leukotoxin and Chronic-Disease

The purpose of this study was to determine to what extent the presence or absence of periodontal pathogens can distinguish between subjects with chronic and aggressive periodontitis.. A systematic review of cross sectional and longitudinal studies providing microbiological data both from patients with chronic periodontitis (ChP) and aggressive periodontitis (AgP) at a subject level. Strict inclusion criteria were applied. The presence or absence of five microorganisms was selected as primary study parameters: Actinobacillus actinomycetemcomitans (AA), Porphyromonas gingivalis (PG), Prevotella intermedia (PI), Bacteroides forsythus (BF), and Campylobacter rectus (CR).. The presence or absence of AA could be evaluated in 11 papers. In seven papers the presence or absence of PG could be analysed. Subject specific data on PI were available from six studies. Two studies could be used regarding the presence or absence of BF, and two regarding CR. Sensitivity and specificity of every microbiological test were individually calculated for each selected study, assuming that the clinical diagnosis of AgP or ChP was the true status the tests attempted to detect. AgP was considered to be the condition of interest and ChP was considered equivalent to 'non-AgP'. Receiver Operator Characteristic (ROC) diagrams were constructed using these data. ROC diagrams indicated the limited discriminatory ability of all of the test parameters to identify subjects with AgP. An additional assessment showed that the highly leukotoxic variant of AA was uniquely associated with patients suffering from aggressive periodontitis. However, in a high proportion of patients diagnosed with AgP the presence of this variant could not be detected.. The presence or absence of AA, PG, PI, BF or CR could not discriminate between subjects with AgP from those with ChP.

Topics: Acute Disease; Aggregatibacter actinomycetemcomitans; Bacteroides; Campylobacter; Chronic Disease; Exotoxins; Humans; Periodontitis; Porphyromonas gingivalis; Prevotella intermedia; ROC Curve; Sensitivity and Specificity

Mechanical debridement results in a shift of the bacterial composition in the periodontal pocket on the species level. It is unknown, however, whether a clonal change within a species could lead to the emergence of strains with different levels of virulence. Therefore, in the present study, the genetic variability of Actinobacillus actinomycetemcomitans was assessed and strains identified which were associated with periodontal disease progression following periodontal therapy, i.e., refractory periodontitis. Twenty adult patients with untreated periodontitis and subgingival colonization of A. actinomycetemcomitans were randomly assigned to receive full-mouth scaling alone or scaling with an adjunctive antimicrobial therapy. Both groups received supportive periodontal therapy at 3, 6, 9, 12, 18, and 24 months. Subgingival plaque samples were taken at every visit; venous blood was obtained at 24 months only. A. actinomycetemcomitans isolates were typed by the RAPD method, and antibody reactivity against outer membrane proteins was assessed by immunoblot analysis. Eleven distinct RAPD patterns were found in 18 patients completing the study. All patients harbored only one A. actinomycetemcomitans genotype, and within each patient this genotype persisted throughout the 24-month observation period. No differences in the expression of antibody reactivity against outer membrane proteins were found between strains isolated at baseline and at 24 months. Three genotypes were associated with reduced survival rates of teeth without probing attachment loss of 2 mm or more. The results indicated that (i) most patients harbored only one A. actinomycetemcomitans genotype; (ii) the genotype persisted following therapy; and (iii) only some genotypes were associated with refractory periodontitis.

Topics: Adult; Aggregatibacter actinomycetemcomitans; Amoxicillin; Anti-Bacterial Agents; Bacterial Outer Membrane Proteins; Bacterial Typing Techniques; Chronic Disease; Clone Cells; Dental Plaque; Disease Progression; DNA Fingerprinting; DNA, Bacterial; Exotoxins; Female; Genetic Variation; Humans; Male; Metronidazole; Middle Aged; Penicillins; Periodontal Pocket; Periodontitis; Random Amplified Polymorphic DNA Technique; Survival Analysis; Virulence

beta2-Glycoprotein I (beta 2GPI) is important in the suppression of coagulation, and antibodies against TLRVYK peptides on the beta 2GPI molecule are related to thrombosis. According to the Swiss-Prot database, Aggregatibacter actinomycetemcomitans leukotoxin c has sequences (SIRVYK) that are homologous to the TLRVYK peptides. The aim of this study was to investigate the effects of A. actinomycetemcomitans infection on the antibody response against SIRVYK peptides in patients with periodontitis.. Serum immunoglobulin G (IgG) antibody and IgG subclass antibody titers against SIRVYK or TLRVYK peptides were measured by enzyme-linked immunosorbent assay in 46 patients with aggressive periodontitis (eight with localized disease, 38 with generalized disease), 28 patients with chronic periodontitis, and 20 periodontally healthy subjects. The presence of A. actinomycetemcomitans in plaque and saliva samples was determined using polymerase chain reaction.. The level of anti-SIRVYK antibodies was significantly higher in patients who were A. actinomycetemcomitans-positive than in A. actinomycetemcomitans-negative patients (P < 0.05) in the chronic periodontitis group. A similar trend was found in the antibody response to TLRVYK peptide; however, no statistically significant difference was seen between A. actinomycetemcomitans-positive and -negative patients. The A. actinomycetemcomitans-positive patients displayed significantly higher levels of anti-SIRVYK IgG2 and IgG3 antibodies than A. actinomycetemcomitans-negative patients (P < 0.05 and P < 0.05, respectively). The level of IgG2 was highest among the four IgG subclasses and it predominantly increased in patients who were A. actinomycetemcomitans-positive. Anti-TLRVYK antibody levels were significantly correlated with anti-SIRVYK IgG antibody levels.. The results suggest that A. actinomycetemcomitans infection may elicit anti-SIRVYK IgG antibodies and modify the anti-TLRVYK antibody response in patients with periodontitis by molecular mimicry with beta2GPI.

Topics: Adult; Aggregatibacter actinomycetemcomitans; Antibodies, Bacterial; Anticoagulants; Bacterial Toxins; beta 2-Glycoprotein I; Chronic Disease; Dental Plaque; Exotoxins; Gingival Hemorrhage; Humans; Immunoglobulin G; Middle Aged; Molecular Mimicry; Peptide Fragments; Periodontal Pocket; Periodontitis; Periodontium; Polymerase Chain Reaction; Saliva

The use of whole saliva has shown to be promising in detecting Actinobacillus actinomycetemcomitans out of the subgingival environment. The objective of the present study was to evaluate the use of unstimulated saliva in detecting A. actinomycetemcomitans and to compare the subgingival and extracrevicular occurrence of this pathogen in Brazilian subjects with chronic periodontitis.. Sixty-six patients (mean age 38.01 9.28 years) with advanced generalized chronic periodontitis were sampled. Subgingival plaque samples were collected from eight sites per patient representing the two deepest sites of each quadrant. Samples of the mucous surfaces, including dorsal surface of the tongue and cheek, were collected with a sterile swab and placed in a microtube containing a reduced solution. Samples of unstimulated saliva were also collected in sterile tubes and 0.1 ml of whole saliva was diluted in 1 ml of reduced solution. The presence of A. actionomycetemcomitans was established using bacterial culture in trypticase soy bacitracin vancomycin selective media. Polymerase chain reaction (PCR) was used to differentiate highly from minimally leukotoxic strains in patients who presented A. actinomycetemcomitans in at least two sampled sites.. A. actinomycetemcomitans was isolated from 63.63% of subgingival samples, 56.06% of saliva samples, and 45.45% of samples from mucous surfaces. No statistical difference was observed between subgingival and salivary occurrence of the microorganism. Linear regression showed an association between subgingival plaque and saliva (r(2) = 0.897; P = 0.015) and mucous membrane and saliva (r(2) = 0.152; P = 0.024). The same A. actinomycetemcomitans leukotoxic profile was observed in all sampled sites for a given patient.. These results suggest that in advanced periodontitis, unstimulated saliva is representative of pooled subgingival plaque samples and its use is appropriate in the oral detection of A. actinomycetemcomitans.

Topics: Adult; Aggregatibacter actinomycetemcomitans; Chronic Disease; Dental Plaque; Exotoxins; Female; Humans; Linear Models; Male; Middle Aged; Mouth Mucosa; Periodontitis; Polymerase Chain Reaction; Saliva

Previous studies suggest differences between geographically and racially distinct populations in the prevalence of periodontopathic bacteria as well as greater periodontal destruction associated with infection by highly leucotoxic Actinobacillus actinomycetemcomitans. The present study examined these hypotheses in Brazilians with aggressive or chronic periodontitis.. Clinical, radiographical, and microbiological assessments were performed on 25 aggressive periodontitis and 178 chronic periodontitis patients including 71 males and 132 females, 15-69 years of age.. The prevalence of Porphyromonas gingivalis was similar to that of other South American populations. The prevalence of A. actinomycetemcomitans and its highly leucotoxic subgroup was higher in Brazilians. Highly leucotoxic A. actinomycetemcomitans was more prevalent in aggressive periodontitis (chi2=27.83) and positively associated with deep pockets (>6 mm, chi2=18.26) and young age (<29 years, chi2=18.68). Greater mean attachment loss was found in subjects with highly leucotoxic A. actinomycetemcomitans than in subjects with minimally leucotoxic (p=0.0029) or subjects not infected (p=0.0001).. These data support the hypothesis of differences between populations in the prevalence of periodontopathic bacteria and of greater attachment loss in sites infected with highly leucotoxic A. actinomycetemcomitans. Detection of highly leucotoxic A. actinomycetemcomitans in children and adolescents may be a useful marker for aggressive periodontitis.

Topics: Acute Disease; Adolescent; Adult; Aged; Aggregatibacter actinomycetemcomitans; Bacteroides; Brazil; Campylobacter rectus; Chronic Disease; Colony Count, Microbial; Cross-Sectional Studies; Dental Plaque; DNA, Bacterial; Exotoxins; Female; Humans; Logistic Models; Male; Middle Aged; Periodontitis; Porphyromonas gingivalis; Prevalence; Prevotella intermedia

The JP2 clone of Actinobacillus actinomycetemcomitans, a high-leukotoxin-producing strain, characterized by a 530-basepair (bp) deletion in the promoter region of the leukotoxin gene operon and mainly found among individuals with African origin, is associated with localized aggressive periodontitis. The objective of the study was to examine the occurrence of periodontal disease in a Moroccan immigrant family living in Denmark in which the oldest son (14 year) was referred and treated for localized aggressive periodontitis. Further, the potential occurrence of the JP2 clone of A. actinomycetemcomitans in the family was examined. Here we present the clinical, radiographic, and microbiological findings from the family. Clinical and radiographic examination of the other family members revealed that 3 of 5 younger siblings had localized aggressive periodontitis, one had gingivitis and the mother had chronic periodontitis. Despite scaling followed by intensive maintenance therapy several family members, including the sibling with gingivitis, had further attachment loss at the 1-year examination. The JP2 clone of A. actinomycetemcomitans was isolated from subgingival plaque samples from 4 children with periodontitis. In contrast, it was not detected in plaque from the oldest boy, who had been treated for localized aggressive periodontitis by surgery combined with antibiotic therapy. The 4 children with periodontitis and colonized with the JP2 clone were treated by scaling and antibiotic administration. One month later the JP2 clone could still be detected in plaque samples. In conclusion, it is confirmed that members of immigrant families with African origin are potential carriers of the JP2 clone and that those families often have multiple family members with localized aggressive periodontitis. It is proposed that those families are given periodontal examination frequently to benefit from early diagnosis and treatment of the disease.

Topics: Actinobacillus Infections; Adolescent; Adult; Aggregatibacter actinomycetemcomitans; Bacterial Toxins; Base Sequence; Child; Chronic Disease; Denmark; Dental Plaque; Emigration and Immigration; Exotoxins; Female; Follow-Up Studies; Gingivitis; Humans; Male; Morocco; Operon; Periodontitis; Promoter Regions, Genetic; Sequence Deletion

A soluble extract from Actinobacillus actinomycetemcomitans (designated strain Y4) caused dose-dependent cytotoxic changes in PMN isolated from the gingival crevices (C-PMN) of normal adults. When the toxin was preincubated with sera from patients with juvenile periodontitis, there was a significant inhibition of toxic activity. In contrast a variety of other sera from normal subjects with healthy gingiva, and from patients with chronic gingivitis, chronic periodontitis, recurrent herpes labialis, rheumatoid arthritis, or ulcerative colitis enhanced the leukotoxic activity. The neutralization of toxin by serum from patients with juvenile periodontitis was probably due to specific antibodies. Since Actinobacillus actinomycetemcomitans organisms can be frequently identified in subgingival plaque from patients with juvenile periodontitis, the capacity of Y4 toxin to kill C-PMN may contribute to the pathogenesis of this disease.

Topics: Actinobacillus Infections; Adult; Animals; Arthritis, Rheumatoid; Chronic Disease; Colitis, Ulcerative; Crohn Disease; Culture Media; Exotoxins; Gingival Diseases; Herpes Labialis; Humans; Neutralization Tests; Neutrophils; Periodontitis; Rabbits