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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., Competing Interests: The authors declare that there is no conflict of interest.

Objective: The microbial eatiology of aggressive perodontitis is different worldwidly. The purpose of this study was to determine the presence or absence of two anaerobic, highly pathogenic bacteria, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis (P.g) in aggressive periodontitis in a Moroccan population., Material and Methods: Our study involved a sample of 32 subjects, 20 with aggressive periodontitis and 12 with a healthy periodontium. A pool of bacterial samples was performed in each patient looking for Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis by the method of bacterial culture., Results and Conclusion: Microbiological analysis showed an association of the presence of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis with aggressive periodontitis in Morocco. Porphyromonas gingivalis would be less present than Aggregatibacter actinomycetemcomitans in aggressive periodontitis in Morocco (30% vs 83%)(p < or = 0.05%). However, given the small sample size other studies are necessary.

Objective: To investigate the presence of A. actinomycetemcomitans, including the highly virulent JP2 clone, in young adult patients with aggressive periodontitis, and associate the findings with the two forms of the disease., Materials and Methods: Seventy Moroccan subjects with aggressive periodontitis, aged less than 35 years, were recruited. Among these, 41 had LAgP and 29 had GAgP. Plaque samples were collected from periodontal pockets and examined using a PCR that detects the presence of A. actinomycetemcomitans and which differentiates between JP2 and non-JP2 genotypes of the bacterium., Results: total of 58 (83%) from the 70 AgP patients were positive for A. actinomycetemcomitans, among whom 77% were positives for the JP2 clone. The JP2 clone was detected in 34 (83%) of the LAgP patients compared to 20 (69%) of the GAgP patients (p = 0.17). Fourteen (20%) of the patients harbored non-JP2 genotypes of A. actinomycetemcomitans, although most of these patients (10/14) also harbored the JP2 clone., Conclusions: The presence of the JP2 clone of A. actinomycetemcomitans is strongly associated with both LAgP and GAgP in young adults in Morocco. This implies that treatment of AgP in this population should include microbiological screening and aim at eradication of the bacterium when present.

Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2-susceptible population and suggests that such individuals may develop immunity to AgP., (© 2010 John Wiley & Sons A/S.)

The JP2 clone of Aggregatibacter actinomycetemcomitans is strongly associated with aggressive periodontitis. To obtain information about colonization dynamics of the JP2 clone, we used PCR to examine its presence in 365 Moroccan juveniles from whom periodontal plaque samples were collected at baseline and after one and two years. Periodontal attachment loss was measured at baseline and at the two-year follow-up. At baseline, 43 (12%) carriers of the JP2 clone were found. Nearly half (44 %) of these were persistently colonized with the clone. The relative risk for the development of aggressive periodontitis, adjusted for the concomitant presence of other genotypes of A. actinomycetemcomitans, was highest for individuals continuously infected by the JP2 clone (RR = 13.9; 95% CI, 9.0 to 21.4), indicating a relationship between infectious dose and disease, which further substantiates the evidence for the JP2 clone as a causal factor in aggressive periodontitis.

We developed a loop-mediated isothermal amplification method that detects the JP2 clone of Aggregatibacter actinomycetemcomitans, which induces aggressive periodontitis in adolescents of North and West African descents. Being independent of special equipment, this specific and sensitive method offers significant advantages for screening of patients on a population basis and in clinical settings.

Background: Periodontitis is a loss of supporting connective tissue and alveolar bone around teeth, and if it occurs in an aggressive form it can lead to tooth loss before the age of 20 years. Although the cause of periodontitis in general remains elusive, a particular clone (JP2) of the gram-negative rod Aggregatibacter (Actinobacillus) actinomycetemcomitans is considered a possible aetiological agent of the aggressive form in adolescents living in or originating from north and west Africa, where the disease is highly prevalent. We did a population-based longitudinal study of adolescents to assess the role of the JP2 clone in the initiation of aggressive periodontitis., Methods: A total of 700 adolescents from public schools in Rabat, Morocco, were enrolled in the study. We used PCR to detect A actinomycetemcomitans in plaque samples (taken from molar and incisor sites) and to differentiate between the JP2 clone and other non-JP2 genotypes of the bacterium. 18 individuals were found to already have periodontitis and were excluded. The 682 periodontally healthy adolescents (mean age 12.5 years; SD 1.0) were classified according to their A actinomycetemcomitans carrier status at baseline. After 2 years, 428 (62.8%) individuals returned for re-examination, which included recording of periodontal attachment loss measured from the cemento-enamel junction to the bottom of the periodontal pockets of all teeth present., Findings: Individuals who carried the JP2 clone of A actinomycetemcomitans alone (relative risk 18.0; 95% CI 7.8-41.2, p<0.0001) or together with non-JP2 clones of A actinomycetemcomitans (12.4; 5.2-29.9, p<0.0001) had a significantly increased risk of periodontal attachment loss. A much less pronounced disease risk was found in those carrying non-JP2 clones only (3.0; 1.3-7.1, p=0.012)., Interpretation: The JP2 clone of A actinomycetemcomitans is likely to be an important aetiological agent in initiation of periodontal attachment loss in children and adolescents. Co-occurrence of non-JP2 clones of A actinomycetemcomitans reduces the risk of development of periodontitis, suggesting competition for the ecological niche between the JP2 and non-JP2 clones of this species.

The JP2 clone of Actinobacillus actinomycetemcomitans has been implicated in the etiology of periodontitis in adolescents. The aim of this two-year longitudinal study was to describe clinical attachment loss (CAL) progression and to assess its association with baseline occurrence of the JP2 and non-JP2 types of A. actinomycetemcomitans. Clinical re-examination of 121 adolescents in Morocco was performed. Progression of CAL > or = 1 mm, > or = 2 mm, > or = 3 mm, and > or = 4 mm on at least one site was found in 58%, 48%, 22%, and 6% of the subjects, respectively. Subjects who, at baseline, harbored the JP2 clone had a significantly higher progression of CAL than did subjects harboring non-JP2 types of A. actinomycetemcomitans. Subjects harboring non-JP2 types displayed a marginally higher CAL progression than did subjects who were culture-negative for A. actinomycetemcomitans.

Background: A clone of Actinobacillus actinomycetemcomitans (JP2) with increased leukotoxin production and characterized by a 530-bp deletion in the leukotoxin gene operon is endemically present in Morocco and strongly associated with the presence of early onset periodontitis (EOP)., Objectives: To compare patterns of attachment loss among EOP-patients with or without JP2-type of A. actinomycetemcomitans in dental plaque., Material and Methods: Among 45 Moroccan adolescents with EOP (i.e. one or more teeth with attachment loss >/= 3 mm) 39 had cultivable plaque samples. Fifteen (38.5%) were culture-positive for A. actinomycetemcomitans of the JP2-type as determined by PCR, and 24 (61.5%) were not (mean age 16.5 years in both groups)., Results: EOP-patients culture-positive for A. actinomycetemcomitans of the JP2-type had significantly more teeth with attachment loss (mean 5.1, median 4.0) than EOP-patients not culture-positive for A. actinomycetemcomitans of the JP2-type (mean 2.8 teeth, median 1.0) (p = 0.02), and higher attachment loss (mean 4.3 mm vs. 3.4 mm; median 4.0 mm vs. 3.0 mm) (p = 0.01). No major differences could be detected between the two groups in the pattern of affected teeth in the dentition., Conclusions: The study demonstrates increased periodontal destruction among EOP-patients culture-positive for A. actinomycetemcomitans of the JP2-type compared with EOP-patients without the JP2-clone.

A particular clone (JP2) of Actinobacillus actinomycetemcomitans with increased leukotoxin production has been isolated from individuals with early-onset periodontitis (EOP). The aim of this study was to determine the frequency of carriers of this clone and its association with EOP in Moroccan schoolchildren. Of 217 plaque samples, 131 (60.4%) were culture-positive for A. actinomycetemcomitans. A total of 19 of these isolates had a 530-bp deletion in the leukotoxin promoter region characteristic of the JP2 clone. A strong association between the presence of A. actinomycetemcomitans with the 530-bp deletion and EOP was found (adjusted OR = 29.4; 95% Cl = 8.3 - 104.4; p < 0.0005), while no association could be demonstrated between the presence of A. actinomycetemcomitans without the deletion and EOP (adjusted OR = 1.3; 95% CI = 0.5 -2.9; p = 0.750). The study demonstrates that the endemic presence, in a human population, of the highly leukotoxic JP2 clone may result in an unusually high prevalence of EOP.