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J J Zambon

Publications and source records attributed to J J Zambon.

At least 19 recordsLinked to original sources
PubMed2002

[Detection of periodontal pathogenic microorganisms in atheromatous plaque. Preliminary results].

INTRODUCTION: Recent studies suggest that chronic infections, including those associated with periodontitis, increase the risk for coronary vascular disease. We hypothesize that oral microorganisms including periodontal bacterial pathogens enter the blood stream during transient bacteremias where they may play a role in the development and progression of atherosclerosis. MATERIALS AND METHODS: To test this hypothesis, 34 human specimens obtained during carotid endarterectomy or bypass procedures were examined by use of specific oligonucleotide primers for Porphyromonas gingivalis, Prevotella intermedia, Actinobacillus actinomycetemcomitans and Bacteroides forsythus in polymerase chain reaction (PCR) assays. RESULTS: Twenty (59%) of the 34 specimens tested positive for bacterial 16S rDNA. Subsequent hybridization of the bacterial 16S rDNA positive specimens with species-specific oligonucleotide probes revealed that 32.4% of the 34 atheromas tested positive for at least one of the target periodontal pathogens. Further analysis of the results in the bacterial positive group (n = 20) shows that 55% of the atheromas tested positive for at least one of the target periodontal pathogens. CONCLUSION: These findings indicate that periodontal pathogens are present in atherosclerotic plaques, where they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.

Adult↗
PubMed2002

Molecular cloning of the fur gene from Actinobacillus actinomycetemcomitans.

In several bacterial species, iron availability in host tissues is coordinated with the expression of virulence determinants through the fur gene product. Initial experiments showed that a cloned Escherichia coli fur gene probe hybridized to Southern blots of Actinobacillus actinomycetemcomitans strain JP2 (serotype b) chromosomal DNA. The A. actinomycetemcomitans fur gene was then cloned utilizing partial functional complementation of the fur mutant in E. coli strain H1780. Analysis of the cloned DNA sequence revealed a 438-bp open reading frame with a deduced 146-amino-acid sequence exhibiting 80% identity to Haemophilus influenzae Fur and 62% identity to E. coli Fur. The pUC Aafur gene probe (generated from JP2 serotype b) hybridized to representatives from all five A. actinomycetemcomitans serotypes as well as to two strains derived from monkeys, suggesting that fur is widely distributed in A. actinomycetemcomitans. Open reading frames having >70% identity with the E. coli and H. influenzae flavodoxin and gyrase A genes, respectively, were found. Expression of the A. actinomycetemcomitans fur gene product repressed fiu expression and siderophore production in E. coli. A gel shift assay demonstrated that the expressed A. actinomycetemcomitans Fur protein bound the bacterial fur consensus sequence. Further characterization of the fur gene product in A. actinomycetemcomitans may improve our understanding of its role in the pathogenesis of periodontal disease and may lead to specific therapeutic modalities.

Aggregatibacter actinomycetemcomitans↗
PubMed2001

Periodontal infections contribute to elevated systemic C-reactive protein level.

BACKGROUND: Periodontitis is a local inflammatory process mediating destruction of periodontal tissues triggered by bacterial insult. However, this disease is also characterized by systemic inflammatory host responses that may contribute, in part, to the recently reported higher risk for cardiovascular disease (CVD) among patients with periodontitis. Moderate elevation of C-reactive protein (CRP) has been found to be a predictor of increased risk for CVD. Elevated CRP levels in periodontal patients have been reported by several groups. In this study, we examined whether CRP plasma levels are increased in periodontitis and if there is a relation to severity of periodontal disease and to the periodontal microflora. METHODS: CRP serum levels were assessed using radial immunodiffusion assay in 174 subjects, 59 with moderate mean clinical attachment loss (AL) (2.39+/-0.29 mm) and 50 with high AL (3.79+/-0.86 mm) as compared to 65 periodontally healthy controls (AL, 1.74+/-0.18 mm). Clinical attachment loss, probing depths, and percentage of periodontal pocket sites > or =5 mm were measured. The presence of periodontal pathogens Porphyromonas gingivalis (P.g.), Prevotella intermedia (P.i.), Campylobacter recta (C.r.), and Bacteroides forsythus (B.f.) in subgingival plaque samples was measured by immunofluorescence microscopy. RESULTS: Statistically significant increases in CRP levels were observed in subjects with periodontal disease when compared to healthy controls (P= 0.036). Subjects with high levels of mean clinical attachment loss had significantly higher mean CRP levels (4.06+/-5.55 mg/l) than controls (1.70+/-1.91 mg/l), P= 0.011. The CRP levels were adjusted for factors known to be associated with elevated CRP, including age, smoking, body mass index (BMI), triglycerides, and cholesterol. Age and BMI were found to be significant covariates. The reported range for CRP as a risk factor for CVD, peripheral vascular diseases, or stroke is 1.34 mg/l to 6.45 mg/l and the mean of this range is 3 mg/l. The percentage of subjects with elevated levels of CRP > or = 3 mm was significantly higher in the high clinical AL group (38%; 95% Cl: 26.7%, 49.3%) when compared to the control group (16.9%; 95% CI: 9.25%, 24.5%), P= 0.011. The presence of periodontal pathogens P.g., P.i., C.r., and B.f. in subgingival samples was positively associated with elevated CRP levels (P= 0.029). CONCLUSIONS: The extent of increase in CRP levels in periodontitis patients depends on the severity of the disease after adjusting for age, smoking, body mass index, triglycerides, and cholesterol. Also, there are elevated levels of CRP associated with infection with subgingival organisms often associated with periodontal disease, including P.g., P.i., C.r., and B.f. Recent investigations emphasized the role of moderate elevated CRP plasma levels as a risk factor for CVD. The positive correlation between CRP and periodontal disease might be a possible underlying pathway in the association between periodontal disease and the observed higher risk for CVD in these patients.

Adult↗
PubMed2000

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Computer-Assisted Instruction↗
PubMed2000

Identification of periodontal pathogens in atheromatous plaques.

BACKGROUND: Recent studies suggest that chronic infections including those associated with periodontitis increase the risk for coronary vascular disease (CVD) and stroke. We hypothesize that oral microorganisms including periodontal bacterial pathogens enter the blood stream during transient bacteremias where they may play a role in the development and progression of atherosclerosis leading to CVD. METHODS: To test this hypothesis, 50 human specimens obtained during carotid endarterectomy were examined for the presence of Chlamydia pneumoniae, human cytomegalovirus, and bacterial 16S ribosomal RNA using specific oligonucleotide primers in polymerase chain reaction (PCR) assays. Approximately 100 ng of chromosomal DNA was extracted from each specimen and then amplified using standard conditions (30 cycles of 30 seconds at 95 degrees C, 30 seconds at 55 degrees C, and 30 seconds at 72 degrees C). Bacterial 16S rDNA was amplified using 2 synthetic oligonucleotide primers specific for eubacteria. The PCR product generated with the eubacterial primers was transferred to a charged nylon membrane and probed with digoxigenin-labeled synthetic oligonucleotides specific for Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Porphyromonas gingivalis, and Prevotella intermedia. RESULTS: Eighty percent of the 50 endarterectomy specimens were positive in 1 or more of the PCR assays. Thirty-eight percent were positive for HCMV and 18% percent were positive for C. pneumoniae. PCR assays for bacterial 16S rDNA also indicated the presence of bacteria in 72% of the surgical specimens. Subsequent hybridization of the bacterial 16S rDNA positive specimens with species-specific oligonucleotide probes revealed that 44% of the 50 atheromas were positive for at least one of the target periodontal pathogens. Thirty percent of the surgical specimens were positive for B. forsythus, 26% were positive for P. gingivalis, 18% were positive for A. actinomycetemcomitans, and 14% were positive for P. intermedia. In the surgical specimens positive for periodontal pathogens, more than 1 species was most often detected. Thirteen (59%) of the 22 periodontal pathogen-positive surgical specimens were positive for 2 or more of the target species. CONCLUSIONS: Periodontal pathogens are present in atherosclerotic plaques where, like other infectious microorganisms such as C. pneumoniae, they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.

Aged↗
PubMed2000

Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis.

BACKGROUND: Actinobacillus actinomycetemcomitans leukotoxin is thought to be an important virulence factor in the pathogenesis of localized juvenile and other forms of early-onset periodontitis. Some highly leukotoxic A. actinomycetemcomitans strains produce 10 to 20 times more leukotoxin than other minimally leukotoxic strains. The distribution, clonality, and intrafamilial transmission of highly leukotoxic A. actinomycetemcomitans were examined in order to determine the importance of leukotoxin in the pathogenesis of periodontitis. METHODS: The polymerase chain reaction (PCR) was used to differentiate highly leukotoxic from minimally leukotoxic strains in examining 1,023 fresh A. actinomycetemcomitans isolates and strains from our culture collection. These were obtained from 146 subjects including 71 with localized juvenile periodontitis (LJP), 4 with early-onset periodontitis, 11 with post-localized juvenile periodontitis, 41 with adult periodontitis, and 19 periodontally normal subjects. The arbitrarily primed polymerase chain reaction (AP-PCR) analysis of 30 oral isolates from each of 25 subjects was used to determine the intraoral distribution of A. actinomycetemcomitans clones. AP-PCR was also used to examine the transmission of A. actinomycetemcomitans in 30 members of 6 families. The clonality of 41 highly leukotoxic A. actinomycetemcomitans strains was evaluated by both AP-PCR and ribotyping. RESULTS: Highly leukotoxic A. actinomycetemcomitans was found only in subjects with localized juvenile and early-onset periodontitis. Fifty-five percent of the LJP subjects harbored highly leukotoxic A. actinomycetemcomitans isolates. Seventy-three percent of the A. actinomycetemcomitans isolates in these subjects were highly leukotoxic. Highly leukotoxic A. actinomycetemcomitans infected younger subjects (mean age 13.95 years, range 5 to 28 years) than minimally leukotoxic (mean age 35.47 years, range 6 to 65 years). Most subjects were infected with only one A. actinomycetemcomitans genotype. However, PCR of whole dental plaques and subsequent analysis of up to 130 individual oral isolates suggested a possible shift in A. actinomycetemcomitans over time in that a few subjects harbored both highly leukotoxic and minimally leukotoxic strains. AP-PCR analysis was consistent with intrafamilial A. actinomycetemcomitans transmission. Ribotyping and AP-PCR analysis confirmed a previous report that highly leukotoxic A. actinomycetemcomitans consists of a single clonal type. CONCLUSIONS: This study suggests that localized juvenile and other forms of Actinobacillus-associated periodontitis are primarily associated with the highly leukotoxic clone of A. actinomycetemcomitans.

Actinobacillus Infections↗
PubMed1998

Rapid chair-side DNA probe assay of Bacteroides forsythus and Porphyromonas gingivalis.

This study compared a rapid, colorimetric DNA probe assay designed to be performed in a dental office within 40 min, with anaerobic culture and indirect immunofluorescence microscopy (IFM) for detection of Bacteroides forsythus and Porphyromonas gingivalis in subgingival plaque samples. The DNA probe assay used the Periodontal Microbial Identification Test (Saigene Corporation, Bothell, Washington, USA). B. forsythus was detected in 46 (52%), 49 (55%) and 39 (44%) of the samples by DNA probe, culture (at levels > or = 10(5)) and IFM, respectively. P. gingivalis was detected in 24 (27%), 18 (20%) and 29 (33%) of the samples by DNA probe, culture (at levels > or = 10(5)) and IFM, respectively. Results from the DNA probe assay were compared to culture. Culture negative, probe positive samples were re-evaluated by IFM, and IFM positive samples were considered positive in "resolved" data. Using resolved data. DNA probe detection sensitivity and specificity values for B. forsythus were 81% and 91% and for P. gingivalis were 80% and 95%, respectively. DNA probe test results were further compared with culture and IFM. For samples negative by both culture and IFM, probe specificity was 92% in 25 B. forsythus samples and 95% in 57 P. gingivalis samples. For samples positive by both reference methods, probe sensitivity was 82% in 27 B. forsythus samples and 73% in 15 P. gingivalis samples. B. forsythus was detected more frequently by culture compared with IFM; the reverse was observed for P. gingivalis. The rapid DNA probe assay for B. forsythus and P. gingivalis was comparable to cultivable and IF analyses.

Adult↗
PubMed1998

Efficacy of a triclosan/NaF dentifrice in the control of plaque and gingivitis and concurrent oral microflora monitoring.

PURPOSE: To compare the effect of a dentifrice containing 0.3% triclosan and 1100 ppm fluoride and a control dentifrice containing 1100 ppm fluoride on plaque, gingiva and the oral microflora in a long-term study simulating clinical usage. MATERIALS AND METHODS: 159 subjects entered the clinical study and 80 were randomly selected to participate in the microbiological evaluation. 71 subjects completed the detailed evaluation of the oral microflora after 6 months use. Plaque was collected at baseline, 3 months, and 6 months, and examined by darkfield microscopy, Gram stain, immunofluorescence, and selective and non-selective media. Changes in antimicrobial susceptibilities were determined for the first 6-month period and for 6 months post-therapy for 68 subjects who completed the entire study. Susceptibilities of whole plaque samples and MIC values for two pre-designated common plaque organisms, A. viscosus and V. parvula were performed. RESULTS: Multivariate ANOVA and non-parametric analyses revealed no statistical differences for any factor tested. No detrimental shifts were found in either; (1) the compositional make up of the normal flora, (2) the periodontopathic or cariogenic flora, or (3) the opportunistic flora in either group of dentifrice users. Both treatments resulted in decreases in Gram positive cocci over time. There was a reduction in spirochetes in the triclosan/fluoride group as compared to the control group. No overgrowth in opportunists, periodontal pathogens, or cariogenic flora was found in either group. No increase in the proportion of the whole plaque flora resistant to triclosan was found nor was an increase in the MIC values of either A. viscosus or V. parvula in either group. Overall, there appeared to be a general decrease in plaque bacteria in both groups over the course of the experiment.

Adolescent↗
PubMed1997

Longitudinal study of prognostic factors in established periodontitis patients.

Numerous indicators for disease progression have been described in the last decade. The purpose of this study was to examine, longitudinally, a large battery of clinical, microbiological, and immunological indicators, to try to determine whether the presence of one or a combination of these parameters at baseline, would correlate positively with increased attachment and or bone loss (true prognostic factors). Following initial screening, 79 patients with established periodontitis were monitored longitudinally for one year. Whole mouth clinical measurements, plaque gingival and calculus indices, together with pocket depth and attachment level measurements, were repeated every three months. Full mouth radiographic survey, performed at baseline and 12 months, served to determine changes in crestal bone height using an image enhancement technique. Subgingival plaque samples were taken at baseline and every 3 months. Immunofluorescence assays were performed for the a battery of target microorganisms. Serum and GCF samples for IgG subclasses analysis were obtained at each visit and assayed using ELISA techniques. Likewise blood, samples were also drawn at each visit for a quantitative analysis of serum cotinine level. The overall mean attachment loss (AL) and bone loss (BL) were almost identical (0.159 mm and 0.164 mm, respectively). Individual patients variation was large (-0.733 to +1.004 mm). An overall 6.89% of sites were active; individual patients' means ranged from 0-28.9%. Mean pocket depth (PD) showed minimal change over the study period (-0.033 mm) thus suggesting that most if not all the AL was accompained by concomitant gingival recession. Smokers exhibited greater AL and radiographic BL compared to non-smokers. Likewise, patients' cotinine level showed direct correlation with outcomes of progressive periodontal breakdown. Past severity of periodontal involvement, as reflected in the patients baseline PD, AL and crestal bone height, showed good correlation with longitudinal changes in the periodontium. This correlation was higher for crestal BL as the outcome variable, while somewhat smaller for change in AL as the outcome variable. Bacteroides forsythus (Bf.), Prevotella intermedia (Pi.) and Porphyromonas gingivalis (Pg.) were frequently found in these patients. The presence of these microorganisms at baseline was associated with further disease progression. Subjects with mean baseline pocket depth equal or greater than 3.2 mm were at greater risk for future bone loss 1 year later (O.R. 2.97; C.I. 1.02-8.70). Smokers were at significantly greater risk for further attachment loss when compared to non-smokers (O.R. 5.41; C.I. 1.50-19.5). Subjects that harbored B. forsythus at baseline, were at seven times greater risk for increased pocket depth (O.R. 7.84; C.I.1.74-35.3). In conclusion, past periodontal destruction, smoking habits, Bf., Pg., & Pi. are prognostic factors for further periodontal breakdown. When designing clinical trials, or when evaluating epidemiological data, it is most important to balance for these factors. Also, treatment strategies should attempt to eliminate or modify these factors.

Adult↗
PubMed1997

Epidemiology and diagnosis of HIV-associated periodontal diseases.

A review of periodontal disease as a manifestation of HIV infection suggests a shift in emphasis over the past 5 years. Initially the focus was on newly described forms of periodontal disease (i.e., HIV-associated gingivitis or linear gingival erythema (LGE); HIV-associated periodontitis or necrotizing ulcerative periodontitis (NUP). While the clinical definition of LGE varies from study to study, an association between LGE and Candida infection has been described. Furthermore, the prevalence of NUP is quite low and this disorder is associated with severe immunosuppression. In contrast, the focus today is on the accelerated rate of chronic adult periodontitis occurring in seropositive patients. While the organisms that characterize adult periodontitis in seronegative individuals are present in subgingival plaque from seropositive individuals, reports suggest that atypical pathogens are also present (i.e., Mycoplasma salivarium, Enterobacter cloacae). Recent studies from our laboratory have identified a novel strain of Clostridium isolated from the subgingival plaque of injecting drug users that has pathologic potential. This organism, however, was found in both seropositive and seronegative individuals in this cohort, suggesting an association with lifestyle rather than serostatus. In addition, data has been published examining the local host response in periodontitis in seropositive individuals. Distinctly elevated levels of IgG in gingival crevicular fluid (GCF) have been observed in seropositive patients. Furthermore, data from our laboratory examining inflammatory mediators in GCF (polymorphonuclear leukocyte lysosomal enzyme beta-glucuronidase and the pro-inflammatory cytokine interleukin-1 beta) suggests an altered response in patients with HIV infection. The alteration manifests as the absence of the expected strong correlation between polymorphonuclear leukocyte activity in the gingival crevice and clinical measures of existing periodontal disease, as well as elevated levels of interleukin-1 beta in sites with deeper probing depths. Therefore, it can be concluded that the progression of periodontal disease in the presence of HIV infection is dependent upon the immunologic competency of the host as well as the local inflammatory response to typical and atypical subgingival microorganisms.

Adult↗
PubMed1997

Principles of evaluation of the diagnostic value of subgingival bacteria.

This paper describes steps in the process of evaluating subgingival bacteria assays for the diagnosis of periodontal disease. The first step examines the infectious etiology of periodontal disease in pointing to specific oral bacteria as periodontal pathogens. Second is characterization of the laboratory test to detect and quantitate these pathogens as to sensitivity, specificity, and positive and negative predictive value. Third is the role of the laboratory test in the diagnosis of the different forms of periodontal disease which is related to the current clinical rather than microbiological definition of these diseases. The fourth and most important step is an analysis of the significance of subgingival bacterial tests in clinical decision-making.

Aggregatibacter actinomycetemcomitans↗
PubMed1997

A microbiological and clinical study of the safety and efficacy of baking-soda dentifrices.

This article reports the results of a study that examined the clinical and microbiological changes associated with regular use of baking-soda dentifrices. Two dentifrice formulations were examined in a 6-month longitudinal study of 101 adult subjects with assessments for plaque, gingival inflammation, and stain at baseline and 3 and 6 months during the active phase of the study, and at 3 months after cessation of product use. One dentifrice contained 52% baking soda and 3% sodium percarbonate (Arm & Hammer PeroxiCare) while the other dentifrice contained 65% baking soda (Arm & Hammer Dental Care). Both dentifrices resulted in statistically significant reductions in dental plaque, gingival inflammation, and stain at all time periods compared to baseline. Dental plaque and buccal soft-tissue samples were obtained for microbiological analysis from a 50-subject subset. Microbiological assays, including bacterial culture, phase-contrast microscopy, and immunofluorescence microscopy, confirmed the safety of both formulations. Beneficial alterations in dental plaque bacteria were noted, including significant reductions in the levels of Actinomyces species. The data from this study indicate that dentifrices containing high levels of baking soda are clinically effective and microbiologically safe.

Adolescent↗
PubMed1996

Colonization by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in adult periodontitis patients as detected by the antibody-based Evalusite Test.

Studies were performed to evaluate the detection of disease-associated bacterial colonization in adult periodontitis patients by the antibody-based Evalusite TestTM (Eastman Kodak Company). The association of test results with disease was assessed by collecting 104 duplicate subgingival plaque samples from 26 patients. Samples were tested for Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia using both microbiological culture and the immunoassay test. The sensitivity and specificity of the 2 methods was calculated using %s of positive results in deep periodontal pockets and negative results in shallow subgingival sites. A cutoff >10(4) cultivable counts yielded the greatest discrimination between health and disease on a cross-sectional basis and established this threshold as clinically relevant for the detection of disease-associated levels of bacterial colonization by these three microorganisms. The clinical detection limit of the immunoassay test was observed to coincide with this threshold of >10(4) cultivable counts. Microbiological testing of the 4 deepest pockets using the immunoassay test was determined to be sufficient to yield a 90% confidence of detecting positive patients in a study with 59 adult subjects. The immunoassay test method was also demonstrated to be effective at detecting bacterial colonization in sets of paper point samples that were pooled for analysis. An overall agreement of 94% (288 of 306) was observed when comparing test results for duplicate sets of pooled and individual samples collected from 51 patients. These studies demonstrate that the Evalusite Test is an effective method for detecting clinically relevant colonization by the test bacteria in patients at risk for periodontal disease.

Adolescent↗
PubMed1996

Cigarette smoking increases the risk for subgingival infection with periodontal pathogens.

Cigarette smoking has been found to increase the risk for periodontitis. The present study examined the association between cigarette smoking and subgingival infection with periodontal pathogens to determine if smokers are more likely to be infected with certain periodontal pathogens than non-smokers. Self-reported data on 1,426 subjects, aged 25 to 74, from the Erie County Study were obtained including data on 798 subjects who were current or former smokers. Mean clinical attachment loss was used to estimate the severity of periodontal destruction. Subgingival infection with target periodontal pathogens was determined by indirect immunofluorescence microscopy. Smokers harbored significantly higher levels and were at significantly greater risk of infection with Bacteroides forsythus than non-smokers. Adjusting for disease severity, the risk of subgingival infection with B. forsythus in current smokers was 2.3 times that of former smokers or non-smokers. The relative risk of B. forsythus infection also increased 1.18 times for every category of smoking as the amount of smoking measured in packyears increased from very light to heavy. Adjusting for disease severity, Porphyromonas gingivalis was also more likely to subgingivally infect smokers than non-smokers; however, there was not a significantly higher relative risk for infection with this bacterium. The data from this study indicate that cigarette smoking increases the likelihood of subgingival infection with certain periodontal pathogens. This may partly explain the increased risk for periodontitis seen in smokers.

Adult↗
PubMed1996

Response to periodontal therapy in diabetics and smokers.

Diabetics and smokers are two patient groups at high risk for periodontal disease who also exhibit impaired wound healing and, therefore, constitute two different groups in whom the relationship between host-parasite interaction, outcome of periodontal therapy, and systemic factors is best represented. The results of two independent clinical trials involving treatment of periodontal disease in diabetics and smokers are presented. A new treatment regimen for the management of periodontal disease associated with diabetes mellitus is proposed. This treatment approach incorporates both antimicrobial agents and pharmacological modulation of the host response. Elimination of periodontal infection and reduction of periodontal inflammation in diabetic patients resulted in a significant short-term reduction in the concentration of glycosylated hemoglobin (HbA1c). Control of chronic infections and modulation of the host response offer a new therapeutic approach in the management of patients with both diabetes and periodontal disease. The effect of smoking on periodontal healing is also discussed. The clinical and microbiological response of smokers to non-surgical periodontal therapy is compared to non-smokers. In addition, possible mechanisms whereby diabetes mellitus and cigarette smoking increase the severity of periodontal disease are discussed.

Adjuvants, Immunologic↗
PubMed1996

Analytical performance of an immunologic-based periodontal bacterial test for simultaneous detection and differentiation of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia.

The analytical performance of a membrane-based immunoassay for the simultaneous detection and differentiation of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia (including Prevotella nigrescens) was investigated. Positive reactions were observed for 71 of 71 reference strains and recent oral isolates of A. actinomycetemcomitans, P. gingivalis, and P. intermedia. No cross-reactivity was observed with 39 other common oral and environmental species. The specificity of the test was unaffected by the presence of potential oral interferents including whole blood, white blood cells, mucin, saliva, toothpastes, and oral rinses. A proficiency test by dental professionals using a standardized set of unknown simulated samples yielded a sensitivity of 97% (116/120) and a 100% specificity (240/ 240). An additional group including dental professionals and high school students was shown to be 99% proficient (1385/1397) in distinguishing proper from improper test function when processing control samples with normal test devices and devices with simulated error conditions. Comparisons to a culture standard for 104 subgingival plaque samples collected from 26 adult periodontitis patients yielded > 98% specificity for each of the test bacteria. In addition, the detection threshold for the test was determined to be equivalent to 10(4) cultivable test bacteria when compared to the culture standard. The data indicate that this membrane immunoassay is a valid and easy-to-use method for the detection of A. actinomycetemcomitans, P. gingivalis, and P. intermedia in subgingival plaque, at levels above the detection threshold of the test.

Adult↗
PubMed1996

Long-term stability of Class II furcation defects treated with barrier membranes.

The present longitudinal study was designed to explore the long-term efficacy of guided tissue regeneration (GTR) in Class II furcation defects and establish the factors that might be responsible for modifying this response. Subjects with two or more mandibular molars, one of which had Class II furcation defects, received the hygienic phase of therapy followed by baseline clinical measurements and subgingival plaque sampling. GTR procedure was performed in furcation defect sites using expanded polytetrafluoroethylene (ePTFE) membranes, while the other non-furcated molars received only scaling and root planning. Twenty-eight subjects (13 females, 15 males) aged 27 to 66 were included in this longitudinal analysis. Post-surgical treatment included routine home care supplemented with daily chlohexidine rinse and systemic tetracycline. Membranes were retrieved 4 to 6 weeks after surgery. During the first year, patients were initially seen bi-weekly and subsequently monthly for professional prophylaxis. At the end of this year, clinical measurements and samples were obtained. For the next 2 years, patients were seen bi-annually for maintenance visits. Clinical measurements and microbiological samples were then repeated. Next, a tighter maintenance protocol was established and patients were seen quarterly for scaling and oral hygiene reinforcement. Final measurements and samples were taken again 1 year later (4 years postoperative). Significant probing reduction (3.00 mm) and gain in horizontal attachment (2.59 mm) were obtained 1 year postsurgery for the GTR sites. These changes were maintained over 4 years with a slight decline at the end of year 3. Changes in probing depth (PD) from year 1 to 4 served to dichotomize the sites into stable (delta PD < or = 0.9 mm), and unstable (PD increase > or = 1 mm). Of the 54 sites available for this analysis only 5 (9.3%) were unstable while 49 (90.7%) were stable or even further improved. Sites which exhibited minimal or no plaque (plaque index [PI] < or = 1) over the tight maintenance period had a further decrease in mean probing depth (0.43 mm) compared with a slight increase (-0.06 mm) in mean probing depth in sites with PI > or = 2 mm (P = 0.0235). The same phenomenon was observed for changes in relative attachment level (RAL): mean gain in RAL was 0.61 mm compared to 0.25 mm for the 2 groups, respectively (P = 0.07). Actinobacillus actinomycetemcomitans was only isolated from 2 sites at year 3, and none at year 4, compared to 21.45% of the sites at baseline. Porphyromonas gingivalis positive sites showed a continual decline over the years: 14.28% at baseline, 10.71% at year 1, and 5.1% at year 4. On the contrary, Prevotella intermedia (Pi) and Bacteroides forsythus (Bf) infected sites remained at approximately the same rate throughout the 4 years of the study (40% to 50% and 30% to 40% for Pi and Bf, respectively). Of these, Pi-infected sites exhibited less favorable clinical results compared to sites which were not infected with this microorganism. In summary, furcation defects treated with membrane barriers can be maintained in health for at least 4 years; however, good oral hygiene and frequent recall visits as part of a complete anti-infective therapy are essential. Finally, once treated, these teeth are comparable to similar molar teeth with no previous history of furcation pathosis.

Adult↗