Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Actinobacillus actinomycetemcomitans isolates from periodontal pockets were examined for restriction fragment-length polymorphism using a characterized 4.7-kb DNA probe. A total of 6 patterns of RFLP was found in 133 isolates originating from 12 subjects. No relatedness was found between RFLP types and serotypes. Different periodontal sites within the same subject and different individuals within the same family sometimes showed only one type of A. actinomycetemcomitans RFLP. When members among the same family showed 2 RFLP types, children were always infected with the A. actinomycetemcomitans strains found in at least one of the parents. These findings support the concept of familial spread of A. actinomycetemcomitans. A. actinomycetemcomitans RFLP type B, corresponding to reference strain JP2, seems to be particularly virulent, as indicated from the presence of RFLP type B in 3 subjects who converted from a healthy periodontal state to localized juvenile periodontitis. RFLP type B was not detected in any of the 21 A. actinomycetemcomitans-infected patients with adult periodontitis. The RFLP method seems to be useful in determining the epidemiology and possibly the potential virulence of periodontal strains of A. actinomycetemcomitans.
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PMID:Genetic approach to the study of epidemiology and pathogenesis of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. 198 6

Actinobacillus actinomycetemcomitans is a gram-negative bacterium that has been implicated in the etiology of several forms of periodontitis, especially localized juvenile periodontitis. A potent leukotoxin (Lkt) is produced by most A. actinomycetemcomitans isolates from patients with periodontal disease, but some isolates are leukotoxin nonproducing (Lkt-). The molecular bases for the differences in leukotoxin expression are being explored to clarify the role of leukotoxin in pathogenesis. We have previously cloned the leukotoxin structural gene, lktA, from the leukotoxin-producing (Lkt+) strain JP2 and have shown that it is linked to three other genes, lktB, lktC, and lktD, whose gene products are thought to be required for activation and localization of the leukotoxin. These genes have now been used in Southern blot analysis to demonstrate that Lkt- strains, like Lkt+ strains, contain all four genes of the lkt gene cluster. While restriction fragment length polymorphisms were detected, they did not correlate with toxin phenotype. RNA blot analysis demonstrated that Lkt+ strains produced two transcripts, one 9.3 kb in length and the other 4.3 kb. They encode lktCABD and lktCA. respectively. Lkt- strains contained significantly lower levels of the 4.3-kb transcript with no discernible 9.3-kb message. The leukotoxic activity of the A. actinomycetemcomitans strains, measured by chromium release assays, correlated with the lkt RNA content. Therefore, a major component of leukotoxin regulation is at the level of RNA transcription or stability. Interestingly, the lkt RNAs in JP2 are regulated during growth phase, being greatly reduced in cells approaching stationary phase. Thus, the regulation of lkt RNA can be affected by both genotype and environment.
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PMID:Regulation of leukotoxin in leukotoxic and nonleukotoxic strains of Actinobacillus actinomycetemcomitans. 200 19

Actinobacillus actinomycetemcomitans is a major periodontal pathogen which is associated with early-onset and adult periodontitis. The organism has been shown to be widely distributed among dentate, healthy individuals as well. It has been demonstrated that A. actinomycetemcomitans shows great genetic diversity. An especially virulent clone of the organism (JP2-like) with a specific 530-base pair (bp) deletion in the promoter region of the leukotoxin gene has been isolated from localized juvenile periodontitis patients and related subjects of African and African-American origin. The aim of the present study was to examine the presence of this specific clone employing specific oligonucleotide primers in a polymerase chain reaction among 51 isolates of A. actinomycetemcomitans recovered from 201, 18- to 25-year-old recruits with no or minor periodontal disease. In addition, clinical isolates from 37 periodontitis patients were analyzed as well as reference strains ATCC 29524, NCTC 9710, Y4 and JP2. Primers amplifying a specific 285-bp amplification product in the ltxA region of the leukotoxin gene and a specific 547-bp amplification product of 16 S rRNA were used to genetically confirm identification of the organisms. Primers amplifying sequences in the leukotoxin promoter region were used to identify the deletion. Species specific primers definitively identified all A. actinomycetemcomitans isolates. No isolates from army recruits or the reference strains displayed the deletion in the leukotoxin promoter region. However, in the periodontitis group, a 24-year-old individual from Ghana with localized juvenile periodontitis was identified with an intraoral infection with highly toxic A. actinomycetemcomitans (JP2-like). Present results confirm previous observations of absence of a highly toxic clone of A. actinomycetemcomitans among periodontally healthy and diseased Caucasians as well as a possible presence in localized juvenile periodontitis in individuals of African origin.
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PMID:Absence of an especially toxic clone among isolates of Actinobacillus actinomycetemcomitans recovered from army recruits. 1080 29

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.
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PMID:Early-onset periodontitis in Morocco is associated with the highly leukotoxic clone of Actinobacillus actinomycetemcomitans. 1149 17

The JP2 clone of Actinobacillus actinomycetemcomitans is associated with early-onset periodontitis in certain ethnic populations of African origin. Here, we describe and evaluate a set of primers for PCR to assay for the presence of A. actinomycetemcomitans and to discriminate between JP2-like strains and other genotypes in subgingival plaque samples.
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PMID:Improved PCR for detection of the highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans in subgingival plaque samples. 1453 34

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.
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PMID:Detection of a highly toxic clone of Actinobacillus actinomycetemcomitans (JP2) in a Moroccan immigrant family with multiple cases of localized aggressive periodontitis. 1470 27

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.
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PMID:The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans and progression of periodontal attachment loss. 1538 16

The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans is strongly associated with aggressive periodontitis in adolescents of African descent. DNA fingerprinting using the frequently cutting restriction enzyme MspI and multilocus sequence typing (MLST) showed that five strains of this clone were genetically virtually identical, although ribotyping of the six rrn genes and EcoRI RFLP analysis of the seven IS150-like elements revealed differences. PCR analyses demonstrated that these multi-copy sequences are subject to intragenomic homologous recombination, resulting in translocations or large inversions. The genome rearrangements were reflected in differences among 25 strains representing the JP2 clone in DNA fingerprinting using the rare-cutting restriction enzyme XhoI and resolved by PFGE. XhoI DNA fingerprinting provides a tool for studying local epidemiology, including transmission of this particularly pathogenic clone of A. actinomycetemcomitans.
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PMID:Intragenomic recombination in the highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans. 1620 19

Actinobacillus actinomycetemcomitans is a Gram negative pathogen that is the etiologic agent of localized aggressive periodontitis (LAP), a rapidly progressing and severe disease of the oral cavity that affects predominantly adolescents. A. actinomycetemcomitans is also found in extraoral infections including infective endocarditis. As one of its many virulence determinants, A. actinomycetemcomitans produces the RTX (repeats in toxin) exotoxin, leukotoxin (LtxA). LtxA specifically kills leukocytes of humans and Old World Monkeys. All of our current knowledge of A. actinomycetemcomitans LtxA is based on the protein from strain JP2, a nonadherent laboratory isolate. Because laboratory isolates can lose virulence properties, we wished to examine LtxA from a clinical isolate, NJ4500. We show that localization patterns of LtxA do not differ between the strains. Subcellular localization studies with NJ4500 revealed that LtxA localizes to the outer membrane and that the interaction between LtxA and the surface of cells is specific. Surface localized LtxA was not removed with NaCl treatment and protease protection experiments revealed that approximately 10 kDa of LtxA is exposed. We purified secreted LtxA from NJ4500 and found that the specific activity of this toxin was greater than that of secreted LtxA from JP2. For other RTX toxins, fatty acid modification affects toxin activity, and A. actinomycetemcomitans LtxA is predicted to be modified. We show by two-dimensional gel electrophoresis that NJ4500 LtxA is more highly modified than JP2 LtxA, suggesting that the difference in activities could be due to differential modification. Studies of A. actinomycetemcomitans pathogenesis should therefore consider LtxA from clinical isolates.
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PMID:Characterization of leukotoxin from a clinical strain of Actinobacillus actinomycetemcomitans. 1641 41

The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans is strongly associated with periodontitis in adolescents. Availability of the DNA sequence of the complete genome of A. actinomycetemcomitans strain HK1651, a representative strain of the JP2 clone (http://www.genome.ou.edu/act.html), has provided new possibilities in basic research regarding the understanding of the pathogenesis of A. actinomycetemcomitans in periodontitis. This case report describes the periodontal treatment of the original source of A. actinomycetemcomitans HK1651, a 16-year-old Ghanaian adolescent girl with aggressive periodontitis. The bacterial examination involved polymerase chain reaction analysis for presence of JP2 and non-JP2 types of A. actinomycetemcomitans. The treatment, including periodontal surgery supplemented by antibiotics, arrested the progression of periodontitis for more than 10 years. Initially, infection by A. actinomycetemcomitans, including the JP2 clone, was detected at various locations in the oral cavity and was not limited to the periodontal pockets. Post-therapy, the JP2 clone of A. actinomycetemcomitans disappeared, while the non-JP2 types of A. actinomycetemcomitans remained a part of the oral microflora.
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PMID:Aggressive periodontitis in a 16-year-old Ghanaian adolescent, the original source of Actinobacillus actinomycetemcomitans strain HK1651 - a 10-year follow up. 1687 36


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