C-reactive protein as a systemic marker of inflammation in periodontitis
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Keywords:
Aggregatibacter actinomycetemcomitans
Clinical attachment loss
Aggressive periodontitis
Periodontal examination
Periodontal pathogen
Background: Initiation and progression of periodontitis correlates with increased quantities of periodontitis‐associated bacteria in periodontal biofilms. In the present study, the aim is to measure Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis amounts in saliva and their antibody (immunoglobulin [Ig]A and IgG) levels in serum and evaluate their diagnostic abilities, together or alone, in chronic periodontitis. Methods: The study population comprised 230 Finnish dentate adults: 84 with generalized chronic periodontitis (GCP), 65 with localized chronic periodontitis (LCP), and 81 controls without periodontitis. General and oral health information was obtained by questionnaires, interviews, and clinical and radiographic examinations. Salivary and serum samples were analyzed by quantitative single copy gene–based real‐time polymerase chain reaction and multiserotype enzyme‐linked immunosorbent assay, respectively. Results: Pathogen carriers suffered mostly from GCP and seldom from LCP. A. actinomycetemcomitans and P. gingivalis quantities in saliva were strongly associated with corresponding serum IgA and IgG values ( P <0.001) and with severity of disease ( P <0.001). P. gingivalis exhibited more straightforward associations among salivary bacterial burdens, corresponding antibody formation, and periodontitis severity than A. actinomycetemcomitans . The combination of information on age, sex, smoking, and P. gingivalis results provided an area under the curve of 0.817 (95% confidence interval 0.76 to 0.87, P <0.001) for GCP. Conclusion: The combination of saliva P. gingivalis quantity with pathogen‐specific host response may be used to diagnose periodontitis with high accuracy.
Aggregatibacter actinomycetemcomitans
Periodontal pathogen
Aggressive periodontitis
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To evaluate the association among serum immunoglobulin G (IgG) responses to Aggregatibacter actinomycetemcomitans (Aa) serotypes a, b and c, Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf) and clinical parameters in Aggressive Periodontitis (AP) subjects. Associations between periodontal pathogens and clinical and immunological parameters were also evaluated.Thirty-eight subjects diagnosed with generalized AP (GAP) and localized AP (LAP) were included. Ten healthy controls were also evaluated. Clinical parameters were assessed and percentages of subgingival levels of Aa, Pg and Tf (beyond bacterial load), were determined by quantitative real-time polymerase chain reaction. Serum IgG antibody levels against Aa, Pg and Tf were evaluated by enzyme-linked immunosorbent assay.Percentages of Aa, Pg and Tf were significantly higher in AP than in controls. The response to Aa serotype c was higher in LAP subjects than in controls. There were no differences in microbial composition or antibodies responses between GAP and LAP, except for IgG response to Tf. Pg levels were correlated with probing depth (PD), BoP and CAL in GAP but not in LAP subjects. Tf levels correlated with PD and CAL in GAP subjects. In GAP, the infection levels of Aa and Pg correlated with the corresponding IgG levels to Aa serotype c and Pg.Given the evidences that IgG response in AP patients correlated with bacterial infection level in GAP, but not in LAP, and that LAP patients lack a response to Tf, despite harbouring this species, our data suggest a difference in host immune defence between these two forms of aggressive periodontitis.
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Tannerella forsythia
Periodontal pathogen
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aggressive periodontitis is a severe and rapidly progressing form of periodontitis [1,2] that affecting supporting tissues of the teeth induced by microbial deposits [3]. Aggregatibacter actinimycetemcomitans is an important pathogen related to aggressively progressive periodontal breakdown in adolescents and adults [4,5]. A. actinomycetemcomitans (A.a.) can be grouped into seven serotypes (a-g) [6,7].
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Periodontal pathogen
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Abstract It has previously been shown that the presence of Aggregatibacter actinomycetemcomitans in subgingival plaque is significantly associated with increased risk for clinical attachment loss. The highly leukotoxic JP2 genotype of this bacterium is frequently detected in adolescents with aggressive forms of periodontitis. The aims of the study were to quantify the levels of JP2 and non‐JP2 genotypes of A. actinomycetemcomitans in saliva of Moroccan adolescents with the JP2 genotype earlier detected in the subgingival plaque. The salivary concentrations of inflammatory proteins were quantified and linked to the clinical parameters and microbial findings. Finally, a mouth rinse with leukotoxin‐neutralizing effect was administrated and its effect on the levels the biomarkers and A. actinomycetemcomitans examined. The study population consisted of 22 adolescents that previously were found to be positive for the JP2 genotype in subgingival plaque. Periodontal registration and sampling of stimulated saliva was performed at baseline. A mouth rinse (active/placebo) was administrated, and saliva sampling repeated after 2 and 4 weeks rinse. The salivary levels of JP2 and non‐JP2 were analyzed by quantitative PCR and inflammatory proteins by ELISA. Both the JP2 and the non‐JP2 genotype were detected in all individuals with significantly higher levels of the non‐JP2. Enhanced levels of the JP2 genotype of A. actinomycetemcomitans was significantly correlated to the presence of attachment loss (≥3 mm). Salivary concentrations of inflammatory biomarkers did not correlate to periodontal condition or levels of A. actinomycetemcomitans . The use of active or placebo leukotoxin‐neutralizing mouth rinse did not significantly interfered with the levels of these biomarkers. Saliva is an excellent source for detection of A. actinomycetemcomitans on individual basis, and high levels of the JP2 genotype were significantly associated with the presence of clinical attachment loss.
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Clinical attachment loss
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To look for clinical signs of periodontal disease in young adults who exhibited radiographic bone loss and detectable numbers of Aggregatibacter actinomycetemcomitans in their primary dentition.Periodontal status and radiographic bone loss were examined in each of the subjects 16 years after the baseline observations. Techniques for anaerobic and selective culture, and checkerboard, were used to detect periodontitis-associated bacterial species. The isolated A. actinomycetemcomitans strains were characterized by polymerase chain reaction.Signs of localized attachment loss were found in three out of the 13 examined subjects. A. actinomycetemcomitans was recovered from six of these subjects and two of these samples were from sites with deepened probing depths and attachment loss. Among the isolated A. actinomycetemcomitans strains, serotypes a-c and e, but not d or f, were found. None of the isolated strains belonged to the highly leucotoxic JP2 clone, and one strain lacked genes for the cytolethal distending toxin.This study indicates that the presence of A. actinomycetemcomitans and early bone loss in the primary dentition does not necessarily predispose the individual to periodontal attachment loss in the permanent dentition.
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Clinical attachment loss
Cytolethal distending toxin
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Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Clinical attachment loss
Bleeding on probing
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Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Actinobacillus
Clinical attachment loss
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Tannerella forsythia
Aggregatibacter actinomycetemcomitans
Forsythia
Aggressive periodontitis
Periodontal pathogen
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Aggregatibacter actinomycetemcomitans is considered a possible etiological agent for aggressive periodontitis. The aim of this study was to determine the prevalence of the JP2 clone and non-JP2 genotypes of A. actinomycetemcomitans in the subgingival plaque of patients with aggressive periodontitis and controls among Sudanese high-school students.In a previous study we examined a large representative sample of students attending high schools in Khartoum, Sudan. In this population, 17 patients with aggressive periodontitis and 17 controls (14-19 years of age) consented to participate in the present study. The subjects underwent a clinical periodontal examination, and subgingival dental plaque samples were collected using paper points. The presence of the A. actinomycetemcomitans JP2 clone and non-JP2 genotypes were assessed using loop-mediated isothermal amplification (LAMP) and the PCR.The JP2 clone of A. actinomycetemcomitans was not detected in the subgingival plaque of either the cases or the controls. Non-JP2 types of A. actinomycetemcomitans were detected in the subgingival plaque of 12 (70.6%) patients with aggressive periodontitis and from only one (5.9%) control subject, showing a significantly higher frequency of detection in cases than in controls (p = 0.0001). The odds ratio for the detection of A. actinomycetemcomitans in the subgingival plaque of the patients with aggressive periodontitis was 38.4 (95% confidence interval: 4.0-373.0; p = 0.002). The PCR and LAMP methods showed identical results pertaining to the identification of non-JP2 types of A. actinomycetemcomitans.The JP2 clone of A. actinomycetemcomitans was not detected in the subgingival plaque of high school subjects in Sudan. The detection of non-JP2 types of A. actinomycetemcomitans may be a useful marker of increased risk for development of aggressive periodontitis in young subjects.
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
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Aggregatibacter actinomycetemcomitans is frequently associated with localized aggressive periodontitis (LAP); however, longitudinal cohort studies relating A. actinomycetemcomitans to initiation of LAP have not been reported. A periodontal assessment was performed on 1,075 primarily African-American and Hispanic schoolchildren, ages 11 to 17 years. Samples were taken from each child for A. actinomycetemcomitans. A cohort of 96 students was established that included a test group of 38 A. actinomycetemcomitans-positive students (36 periodontally healthy and 2 with periodontal pockets) and 58 healthy A. actinomycetemcomitans-negative controls. All clinical and microbiological procedures were repeated at 6-month intervals. Bitewing radiographs were taken annually for definitive diagnosis of LAP. At the initial examination, clinical probing attachment measurements indicated that 1.2% of students had LAP, while 13.7% carried A. actinomycetemcomitans, including 16.7% of African-American and 11% of Hispanic students (P = 0.001, chi-square test). A. actinomycetemcomitans serotypes a, b, and c were equally distributed among African-Americans; Hispanic students harbored predominantly serotype c (P = 0.05, chi-square test). In the longitudinal phase, survival analysis was performed to determine whether A. actinomycetemcomitans-positive as compared to A. actinomycetemcomitans-negative students remained healthy ("survived") or progressed to disease with attachment loss of >2 mm or bone loss (failed to "survive"). Students without A. actinomycetemcomitans at baseline had a significantly greater chance to remain healthy (survive) compared to the A. actinomycetemcomitans-positive test group (P = 0.0001). Eight of 38 A. actinomycetemcomitans-positive and none of 58 A. actinomycetemcomitans-negative students showed bone loss (P = 0.01). A. actinomycetemcomitans serotype did not appear to influence survival. These findings suggest that detection of A. actinomycetemcomitans in periodontally healthy children can serve as a risk marker for initiation of LAP.
Aggregatibacter actinomycetemcomitans
Aggressive periodontitis
Clinical attachment loss
Longitudinal Study
Actinobacillus
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