Clinical immunologic and microbiologic features of active disease sites in juvenile periodontitis

Mandell, Robert L.; Ebersole, Jeffrey L.; Socransky, S. S.

doi:10.1111/j.1600-051x.1987.tb00996.x

Cited by 114 publications

(83 citation statements)

References 36 publications

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“…The ease of de novo colonization may be influenced by the presence of periodontal disease or other subgingival bacterial species. In this regard, Mandell and colleagues (15,16) reported a synergistic relationship between E. corrodens and A. actinomycetemcomitans. We noted an association between the clonal diversity of E. corrodens and coinfection with P. gingivalis at the same sites.…”

Section: Discussionmentioning

confidence: 99%

Clonal Diversity and Stability of Subgingival Eikenella corrodens

et al. 2004

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Eikenella corrodens is a commensal subgingival bacterium commonly found in both periodontally nondiseased and diseased subjects. The present study examined the clonal diversity and stability of subgingival E. corrodens over time. Ninety-five subjects were enrolled at the baseline examination, including 44 periodontally nondiseased subjects and 51 subjects with aggressive periodontitis. Twenty-two nondiseased subjects and 11 subjects with aggressive periodontitis were subsequently reexamined after an average interval of 14 months. Two subgingival plaque samples were obtained from each subject to determine the total cultivable bacteria. In addition, multiple E. corrodens isolates from each sample were recovered for clonal analysis by arbitrarily primed PCR. The mean numbers of distinct E. corrodens clones harbored by nondiseased subjects and subjects with aggressive periodontitis were 1.3 and 3.0, respectively. Thirty-nine percent of the nondiseased subjects and 63% of the subjects with aggressive periodontitis harbored multiple clones of E. corrodens. The numbers of distinct E. corrodens clones increased significantly (Mann-Whitney ranking test, P < 0.05) in sites from patients with aggressive periodontitis, in sites with pocket depths of 4 mm or greater, in sites with a clinical attachment loss of 2 mm or greater, and in sites coinfected with Porphyromonas gingivalis. Comparison of E. corrodens clones recovered at the baseline and those recovered at the follow-up examination showed that E. corrodens colonization was not stable. Thirty-eight of the 66 follow-up samples (58%) showed a complete change (including de novo colonization of the sites or complete elimination of the organism from the sites) of the subgingival E. corrodens clonal types between the baseline and the follow-up examinations. Our results suggest a complexity of subgingival microbiota not seen previously.

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Section: Discussionmentioning

confidence: 99%

Clonal Diversity and Stability of Subgingival Eikenella corrodens

et al. 2004

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“…12 In a large study in the United States, A. actinomycetemcomitans was detected in nearly all the analyzed LAgP patients, and in contrast in fewer healthy (16.9%) or chronic periodontitis subjects (20.8%) as assessed by culture and immunofluorescence serotyping. 13 A more established role for A. actinomycetemcomitans became clearer with the evidence of a correlation of its elimination with treatment response 14 and the finding of an elevated serum antibody response to this bacterium in patients with LAgP. 15,16 The next milestone was represented by the discovery, in a young case of LAgP, of the A. actinomycetemcomitans JP2 clone, 17 characterized by a 530-base-pair deletion in the leukotoxin operon, associated with increased leukotoxic activity.…”

Section: Agp-microbiological Studiesmentioning

confidence: 99%

Aggressive Periodontitis: microbes and host response, who to blame?

Nibali

2015

Virulence

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“…But with the identification of A. actinomycetemcomitans as a putative periodontal pathogen, emphasis shifted from anaerobes to this micro-aerophilic species. Selective media were developed that allowed it to be detected even when it was greatly outnumbered by other plaque species (Slots, 1982;Mandell et al, 1987). As a result, it was implicated, on the basis of association-type studies, as a putative periodontal pathogen in refractory periodontitis, early-onset periodontitis, and in the rapidly deteriorating lesion (Tanner et al, 1979;Dzink et al, 1988;van Winkelhoff et al, 1989;Slots et al, 1990a;Haffajee and Socransky, 1994).…”

Section: (A) the Non-specific Plaque Hypothesismentioning

confidence: 99%

The Antimicrobial Treatment of Periodontal Disease: Changing the Treatment Paradigm

Loesche

1999

Critical Reviews in Oral Biology & Medicine

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Over the last 100 years, methods of surgical periodontal treatment have enjoyed a history of success in improving oral health. The paradigm of care is based on the "non-specific plaque hypothesis"-that is, the overgrowth of bacterial plaques cause periodontal disease, and the suppression of this overgrowth reduces disease risk. The central feature of this approach to care is the removal of inflamed gingival tissue around the teeth to reduce periodontal pocket depth, thereby facilitating plaque removal by the dentist and by the patient at home. Over the last 30 years, with the recognition that periodontal disease(s) is caused by specific bacteria and that specific antimicrobial agents can reduce or eliminate the infection, a second paradigm has developed. This new paradigm, the "specific plaque hypothesis", focuses on reducing the specific bacteria that cause periodontal attachment loss. The contrast between the two paradigms can be succinctly stated as follows: The antimicrobial therapy reduces the cause, while the surgical therapy reduces the result of the periodontal infection. The specific plaque hypothesis has two important implications. First, with the increasing attention to evidence-based models for prevention, treatment, outcome assessment, and reimbursement of care, increasing attention and financial effort will be channeled into effective preventive and treatment methods. Second, the recent observations that periodontal infections increase the risk of specific systemic health problems, such as cardiovascular disease, argue for the prevention and elimination of these periodontal infections. This review highlights some of the evidence for the specific plaque hypothesis, and the questions that should be addressed if antimicrobial agents are to be used responsively and effectively.

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Clinical immunologic and microbiologic features of active disease sites in juvenile periodontitis

Cited by 114 publications

References 36 publications

Clonal Diversity and Stability of Subgingival Eikenella corrodens

Clonal Diversity and Stability of Subgingival Eikenella corrodens

Aggressive Periodontitis: microbes and host response, who to blame?

The Antimicrobial Treatment of Periodontal Disease: Changing the Treatment Paradigm

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