Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

OBJECTIVE: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP). SUBJECTS AND METHODS: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR. RESULTS: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29. CONCLUSION: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals.

Detection of specific periodontal microorganisms from bacteraemia samples after periodontal therapy using molecular-based diagnostics.

AIM: The aim of this study was to assess the presence of subgingival pathogens in peripheral blood samples from periodontitis patients before and after scaling and root planing (Sc/RP) using nested polymerase chain reaction (nested PCR). MATERIALS AND METHODS: Peripheral blood samples were obtained from 42 patients with severe generalized chronic or aggressive periodontitis. In each patient, four samples of peripheral blood were drawn at different times: immediately before the Sc/RP procedure; immediately after Sc/RP; 15 and 30 min. post-Sc/RP. Blood samples were analysed for bacteraemia with anaerobic culturing and nested PCR, using universal bacterial primers that target the 16S-rRNA gene of most bacteria, subsequently re-amplified with specific primers to Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Eikenella corrodens, Campylobacter rectus and Prevotella intermedia, using a modified phenol-chloroform method for DNA extraction. RESULTS: Presence of specific periodontal pathogens in peripheral blood after treatment was detected in 54.8% of the patients, in 47.6% with anaerobic culturing and in 19% with nested PCR. In 16.6%, the periodontal pathogens were detected before Sc/RP. P. gingivalis and A. actynomicetemcomitans were the pathogens most frequently detected in the bloodstream before and after Sc/RP. CONCLUSIONS: Nested PCR demonstrated the presence of DNA from periodontal pathogens in blood samples in severe periodontitis patients before, during and after periodontal therapy. The use of these molecular-based techniques may improve the accuracy from the results obtained by haemoculture.

Aggressive and chronic periodontitis correlate with distinct cellular sources of key immunoregulatory cytokines.

BACKGROUND: Chronic periodontitis (CP) and aggressive periodontitis (AP) are inflammatory diseases and the main cause of dental loss in adults. We aimed to investigate the expression of adhesion molecules and the source of proinflammatory and anti-inflammatory cytokines in circulating mononuclear cells from patients with CP and AP. METHODS: Peripheral blood mononuclear cells from healthy controls and CP or AP patients were collected. The expression of the cell adhesion molecules CD11a and CD11b, and the cellular sources of interleukin (IL)-4, IL-10, IL-12, interferon-γ, and tumor necrosis factor-α by distinct subpopulations of circulating leukocytes were determined using flow cytometry. RESULTS: The expression of CD11a, but not CD11b, was significantly higher within the CD4(+) and CD8(+) T cells in CP and AP than in healthy controls. The frequencies of tumor necrosis factor-α-expressing CD4(+) T cells and CD14(+) cells were higher in AP and CP, compared to healthy controls, respectively. Moreover, the frequency of IL-10 expressing CD14(+) cells was higher in CP, but not AP, compared to healthy controls CD4(+) T cells committed to IL-4 production was higher in CP than in healthy controls. CONCLUSION: These results suggest the participation of CD11a in the pathogenesis of periodontal lesions and show distinct cellular sources of immunoregulatory cytokines in AP versus CP.

Serum levels of cytokines in subjects with generalized chronic and aggressive periodontitis before and after non-surgical periodontal therapy: a pilot study.

BACKGROUND: The emergence of periodontal medicine has increased interest in defining the serologic profiles of inflammatory mediators in subjects with periodontitis. Thus, the aim of this pilot study is to evaluate the serum levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, and interleukin (IL)-4, -17, and -23 in subjects with generalized chronic periodontitis (GCP) and generalized aggressive periodontitis (GAgP) before and after non-surgical periodontal therapy. METHODS: Cytokines were measured by enzyme-linked immunosorbent assay in serum samples taken from 42 systemically healthy subjects divided according to periodontal status into subjects with GAgP (n = 14) and GCP (n = 14) and periodontally healthy (PH) subjects (n = 14). In addition, the levels of cytokines were reassessed at 6 months after periodontal therapy in the periodontitis groups. Clinical parameters were also evaluated at baseline and 6 months post-therapy. RESULTS: After therapy, both periodontitis groups demonstrated a significant improvement in clinical periodontal status (P <0.05). At baseline, concentrations of TNF-alpha (P = 0.0006) and IL-17 (P = 0.02) were significantly higher in the GAgP group compared to the other groups. There was a significant decrease in serum concentrations of TNF-alpha (P = 0.03) and IL-17 (P = 0.04) at 6 months post-therapy in the GAgP group (P <0.05). The concentration of TNF-alpha remained elevated in the GAgP group compared to the PH group at 6 months post-therapy (P = 0.04). CONCLUSIONS: Subjects with GAgP presented higher levels of TNF-alpha and IL-17 than subjects with GCP and PH subjects. In addition, although the serum levels of these cytokines improved significantly as a result of periodontal therapy, the levels of TNF-alpha remained higher in subjects with GAgP compared to PH subjects.

[Anti-leukotoxin antibodies against Actinobacillus actinomycetemcomitans in serum and saliva samples from patients with localized juvenile periodontitis]. / Anticorpos antileucotoxina contra Actinobacillus actinomycetemcomitans em amostras de soro e saliva de pacientes com periodontite juvenil localizada.

The leukotoxin produced by Actinobacillus actinomycetemcomitans is considered the major virulence factor with potential to cause damage to the host defenses. The present work analyzed the serumal and salivary levels of antibodies against the leukotoxin produced by A. Actinomycetemcomitans, in patients with Localized Juvenile Periodontitis (LJP) and in healthy controls. Additionally, analysis of the immune complex (IC) was carried out in saliva samples. The classic ELISA method, with leukotoxin obtained through Sephadex G-200 gel filtration, and the capture ELISA method, using rabbit anti-A. Actinomycetemcomitans (leukotoxic, FDC Y4, IgG) adsorbed with a non-leukotoxic strain of A. actinomycetemcomitans, were used. The results obtained demonstrated significantly higher serumal levels of IgG in patients with LJP, when they were compared with the healthy controls, both for the classic and capture ELISA methods (p < 0.05). However, no significant differences were observed between the salivary levels of IgG, SIgA and IC in the examined individuals. These results suggest that even though A. actinomycetemcomitans presents virulence factors that affect the immune response, there is immune response to leukotoxin in LJP patients. This increase of IgG in the blood stream might contribute to host defense, limiting the lesion to the periodontal regions already colonized by A. actinomycetemcomitans.

Neutrophil chemotaxis and serum factor modulation in Brazilian periodontitis patients.

The polymorphonuclear neutrophil (PMN) chemotaxis index and modulation of serum factors in 15 Brazilian periodontal patients (five localized juvenile and ten adult periodontitis) and ten healthy subjects were examined. Adult periodontitis patients showed a normal chemotaxis index, Localized juvenile periodontitis LJP patients showed diminished chemotaxis and serum cell-directed inhibitor activity. The results suggest that PMN abnormalities could not be caused by only the neutrophils themselves, but also by modulation of serum factors acting on this LJP disease.

No association between secretor status of ABO blood group antigens and juvenile periodontitis.

The aim of this study was to determine the association between secretor status of ABO blood group antigens and localized juvenile periodontitis (LJP). Forty-three patients with LJP (mean age 20.8 years) diagnosed according to Baer's criteria were selected. Thirty two periodontally healthy normal subjects (mean age 24.7 years) were use as control. Samples of blood and saliva were collected from patients and from control subjects. ABO blood group was determined by agglutination of erythrocytes with appropriate antisera. Determination of soluble ABO antigens in saliva was made by the haemagglutination inhibition assay. Subjects with O blood group were most frequent in both groups. The distribution of blood groups, and secretor and non-secretor status of ABO group antigens in LJP patients and control subjects was not significant. The results provide support for the hypothesis that there is no association between non-secretor status and LJP.