The periodontal pathogen Actinobacillus actinomycetemcomitans produces a leukotoxin that is considered a primary virulence factor in localized juvenile periodontitis (LJP). Select strains of the bacterium contain a 530‐bp deletion in the promoter region of the leukotoxin gene operon which results in enhanced transcription of the leukotoxin. DNA hybridization and polymerase chain reaction (PCR) were used to examine genetic variants of A. actinomycetemcomitans in 24 LJP‐susceptible children from 21 families having a history of the disease and 34 control children from non‐LJP families. A significant association was found between the detection of variants that had a deletion in the leukotoxin promoter region, indicative of a high level expression leukotoxin genotype, and conversion from a healthy periodontal status to disease. Subjects harboring A. actinomycetemcomitans of this genotype were more likely to convert to LJP than those subjects who had variants containing the full length leukotoxin promoter region (odds ratio = 22.50, 95% C.I.). These findings support the concept that highly virulent strains or clonai types of periodontal pathogens play a major role in the initiation of periodontal disease in susceptible hosts. J Periodontol 1998;69:998–1007.
Early mutans streptococci (MS) infection has been associated with higher caries activity in childhood. Since colonization with MS does not always lead to caries activity, additional factors may be involved in MS cariogenicity. For example, MS may differ in virulence traits such as the potential to synthesize glucan polymers from sucrose. In the present study, we tested the hypothesis that caries activity can be associated with variations in virulence factor expression of MS-infecting strains. At baseline, levels of MS obtained by the tongue-blade sampling method, and the presence of visible plaque on upper incisors, were measured in 101 12- to 30-month-old children. Dental caries lesions were diagnosed at baseline and after one year. Caries incidence data were then used to select ten caries-free and nine caries-active children from whom a total of 20 MS fresh isolates was studied. Water-insoluble glucan (WIG) synthesis, final pH, and sucrose-dependent adherence on glass surfaces were measured in these MS isolates. Concentrated culture supernatants were separated in duplicate SDS-PAGE gels, which were then either stained for protein or incubated with 5% sucrose. The intensities of the WIG bands developed in the 5% sucrose PAGE gels and the corresponding protein-stained GTF bands were measured by scanning densitometry. High MS levels (> or = 100 CFU) were associated with high caries incidence (p < 0.01). The presence of visible plaque did not correlate with caries incidence. The intensities of WIG bands were positively correlated with caries incidence (p < 0.05) and with the ability of MS to adhere to glass surfaces (p < 0.05). Analysis of our data suggests that the ability to synthesize WIG is an important virulence factor in initial caries development by increasing MS adherence and accumulation in the plaque of young children.
A genetic locus for a cytolethal distending toxin (CDT) was identified in a polymorphic region of the chromosome ofActinobacillus actinomycetemcomitans, a predominant oral pathogen. The locus was comprised of three open reading frames (ORFs) that had significant amino acid sequence similarity and more than 90% sequence identity to the cdtABC genes of some pathogenicEscherichia coli strains and Haemophilus ducreyi, respectively. Sonic extracts from recombinant E. coli, containing the A. actinomycetemcomitans ORFs, caused the distension and killing of Chinese hamster ovary cells characteristic of a CDT. Monoclonal antibodies made reactive with the CdtA, CdtB, and CdtC proteins of H. ducreyi recognized the corresponding gene products from the recombinant strain. CDT-like activities were no longer expressed by the recombinant strain when an ΩKan-2 interposon was inserted into the cdtA andcdtB genes. Expression of the CDT-like activities inA. actinomycetemcomitans was strain specific. Naturally occurring expression-negative strains had large deletions within the region of the cdt locus. The cdtABC genes were flanked by an ORF (virulence plasmid protein), a partial ORF (integrase), and DNA sequences (bacteriophage integration site) characteristic of virulence-associated regions. These results provide evidence for a functional CDT in a human oral pathogen.
Accumulated lines of evidence suggest that hyperimmune responses to periodontal bacteria result in the destruction of periodontal connective tissue and alveolar bone. The etiological roles of periodontal bacteria in the onset and progression of periodontal disease (PD) are well documented. However, the mechanism underlying the engagement of periodontal bacteria in RANKL-mediated alveolar bone resorption remains unclear. Therefore, this review article addresses three critical subjects. First, we discuss earlier studies of immune intervention, ultimately leading to the identification of bacteria-reactive lymphocytes as the cellular source of osteoclast-induction factor lymphokine (now called RANKL) in the context of periodontal bone resorption. Next, we consider (1) the effects of periodontal bacteria on RANKL production from a variety of adaptive immune effector cells, as well as fibroblasts, in inflamed periodontal tissue and (2) the bifunctional roles (upregulation vs. downregulation) of LPS produced from periodontal bacteria in a RANKL-induced osteoclast-signal pathway. Future studies in these two areas could lead to new therapeutic approaches for the management of PD by down-modulating RANKL production and/or RANKL-mediated osteoclastogenesis in the context of host immune responses against periodontal pathogenic bacteria.
Propolis extract antimicrobial activity against periodontopathic (ATCC) bacteria was investigated "in vitro". Bacterial strains tested were: Prevotella intermedia, Prevotella melaninogenica, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Capnocytophaga gingivalis and Fusobacterium nucleatum. Minimal inhibitory concentration (MIC) for the strains tested was determined using the method of broth dilution with the propolis extract in serial concentrations. Results showed MIC of 1 µg/ml for Actinobacillus actinomycetemcomitans and Capnocytophaga gingivalis; and 0.25 µg/ml for Prevotella intermedia, Prevotella melaninogenica, Porphyromonas gingivalis and Fusobacterium nucleatum. Some superinfectant organisms were also tested: Candida albicans susceptibility to propolis ethanolic extract was demonstrated at a concentration of 12 µg/ml. The MIC for Pseudomonas aeruginosa, Escherichia coli and Staphylococcus aureus (wild types) was 14 µg/ml. All periodontal pathogens and superinfectants tested were susceptible to the propolis extract. The positive results suggest that the propolis extract should be further tested as an adjuvant to periodontal therapy.
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