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Objective: Aggregatibacter actinomycetemcomitans is known to be a major cause of localized aggressive periodontitis. Previous research has suggested that A. actinomycetemcomitans can damage many types of host cells. There is evidence for the ability of this organism to invade endothelial and epithelial cells, but information pertaining to its potential for invading gingival fibroblasts is very limited. Internalization of bacteria is not only responsible for damaging host tissue but also a means to evade the host immune response. It was hypothesized that A. actinomycetemcomitans can invade and reside in human gingival fibroblasts (HGF)., Methods: Primary cultures of HGF were infected with A. actinomycetemcomitans at a ratio of 1:100. Bacterial internalization was determined by an antibiotic protection assay. Bacterial-fibroblast interaction was examined using phase-contrast, scanning and transmission electron microscopy., Results: It was demonstrated that A. actinomycetemcomitans was internalized into HGF at an efficiency of 0.084%. Transmission electron microscopic study showed the presence of A. actinomycetemcomitans in the cytoplasm of HGF without the surrounding membrane. Scanning electron micrographs revealed the sloughing of HGF surfaces on which A. actinomycetemcomitans adhered. Rounded cells, attachment loss and damaged cells were also observed., Conclusions: It is concluded that the attachment and invasion of A. actinomycetemcomitans into human gingival fibroblasts play a role in periodontal tissue damage and may also be a means of immune evasion., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Periodontitis is initiated by the subgingival occurrence of periodontopathogens. It is triggered by a specific host-dependent immune response that is influenced by genetic predisposition. Polymorphisms in the interleukin-1 (IL-1) gene cluster have been suggested to influence the pathogenesis of periodontitis. A total of 159 periodontitis patients (chronic disease: n = 73, aggressive disease: n = 86) and 89 periodontitis-free controls were included in the study. Polymorphisms IL-1α (rs1800587), IL-1β (rs16944, rs1143634), IL-1 receptor (rs2234650), and IL-1 receptor antagonist (rs315952) were determined by polymerase chain reaction with sequence-specific primers (PCR-SSP). Subgingival bacterial colonization was assessed using a polymerase chain reaction/DNA probe test (micro-Ident). Haplotype block structure was determined using Haploview 4.2. Statistical analyses were performed applying SPSS 17.0 considering dominant, recessive, and codominant genetic models. In this case-control study, no association between genomic variants of the IL-1 gene cluster and the incidence of severe periodontitis could be shown. Carriers of the rare genotypes of rs1800587 (p(corr) = 0.009), rs1143634 (p(corr) = 0.009) and composite genotype (rs1800587+rs1143634) (p(corr) = 0.031) had a twofold higher risk for subgingival occurrence of Aggregatibacter actinomycetemcomitans. In forward stepwise binary logistic regression analyses considering age, gender, smoking, and approximal plaque index as potential confounders these significant associations were demonstrated. Despite the genetic background of IL-1 gene cluster could be shown to be associated with subgingival colonization of A actinomycetemcomitans, there is no evidence that it is an independent risk indicator for periodontitis., (Copyright © 2011 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.)

Localized juvenile periodontitis (LJP) causes severe alveolar bone loss and early tooth loss in adolescents and young adults. If it is not appropriately treated as an infection in association with Actinobacillus actinomycetemcomitans, treatment failure is likely. This review of clinical trials of treatment of LJP uses those trials to construct guidelines for LJP treatment.

Human serum antibody responses to antigens from a suspected oral pathogen, Actinobacillus actinomycetemcomitans (Aa), were studied. IgG and IgM isotype antibodies to four antigen preparations, sonicate antigen (SA), leukotoxin (LT), group carbohydrate (LG), and lipopolysaccharide (LPS), were determined using an ELISA. An ELISA inhibition technique was developed to show that human serum antibodies reacting with the LT, LG, or LPS materials were binding to different antigenic moieties in each preparation. Cross-sectional studies of serum IgG antibodies showed that patients with localized juvenile periodontitis (LJP) had a greater frequency of occurrence and a higher level of antibodies to the SA (82%), LT (70%), and LG (62%) antigens compared to all other diseased (11-46%) or normal (4-13%) groups. Serum IgM antibodies to LPS were increased in LJP, generalized juvenile periodontitis, and adult periodontitis patients compared to all other groups. Therefore, while both IgG and IgM antibodies were found against various Aa antigens, the detection of IgG antibodies was most clearly associated with the specific disease classification of LJP. Blocking studies suggested that the human serum responses were specific for the Aa antigens and that the LT, LG, and LPS comprise major antigenic determinants on the organisms to which human serum antibody reacts.

The different forms of periodontitis are all associated with a distinct bacterial flora. However, a clear relationship is described between localized juvenile periodontitis (LJP) and Actinobacillus actinomycetemcomitans. Eleven LJP patients all harboured A. actinomycetemcomitans. The arrest of LJP is often impossible, due to the inability to eliminate A. actinomycetemcomitans. Therefore, antibiotic treatment was introduced in combination with the initial treatment. We studied the effect of periodontal treatment on the microflora and clinical status of periodontal disease patients using different therapies. Group 3 attained the best results (initial treatment and a combination metronidazole and amoxicillin), the group to eliminate A. actinomycetemcomitans effectively.