IL-17 in sera from patients with aggressive periodontitis.

Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis. IL-17 was barely detectable in sera from periodontally healthy individuals (1.9 +/- 2.0 pg/mL), but was present at significantly higher concentrations in sera from those with LAgP (7.6 +/- 2.2 pg/mL) and GAgP (17.1 +/- 2.3 pg/mL). Multivariate analyses demonstrated associations of IL-17 concentrations with periodontal attachment loss, but not with current smoking. Therefore, Th17 responses may be characteristic of AgP, and IL-17 may play a role in the pathogenesis of aggressive periodontitis.

Anti-cardiolipin antibodies in sera from patients with periodontitis.

Antiphospholipid antibodies are commonly found in patients with systemic lupus erythematosus or the antiphospholipid syndrome, and a subset of such antibodies is associated with prothrombotic events such as stroke and with adverse pregnancy outcomes and fetal loss. We examined sera from 411 patients who were clinically characterized as to their periodontal disease status for serum levels of beta2-glycoprotein I-dependent anti-cardiolipin autoantibodies (anti-CL). The prevalence of patients with chronic periodontitis (CP) and generalized aggressive periodontitis (GAgP) positive for anti-CL (16.2% and 19.3%, respectively) was greater than that in healthy controls (NP) and localized aggressive periodontitis (LAgP) patients (6.8% and 3.2%). Patients with these autoantibodies demonstrated increased pocket depth and attachment loss compared with patients lacking the antibodies. Analysis of the data indicates that patients with generalized periodontitis have elevated levels of autoantibodies reactive with phospholipids. These antibodies could be involved in elevated risk for stroke, atherosclerosis, or pre-term birth in periodontitis patients.

Evidence of a substantial genetic basis for IgG2 levels in families with aggressive periodontitis.

IgG2 is elevated in localized but not in generalized aggressive periodontitis (AgP). Exposure to pathogenic bacteria is essential for disease. Immune responses are dominated by IgG2 reactive with bacterial surface carbohydrates. We used variance component analyses to assess IgG2 heritability and determine whether genes that influence IgG2 are the same genes that influence disease susceptibility. We studied 17 Caucasian and 43 African American families with two or more localized or generalized AgP-affected members (274 subjects with IgG2 measurements). Only 16% of the variance in IgG2 was attributable to age, race, and smoking. Even with the addition of localized AgP, the model still explained only 19% of IgG2 variance. By contrast, heritability of IgG2 levels was estimated to be 38% and highly significant (P = 0.0006), demonstrating a substantial genetic basis. Bi-trait variance component analyses of IgG2 and quantitative measures of AgP indicate that different genes appear to control IgG2 levels and disease susceptibility.

Phosphorylcholine-dependent cross-reactivity between dental plaque bacteria and oxidized low-density lipoproteins.

Antibodies reactive with phosphorylcholine (PC) are ubiquitous in human sera, but the antigens stimulating their production and their function are not clear. Previous studies have shown that a significant proportion of dental plaque bacteria contain PC as determined by reactivity with PC-specific mouse myeloma proteins and monoclonal antibodies. Additionally, serum antibody concentrations of immunoglobulin (IgG) G anti-PC are higher in sera of individuals who have experienced periodontal attachment loss than those who are periodontally healthy. These data implicate the oral microflora as a source of antigen-stimulating anti-PC responses. Recent data also indicate that antibodies with specificity for PC are elevated in ApoE-deficient mice, a model for studies of athersclerosis, and that such antibodies bound oxidized low-density lipoproteins (LDL) (oxLDL) in atherosclerotic plaques. These data prompted the hypothesis that human anti-PC could bind to both oral bacteria and human oxLDL, and that these antigens are cross-reactive. We therefore examined the ability of human anti-PC to bind to PC-bearing strains of oral bacteria using enzyme-linked immunosorbent inhibition assays and by assessment of direct binding of affinity-purified human anti-PC to PC-bearing Actinobacillus actinomycetemcomitans. Our results indicated that PC-bearing strains of Streptococcus oralis, Streptococcus sanguis, Haemophilus aphrophilus, Actinomyces naeslundii, Fusobacterium nucleatum, and A. actinomycetemcomitans, as well as a strain of Streptococcus pneumoniae, absorbed up to 80% of anti-PC IgG antibody from human sera. Furthermore, purified anti-PC bound to a PC-bearing strain of A. actinomycetemcomitans but only poorly to a PC-negative strain. OxLDL also absorbed anti-PC from human sera, and oxLDL but not LDL reacted with up to 80% of the anti-PC in human sera. Furthermore, purified anti-PC bound directly to oxLDL but not to LDL. The data indicate that PC-containing antigens on a variety of common oral bacteria are cross-reactive with neoantigens expressed in oxLDL. We propose that PC-bearing dental plaque microorganisms may induce an antibody response to PC that could influence the inflammatory response associated with atherosclerosis.

Evidence of a substantial genetic basis for risk of adult periodontitis.

BACKGROUND: A few previous studies have suggested that risk for adult periodontitis (AP) has a genetic (heritable) component. We estimated genetic and environmental variances and heritability for gingivitis and adult periodontitis using data from twins reared together. METHODS: One hundred seventeen (117) pairs of adult twins (64 monozygotic [MZ] and 53 dizygotic [DZ] pairs) were recruited. Probing depth (PD), attachment loss (AL), plaque, and gingivitis (GI) were assessed on all teeth by two examiners. Measurements were averaged over all sites, teeth, and examiners. Extent of disease in subjects was defined at four thresholds: the percentage of teeth with AL > or = 2, AL > or = 3, PD > or = 4, or PD > or = 5 mm. Genetic and environmental variances and heritability were estimated using path models with maximum likelihood estimation techniques. RESULTS: MZ twins were more similar than DZ twins for all clinical measures. Statistically significant genetic variance was found for both the severity and extent of disease. AP was estimated to have approximately 50% heritability, which was unaltered following adjustments for behavioral variables including smoking. In contrast, while MZ twins were also more similar than DZ twins for gingivitis scores, there was no evidence of heritability for gingivitis after behavioral covariates such as utilization of dental care and smoking were incorporated into the analyses. CONCLUSIONS: These results confirm previous studies and indicate that approximately half of the variance in disease in the population is attributed to genetic variance. The basis for the heritability of periodontitis appears to be biological and not behavioral in nature.

The use of the Mini-Nutritional Assessment (MNA) tool in elderly orthopaedic patients.

OBJECTIVE: To assess the use of the Mini-Nutritional Assessment (MNA) in elderly orthopaedic patients. DESIGN: An observation study assessing the nutritional status of female orthopaedic patients. SETTING: The orthopaedic wards of the Royal Surrey County Hospital. SUBJECTS: Forty-nine female patients aged 60-103 y; dietary records were obtained for 41 subjects and 36 subjects gave a blood sample for biochemical analysis. MAJOR OUTCOME METHODS: MNA questionnaire, anthropometry, plasma albumin, transferrin, C-reactive protein (CRP) levels and dietary analyses. RESULTS: The group as a whole had low mean values for body weight, albumin and transferrin and high CRP levels. In addition, the group had mean energy intakes well below the estimated average requirement (EAR) and mean intakes of vitamin D, magnesium, potassium, selenium and non-starch polysaccharides (NSP) were below the lower reference nutrient intakes (LRNI). The MNA screening section categorized 69% of the patients as requiring a full assessment (scored 11 or below), but for the purposes of the study the MNA was completed on all patients. The MNA assessment categorized 16% of the group as 'malnourished' (scored<17 points), 47% as 'at risk' (scored 17.5-23.5) and 37% as 'well nourished' (scored>23.5). Significant differences were found between the malnourished and well nourished groups for body weight (P<0.001), body mass index (BMI) (P<0.001), demiquet (P<0.001) and mindex (P<0. 001). Mean values for energy and nutrient intakes showed a clear stepwise increase across the three groups for all nutrients except sodium, with significant differences for protein (P<0.05), carbohydrate (P<0.05), riboflavin (P<0.05) niacin (P<0.05), pyridoxine (P<0.05), folate (P<0.05), calcium (P<0.05), selenium (P<0.05), iron (P<0.05) and NSP (P<0.05) intakes. Stepwise multiple regression analysis indicated that anthropometric assessments were the most predictive factors in the total MNA score. The sensitivity and specificity of the MNA was assessed in comparison with albumin levels, energy intake and mindex. The sensitivity of the MNA classification of those scoring less than 17 points in comparison with albumin levels, energy intake and mindex varied from 27 to 57% and the specificity was 66-100%. This was compared with the sensitivity and specificity of using a score of less than 23.5 on the MNA to predict malnourished individuals. Using this cut-off the sensitivity ranged from 75 to 100%, but the specificity declined to between 37 and 50%. CONCLUSIONS: The results suggest that the MNA is a useful diagnostic tool in the identification of elderly patients at risk from malnutrition and those who are malnourished in this hospital setting. SPONSORSHIP: Nestlé Clinical Nutrition, Croydon, Surrey.

The quantitation of lipoprotein lipase mRNA in biopsies of human adipose tissue, using the polymerase chain reaction, and the effect of increased consumption of n-3 polyunsaturated fatty acids.

OBJECTIVE: To examine the effects of the consumption of fish oils on the gene expression of lipoprotein lipase (LPL, EC 3.1.1.34) in human adipose tissue. In order to measure LPL mRNA in adipose tissue samples obtained by needle biopsy from human volunteers a competitive, reverse transcriptase PCR (RT-PCR) protocol was developed. DESIGN: A randomised controlled, single blind cross over dietary study which compared the effects of a low level n-3 polyunsaturated fatty acids (PUFA) using normal foods enriched with eicosapentaenoic (EPA) and docosahexaenoic (DHA) (test diet), with non-enriched but otherwise identical foods (control). The diets were consumed for a period of 22 d with a wash out period of 5 months between the diets. SETTING: Free-living individuals associated with the University of Surrey. SUBJECTS: Six male subjects with a mean (+/- sd) age of 51.2+/-3.6 y were recruited. MAJOR OUTCOME MEASURES: Pre- and postprandial blood samples were taken for the measurement of triacylglycerol (TAG), postheparin LPL activity and adipose tissue samples for the measurement of LPL mRNA levels. RESULTS: Mean LPL expression values were 4.12 x 10(5) molecules of LPL mRNA per ng total RNA on the control diet and 4.60 x 10(5) molecules of LPL mRNA per ng total RNA on the n-3 PUFA enriched (test) diet. There was no significant difference between the levels of LPL expression following each diet, consistent with the lack of change in TAG levels in response to increased dietary n-3 PUFA intake. However, the change in LPL expression (Test-Control diet) correlated significantly with the change in fasting TAG levels (P = 0.03, R = -0.87 and R2 = 0.75) and with the total area under the TAG-time response curve (P = 0.003, R = -0.96 and R2 = 0.92) in individuals. CONCLUSIONS: These findings, although based on a small number of subjects, suggest that LPL expression may be a determinant of plasma TAG levels. The development of this methodology should allow further elucidation of the effects of dietary manipulation and disease processes on lipid clearance and regulation in human subjects.

Linkage disequilibrium of interleukin-1 genetic polymorphisms with early-onset periodontitis.

BACKGROUND: Genetic polymorphisms at interleukin (IL)-1alpha and IL-1beta were recently suggested to be associated with severity of adult periodontitis. We evaluated whether these polymorphisms might also be associated with early-onset periodontitis (EOP) in 28 African American families and 7 Caucasian American families with 2 or more affected members. METHODS: Genomic DNA from peripheral blood was amplified, followed by restriction endonuclease digestion and acrylamide gel electrophoresis to distinguish alleles of different fragment sizes. Genetic epidemiological methods suitable for family data were used that are robust to false-positive findings due to mismatching of cases and controls or mixed subpopulations of different ethnic or geographic origin. The 2 major EOP subtypes, localized juvenile periodontitis (LJP), and generalized early-onset periodontitis (G-EOP, encompassing rapidly progressive periodontitis and generalized juvenile periodontitis), were analyzed both separately and together. RESULTS: We obtained highly significant evidence of linkage disequilibrium for both African American and Caucasian G-EOP subjects. A similar trend was noted for LJP. The IL- alleles associated with high risk of EOP had been suggested previously to be correlated with low risk for severe adult periodontitis. Disequilibrium with G-EOP was equally strong for smoking and non-smoking subjects. IL-1alpha and IL-1beta polymorphisms were in strong disequilibrium with each other in Caucasians, but not in African Americans. Haplotype analyses evaluating both polymorphisms simultaneously indicated that the IL-1beta variant is likely to be most important for EOP risk. Sibpair linkage analyses, by contrast, provided only marginal support for a gene of very major effect on EOP risk attributable to these IL-1 polymorphisms. CONCLUSIONS: Recent theoretical analyses indicate that our findings are most consistent with an interpretation of EOP as a complex, oligogenic disorder, with IL-1 genetic variation contributing an important but not exclusive influence on disease risk.

Markers of intestinally-derived lipoproteins: application to studies of altered diet and meal fatty acid compositions.

BACKGROUND AND AIM: The atherogenic potential of dietary derived lipids, chylomicrons (CM) and their remnants (CMr) is now becoming more widely recognised. To investigate factors effecting levels of CM and CMr and their importance in coronary heart disease risk it is essential to use a specific method of quantification. Two studies were carried out to investigate: (i) effects of increased daily intake of long chain n-3 polyunsaturated fatty acid (LC n-3 PUFA), and (ii) effects of increasing meal monounsaturated fatty acid (MUFA) content on the postprandial response of intestinally-derived lipoproteins. The contribution of the intestinally-derived lipoproteins to total lipaemia was assessed by triacylglycerol-rich lipoprotein (TRL) apolipoprotein B-48 (apo B-48) and retinyl ester (RE) concentrations. METHODS AND RESULTS: In a randomised controlled crossover trial (placebo vs LC n-3 PUFA) a mean daily intake of 1.4 g/day of LC n-3 PUFA failed to reduce fasting and postprandial triacylglycerol (TAG) response in 9 healthy male volunteers. Although the pattern and nature of the apo B-48 response was consistent with the TAG response following the two diets, the postprandial RE response differed on the LC n-3 PUFA diet with a lower early RE response and a delayed and more marked increase in RE in the late postprandial period compared with the control diet, but the differences did not reach levels of statistical significance. In the meal study there was no effect of MUFA/SFA content on the total lipaemic response to the meals nor on the contribution of intestinally derived lipoproteins evaluated as TAG, apo B-48 and RE responses in the TRL fraction. In both studies, the RE and apo B-48 measurements provided broadly similar information with respect to lack of effects of dietary or meal fatty acid composition and the presence of single or multiple peak responses. However the apo B-48 and RE measurements differed with respect to the timing of their peak response times, with a delayed RE peak, relalive to apo B-48, of approximately 2-3 hours for the LC n-3 PUFA diet (p = 0.002) study and 1-1.5 hours for the meal MUFA/SFA study. CONCLUSIONS: It was concluded that there are limitations of using RE as a specific CM marker, apo B-48 quantitation was found to be a more appropriate method for CM and CMr quantitation. However it was still considered of value to measure RE as it provided additional information regarding the incorporation of other constituents into the CM particle.

The effect of smoking on individuals with minimal periodontal destruction.

Recent studies have demonstrated that smoking is associated with periodontal destruction. The majority of these studies have focused on periodontal disease groups with moderate or severe periodontal destruction. Additionally, there have been few reports investigating the relationship between smoking and gingival recession. The goal of this report was to investigate the effect of smoking on periodontal destruction and recession in subjects with minimal or no interproximal attachment loss. This is a cross-sectional study of 142 non-smoking subjects and 51 smoking subjects. Subjects could have no more than one tooth with a site of interproximal attachment loss > or =2 mm. Subjects could, however, have attachment loss associated with recession. For three different methods of summarizing attachment loss measurements at a subject level, including average attachment loss, percentage of teeth with one site of 2 mm of attachment loss, and the percentage of teeth with one site of 5 mm of attachment loss, smoking subjects had approximately twice as much attachment loss than their non-smoking counterparts. Smoking subjects also had significantly greater recession (P < 0.05) [0.056+/-0.017 mm] than non-smoking subjects (0.025+/-0.005 mm). Recession sites occurred primarily on the facial surface of maxillary molars and bicuspids and mandibular central incisors and bicuspids. The results suggest a strong association between smoking and both attachment loss and recession in subjects who have minimal or no periodontal disease.

A longitudinal comparison of tooth whitening resulting from dentifrice use.

The effect of twice-daily brushing with one of three different dentifrices (Arm & Hammer Dental Care, Arm & Hammer Dental Care Extra Whitening, Crest) on stain removal and tooth whitening was examined in 115 volunteers over a period of 12 weeks. The facial surfaces of 12 anterior teeth were assessed for stain using a published, modified version of a standard stain index. Whiteness was measured on teeth 8 and 9 using a single Vita Lumin-Vaccum Shade Guide for consistency. At baseline, the mean facial stain scores were significantly higher (p < 0.05-0.01) for both Arm & Hammer dentifrices than for Crest. In addition, the tooth shades, as indicated by the stain guide, specifically the b* values representing yellowness, were quantified using a Minolta spectrophotometer. Arm & Hammer Dental Care Extra Whitening formula was found to be significantly better than Crest at removing naturally occurring extrinsic stain. The difference between Arm & Hammer Dental Care Extra Whitening and Crest became significant (p < 0.01) after two weeks of use, and remained intact during the balance of the study, achieving p values of 0.0002 for at least one of the three assessed parameters (total stain, proximal, and facial) at weeks 4 and 12. The study also found that Arm & Hammer Dental Care produced a significant increase in tooth whiteness by week 12, whereas Crest showed no such increase at any time during the study. These results suggest that the two Arm & Hammer Baking Soda products are more effective in reducing stain and increasing whiteness than the standard silica-based dentifrice. Their effectiveness is not related to abrasivity since they are less abrasive to tooth enamel than the silica-based product tested.

Use of manufactured foods enriched with fish oils as a means of increasing long-chain n-3 polyunsaturated fatty acid intake.

The objectives of the present study were to determine the feasibility of using manufactured foods, enriched with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as a means of increasing the intake of these n-3 polyunsaturated fatty acids (PUFA), and to determine the effect of the consumption of these foods on postprandial lipaemia and other metabolic responses to a high-fat mixed test meal. Nine healthy, normotriacylglycerolaemic, free-living male volunteers (aged 35-60 years) completed the randomized, controlled, single-blind, crossover study. The study consisted of two periods (each of 22 d) of dietary intervention, separated by a 5-month washout period. During these two periods the subjects were provided with the manufactured foods enriched with EPA and DHA (n-3 enriched) or identical but unenriched foods (control). A mixed test meal containing 82 g fat was given to the fasted subjects on day 22 of each dietary intervention period. Two fasting, and thereafter hourly, blood samples were collected from the subjects for an 8 h period postprandially. Plasma triacylglycerol, total and HDL-cholesterol, non-esterified fatty acids (NEFA), glucose and immunoreactive insulin levels, post-heparin lipoprotein lipase (EC 3.1.1.34) activity and the plasma free fatty acid and phospholipid fatty acid compositions were measured. A mean daily intake of 1.4 g EPA+DHA (0.9 g EPA, 0.5 g DHA) was ingested during the n-3-enriched dietary period, which was significantly higher than the intake during the habitual and control periods (P < 0.001) assessed by a 3 d weighed food intake. A significantly higher level of EPA+DHA enrichment of the plasma fatty acids and phospholipids (P < 0.001) after the n-3-enriched compared with the control intervention periods was also found. The energy intake on both of the dietary intervention periods was found to be significantly higher than on the habitual diet (P < 0.001), with an increase in body weight of the subjects, which reached significance during the n-3 PUFA-enriched dietary intervention period (P < 0.04). The palatability of the enriched foods was not significantly different from that of the control foods. Significantly higher fasting plasma HDL-cholesterol and glucose concentrations were found after the n-3 PUFA-enriched compared with the control intervention period (P < 0.02 and P < 0.05 respectively). No significant differences were found for the postprandial lipid and hormone measurements, except for significantly lower levels of NEFA at 60 min after the n-3-enriched intervention period (P < 0.04). Enriched manufactured foods were a feasible vehicle for increasing n-3 PUFA intake. However the nature of the foods provided as the n-3 vehicle may have contributed to the increased body weight and higher energy intakes which were adverse consequences of the intervention. These factors, together with the short duration of the study may have been responsible for the failure to observe significant plasma triacylglycerol reductions in response to daily intakes of 1.4 g EPA+DHA.

Periodontal therapy in young adults with severe generalized periodontitis.

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.

Maintenance therapy in young adults with severe generalized periodontitis.

The purpose of this study was to evaluate one year of maintenance therapy in young adults with severe periodontitis (SP) who had previously received periodontal therapy consisting of root planing and scaling followed by open flap debridement. Subjects were evaluated with clinical and microbiological measurements at 3, 6, 9, and 12 months following the completion of active therapy. Subjects were included in the study if they completed a minimum of two evaluation appointments. Monitoring of these subjects during the maintenance phase was analyzed by three methods. First, changes in mean attachment level and mean probing depth were calculated at 3-month intervals to determine if the subjects continued to lose or gain attachment and/or had periodontal pockets of increasing or decreasing depth. Second, the frequency of periodontal breakdown was determined and compared to breakdown rates of subjects in other patient populations. Third, future changes in attachment level were related to the presence or absence of two putative periodontal pathogens, Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in subgingival plaque. Mean attachment level remained constant in 13 subjects who completed one year of maintenance therapy. However, mean probing depth increased at a yearly rate of 0.19 mm and in periodontally-involved sites pocket depth increased at a yearly rate of 0.65 mm both of which were statistically significantly different from 0 (P < .05). The frequency of periodontal breakdown in this study was higher than reported in other similar studies of different periodontitis patient populations. The remainder of the data in the study was from 21 subjects who had completed at least two recall appointments.(ABSTRACT TRUNCATED AT 250 WORDS)

Investigation of the influences of puberty, genetics, and environment on the composition of subgingival periodontal floras.

The classical twin model was utilized in this study in an attempt to determine the importance of host genetics to the composition of the subgingival flora. Simultaneously, the effect of puberty on the flora composition was assessed. The compositions of the floras were significantly different at ages 11 and 14 in the same people, indicating that transition to an adult flora composition may be initiated during puberty. However, the numbers of subjects who had prepubertal and postpubertal testosterone levels in this study were too small to demonstrate significant differences based solely on testosterone level (P = 0.053 and 0.11 for tests of unrelated members, i.e., all twins "a," the first twin of each pair, and all twins "b," the second twin of each pair). Sixteen unrelated 11-year-old subjects had prepubertal levels of less than 30 ng of testosterone per dl of serum, and only six of these unrelated subjects had levels above 300 ng/dl by age 14. Of their twin siblings, who formed the second group of unrelated individuals, 15 had prepubertal levels and only 5 reached postpubertal levels. Unpaired t tests indicated that Veillonella atypica, Prevotella denticola, and Prevotella melaninogenica were among the species that contributed most to changes in flora composition during puberty. The compositions of subgingival floras of 11-year-old monozygous and dizygous male twins were significantly more similar than those of unrelated subjects in the study (P = 0.004 and 0.009, respectively). At 12.5 years of age, the floras of monozygous twins remained more similar than those of unrelated subjects (P = 0.001), but the dizygous-twin floras were not significantly more similar than those of unrelated people. This difference corresponded with moderate and varied testosterone levels within dizygous-twin pairs at age 12.5. By age 14 both monozygous and dizygous twins again had floras with compositions more similar than those of unrelated people (P = 0.008 and 0.002, respectively). Estimates of the genetic contributions to the increased similarity of the floras of twins as compared with floras of unrelated people indicated that the concentrations of several species in the flora may be influenced by host genetic factors. The prevalence of certain other species appeared to be controlled primarily by environment.

The influence of race and gender on periodontal microflora.

Previous studies have demonstrated that demographic characteristics of subject populations influence both the incidence of periodontal diseases and various aspects of host responses to periodontal bacteria. In this study we analyzed the components of the subgingival microflora from individuals with adult periodontitis, early onset periodontitis, gingivitis, and periodontal health as a function of gender and race (black and white). Clinical categories were analyzed individually so that there were no differences in the clinical characteristics of the sampled sites. No significant differences were noted in the subgingival microflora between males and females. When either the first two bacterial samples from each subject or all bacterial samples taken from each subject were included in the analysis, it was found that Porphyromonas gingivalis was more significantly associated with black subjects in the adult periodontitis group. When all samples were considered in the analysis, it was found that Peptostreptococcus anaerobius was associated with black subjects in the adult periodontitis group, while Fusobacterium nucleatum was associated with white subjects in both the adult periodontitis and early onset periodontitis groups. Thus a limited number of important bacterial components of the subgingival microflora are influenced by the race and diagnosis of the subject group.

Periodontal microflora of HIV positive subjects with gingivitis or adult periodontitis.

The subgingival microflora of 39 HIV+ subjects with gingivitis or adult periodontitis was cultured quantitatively anaerobically for bacteria, spirochetes, and mycoplasma and aerobically for yeasts. Isolates were characterized by conventional biochemical tests, polyacrylamide gel electrophoresis of soluble proteins, cellular fatty acid profiles, immunofluorescence, and immunodiffusion. In general, the same types of bacteria were isolated from the subgingival crevice of HIV+ subjects as we previously had isolated from the subgingival crevice of non-HIV subjects. A statistically significant difference was found between the composition of the flora of HIV+ subjects with adult periodontitis (AP) and concurrent studies of a non-HIV+ AP population. Mycoplasma salivarium was significantly elevated in the HIV+ subjects examined. Yeasts were isolated from only 10% of the samples and from 13% of the HIV-positive subjects at 0.05 to 0.0002% of the total cultivable count when present.

No female preponderance in juvenile periodontitis after correction for ascertainment bias.

Juvenile periodontitis (JP) is generally recognized to exist in 2 clinical forms: localized and generalized. Historically, females have been reported to be affected by both forms of JP at rates of 2 to 10 times greater than males. However, evidence suggests that females are more likely than males to seek dental care. If this is true, females will be diagnosed with JP more often than males even if juvenile periodontitis is equally prevalent among males and females in the general population. Thus, previous reports of a female predominance for JP may simply reflect this selection bias. The purpose of this study was to test our hypothesis that juvenile periodontitis occurs with equal frequency in males and females after correcting for selection bias. Twenty-four juvenile periodontitis probands were ascertained from the VCU/MCV dental clinics. The families of these individuals were examined to determine the relative prevalence of JP among male and female relatives of these probands. Our results indicate that while females are 3 times more likely than males to be initially ascertained as juvenile periodontitis probands, among relatives of probands the proportion of affected males and females is equal.

Reliability of attachment loss measurements in a longitudinal clinical trial.

In order to appropriately carry out a longitudinal assessment of periodontal attachment loss in individuals with untreated periodontitis, reliable criteria for determining "real" changes in attachment level (AL) are required. In the present study, 25 subjects were to be examined every 2 months for up to 2 years to determine changes in AL and to relate clinical and laboratory criteria to such changes. Trained examiners for the study underwent calibration trials to determine inter-examiner and intra-examiner reliability both before the study and at intervals during the study. It was found that AL measurements were in agreement within 2 mm more than 95% of the time. The calibration trials provided an estimate of the error in attachment loss measurements, since no "real" attachment loss had occurred. From estimates of measurement error, the probability of false positive changes were determined. It was found that acceptable false positive rates (less than 5%) could be achieved if 2 examiners each detected 3 mm change at a given site or if 2 examiners each detected 2 mm change at a site and verified that this change persisted at a subsequent examination. The results of the longitudinal trial were then compared to the probability estimates calculated from the calibration trials. It was found that probabilities of AL changes detected during the longitudinal trial for less stringent conditions than described above (e.g., single examiner, 2 examiners unconfirmed) were similar to to previously estimated false positive rates.(ABSTRACT TRUNCATED AT 250 WORDS)