions of periodontal treatment (T1), and 6 months after treatment (T2). (3) Results: Periodontal therapy improved clinical periodontal measurements and oxidative stress markers in both analyzed groups, with supplementary benefits for laser- and PDT-treated periodontal pockets. (4) Conclusions: The analyzed oxidative stress markers decreased significantly following non-surgical periodontal therapy in both rheumatoid arthritis and systemically healthy patients. All the periodontal disease treatment possibilities analyzed in this study offered clinical and paraclinical improvements; however, the association of laser with SRP and photodisinfection with SRP yielded the best clinical and paraclinical outcomes when compared to SRP alone.

The study is aimed at assessing the impact that periodontal disease and chronic hepatitis C could have on gingival crevicular fluid levels of the NLRP3 inflammasome, caspase-1 (CASP-1), and interleukin-18 (IL-18) and at evaluating whether the increased local inflammatory reaction with clinical periodontal consequences is correlated to their upregulation. Patients were divided into four groups, according to their periodontal status and previously diagnosed hepatitis C, as follows: (i) CHC group, chronic hepatitis C patients; (ii) P group, periodontal disease patients, systemically healthy; (iii) CHC + P group, patients suffering from both conditions; and (iv) H group, systemically and periodontally healthy controls. Gingival crevicular samples were collected for quantitative analysis of the NLRP3 inflammasome, CASP-1, and IL-18. CHC + P patients expressed the worse periodontal status and the highest NLRP3, CASP-1, and IL-18 levels, the difference being statistically significant ( p < 0.05 ). The P group patients also expressed significantly more elevated NLRP3, CASP-1, and IL-18 levels, as compared to nonperiodontal patients (CHC and H groups). Chronic hepatitis C and periodontal disease could have a significant influence on the upregulation of NLRP3 inflammasome and its components, possibly contributing to an increased local inflammatory reaction and clinical periodontal consequences.