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Periodontal regeneration-treatment that results in new alveolar bone, cementum, and a functional periodontal ligament-is successful in class II furcation defects. This article examines one aspect of periodontal regeneration-alveolar bone growth in furcation defects-in trying to answer the question, Can bone lost from furcations be regenerated? The best evidence for bone growth is histology but there is limited histologic evidence for bone growth in human furcation defects. There is more evidence from intraoperative measurements for hard tissue growth in treated furcation defects, but the nature of the hard tissue needs to be determined histologically.

Aim: Oral malodor (halitosis) is a widespread condition caused by oral bacteria, particularly sulfur compound-producing species. This study assessed the effect of a triclosan/copolymer-containing dentifrice and a novel toothbrush with attached tongue cleaner on oral malodor and on the bacteria colonizing the dorsal surface of the tongue. Materials and Methods: 14 adult subjects with oral malodor defined as organoleptic scores ≥ 3 (scale 0 - 5) and mouth air sulfur levels ≥ 250 ppb participated in this study. Subjects were examined at baseline and after 28 days use of the triclosan dentifrice and toothbrush/tongue cleaner for: 1) organoleptic assessment; 2) mouth air sulfur levels; 3) tongue coating; and, 4) dorsal tongue surface microorganisms. Total bacterial numbers were assayed by microscopy. Dot-blot hybridization was used to assess a panel of 20 oral bacteria. Results: After 28 days, all subjects had significantly reduced organoleptic scores and mouth air sulfur levels compared to baseline (p 70% reduction in microbial numbers (p Enterococcus faecalis (p Peptostreptococcus micros (p Prevotella melaninogenica (p Porphyromonas gingivalis (p Solobacterium moorei (p

This study evaluated the antimicrobial activity of two commercially available 0·05% cetylpyridinium chloride (CPC) mouthrinses with or without alcohol and examined its antimicrobial activity on oral bacterial species including fresh clinical isolates compared to a chlorhexidine mouthrinse and a control fluoride mouthrinse without CPC. Two different approaches were used to evaluate antimicrobial activity. First, the minimum inhibitory concentration (MIC) was determined for each mouthrinse against a panel of 25 micro-organisms including species associated with dental caries, gingivitis and periodontitis. Second, supragingival dental plaque obtained from 15 adults was incubated with the four mouthrinses to evaluate antimicrobial activity on micro-organisms in oral biofilms. Both CPC mouthrinses exhibited lower MIC's, that is, greater antimicrobial activity, against oral Gram-negative bacteria especially periodontal pathogens and species implicated in halitosis such as Aggregatibacter actinomycemcomitans, Campylobacter rectus, Eikenella corrodens, Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei than the control mouthrinse. Ex-vivo tests on supragingival plaque micro-organisms demonstrated significantly greater antimicrobial activity by the CPC mouthrinses (>90% killing, P 98% killing, P

To cite this article: Int J Dent Hygiene9, 2011; 136–142 DOI: 10.1111/j.1601-5037.2010.00465.x Sreenivasan PK, Haraszthy VI, Zambon JJ.The effect of a microbead dentifrice on microbial load in oral microenvironments. Abstract: Objectives: The human oral cavity contains several microenvironments or ecologic niches. While mechanical plaque control is well known to reduce the number of supragingival dental plaque bacteria, there is little data on antimicrobial effects in other oral ecologic niches. The present study examined the effects of mechanical plaque control using a microbead dentifrice on bacteria colonizing oral ecologic niches. Methods: Twenty-two adults (aged 18–70 years) including nine generalized moderate chronic periodontitis subjects and 13 periodontally healthy subjects having average gingival indices ≥1 and plaque indices ≥1.5 completed a 1 week washout phase and refrained from oral hygiene the morning of baseline sample collection. Microbial samples from supragingival dental plaque, buccal mucosa, dorsal surface of the tongue and whole mixed saliva were obtained. Subjects brushed with a microbead dentifrice and, after 10 min, sampling was repeated. The number of anaerobic bacteria was determined by culture on non-selective media and transformed to log10 for statistical analyses. Results: Mechanical plaque control using the microbead dentifrice resulted in statistically significant reductions in bacterial numbers in each ecologic niche (P

Dentists and other health care professionals are familiar with the impact of tobacco on oral and general health. However, oral health care professionals do not often provide tobacco-cessation counseling to their patients, thus reflecting a significant disconnect between research and clinical practice. This report demonstrates the benefits of tobacco cessation in resolving oral lesions and improving overall periodontal and oral health.A 51-year-old white male presented to the University at Buffalo, School of Dental Medicine clinic requesting an oral and periodontal examination as part of a presurgical protocol prior to cardiac surgery. A review of the patient's history from a health questionnaire revealed that he was using smokeless tobacco every day. An oral examination revealed several white lesions (5 x 10 mm) on the maxillary right and left labial mucosa. The patient was provided with tobacco-cessation counseling as well as oral hygiene instructions and professional dental prophylaxis.An oral examination 2 weeks after tobacco cessation revealed complete resolution of the oral lesions and overall improvement of periodontal and oral health.Although the findings presented in this article are based only on a single case report, the improvement in the patient's oral health after cessation of tobacco use was dramatic and reinforces the belief that tobacco-cessation counseling should be a routine component of the standard of care for tobacco-using patients.

Background The authors examined the tongue bacteria associated with oral halitosis (bad breath originating from the oral cavity), focusing on noncultivable bacteria—bacteria that cannot be identified by bacterial culture techniques. Methods The authors took samples from the dorsal tongue surface of eight adult subjects with halitosis and five control subjects who did not have halitosis. They identified the bacteria in these samples by using both anaerobic culture and direct amplification of 16S ribosomal DNA, a method that can identify both cultivable and noncultivable microorganisms. They analyzed the resulting microbiological data using χ 2 and correlation coefficient tests. Results Clinical measures of halitosis were correlated highly with each other and with tongue coating scores. Of 4,088 isolates and phylotypes identified from the 13 subjects, 32 species including 13 noncultivable species were found only in subjects with halitosis. Solobacterium moorei was present in all subjects with halitosis but not in any control subjects. Conclusions Subjects with halitosis harbor some bacterial species on their dorsal tongue surfaces that are distinct from bacterial species found in control subjects. This finding is consistent with the hypothesis that halitosis has a microbial etiology. Clinical Implications Like other oral diseases with microbial etiology, halitosis may be amenable to specific and nonspecific antimicrobial therapy targeted toward the bacteria associated with it.

Made available in DSpace on 2019-09-12T16:56:44Z (GMT). No. of bitstreams: 0 Previous issue date: 2005 Objectives: 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. Materials and Methods: 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. Results: 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 (chi(2) = 527.83) and positively associated with deep pockets (46 mm, chi(2) = 18.26) and young age (< 29 years, chi(2) = 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). Conclusion: 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. SUNY Buffalo, Sch Dent Med, Buffalo, NY 14214 USA; Universidade de Taubaté (Unitau), Sao Paulo, Brazil

In der vorliegenden Studie wurden von 62 Patienten (18 Frauen und 44 Manner) 93 Proben aus verschiedensten Gefasen und Gefasabschnitten wahrend der Gefasoperation entnommen und auf bakterielle 16S rDNS sowie—mittels spezifischen Oligonukleotidprimern—auf die mit Parodontitis assoziierten Keime P. gingivalis, P. intermedia, A. actinomycetemcomitans, C. rectus und B. forsythus untersucht. In 76,34% der 93 untersuchten Gefaswandpraparate waren Bakterien nachzuweisen, in 40,86% einer oder mehrere der parodontalpathogenen Erreger. Diese kamen so gut wie immer (mit einer Ausnahme) zusammen mit anderen Bakterien vor. C. pneumoniae fanden sich in 22,58% der Proben. Ihr Auftreten stand signifikant mit dem Vorkommen von parodontalpathogenen Keimen in Zusammenhang. Herpes-simplex- und Zytomegalieviren kamen in 24,73% bzw. 30,11% der Proben vor, ohne dass ein Zusammenhang mit Parodontalkeimen bestand. Diese Ergebnisse stehen im Einklang mit der Hypothese, dass Mikroorganismen, die mit Parodontitis assoziiert sind, bei der Atiologie und Pathogenese der Arteriosklerose eine wichtige Rolle spielen.

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.

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.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 sitesor =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.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 CRPor = 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).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.

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.

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.

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 PDor = 0.9 mm), and unstable (PD increaseor = 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 PIor = 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.

The purpose of this study was to assess the prevalence of A. actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia, and their association with periodontal disease states in a population sample from Sri Lanka. Based on clinical parameters, a total of 536 sites in 268 male Sri Lankan tea workers were categorized as healthy, or showing gingivitis only, moderate or advanced periodontitis. Bacterial samples were obtained from all sites and the three target bacteria identified by indirect immunofluorescence. P. intermedia, P. gingivalis and A. actinomycetemcomitans were found in 76%, 40% and 15% of the subjects, respectively. Of the 536 periodontal sites, 10.5% were categorized with "no disease", 14% "gingivitis only": 59% with moderate and 16% with advanced periodontitis. The prevalence of P. gingivalis and P. intermedia was significantly higher in sites with moderate and advanced periodontitis than in sites with no disease or gingivitis only. A. actinomycetemcomitans was not found in healthy sites, but occurred with equal frequency in sites with gingivitis, moderate and advanced periodontitis. The association between these three bacteria and periodontal diseases in Sri Lankan tea laborers was similar to that described for other non-industrialized and industrialized countries.

A total of 325 subjects were entered into a double-blind, stratified 2-treatment clinical study that examined the effects of a dentifrice containing 0.3% triclosan, 2% Gantrez copolymer and 0.243% sodium fluoride on supragingival dental plaque and gingivitis. A subset of 159 subjects including 72 men and 87 women participated in the microbiological component of this study, which was designed to detect shifts in supragingival bacterial species in response to triclosan. Subjects were divided into two groups: one performed normal oral hygiene with the triclosan/copolymer dentifrice and a control group used a placebo dentifrice without triclosan. At baseline, 3 and 6 months during treatment and at 6, 12, 18 and 24 weeks post-treatment, supragingival dental plaque was collected from the buccal and lingual surfaces of the 4 first molar teeth and assayed for: 1) bacterial morphotypes by phase-contrast microscopy; 2) select bacterial groups and bacterial species by culture; and 3) target periodontal pathogens including Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Porphyromonas gingivalis and Prevotella intermedia by immunofluorescence microscopy. There were few statistically significant differences between treatment groups in any of the 90 microbiological parameters measured at the 7 different time points. The control group demonstrated significantly higher levels of cultivable Neisseria and higher proportions at the 3-month treatment period of P. gingivalis-infected subjects and mean cells. After 6 months of treatment, the triclosan group demonstrated higher levels of fusiforms. Analysis of triclosan resistance data failed to detect a shift towards increased proportions of bacteria resistant to triclosan, and both treatment groups demonstrated triclosan-resistant strains, predominantly Veillonella dispar. This study confirms the microbiological safety of triclosan-containing dentifrices and suggests that continued use can be associated with beneficial alterations in the bacterial composition of supragingival dental plaque.

This study examined the risk indicators for alveolar bone loss associated with periodontal infection. A cross-section of 1,361 subjects aged 25 to 74 years, from Erie County, NY were evaluated for interproximal alveolar bone loss and potential explanatory variables including age, gender, history of systemic diseases, smoking, and presence of 8 subgingival bacteria. Interproximal alveolar bone loss was measured from the alveolar crest to the CEJ and a mean computed for each subject. The mean bone loss per subject (BL) ranged from 0.4 to 8.8 mm, and this outcome variable was grouped into 4 ordered categories. The degree of association between the explanatory variables and BL was examined utilizing an ordinal stepwise logistic regression model. Factors which were positively associated with more severe bone loss included subgingival colonization with B. forsythus (O.R. 2.52; 95% CI: 1.98 to 3.17) or P. gingivalis (O.R. 1.73; 95% CI: 1.27 to 2.37), race (Native American, Asian, or Pacific Islanders) with an O.R. 2.40 (95% CI: 1.21 to 4.79), and gender with males having higher odds than females. Smokers had greater odds for more severe bone loss compared to non-smokers ranging from 3.25 (95% CI: 2.33 to 4.54) to 7.28 (95% CI: 5.09 to 10.31) for light and heavy smokers, respectively. Individuals at older ages also showed more severe levels of bone loss. History of kidney disease (O.R. 0.55; 95% CI: 0.35 to 0.89) and history of allergies (O.R. 0.76; 95% CI: 0.59 to 0.98) were inversely associated with severity of bone loss.(ABSTRACT TRUNCATED AT 250 WORDS)

This article describes the baseline findings from a study designed to compare the oral manifestations of HIV infection in homosexual men and intravenous drug users. Both seropositive and seronegative persons were studied. A standard examination instrument was developed to record indexes of oral disease as well as to record the presence of oral lesions. The two groups differed in terms of education, race, socioeconomic status, employment status, housing, and smoking experience. The prevalence and type of oral lesions differed in the two seropositive groups. In seropositive homosexual men, white lesions on the tongue (28.4%) predominated; whereas for the seropositive intravenous drug users, oral candidiasis (43.0%) and gingival marginal erythema (33.3%) were most often detected. We also observed that seronegative intravenous drug users displayed a greater number of oral lesions than seronegative homosexual men. For seropositive homosexual men, lesion presence was significantly associated with decreased levels of CD4; positive associations were seen with current smoking, antiviral drug use, and antibiotic use, and a negative association was observed with current employment. In contrast, only exposure to antiviral drugs was significantly correlated with lesion presence for seropositive intravenous drug users. This baseline analysis from our longitudinal study suggests clear differences in oral manifestations of HIV infection between seropositive homosexual men and intravenous drug users and between seronegative homosexual men and intravenous drug users. Among other parameters, it is apparent that lifestyle, access to health care, and the condition of the oral cavity before infection influence the development of oral lesions in persons with HIV infection.

144 subjects completed a 6-month, double-blind study which examined the effects of a 0.3% triclosan/2% copolymer/0.243% sodium fluoride dentifrice on the microflora of supragingival dental plaque. The subjects were randomly assigned to use, in an oral hygiene program, either the triclosan/copolymer/fluoride test dentifrice or a control dentifrice. The latter had the same formulation as the test dentifrice except it did not contain triclosan. Supragingival plaque was collected from the buccal and lingual surfaces of 4 teeth at baseline, 3 months, and 6 months, and microbiological examined by darkfield microscopy, gram stain morphology', immunofluorescence, and selective and non-selective media. Antimicrobial susceptibilities were determined by agar dilution and whole plaque susceptibility methodologies on plaque samples from 136 subjects at each of the above sample periods and at 6-week intervals for an additional 6 months post-therapy. Both dentifrices resulted in highly statistically significant reductions in the total cultivable flora obtained at both the 3 and 6-month samples relative to baseline as well as at 6 months relative to the 3-month sample. The relative decrease in total anaerobic counts and in strict anaerobes, while not statistically significant, was more pronounced at both the 3- and 6-month sample periods in subjects receiving the triclosan dentifrice than for the controls. Neither dentifrice resulted in detrimental shifts in the microbial composition of the normal flora nor led to the emergence of periodontal or opportunistic pathogens. There was no difference in the relative proportions of the microflora resistance to triclosan or in the number of subjects harboring triclosan-resistant micro-organisms regardless of whether the subjects received the triclosan dentifrice or the control. The proportion of the cultivable flora resistant to triclosan was higher at baseline than at any other sample period. This study demonstrates that the extended use of the 03% triclosan/2% copolymer/fluoride dentifrice does not disrupt the normal microflora associated with supragingival plaque, favor the growth or colonization of periodontal or opportunistic pathogens, or promote the acquisition of microbial resistance.

This study evaluated the effect of periodontal therapy on clinical and microbiological parameters in 23 subjects with severe generalized early onset periodontitis. Therapy consisted of oral hygiene instruction and root planing and scaling, followed 3 months later by open flap debridement. Subjects were monitored for both clinical measures and levels of Actinobacillus actinomycetemcomitans and Porphyromas gingivalis as identified by indirect immunofluoresence. Clinical and microbiological evaluations were done at the start of the study, 3 months after the completion of root planing and scaling and 3 months after open flap debridement. Mean probing depth was reduced by both root planing and scaling and open flap debridement and the level of reduction demonstrated by both phases of therapy was similar to reductions found in studies that utilized subjects with chronic adult periodontitis. In contrast, reductions in attachment level due to the two phases of therapy, demonstrated in previous studies of subjects with adult periodontitis were not found in the young adult subjects with severe periodontal disease utilized in this study. Levels of A. actinomycetemcomitans were not significantly affected by root planing and scaling, but were reduced by open flap debridement. P. gingivalis was virtually eliminated by root planing and scaling, demonstrating that the two bacterial types respond differently to periodontal therapy. These changes in microbiological parameters were similar to those found in studies of localized juvenile periodontitis subjects, where surgery or antibiotics have been shown to be necessary to reduce levels of A. actinomycetemcomitans.

Specific risk indicators associated with either susceptibility or resistance to severe forms of periodontal disease were evaluated in a cross-section of 1,426 subjects, 25 to 74 years of age, mostly metropolitan dwellers, residing in Erie County, New York, and surrounding areas. The study sample exhibited a wide range of periodontal disease experience defined by different levels of attachment loss. Therefore, it was possible to accurately assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old ranging from 1.72 (95% CI: 1.18 to 2.49) to 9.01 (5.86 to 13.89) for subjects 65 to 74 years old. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.32 (95% CI: 1.17-4.60). Smoking had relative risks ranging from 2.05 (95% CI: 1.47-2.87) for light smokers increasing to 4.75 (95% CI: 3.28-6.91) for heavy smokers. The presence of two bacteria, Porphyromonas gingivalis and Bacteroides forsythus, in the subgingival flora represented risks of 1.59 (95% CI: 1.11-2.25) and 2.45 (95% CI: 1.87-3.24), respectively. Our results show that age, smoking, diabetes mellitus, and the presence of subgingival P. gingivalis and B. forsythus are risk indicators for attachment loss. These associations remain valid after controlling for gender, socioeconomic status, income, education, and oral hygiene status expressed in terms of supragingival plaque accumulation and subgingival calculus. Longitudinal, intervention, and etiology-focused studies will establish whether these indicators are true risk factors.

The primary objectives of this double-blind, controlled clinical trial were to assess factor(s) which affect the success of guided tissue regeneration (GTR) procedures in mandibular Class II buccal furcation defects. Thirty subjects, with mandibular Class II furcation defects, were randomly assigned to one of two treatment groups; patients in Group A received oral hygiene instructions with scaling and root planing, while subjects in Group B received similar treatment but without subgingival scaling and root planing at the affected site. After initial oral hygiene instructions and scaling and root planing, GTR surgery was performed using ePTFE barrier membranes. Membranes were retrieved at 6 weeks and subjected to histological examination. Twelve months after regenerative therapy, clinical measurements and re-entry surgical measurements were repeated. Probing reduction (2.61 mm), horizontal probing attachment gain (2.59 mm), and vertical probing attachment gain (0.95 mm) were all significantly better compared to baseline. Likewise, significant improvements in furcation volume (8.0 microliters) and in bone measurements were observed at re-entry. There was no discernible difference between subjects for whom complete anti-infective therapy was deferred to the time of the surgery (Group B) compared to subjects in whom complete anti-infective therapy was performed as part of the hygienic phase of therapy (Group A). Pre-operative pocket depth was directly correlated with the magnitude of attachment gain as well as the amount of new bone formation in the furcation area. Subjects who maintained good oral hygiene and who had minimal gingival inflammation throughout the study demonstrated consistently better regenerative response.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of the present study was to evaluate the effect of anti-infective therapy on the success of periodontal regeneration in mandibular Class II furcation defects. Eighteen patients with mandibular bilateral Class II furcation defects were enrolled. Following an initial hygienic phase, guided tissue regeneration (GTR) was performed using an expanded polytetrafluoroethylene (e-PTFE) membrane barrier. The area was surgically exposed, thoroughly root planed, and irrigated with either tetracycline (100 mg/ml) or 0.9% saline. Post-operative care included systemic tetracycline (250 mg q.i.d.) and chlorhexidine 0.12% mouthwash twice daily. Patients were maintained on a prophylaxis schedule of every 2 weeks for the first 3 months, and monthly thereafter. Clinical parameters of probing depth (PD), probing attachment level - vertical (PAL-v), probing attachment level - horizontal (PAL-h), and target periodontal pathogens were monitored at baseline and quarterly for one year. An overall improvement in all clinical parameters was observed in both groups: probing reduction (3.1 mm), PAL-h gain (2.3 mm), and PAL-v gain (1.2 mm) were all statistically significant compared to baseline measurements. Vertical measurements were performed parallel to the long axis of the tooth with no attempt to angulate the probe into the furcation. There was no significant difference in sites receiving tetracycline. A strong positive correlation was noted between initial PD and pocket reduction (r = 0.77, P < 0.0001) and between initial PD and PAL-h gain (r = 0.54) and PAL-v gain (r = 0.45) suggesting that initial probing depth might be used to assess the regenerative potential of a given site.(ABSTRACT TRUNCATED AT 250 WORDS)

The current study assessed the clinical and microbiological effects of systemic antimicrobial therapy alone in Actinobacillus actinomycetemcomitans-infected adolescents with periodontal disease. The study involved 6 localized juvenile periodontitis patients 13-18 years of age, who harbored high numbers of A. actinomycetemcomitans in subgingival plaque samples. The periodontal lesions were microbiologically monitored by selective culture, and clinically assessed for probing pocket depth and periodontal attachment level 3 months prior to baseline, and at 3, 6, 12, and 24 months posttreatment. Tetracycline-HCl (250 mg/QID) was prescribed until 1 week after subgingival A. actinomycetemcomitans was no longer detectable or for a maximum of 8 weeks. During 3 months prior to treatment, pocket depth was unchanged, and was then significantly reduced from an average of 7.1 mm to 5.1 mm 12 months after treatment (p = 0.02). The mean change in clinical attachment level was a gain of 1.4 mm between baseline and 12 months (p = 0.02). 3 of the 6 patients were still infected with A. actinomycetemcomitans after 8 weeks of antibiotic therapy and 4 subjects were infected at 12 months. Numbers of A. actinomycetemcomitans were still suppressed in most lesions. There was a strong association between mean numbers of A. actinomycetemcomitans in periodontal pockets and mean change in probing attachment level at any given time point. For 22 available comparisons, derived from all time points, there was a strong association (r = 0.68) between subgingival A. actinomycetemcomitans and change in probing attachment level.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical measurements of periodontal attachment loss, while not always representing the histological changes, are used to establish the diagnosis of adult periodontitis. Such measurements are difficult to perform accurately and are labor intensive. To counter these problems, index teeth and index sites have been employed in an attempt to estimate the severity of the periodontal condition without the need to resort to elaborate attachment measurements. Unfortunately, such indices usually tend to underestimate prevalence while often overestimating severity. The purpose of the present study was to examine the correlation of alternative clinical, radiographic and microbiological parameters, with periodontal disease using the diagnostic criteria of established periodontitis. 508 adults included in this study received thorough periodontal examination which included probing pocket depth, clinical attachment level, plaque, gingival and calculus scores, together with radiographic analysis and assays of subgingival periopathogenic microorganisms. Radiographic alveolar bone loss and probing pocket depth had the highest correlation with clinical attachment loss (phi = 0.72 and phi = 0.75 respectively). Plaque scores (phi = 0.17), like gingival scores (phi = 0.06) and calculus scores (phi = 0.42) had poor correlation with established periodontitis. Periodontopathogenic species demonstrated high specificity and negative predictive values; but low sensitivity and positive predictive values make for an overall low correlation of these species with established periodontitis. However, when used in a logistic regression model, the presence of P. gingivalis (odds ratio = 6.25) has shown to contribute significantly to the estimate of probability for established periodontitis. The use of these various alternative parameters for screening of periodontal disease is discussed in light of their sensitivity, specificity and predictive value.

The association between specific plaque microorganisms and periodontal diseases has been the subject of much recent interest due to its potential importance in the diagnosis and classification of these diseases. In order to optimize microbiological tests in periodontal therapy, it is important to know how many subgingival plaque samples must be assayed from a single patient in order to ascertain infection with a periodontal pathogen. To answer this question the present study assessed the distribution of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, and Prevotella intermedia in multiple subgingival plaque samples. The samples were quantitatively assessed for specific bacteria by indirect immunofluorescence, a technique previously found to correlate well with cultural assessment of these same organisms. Subgingival plaque from the mesial pockets/sulci of all teeth except third molars was sampled in 12 patients with adult periodontitis, 22 to 28 sites/patient for a total of 315 samples. These patients demonstrated an average mesial probing depth and loss of attachment of 3.7 +/- 1.2 mm and 3.1 +/- 1.5 mm, respectively (mean +/- SD). P. gingivalis, P. intermedia, and B. forsythus were demonstrated in one or more sites from all patients, while A. actinomycetemcomitans was found in one or more sites in 8 of 12 patients. The proportion of positive sites per subject varied, but it was, on average, similar for the 3 black-pigmented organisms and ranged from 44% to 54%. In contrast, A. actinomycetemcomitans was identified, on average, in only 11.4% of the sites in these same patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Antony van Leeuwenhoek first described oral bacteria. However, not until almost 200 years later was the famous Koch postulate introduced. Since then, research has extensively been performed regarding the development and microbiology of dental plaques. In spite of the complexity of the developing flora of supragingival plaque, culture studies have shown a remarkably orderly succession of organisms. Lately, the concept of microbial specificity in the etiology of periodontal diseases has been widely suggested, i.e., that different forms of periodontal disease are associated with qualitatively distinct dental plaques. Cross-sectional and longitudinal studies of the predominant cultivable microflora reveal that only a small number of the over 300 species found in human subgingival plaques are associated with periodontal disease. Among the commonly mentioned are: Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, Bacteroides intermedius, Capnocytophaga sp., Eikenella corrodens, Fusobacterium nucleatum, and Wolinella recta, as well as certain gram-positive bacteria such as Eubacterium species. Anti-infective therapy for many systemic infections equals the use of antimicrobial drugs. However, for localized infections like periodontal diseases, treatment may consist of a combination of mechanical wound debridement and the application of an antimicrobial agent. The general effectiveness of mechanical anti-infective therapy and successful oral hygiene in the management of periodontal disease is well established in the literature and has met the test of success in clinical practice for most cases of periodontitis in adults. The definition of periodontal pathogens as either opportunistic pathogens, or as exogenous pathogens carries with it significant implications.(ABSTRACT TRUNCATED AT 250 WORDS)

Two unique forms of periodontal disease, HIV-gingivitis and HIV-periodontitis, have been described in patients with Acquired Immunodeficiency Syndrome (AIDS). In order to determine the bacterial species associated with periodontitis in AIDS patients, the predominant cultivable microflora was examined in 21 subgingival plaque samples from 11 AIDS patients with periodontitis. The presence of putative periodontal pathogens including Actinobacillus actinomycetemcomitans, Bacteroides intermedius, Porphyromonas gingivalis (formerly B. gingivalis), and Wolinella recta was examined by immunofluorescence in 128 subgingival dental plaque samples from 50 AIDS patients including 32 patients with periodontitis. Of 666 bacterial strains isolated from the 21 subgingival plaque samples, Streptococcus sanguis II was the most frequently recovered species comprising 18.5% of the total number of isolates followed by Lactobacillus acidophilus (12.2%), Porphyromonas gingivalis (12%), Fusobacterium nucleatum (11.4%), Staphylococcus epidermidis (8.7%), Actinomyces naeslundii (7.5%), and Actinomyces viscosus (4.7%). Fusobacterium nucleatum was the most prevalent species and was found in 76% of the sites and 91% of the patients. Enteric species including Enterococcus avium and Enterococcus faecalis, Clostridium clostridiiforme and Clostridium difficle as well as Klebsiella pneumoniae also were recovered. Immunofluorescence assays detected similar carriage rates of A. actinomycetemcomitans, B. intermedius, and P. gingivalis in both gingivitis patients and periodontitis patients, while four times more periodontitis patients demonstrated W. recta. Subgingival yeast was a frequent finding in these AIDS patients, present in 62% of the subjects and 55% of the sites. This study indicates that subgingival plaque in AIDS patients with periodontitis can harbor high proportions of the same periodontal pathogens as are associated with periodontitis in non-HIV infected subjects as well as high proportions of opportunistic pathogens.

The CO2 laser prevents bleeding by sealing blood and lymph vessels as it vaporizes tissue. Bacteremia following oral surgery might not occur under these conditions. To test this hypothesis, a 0.2-mm-deep incision 1 cm long was made in the right buccal cheek pouch of hamsters using either laser, electrosurgery, or a scalpel. Twenty minutes later, 1 mL of blood was taken from each animal by cardiac puncture, inoculated on a blood agar medium, and incubated anaerobically for 4 days; then the colonies were counted. Using an operational definition of bacteremia as five colonies or more per plate, there were no positive results out of 18 trials (0/18) for laser surgery, 7/8 for electrosurgery, and 8/12 for scalpel surgery. Based on the Student t test using the binomial distribution, the laser produced statistically less bacteremia than the other two methods (P less than .01). Because the five-colony cutoff was arbitrary, the nonparametric Wilcoxon Rank test was also used. Colony formation from blood from the laser group was significantly less than from the electrosurgery group (P less than .01) and the scalpel group (P less than .05). The laser surgery group was not statistically different from the control (nonsurgerized) group. These results suggest that there is a considerable bacteremia following scalpel and electrosurgery, but that laser surgery produces no bacteremia.

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.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.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.This study suggests that localized juvenile and other forms of Actinobacillus-associated periodontitis are primarily associated with the highly leukotoxic clone of A. actinomycetemcomitans.

Longitudinal assessment of risk factors for periodontal disease is necessary to provide evidence that a putative risk factor or risk indicator is a true risk factor. The purpose of the present study was to explore longitudinally a variety of markers as possible periodontal risk factors in subjects with little or no periodontal disease at baseline. 415 subjects with mild or little periodontal disease were examined: medical and dental history; socioeconomic profile, clinical measurements, microbial samples and radiographic assessment of bone height were performed at baseline, and at a follow-up examination 2 to 5 years later. Mean probing pocket depth (PPD) at baseline was 1.99±0.37 mm while mean overall change was 0.1 mm which amounts to an annual rate of 0.04 mm. Overall mean clinical attachment level (1.75±0.6 mm) at baseline resulted in mean attachment change of 0.28 mm (0.12 mm. annually). Alveolar crestal height (ACH) at baseline (mean 2.05±0.85 mm) resulting in a mean net loss of 0.1 mm. Approximately 10% of all sites presented for the second visit with attachment loss exceeding the threshold (4.4% annually), while only 2.2% of all sites exhibited attachment gain (0.88% annually). Older individuals exhibited greater mean bone loss but the least amount of attachment loss. Current smokers exhibited greater disease progression compared to non-smokers. Tooth morbidity (0.17 teeth/patient/year) was associated with greater baseline CAL and ACH loss, and an assortment of systemic conditions. Subjects who harbored Bacteroides forsythus (Bf) at baseline had greater loss in ACH; likewise, these subjects experienced greater proportions of losing sites and twice as much tooth mortality compared to Bf-negative patients. Baseline clinical parameters correlated strongly with the outcome, i.e., subjects with deeper mean pocket depth at baseline exhibited greater increase in pocket depth overtime; while subjects with greater attachment loss at baseline exhibited greater attachment loss between the 1st and 2nd visits.

This study investigated the effect of cigarette smoking on 143 patients' clinical and microbiological responses to mechanical therapy. Treatment included four to six sessions of subgingival scaling and root planing and instruction in oral hygiene. Results indicate that current smokers have less healing and reduction in subgingival Bacteroides forsythus and Porphyromonas gingivalis after treatment compared to former and nonsmokers, suggesting that smoking impairs periodontal healing. As the healing and microbial response of former smokers is comparable to that of nonsmokers, smoking cessation may restore the normal periodontal healing response.

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.

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. J Periodontol 1996;67:1094-1102.

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. J Periodontol 1996;67:1050-1054.

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.

Periodontal status was evaluated in two cohorts participating in a study of the natural history of human immunodeficiency virus (HIV) infection. One cohort consisted of 77 seropositive and 44 seronegative homosexual men, and the other cohort was comprised of 44 seropositive and 39 seronegative parenteral drug users (PDU). No differences were observed between seropositive and seronegative individuals within a cohort in terms of clinical periodontal parameters (percent of sites with > or = 4 mm probing depth, percent of sites exhibiting bleeding on probing, mean oral hygiene index). The PDU displayed more existing periodontal disease than the homosexual men. Periodontal disease in the seropositive individuals in both cohorts was not strictly related to the number of CD4+ lymphocytes. Linear gingival erythema (LGE), defined as an erythematous band of at least 2 mm extending between adjacent papilla, was observed in all 4 groups. Seropositive homosexual men displayed more LGE than seronegative homosexual men (16.6% vs. 11.4%) and seronegative PDU displayed more LGE than seropositive PDU (38.5% vs. 29.5%), but neither difference was significant. LGE tended to be related to reduced numbers of CD4+ lymphocytes, but this relationship did not reach statistical significance. A statistically-significant relationship was found between the presence of intraoral candidiasis and LGE in seropositive homosexual men: 42.9% of these subjects with candidiasis had LGE, while only 12.7% of the subjects without candidiasis had LGE (P < .05). For the seropositive PDU, 35.3% of the individuals with candidiasis had LGE and 25.9% of the subjects without candidiasis displayed LGE, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

In a random sample of subgingival dental plaque samples from 375 blacks and 300 whites aged 65 and older, immunofluorescence assays for 3 target pathogens including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia, and BANA enzyme analysis were carried out. Blacks had significantly greater proportions of P. gingivalis and P. intermedia in their subgingival plaque and had significantly higher BANA scores. These assay results were investigated for concordance with each other and with 2 cariogenic salivary bacteria, Streptococcus mutans and lactobacilli. In general for both races, the periodontal pathogens were more likely to occur in combination with each other than with either S. mutans or lactobacilli. P. gingivalis and P. intermedia were more frequently associated with each other than with A. actinomycetemcomitans. There was a significant negative concordance between BANA and A. actinomycetemcomitans in whites and a significant positive concordance between BANA and P. intermedia in blacks.

The objective of The Present study was to define criteria for the diagnosis of "established periodontitis." This term will define subjects who have demonstrated clinical attachment loss, and as such can be considered to have periodontitis. Using these criteria, healthy and established periodontitis subjects were compared with respect to gender, race, and age. Five hundred and eight subjects including 248 females and 260 males between the ages of 25 to 73 (mean 44.6 years), were examined in this study. The clinical examination included: plaque assessment index (PAI); gingival assessment index (GAI); probing pocket depth (PPD); and clinical attachment level (CAL). The mean and frequency distribution of these parameters were analyzed by age and gender. CAL (mean 2.12 mm) showed constant and significant increases with age, ranging from a mean of 1.63 mm in subjects 25 to 34 years of age to a mean of 2.65 mm in subjects 65 to 74 years of age. Males exhibited higher mean values than females for all the measured parameters, which were statistically significant for PAI, PPD, and CAL. The frequency distribution of subjects with PPD and CAL beyond certain threshold levels showed an exponential decline and was correlated to both the severity of the most involved site as well as the number of sites beyond threshold levels. The clinical entity of "established periodontitis" is suggested based on the presence of CAL greater than or equal to 6 mm in 2 or more teeth and one or more sites with PPD greater than or equal to 5 mm. In the present study, 30.5% of the subjects fell into this category.(ABSTRACT TRUNCATED AT 250 WORDS)

The prevalence of people and sites with attachment loss, pocket depth, Actinobacillus actinomycetemcomitans, Prevotella intermedia, and Porphyromonas gingivalis are described for a random sample of 366 black and 297 white community-dwelling adults, aged 65 or over, residing in five counties in North Carolina. In addition, relationships between sites harboring these microorganisms and loss of attachment (LA) and pocket depth (PD) are presented in a manner that considers the lack of independence of sites within each person. Pocket depths and recession were measured on all teeth by trained examiners during household visits. Immunofluorescent assays for A. actinomycetecomitans, P. intermedia, and P. gingivalis were conducted on subgingival plaque samples obtained from the mesiobuccal aspect of the four first molar teeth using paper points. The prevalences of A. actinomycetemcomitans, P. intermedia, and P. gingivalis were greater in blacks than in whites. The most striking difference was seen for P. gingivalis, which was found in 38.8% of blacks and 9.4% of whites. Similar relationships were found when the percent of sites with these organisms were assessed. Blacks with P. gingivalis or P. intermedia had a higher prevalence of sites with LA greater than or equal to 7 mm as compared to blacks not infected with P. gingivalis or P. intermedia. The same was true for whites. Similar relationships between P. gingivalis or P. intermedia and PD greater than or equal to 6 mm were found for both blacks and whites.(ABSTRACT TRUNCATED AT 250 WORDS)

This study describes the relationship between varying ascorbate intake, periodontal status, and subgingival microflora as part of a multidisciplinary investigation of ascorbic acid (AA) metabolism in young men housed for 13 weeks in a nutrition suite that provided controlled periods of ascorbic acid depletion and repletion. Twelve medically healthy non-smoking men, aged 25 to 43 years, ate a rotating four-day diet adequate in all nutrients except ascorbic acid. Following an initial baseline period during which the subjects received 250 mgAA/day, the subjects received 5 mgAA/day for a 32-day depletion period. Eight of the 12 subjects participated in a subsequent 56-day repletion period designed to replace the reduced body AA pool slowly. Plasma and leukocyte ascorbate levels, Plaque Index, Gingival Index, probing depths, and attachment level were monitored at the beginning and end of the depletion and repletion periods. Subgingival plaque samples were obtained and examined for selected organisms by indirect immunofluorescence microscopy. A uniform oral hygiene program was reinforced after each examination. Ascorbate concentrations in plasma and leukocytes responded rapidly to changes in vitamin C intake. There were no significant changes in plaque accumulation, probing pocket depth, or attachment level during the study. In contrast, gingival bleeding increased significantly after the period of AA depletion and returned to baseline values after the period of AA repletion. However, no relationship could be demonstrated between either the presence or proportion of target periodontal micro-organisms and measures of gingival bleeding or ascorbate levels.

The purpose of this study was to determine the prevalence of Actinobacillus actinomycetemcomitans (Aa) in individuals from families where at least one individual has an early onset form of periodontitis. Twenty-three families with 73 subjects were evaluated in this study. Forty-seven early onset periodontitis subjects outside the 23 families were also studied. Prevalence of detection of Aa in family members ranged from 49% to 66% among groups constituted by clinical findings indicative of no loss of attachment, adult periodontitis, generalized severe juvenile periodontitis, or localized juvenile periodontitis. Whether the data were analyzed by subject or by site, no statistical differences could be found in prevalence (proportion of positive samples) among those clinical groups. The only significant difference was that localized juvenile periodontitis subjects had higher concentrations of Aa in their Aa-positive sites than did the other clinical groups. The prevalence of Aa-positive sites in subjects without attachment loss, but who are members of families in which early onset periodontitis is represented, was much higher than in other reports where periodontally healthy subjects were not related to early onset periodontitis cases. This suggests that Aa may be transmitted among members of families in which one or more members has an early onset form of periodontitis.

Study objectives: Poor dental hygiene has been linked to respiratory pathogen colonization in residents of long-term care facilities. We sought to investigate the association between dental plaque (DP) colonization and lower respiratory tract infection in hospitalized institutionalized elders using molecular genotyping. Methods: We assessed the dental status of 49 critically ill residents of long-term care facilities requiring intensive care treatment. Plaque index scores and quantitative cultures of DPs were obtained on ICU admission. Protected BAL (PBAL) was performed on 14 patients who developed hospital-acquired pneumonia (HAP). Respiratory pathogens recovered from the PBAL fluid were compared genetically to those isolated from DPs by pulsed-field gel electrophoresis. Measurements and results: Twenty-eight subjects (57%) had colonization of their DPs with aerobic pathogens. Staphylococcus aureus (45%) accounted for the majority of the isolates, followed by enteric Gram-negative bacilli (42%) and Pseudomonas aeruginosa (13%). The etiology of HAP was documented in 10 patients. Of the 13 isolates recovered from PBAL fluid, nine respiratory pathogens matched genetically those recovered from the corresponding DPs of eight patients. Conclusions: These findings suggest that aerobic respiratory pathogens colonizing DPs may be an important reservoir for HAP in institutionalized elders. Future studies are needed to delineate whether daily oral hygiene in hospitalized elderly would reduce the risk of nosocomial pneumonia in this frail population. (CHEST 2004; 126:1575–1582)

An actinomycetemcomitans can cause localized juvenile periodontitis and certain types of adult periodontitis. Optimal treatment of periodontal disease caused by this microorganism requires systemic antibiotic therapy in addition to mechanical debridement of the infected gingival tissues. Laboratory techniques are available to assist the practitioner in identifying this microorganism in dental plaque samples.

Human oral spirochetes are prominent inhabitants of subgingival plaque in patients with periodontal disease. Measurements of serum antibody titers to these micro-organisms have been used to illuminate the role of human oral spirochetes in periodontal disease. In the present study, rabbit antisera to four oral spirochetes (including Treponema denticola ATCC33520 and three clinical isolates) were examined for reactivity to cell lysates. Western blotting demonstrated that the major treponemal antigens reactive with the rabbit antisera to T. denticola ATCC33520 and to strains 42, 48, and 57 possessed 53-kDa, 53-kDa, 56-kDa, and 56-kDa molecular weights, respectively. Human sera from patients with acute necrotizing ulcerative gingivitis (ANUG) and localized juvenile periodontitis (LJP) were also reactive with these antigens, particularly the 53-kDa antigen of T. denticola ATCC33520. A membrane-rich preparation was obtained from the cell lysate of T. denticola ATCC33520 by column chromatography and centrifugation, and applied to an SDS-polyacrylamide gel. The 53-kDa major peptide band was found. The membrane vesicles in an axial filament-membrane-containing fraction were agglutinated in the presence of the rabbit antiserum to T. denticola ATCC33520. Western blot analysis indicated that the 53-kDa antigen reacted strongly with the rabbit antiserum to T. denticola ATCC33520. These findings suggest that polypeptide antigens, such as the 53-kDa antigen from human oral spirochetes, play an important role in production of humoral antibodies associated with periodontal disease.

The prevalence and distribution of the putative periodontal pathogen Eikenella corrodens in the human oral cavity was examined. A total of 508 oral bacterial samples were taken from 10 periodontally healthy adults (PH), 11 adult periodontitis patients (AP), and 6 localized juvenile periodontitis patients (LJP). From each subject, samples of supra- and subgingival plaque were obtained from six to eight teeth as well as samples from buccal mucosa, lateral and dorsal surfaces of tongue, tonsil, and saliva. E. corrodens was cultured from 70% of healthy subjects and 100% of periodontitis patients. Dental plaque appears to be the main oral ecological niche of E. corrodens in PH subjects since it was found in, respectively, 26% and 31% of supra- and subgingival plaque samples and rarely found in other oral sites in these subjects. It was found in 59% of both supra- and subgingival plaque samples from AP subjects, as well as 48% and 64% of supra- and subgingival plaque samples of LJP subjects. In contrast to healthy subjects, E. corrodens was found on the buccal mucosa, tongue, tonsil and in the saliva of patients with periodontitis. The microorganism constituted, on average, 1% to 2% of the total cultivable bacteria in supra- and subgingival plaque samples. The prevalence of E. corrodens in plaque samples was higher in AP and LJP subjects and was significantly different from PH subjects. Within the AP group, the prevalence of E. corrodens in subgingival plaque is significantly higher from sites with GI greater than or equal to 2. These data suggest that E. corrodens is an indigenous oral microorganism which may be an opportunistic pathogen associated with gingival inflammation.