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Aim To study whether cytokine levels and bacterial counts in p atients with peri-implantitis reflect clinical treatment outcome following non-surgical management. Materials and Methods Luminex magnet bead technology and checkerboard DNA–DNA hybridization were used to assess treatment outcome after treatment at the implant with the most severe peri-implantitis in 41 participants. Results Study group mean age was 40.3 years (SD ± 9.9). Stable treatment outcome after 6 months (no further bone loss, probing pocket depth decrease ≥0.5 mm, no bleeding/suppuration) was identified in 9 of 41 (22%) participants. Peri-implant crevicular fluid (PICF) levels were also lower for Il-1β (P

Rationale Chronic kidney disease (CKD) and periodontitis (PD) are important health issues. There is a large variety of microorganisms related to the pathogenesis of periodontitis, and optimising the time and the cost of laboratory assays to detect these organisms is highly valuable in the medical field. Methods Bacteria were isolated from saliva and oral biofilm of 30 adolescents and young adults with definite medical and dental diagnosis of CKD and PD, respectively, and proteins were extracted for microorganism identification by means of the matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOFMS) technique. Results The results showed that the most incident microorganisms were Actinomyces dentalis (43%), Acinetobacter ursingi (60%), Aggregatibacter actinomycetencomitans (60%), Corynebacterium argentoctens (63%), Staphylococcus aureus (93%), Streptococcus salivarius (97%) and Tannerella forsythensis (43%). The analysis of oral biofilm showed higher incidences for Actinomyces dentalis (33%), Acinetobacter ursingi (50%), Aggregatibacter actinomycetencomitans (50%), Corynebacterium argentoctens (70%), Pseudomonas aeruginosa (40%), Staphylococcus aureus (73%) and Streptococcus salivarius (87%). Conclusions Based on these results, we concluded that the MALDI Biotyper protocol proves useful as a rapid and reliable assay for distinguishing different microorganisms possibly related to CKD and PD. Copyright © 2016 John Wiley & Sons, Ltd.

Objectives To determine in vivo association between Aggregatibacter actinomycetemcomitans (Aa) and Streptococcus mutans (Sm) in aggressive periodontitis patients (AgP) and the in vitro influence on Sm of saliva and of Aa strains isolated from individual Aa-positive patients. Materials and Methods Clinical indices and saliva samples were taken from 30 AgP patients. Aa and mutans streptococci levels were determined. Antibacterial effect of saliva from 12 Aa-positive patients, and their individual Aa strain, was checked turbidimetrically in vitro on Sm. Results Aa salivary level was inversely correlated with levels of mutans streptococci and directly correlated with pockets of ≥7 mm. During exponential growth phase: (i) All Aa-positive and Aa-negative saliva samples showed no significant influence on Sm growth. (ii) Each individually isolated Aa strain presented significant inhibitory effect on Sm growth. During stationary growth phase, all the above demonstrated an inhibitory effect on Sm growth, with significantly greater influence of Aa individual strains. Conclusion Saliva of each AgP Aa-positive subject had an inhibitory effect on Sm growth, which is most likely derived from Aa bacterial physiology. This research raises the possibility that suppression of Aa due to periodontal treatment may increase Sm levels and hence caries incidence.

It is critical to understand the underlying host responses in aggressive periodontitis to provide a better appreciation of the risk and susceptibility to this disease. Such knowledge may elucidate the etiology and susceptibility to aggressive periodontitis and directly influence treatment decisions and aid diagnosis. This review is timely in that several widely held tenets are now considered unsupportable, namely the concept that Aggregatibacter actinomycetemycomitans is the key pathogen and that chemotactic defects in polymorphonuclear leukocytes are part of the etiopathology. This review also serves to put into context key elements of the host response that may be implicated in the genetic background of aggressive periodontitis. Furthermore, key molecules unique to the host response in aggressive periodontitis may have diagnostic utility and be used in chairside clinical activity tests or as population screening markers. It is becoming increasingly appreciated that the microbial etiology of aggressive periodontitis and the histopathology of this disease are more similar to than different from that of chronic periodontitis. An important therapeutic consideration from the lack of support for A. actinomycetemycomitans as a critical pathogen here is that the widely held belief that tetracycline had a role in aggressive periodontitis therapy is now not supported and that antibiotics such as those used effectively in chronic periodontitis (metronidazole and amoxicillin) are not contraindicated. Furthermore, A. actinomycetemycomitans-related molecules, such as cytolethal distending toxin and leukotoxin, are less likely to have utility as diagnosis agents or as therapeutic targets.

This cross-sectional study characterizes the association between subgingival bacterial profile and periodontal parameters in patients assigned to coronary angiography because of cardiologic problems, which may affect the oral microbiota.Pooled subgingival bacterial samples were collected from 477 dentate individuals during the oral examinations, along with periodontal probing depth (PD) and assessments of bleeding on probing (BOP) and radiographic alveolar bone loss (ABL). The checkerboard DNA-DNA hybridization assay was used to determine the levels of 29 oral bacteria, which were divided into three bacterial complexes.All bacterial combinations from the etiologic bacterial group and each species from the red complex were significantly associated (P0.001) with grade of ABL. The prevalence of the etiologic bacterial group and the level of each species were also associated strongly with the proportion of sites with PD 4 to 5 mm and ≥ 6 mm, BOP, and ABL, except Aggregatibacter actinomycetemcomitans. Levels of Gram-negative oral bacteria correlated significantly with those of Gram-positive species (r = 0.840, P0.001). In multiple logistic regression analysis, the prevalence of the etiologic bacterial group, levels of Gram-negative bacteria and Treponema denticola, and the prevalence of Porphyromonas gingivalis and T. denticola associated significantly with ABL, whereas other bacterial complexes and levels of Gram-positive species did not.Although levels of Gram-negative and -positive species paralleled periodontal parameters, only the species considered etiologic were associated with ABL.

Tavares WLF, Neves de Brito LC, Teles RP, Massara MLA, Ribeiro Sobrinho AP, Haffajee AD, Socransky SS, Teles FR. Microbiota of deciduous endodontic infections analysed by MDA and Checkerboard DNA–DNA hybridization. International Endodontic Journal 44, 225–235, 2011. Abstract Aims To evaluate the microbiota of endodontic infections in deciduous teeth by Checkerboard DNA–DNA hybridization after uniform amplification of DNA in samples by multiple displacement amplification (MDA). Methodology Forty samples from the root canal system of deciduous teeth exhibiting pulp necrosis with or without radiographically detectable periradicular/interradicular bone resorption were collected and 32 were analysed, with three individuals contributing two samples; these were MDA-amplified and analysed by Checkerboard DNA–DNA hybridization for levels of 83 bacterial taxa. Two outcome measures were used: the percentage of teeth colonized by each species and the mean proportion of each bacterial taxon present across all samples. Results The mean amount of DNA in the samples prior to amplification was 5.2 (±4.7) ng and 6.1 (±2.3) μg after MDA. The mean number of species detected per sample was 19 (±4) (range: 3–66) to the nearest whole number. The most prevalent taxa were Prevotella intermedia (96.9%), Neisseria mucosa (65.6%), Prevotella nigrescens (56.2%) and Tannerella forsythia (56.2%). Aggregatibacter (Haemophilus) aphrophilus and Helicobacter pylori were not detected. P. intermedia (10%), Prevotella tannerae (7%) and Prevotella nigrescens (4.3%) presented the highest mean proportions of the target species averaged across the positive samples. Conclusion Root canals of infected deciduous teeth had a diverse bacterial population. Prevotella sp. were commonly found with P. intermedia, Prevotella tannerae and Prevotella nigrescens amongst the most prominent species detected.

This study examined the distribution pattern of Aggregatibacter actinomycetemcomitans serotypes in the subgingival plaque of subjects residing in the United States. A. actinomycetemcomitans was identified in 256 subgingival plaque samples from 161 subjects. For 190 of the 256 samples, the total cultivable bacteria and selected periodontal pathogenic species were determined. A. actinomycetemcomitans isolates were confirmed by a16S rDNA-based PCR analysis, genotyped by arbitrarily-primed PCR, and serotyped by PCR analysis of serotype-specific gene clusters. A total of 82 distinct A. actinomycetemcomitans strains were identified. The serotype distribution pattern of the strains was 21 (25.6%) serotype a, 12 (14.6%) b, 41 (50%) c, 6 (7.3%) e, 1 (1.2%) f, and 1 (1.2%) non-typeable. For 14 subjects where multiple colonies of A. actinomycetemcomitans were identified, 11 subjects (78.6%) were each infected by a single serotype, while the remaining three subjects (21.3%) were each infected by two serotypes of A. actinomycetemcomitans. There was an inverse relationship between the level of cultivable A. actinomycetemcomitans and Porphyromonas gingivalis. Within subgingival plaque of study cohort A. actinomycetemcomitans serotype c was the dominant serotype and comprised 50% of all strains, followed by (in order of detection frequency) serotypes a and b. Serotypes d, e, and f strains were either not detected or less frequently found. Serotype distribution patterns of subgingival A. actinomycetemcomitans may vary among subjects of different race orethnicity.

Animal studies suggest that inducible nitric oxide synthase (iNOS) may be associated with destructive periodontal disease. l-N6-(1-Iminoethyl)-lysine (l-NIL) has been shown to inhibit iNOS in a selective manner, and hence the aim of the present study was to test the hypothesis that treatment with l-NIL may induce a T-cell helper 1 (Th1)-like immune response by Aggregatibacter (Actinobacillus) actinomycetemcomitans lipopolysaccharide (LPS)-stimulated murine spleen cells in vitro. BALB/c mice were either sham-immunized or immunized with A. actinomycetemcomitans LPS. Spleen cells were stimulated with A. actinomycetemcomitans LPS in the presence or absence of l-NIL. Nitric oxide (NO), iNOS activity, specific IgG subclass antibodies, interferon-γ (IFN-γ), and interleukin-4 (IL-4) levels and cell proliferation were determined. The results showed that treatment with l-NIL suppressed both NO production and iNOS activity but enhanced specific IgG2a, IFN-γ levels, and increased cell proliferation following stimulation with A. actinomycetemcomitans LPS-stimulated cells. The results of the present study suggest that inhibition of iNOS activity by l-NIL may skew the A. actinomycetemcomitans LPS-stimulated murine splenic immune response towards the Th1-like immune profile in vitro.

Aim: To evaluate and compare the microbiological effects of hand instruments, Er:YAG-laser, sonic, and ultrasonic scalers in patients with chronic periodontitis. Patient perception of each treatment was documented. Material and Methods: From 72 patients, bacterial samples were collected from the deepest pocket in each quadrant (total: 288 sites). A polymerase chain reaction kit estimated the amount of Aggregatibacter (Actinobacillus) actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tannerella forsythensis (Tf), and Treponema denticola (Td) at baseline as well as 3 and 6 months after therapy. One quadrant in each patient was randomly assigned to curettes (H-group), Er:YAG laser (L-group), sonic device (S-group), or ultrasonic device (U-group). Results: Three months post-operatively, the amounts of Pg, Pi, Tf, and Td were significantly reduced in all groups. Laser and sonic instrumentation failed to reduce Aa. Six months after therapy, significant differences were still detected for Pg (L- and U-group), for Pi and Tf (S-group), and for Td (L-, S- and U-group). Patients rated ultrasonic treatment as more preferable than hand and laser instrumentation. Conclusion: The various treatment methods resulted in a comparable reduction of the evaluated periodontal pathogens, and bacterial increase was only partially different 6 months post-operatively. Ultrasonic instrumentation caused less discomfort.