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Smoking increases the risk for periodontal disease and reduces the healing response. We examined the antimicrobial and clinical effects of scaling and root planing (SRP) with and without minocycline HCl 1 mg microspheres (MM) relative to smoking status in subjects with periodontitis.A total of 127 subjects (46 never smokers, 44 former smokers, and 37 current smokers) with moderate to advanced periodontitis were randomized to receive MM + SRP (N = 62) or SRP alone (N = 65). Subgingival plaque samples collected at baseline and day 30 were examined for the presence of 40 periodontal bacteria by DNA probe analysis.MM + SRP reduced red-complex bacteria (RCB) numbers and proportions to a greater extent than SRP alone, irrespective of smoking status. RCB numbers were not reduced by SRP in current smokers. The difference in the reduction in numbers of RCB by SRP relative to MM + SRP in current smokers was statistically significant (P0.05). Numbers and proportions of orange complex bacteria (OCB) were reduced in all groups treated with MM + SRP. Proportions of OCB increased in current smokers treated with SRP alone. In current smokers, MM + SRP significantly reduced probing depth (PD), increased clinical attachment level (CAL), and reduced bleeding on probing (BOP) to a greater extent than SRP alone (P0.05).SRP alone was ineffective at reducing numbers or proportions of RCB or OCB in current smokers, whereas MM + SRP significantly reduced both. MM + SRP also improved PD, BOP, and CAL to a greater extent than SRP alone independent of smoking status.

Background: The objective of this trial was to measure the antimicrobial effects of a minocycline HCl microsphere (MM) local drug-delivery system when used as an adjunct to scaling and root planing (SRP). DNA probe analysis for 40 bacteria was used to evaluate the oral bacteria of 127 subjects with moderate to advanced chronic periodontitis. Methods: Subjects were randomly assigned to either SRP alone (N = 65) or MM + SRP (N = 62). The primary endpoints of this study were changes in numbers and proportions of the red-complex bacteria (RCB) and the sum of Porphyromonas gingivalis, Tannerella forsythia (formally T. forsythensis), and Treponema denticola relative to 40 oral bacteria at each test site from baseline to day 30. Numbers of RCB from the five test sites were averaged to provide a value for each subject. Results: MM + SRP reduced the proportion of RCB by 6.49% and the numbers by 9.4 · 10 5 . The reduction in RCB proportions and numbers by SRP alone (5.03% and 5.1 · 10 5 , respectively) was significantly less. In addition, MM + SRP reduced probing depth by 1.38 mm (compared to 1.01 mm by SRP alone), bleeding on probing was reduced by 25.2% (compared to 13.8% by SRP alone), and a clinical attachment level gain of 1.16 mm (compared to 0.80 mm by SRP alone) was achieved. Conclusion: These observations support the hypothesis that RCBs are responsible for periodontal disease and that local antimicrobial therapy using MM + SRP effectively reduces numbers of RCBs and their proportions to a greater extent than SRP alone. J Periodontol 2007;78:1568-1579.

We present an approach to examiner calibration study design where the number of calibration subjects is based on a specified margin of error (half-width of the 95% confidence interval [CI]) of the percentage of agreement (exact and within 1 mm) for both intra- and interexaminer reliability assessments.An experienced standard examiner (S) trained three dental hygienists (A, B, and C) in correct procedures for obtaining a variety of periodontal measures. Duplicate measurements of probing depth (PD [mm]) and the free gingival margin to the cemento-enamel junction (CEJ-GM [mm]) were obtained in a pilot study to design a formal examiner calibration study, where sample sizes were adjusted for the effects of within-subject clustering of binary indices of agreement.Within-subject clustering of agreement indices resulted in an approximate four-fold increase in the variance of the estimates of percentage of agreement with the standard. PD and CEJ-GM percentage of exact agreement measurements (95% CI) for each examiner-standard pair, respectively, were as follows: AS=55% (48%, 61%) and 70% (62%, 78%); BS=52% (45%, 59%) and 73% (63%, 82%); and CS=55% (50%, 61%) and 72% (65%, 79%). The corresponding 95% CIs unadjusted for the effects of clustering underestimated the margin of error associated with the estimates of exact agreement by as much as 57% for PD and 68% for CEJ-GM.Failure to account for dependence among site-level agreement indices results in a false sense of precision in the resulting reliability estimates and can lead to faulty inference.

Bacterial interactions in response to local and systemic factors may explain important features of the pathogenesis of periodontal disease. This study evaluates the role of supragingival plaque level on the relationship between subgingival microorganisms and the risk of attachment loss.The study population consisted of 386 white women aged 45 years and older who had at least seven teeth. Subgingival plaque samples were taken from the mesio-buccal surface of six maxillary and six mandibular teeth using paper point technique. The samples were pooled, and immunofluorescence microscopy was performed to identify the following target microorganisms: Actinobacillus actinomycetemcomitans (Aa), Tannerella forsythensis (Tf), Campylobacter rectus (Cr), Prevotella intermedia (Pi), Capnocytophaga species (Cs), Porphyromonas gingivalis (Pg), Eubacterium saburreum (Es), and Fusobacterium nucleatum (Fn). The presence or absence of supragingival plaque and clinical attachment loss (CAL) were assessed at the same 12 sites where subgingival plaque samples were taken. The association of each microorganism with CAL was tested using multiple logistic regressions controlling for age, smoking status, and diabetes. Odds ratios (OR) and their 95% confidence intervals (CI) were calculated.At low supragingival plaque levels, only the presence of Pg was significantly associated with CAL (OR: 6.41, 95% CI: 1.30 to 31.70); all remaining microorganisms were also associated with increased but non-significant risk of CAL. At high supragingival plaque levels, the presence of Tf (OR: 2.40, 95% CI: 1.42 to 4.04) and Pg (OR: 3.71, 95% CI: 1.63 to 8.42) was significantly associated with increased risk of attachment loss. By contrast, the presence of Cs (OR: 0.55, 95% CI: 0.30 to 1.01) and Es (OR: 0.35, 95% CI: 0.15 to 0.82) was associated with decreased risk of attachment loss. Fn, Pi, and Cr were not significantly associated with CAL at either low or high supragingival plaque levels.This study suggests that the association of certain subgingival microorganisms with CAL changes in relation to supragingival plaque levels in older adult women. It also suggests that the overall effect of dental plaque is a function of the balance between pathogenic and other microorganisms that colonize this environment. Therefore, all microorganisms in the biofilm, including those with no apparent association with overt disease and those with negative associations, may play roles in the pathogenesis of periodontal diseases.

But: Le P-113, un peptide contenant de l'histatine a ete evalue dans un bain de bouche pour sa securite et son efficacite dans une etude multicentrique phase 2. Methode. 294 sujets sains ont arrete toute hygiene buccale et se sont rince avec soit 15 ml de P-113 0.01%, 15 ml de P-113 0.03% ou 15 ml d'une solution placebo 2× par jour durant une periode de 4 semaines. Pendant ce temps, les effets anti-plaque et anti-gingivite, la securite ont ete evalues. Resultats: Il y avait une reduction significative entre l'examen de depart et le jour 22 dans le saignement au sondage dans le groupe P-113 0.01% (p=0.049). Aucune tendance significative dans la reduction des autres parametres n'a ete observee dans cette population (p≥0.159). Un sous-groupe de sujets qui developpaient des niveaux significatifs de maladie durant ces 4 semaines a ete identifie sur base de leur indice gingival initial ≥0.75. Des decouvertes significatives ont ete observees pour le saignement au sondage, l'indice gingival et l'indice de plaque dentaire dans cette population (p

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.

Systemic bone loss has been proposed as a risk factor for periodontal disease; however, the relationship between these two diseases is still not clear. The objective of this study was to assess the relationship between systemic bone mineral density and periodontal disease, controlling for known confounders.The study population included 70 postmenopausal Caucasian women aged 51 to 78 (mean +/- SD: 62.10 +/- 7.1 years). Skeletal bone mineral density (BMD) was assessed by dual energy x-ray absorptiometry (DXA) at the neck, trochanter, intertrochanter, Ward's triangle, and total regions of the femur, and from the anterior-posterior view of the lumbar spine. Periodontal disease severity was represented by clinical attachment loss (CAL) and interproximal alveolar bone loss (ABL). Other measures of periodontal status included probing depth (PD), supragingival plaque, gingival bleeding on probing, and calculus. DXA and oral examinations were performed by calibrated examiners. Partial correlation coefficients (r) were obtained from multiple linear regression analysis adjusting for age, age at menopause, estrogen supplementation, cigarette smoking, body mass index, and supragingival plaque.Mean ABL was significantly correlated with BMD of the trochanter (r =- 0.27), Ward's triangle (r = -0.26), and total regions of the femur (r = -0.25). Mean CAL appeared to be related to BMD consistently at all regions of the skeleton, although the association did not reach statistical significance.We can conclude that skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical attachment loss, implicating postmenopausal osteopenia as a risk indicator for periodontal disease in postmenopausal Caucasian women.

Vitamin C has long been a candidate for modulating periodontal disease. Studies of scorbutic gingivitis and the effects of vitamin C on extracellular matrix and immunologic and inflammatory responses provide a rationale for hypothesizing that vitamin C is a risk factor for periodontal disease.We evaluated the role of dietary vitamin C as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III) which is representative of the U.S. civilian, non-institutionalized population.A sample of 12,419 adults (20 to 90+ years of age), with dental measurements and assessment of dietary information as well as demographic and medical histories were included in the studies. Dietary vitamin C was estimated by a 24-hour dietary record. Individuals with periodontal disease were arbitrarily defined as those who had mean clinical attachment levels ofor =1.5 mm. Using multiple logistic regression analysis, we found a relationship between reduced dietary vitamin C and increased risk for periodontal disease for the overall population (odds ratio [OR] = 1.19; 95% CI: 1.05 to 1.33). Current and former tobacco users who were taking less dietary vitamin C showed an increased risk of periodontal disease with OR of 1.28, 95% CI: 1.04 to 1.59 for former smokers, and an OR of 1.21, 95% CI: 1.02 to 1.43 for current tobacco users. There was a dose-response relationship between the levels of dietary vitamin C and periodontal disease with an OR of 1.30 for those taking 0 to 29 mg of vitamin C per day, to 1.16 for those taking 100 to 179 mg of vitamin C per day as compared to those taking 180 mg or more of vitamin C per day.Dietary intake of vitamin C showed a weak, but statistically significant, relationship to periodontal disease in current and former smokers as measured by clinical attachment. Those taking the lowest levels of vitamin C, and who also smoke, are likely to show the greatest clinical effect on the periodontal tissues.

The exclusive use of mean measurements in periodontal research might at times be misleading, as changes in different sites in the same individual might nullify each other. The purpose of the present study was to compare disease progression and response to periodontal therapy using both individual site activity with thresholds and mean patient changes.Seventy-nine (79) subjects with established periodontitis were monitored for 1 year (no treatment [NTx] group); 108 subjects who received scaling, root planing, and quarterly prophylaxis were observed in a similar time interval (treatment [Tx] group). Probing depth (PD), attachment level (AL) and alveolar crestal height (ACH) were measured at baseline and 1 year using pressure-sensitive probes and computer-assisted image analysis of radiographs.Mean reduction in PD (0.50 mm) was observed in the Tx group compared to a small increase (-0.04 mm) in the NTx group (P= 0.0001). Treatment resulted in mean AL gain (0.44 mm) compared to net AL loss (-0.21 mm) in the NTx group (P= 0.0001). Subjects in the Tx group had twice as many sites with AL gain (beyond the threshold) compared to NTx subjects (16.64+/-1.07% versus 8.11+/-0.68%) which was highly significant (P = 0.0001, Student t test). Similarly, although in the opposite direction, percentage of sites with AL loss beyond threshold was 6.21+/-0.47% (Tx group) and 14.02+/-1.15% (NTx group) which was also highly significant (P = 0.0001, Student t test). Change in ACH was minimal for the Tx group (-0.07+/-0.03 mm) while NTx subjects experienced greater bone loss throughout the year (-0.16+/-0.02 mm); percentage of sites with ACH loss was similar for both groups, while the Tx group had 3 times the number of sites with ACH gain (11.76% versus 3.42%), suggesting that the reduction in mean bone loss in the Tx group did not result from a reduction in losing sites, but rather from an increase in gaining sites. The use of both means and binary data seems to supplement the information regarding the nature and mechanism of disease progression and arrest.The characteristics of periodontal disease with its multifactorial patient, local, and site-related etiology support the use of both mean and site-based changes in clinical studies of periodontal disease and treatment.

The association of stress, distress, and coping behaviors with periodontal disease was assessed.A cross-sectional study of 1,426 subjects between the ages of 25 and 74 years in Erie County, New York, was carried out to assess these relationships. Subjects were asked to complete a set of 5 psychosocial questionnaires which measure psychological traits and attitudes including discrete life events and their impact; chronic stress or daily strains; distress; coping styles and strategies; and hassles and uplifts. Clinical assessment of supragingival plaque, gingival bleeding, subgingival calculus, probing depth, clinical attachment level (CAL) and radiographic alveolar crestal height (ACH) was performed, and 8 putative bacterial pathogens from the subgingival flora measured.Reliability of subjects' responses and internal consistencies of all the subscales on the instruments used were high, with Cronbach's alpha ranging from 0.88 for financial strain to 0.99 for job strain, uplifts, and hassles. Logistic regression analysis indicated that, of all the daily strains investigated, only financial strain was significantly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09 to 2.65 and OR = 1.68, 95% CI = 1.20 to 2.37, respectively) after adjusting for age, gender, and cigarette smoking. When coping behaviors were evaluated, it was found that those with more financial strain who were high emotion-focused copers (a form of inadequate coping) had a higher risk of having more severe attachment loss (OR = 2.24, 95% CI = 1.15 to 4.38) and alveolar bone loss (OR = 1.91, 95% CI = 1.15 to 3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. Similar results were found among the low problem-focused copers for AL (OR = 2.21, 95% CI = 1.11 to 4.38) and ACH (OR = 2.12, 95% CI = 1.28 to 3.51). However, subjects with high levels of financial strain who reported high levels of problem-based coping (considered adequate or good coping) had no more periodontal disease than those with low levels of financial strain, suggesting that the effects of stress on periodontal disease can be moderated by adequate coping behaviors.We find that psychosocial measures of stress associated with financial strain and distress manifest as depression, are significant risk indicators for more severe periodontal disease in adults in an age-adjusted model in which gender (male), smoking, diabetes mellitus, B. forsythus, and P. gingivalis are also significant risk indicators. Of considerable interest is the fact that adequate coping behaviors as evidenced by high levels of problem-based coping, may reduce the stress-associated risk. Further studies also are needed to help establish the time course of stress, distress, and inadequate coping with respect to the onset and progression of periodontal disease, and the mechanisms that explain this association.

Mechanical periodontal therapy is widely used for a variety of periodontal conditions. While the clinical efficacy of this treatment has been validated, the radiographic response has not been studied in depth. The purpose of the present study was to examine the clinical and radiographic response to mechanical periodontal therapy, and assess the factors associated with these changes. One hundred and eight patients, with established periodontitis, received oral hygiene instruction and mechanical periodontal therapy for a period of 4 to 5 weeks. Scheduled maintenance visits were performed at 3, 6, 9, and 15 months. Probing depth (PD) and attachment level (AL) measurements were performed at baseline, and at 3 and 15 months. Intraoral radiographs were taken at baseline and 12 to 15 months postsurgery using a Rinn alignment system. Alveolar crestal height (ACH) measurements were performed on a pair of digitized images of the previously taken radiographs. An overall mean of patients' changes for PD, AL, and ACH was initially computed. Active sites (gainers and losers) were determined using a threshold method, and expressed as patient's percentage of active sites (number of active sites of the total sites measured in each patient). Mean overall probing reduction and AL gain was 0.5 mm and 0.44 mm, respectively. Of all sites measured, 16.6% exhibited AL gain, while only 6.2% of all sites exhibited AL loss. Mean overall change in ACH was -0.07 mm, of which 11.8% of all sites exhibited ACH gain, while 15.1% exhibited loss beyond the threshold. Non-smokers presented no change in bone loss, while smokers continued to lose bone at an annual rate of 0.17 mm, despite treatment (P0.005). Likewise, the average percent of sites per patients showing attachment gain beyond the threshold were much greater in non-smokers (13.9%) compared to 9.0% in smokers (P0.01). Mean probing reduction was 50% greater among non-smokers (0.6 mm) when compared to smokers (0.4 mm), which was also statistically significant (P0.05). A positive and significant correlation was established between the percentage of sites with AL gain and sites with ACH gain (Rho =0.40; P=0.0001). It is suggested that monitoring sites for AL and ACH gain expressed as changes beyond a selective threshold is an important outcome variable in treatment studies.

Change in clinical attachment level (CAL) and radiographic change in crestal bone height are often used to assess periodontal breakdown and disease progression. These two variables are also used to monitor the effect of treatment. The purpose of the present longitudinal study was to evaluate the correlation between changes in CAL and alveolar bone loss. Following initial screening, 79 subjects with established periodontitis were monitored quarterly for 1 yr, using a pressure-sensitive automated probe. CAL and relative attachment level (RAL) were recorded at 6 sites for each tooth. Radiographs were obtained at baseline and 1 yr. Crestal bone changes were determined using an image enhancement technique. Mean change in attachment level was 0.16 mm. Similarly, mean proximal bone loss measured radiographically was 0.16 mm. In 6.9% of all the sites, and 13.7% of all pooled interproximal sites, AL loss was in excess of the threshold defined as 2 s.d. of repeated measurements (mean 1.54 mm). Similar percentages of sites (12.9%) had radiographic evidence of proximal bone loss exceeding the threshold (0.55-1.08 mm). A site-based analysis of active sites revealed an overall poor correlation between the 2 variables (kappa value = 0.03) which was the result of a very poor sensitivity (0.16) despite a relatively good specificity (0.81). A patient-based comparison of clinical and radiographical changes revealed an overall kappa value of 0.08, with sensitivity and specificity of 0.51 and 0.56, respectively. However, baseline CAL and crestal bone height showed good correlation (r = 0.73; p = 0.0001). It is suggested that changes in CAL and radiographic bone level progress somewhat independently. Over a short-term period of time they might not follow the same course; however, in the long term, these differences seem to level off. For longitudinal monitoring of disease progression and response to therapy both methods may be needed; while for cross-sectional evaluation and long-term prospective studies, either variable may be used alone.

Periodontal disease is a common infection-induced inflammatory disease among individuals suffering from diabetes mellitus. The purpose of this study was to assess the effects of treatment of periodontal disease on the level of metabolic control of diabetes. A total of 113 Native Americans (81 females and 32 males) suffering from periodontal disease and non-insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups. Periodontal treatment included ultrasonic scaling and curettage combined with one of the following antimicrobial regimens: 1) topical water and systemic doxycycline, 100 mg for 2 weeks; 2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; 3) topical povidone-iodine and systemic doxycycline, 100 mg for 2 weeks; 4) topical 0.12% CHX and placebo; and 5) topical water and placebo (control group). Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbA1c). After treatment all study groups showed clinical and microbial improvement. The doxycycline-treated groups showed the greatest reduction in probing depth and subgingival Porphyromonas gingivalis compared to the control group. In addition, all 3 groups receiving systemic doxycycline showed, at 3 months, significant reductions (P < or = 0.04) in mean HbA1c reaching nearly 10% from the pretreatment value. Effective treatment of periodontal infection and reduction of periodontal inflammation is associated with a reduction in level of glycated hemoglobin. Control of periodontal infections should thus be an important part of the overall management of diabetes mellitus patients.

This study determined the relative contribution to probing measurement reliability of several factors, compared with that of random error. Probing measurements were performed by examiners properly trained and calibrated. A total of 5771 pairs of replicate pocket depth (PD) and relative attachment level (RAL) measurements were performed with the Florida Probe. A total of 1488 replicate clinical attachment level (CAL) measurements were performed with the North Carolina 15 mm probe. In addition, longitudinal replicate measurements of RAL were performed at 0 and 12 months on 816 sites in 11 patients utilizing the Florida Probe 20 mm disk probe. Measurement reliability with the Florida Probe resulted in mean intraexaminer variances of 0.21 and 0.33, for PD and RAL, respectively (s.e.m. 0.46 mm for PD and 0.57 mm for RAL). Measurement reliability with the conventional probe resulted in mean intra-examiner variances of 0.19 for PD and 0.32 for CAL (s.e.m. 0.44 mm and 0.56 mm). Pocket depth contributed to = 5% of the variability of the intra-examiner variance with both probes with other contributing factors being the individual patient, tooth and site location. Mean intra-examiner reproducibility for duplicate RAL measurement performed at 0 and 12 months was 0.24 and 0.19, respectively (s.e.m. 0.49 mm and 0.43 mm). In conclusion, a mean intra-examiner variance of < or = 0.24 can be achieved for replicate measurements with both electronic and conventional probes for moderate and severe periodontitis patients. Individual examiner, individual patient and site location contribute up to 10% to the overall variance. Hence, the pattern of variability for intra-examiner variance of probing measurements performed with either electronic or conventional probes by trained and calibrated examiners is mostly random error.

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.

Cigarette smoking and tobacco use have been the subjects of numerous studies for many years. Smoking has also been associated with periodontal disease. However, no relationship between a reliable biochemical marker and increased severity of the periodontal condition has yet been described. It was thus the aim of this study to apply the measurement of cotinine, the major metabolite of nicotine, as a quantitative method to assess levels of smoking, and to correlate serum levels of cotinine with severity of periodontal disease. The degree of association between smoking and periodontal attachment loss was investigated in a study including 79 patients 25 to 64 years old suffering from periodontitis. Patients were examined and the following parameters recorded: Gingival Assessment (GA), Probing Pocket Depth (PPD), Clinical Attachment Level (CAL), and Bone Crest Height (BCH). In addition, self-reported histories of tobacco use as well as blood samples for quantitative analysis of serum levels of cotinine were taken. The serum samples were analyzed for cotinine content by means of a competitive-inhibition ELISA technique. The differences in mean cotinine levels were statistically significant (p = 0.0001) between smokers and non-smokers, showing no overlap between the groups. Severity of periodontal attachment loss was positively correlated with serum levels of cotinine for both measures of periodontal disease (CAL p = 0.005; BCH p = 0.008). Results from the present study indicate that serum cotinine levels used as a biochemical marker of smoking status are correlated with severity of periodontal attachment loss.

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)

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.

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 prevalence of dental caries and gingivitis was assessed in schoolchildren of the Tlalpan region in Mexico City. A total of 700 children (age range: 11–17 yr) of both sexes were examined. The sample population included children attending the Middle-School System, where two shifts are run (A.M. and P.M.). Decayed, missing and filled surfaces (DMFS), and Gingival Index (GI) were recorded for all existing teeth. Analysis of the data showed that mean DMFS scores increased with chronological age in both genders, were higher in the P.M. session, and more elevated in females. Similarly the mean GI scores also increased with age, and were higher in the P.M. session. In contrast to the DMFS scores, males presented higher GI scores than females at all age intervals. The results of our study indicated a distinctively high prevalence of caries and gingivitis in Mexican schoolchildren.

The objective of this study was to investigate the association between the antimicrobial and clinical efficacy of minocycline hydrochloride microspheres when used adjunctively with scaling and root planing.127 subjects with moderate-to-advanced chronic periodontitis were randomly assigned to receive either minocycline microspheres plus scaling and root planing (n = 62) or scaling and root planing alone (n = 65). Deoxyribose nucleic acid analysis and clinical data were obtained at baseline and 30 days after treatment. End points included changes in the mean sum of red complex bacteria, pocket depth, number of deep pockets, bleeding on probing, and clinical attachment level from baseline to day 30. Regression analysis determined the association between microbiological and clinical efficacy.Minocycline microspheres plus scaling and root planing reduced pocket depth, the number of deep pockets and bleeding on probing, and increased clinical attachment level significantly more than scaling and root planing alone (p0.05). Comparing minocycline microspheres plus scaling and root planing with scaling and root planing alone, the number needed to treat for a 2 mm pocket depth reduction difference was 6.5. Pocket depth reduction correlated significantly with a decrease in the numbers and proportions of red complex bacteria. Minocycline microspheres significantly improved all clinical parameters compared to scaling and root planing alone.The addition of minocycline microspheres to scaling and root planing led to a greater reduction in the proportions and numbers of red complex bacteria. The reduction in pocket depth was significantly correlated with the reduction of the proportions and numbers of red complex bacteria. Additionally, there were statistically greater improvements in all clinical parameters examined.

A method is presented for histological examination of undecalcified ground sections of tooth roots affected with periodontal disease. The roots were placed in Karnovsky's fixative overnight, postfixed in 2% buffered osmic acid, and dehydrated in an ascending series of ethanol. The specimens were then infiltrated with propylene-oxide and Epon-Araldite resin, embedded in Epon-Araldite, and sections were prepared using a cutting and grinding system. The resulting ground sections were 8-12 microns thick. The sections were allowed to air dry at room temperature. When thoroughly dried, a coverglass was applied using resinous mounting medium DPX. The specimens were examined by phase-contrast microscopy. The method is useful for simultaneous examination of mineralized dental tissue and bacterial morphotypes covering the root surface of teeth involved with periodontal disease.

Background- In the Periodontitis and Vascular Events (PAVE) pilot study periodontal therapy was provided as an intervention in a secondary cardiac event prevention model through five coordinated cardiac-dental centers. Methods- Subjects were randomized to either community care or protocol provided scaling and root planing to evaluate effects on periodontal status and systemic levels of high-sensitivity Creactive protein (hs-CRP). Results- After 6 months there was a significant reduction in mean probing depth and extent of 4- or 5-mm pockets. However there were no significant differences in attachment levels bleeding upon probing or extent of subgingival calculus comparing subjects assigned to protocol therapy (n = 151) to those assigned to community care (n = 152). Using intent-to-treat analyses there was no significant effect on serum hs-CRP levels at 6 months. However 48% of the subjects randomized to community care received preventive or periodontal treatments. Secondary analyses demonstrated that consideration of any preventive or periodontal care (i.e. any treatment) compared to no treatment showed a significant reduction in the percentage of people with elevated hs-CRP (values >3 mg/l)at 6 months. However obesity nullified the periodontal treatment effects on hs-CRP reduction. The adjusted odds ratio for hs-CRP levels >3 mg/l at 6 months for any treatment versus no treatment among non-obese individuals was 0.26 (95%confidence interval: 0.09 to 0.72) adjusting for smoking marital status and gender. Conclusion- This pilot study demonstrated the critical role of considering obesity as well as rigorous preventive and periodontal care in trials designed to reduce cardiovascular risk. Originally published Journal of Periodontology Vol. 80 No. 2 Feb 2009

The effect of age on the humoral response to Porphyromonas gingivalis was assessed in groups of adults (25 to 54 years and 55 to 74 years) with periodontal disease and compared with that in age-matched healthy controls. To determine whether there was an antibody response against P. gingivalis, we measured serum antibodies against whole cells of P. gingivalis 381, A7A1-28, and W50. In addition, antibody levels against purified P. gingivalis outer membrane proteins (i.e., the 43-kDa fimbrial protein and a 75-kDa protein) were also evaluated. Elderly subjects showed the same response to P. gingivalis as younger subjects. Immunoglobulin G (IgG) antibodies to both purified proteins were also elevated in both diseased groups as compared with the normal groups. Total serum IgG, IgA, and IgM levels were also determined by an enzyme-linked immunosorbent assay for all four groups. Total serum IgG levels were elevated in older adults with periodontitis and total IgA levels were elevated in both groups of older adults compared with the younger groups of similar disease status. Total serum IgM levels were comparable for the four groups. Antinuclear antibody titers were assessed in the two groups of older adults and were also found to be higher for the group with periodontitis. These studies show that older adults as well as younger adults have markedly elevated specific antibodies of the IgG and IgA classes to antigens of P. gingivalis, a putative pathogen in both groups. Furthermore, older adults with periodontitis have significantly elevated levels of total serum IgG which may possibly be related to higher levels of autoantibodies.

g b t o t p c o m m p A M S P D C n response to the calls for action that dental caries is the most prevalent infectious disease in our nation’s children, the American Academy of Pediatrics (AAP) in artnership with the Federal Maternal and Child Health ureau (MCHB), with the endorsement of the American ental Association, the American Academy of Pediatric entistry, and supporting organizations such as Bright Fuures, and other children’s health organizations have impleented the AAP Oral Health Initiative. The purpose of this rogram is to engage the pediatric community in addressing he need to increase oral health services to children and reduce ral health disparities. This program promotes improvement n children’s oral health by offering child health care profesionals the tools and support they need to provide communiy-based collaborative care. The AAP policy statement recmmends that pediatricians perform the Oral Health Risk ssessment and Establishment of the Dental Home by the ge of 12 months. Along with these initiatives, advocacy ampaigns supporting oral health in pediatric primary care ave been implemented, resulting in increased awareness of he importance of oral health and, more importantly, that the edical community can play a significant role in reducing oral ealth disparities. This paradigm change in the relationship etween medicine and dentistry, although still in its infancy, as swung the pendulum toward pediatricians working much ore closely with dental professionals. However, a limitation n this partnership has been that children’s oral health has een regarded by the medical profession mostly as a tooth ecay problem. Accordingly much of the participation of peditricians in screening of oral disease has been limited to early ental caries and preventive measures have been largely limited o the fluoride varnish program. Much work remains to be done f we are to engage the medical community in oral health romotion and prevention of dental diseases in children.

Population-based clinical and laboratory studies have reported findings providing support for a possible relationship between periodontal disease and cardiovascular disease. The Periodontitis and Vascular Events (PAVE) pilot study was conducted to investigate the feasibility of a randomized secondary prevention trial to test whether treatment of periodontal disease reduces the risk for cardiovascular disease.Five clinical centers recruited participants who had documented coronary heart disease and met study criteria for periodontal disease. Eligible participants were randomized to receive periodontal therapy provided by the study or community dental care. Follow-up telephone calls and clinic visits were planned to alternate at 3-month intervals after randomization, with all participants followed until at least the 6-month clinic visit. Participants were followed for adverse events and periodontal and cardiovascular outcomes.A total of 303 participants were randomized. Recruitment that involved active participation of a cardiologist with responsibility for the patients worked best among the strategies used. Of those who had not withdrawn, 93% completed the 6-month contact. During follow-up, 11% of the 152 subjects in the community dental care group reported receiving periodontal therapy outside of the study.If appropriate recruitment strategies are used, this pilot study demonstrated that it is feasible to conduct a secondary prevention trial of periodontal therapy in patients who have had coronary heart disease. If a community dental care group is used, sample size estimation needs to take into account that a non-trivial proportion of participants in this group may receive periodontal therapy outside of the study.

During the last 15 years, a substantial number of population-based, clinical, laboratory, and animal studies have been published that reported findings on the relationship between periodontal disease and cardiovascular disease. The Periodontitis and Vascular Events (PAVE) pilot study was conducted to investigate the feasibility of a randomized secondary prevention trial to test whether treatment of periodontal disease reduces the risk for cardiovascular disease. This article describes the occurrence of adverse events during the pilot study.The PAVE pilot study was a multicenter, randomized trial comparing periodontal therapy to community dental care. Baseline and follow-up clinic visits included a periodontal examination; blood, subgingival plaque, and crevicular fluid specimen collection; and medical and dental histories. Telephone follow-up contacts were scheduled to occur 3 months after randomization and every 6 months thereafter to assess adverse events or endpoints.Cardiovascular adverse events occurred with similar frequency (23 versus 24 [P = 0.85] in the community control and the treatment groups, respectively). There were 15 serious adverse events (SAEs) with a non-significantly higher percentage occurring in the community care group (6.6% versus 3.3%; P = 0.19). A time-to-event analysis of patterns of SAEs indicated that subjects in the periodontal therapy group tended to be less likely to experience an SAE over the entire 25 months of the study.For those individuals who remained in the study, it appears that provision of periodontal scaling and root planing treatment to individuals with heart disease resulted in a similar pattern of adverse events as seen in the community care group, which also received some treatment.

Background: Public health and other population-based studies often depend on participants' self-reported disease status to assess prevalence, incidence, and disease trends. We sought to assess the feasibility of self-reported periodontal disease measures using dental history questions combined with demographic and medical history to predict periodontal disease. Methods: We evaluated results from two separate population-based studies carried out at the University at Buffalo, Buffalo, New York, i.e., the “Periodontal Infection and Risk for Myocardial Infarction Study,” a study of 1,578 adults assessing the association between periodontal disease and myocardial infarction and the “Periodontal Disease Research Center” (the Erie County Study), an epidemiologic risk assessment study of 1,438 adults. In each study, an extensive list of oral health questions was asked, and a comprehensive medical history, blood analysis using chemistry and hematology tests, and demographic data were collected. Results: Using a predefined measure of severity of periodontal disease, we compared patients with severe disease to all others (i.e., those with moderate and no or mild disease). We examined areas under the curve (AUC) of the receiver operating curve to determine the best models, adding one, two, or three dental variables in all possible combinations. The AUC maximized at 0.76, and the combined sensitivity and specificity maximized at 142 and were comparable in both studies. Conclusions: Self-reported measures of periodontal disease are moderately predictive of clinical attachment loss. The demographic variables of age, race, smoking, gender, and diabetes mellitus accounted for much of the predictive power for self-reported periodontal disease; however, increases in sensitivity and specificity in the C statistics occurred when questions, including “Gum surgery in the past?,” “Sore gums in the past?,” “Scaling in the past?,” “Bleeding gums now?,” “Periodontal surgery in the past 2 years?,” and “Chewing satisfaction?,” were added to the model.

Background: The role of periodontal disease as a predictor of incident tooth loss in postmenopausal women has not been determined. The aim of this cohort study was to determine the extent of the association between baseline periodontal status and incident tooth loss in a population of postmenopausal women. Methods: The study population included 106 dentate white postmenopausal women who participated in a cross-sectional study between 1989 and 1991 who were willing and eligible to have a repeat examination after 10 to 13 years. At baseline, full-mouth assessment of periodontal status was performed clinically and radiographically. Assessment of tooth loss during follow-up was assessed clinically by a periodontist. Odds ratio (OR) and its 95% confidence interval (CI) for each periodontal variable was obtained from separate multiple logistic regression analyses adjusting for the effect of age, household income, smoking, hormone therapy, snack consumption, and number of decayed teeth. Results: Sixty-one (57.5%) subjects lost at least one tooth during follow-up. Mean tooth loss per person was 1.81 ± 2.77. After adjusting for confounders, each millimeter of alveolar bone loss at baseline increased the risk of tooth loss 3-fold (OR = 3.26; 95% CI: 1.60 to 6.64). The risk of tooth loss also increased 2.5 times for each millimeter of clinical attachment loss (OR = 2.50; 95% CI: 1.24 to 5.07). Probing depth (OR = 2.53; 95% CI: 0.98 to 6.53), gingival bleeding (OR = 1.99; 95% CI: 0.21 to 18.94), calculus (OR = 2.05; 95% CI: 0.91 to 4.61), and plaque (OR = 0.70; 95% CI: 0.13 to 3.34) were not significantly associated with incident tooth loss. Conclusion: Periodontal disease, especially measured by alveolar bone loss, is a strong and independent predictor for incident tooth loss in postmenopausal women. J Periodontol 2005;76:1123-1128.

Obesity is an important risk factor for diabetes, cardiovascular disease, and periodontal disease. Adipocytes appear to secrete proinflammatory cytokines which may be the molecules linking the pathogenesis of these diseases. We evaluated the relationship between obesity, periodontal disease, and diabetes mellitus insulin resistance as well as the plasma levels of tumor necrosis factor alpha (TNFalpha) and its soluble receptors (sTNFalpha) to assess the relationship of inflammation to obesity, diabetes, and periodontal infections.The relationship between periodontal disease, obesity, and insulin resistance was examined in the Third National Health and Nutrition Examination Survey (NHANES III). In a population of 12,367 non-diabetic subjects, the variable body mass index (BMI) was used as an assessment of obesity and periodontal disease was assessed by mean clinical attachment loss. The plasma levels of TNFalpha and sTNFalpha were assessed in subsets of 1,221 adults from Erie County, New York, who represented the highest and lowest quartile of BMI. These subjects had extensive periodontal and medical evaluations.In the NHANES III portion of the study, BMI was positively related to severity of periodontal attachment loss (P0.001). Weighted multiple logistic regressions showed that this relationship is likely mediated by insulin resistance, since overweight individuals (with BMIor=27 kg/m2) with high levels of insulin resistance (IR) exhibited an odds ratio of 1.48 (95% confidence interval 1.13 - 1.93) for severe periodontal disease as compared to overweight subjects with low IR. In the Erie County adult population, the highest levels of TNFalpha and sTNFalpha receptors were found in those individuals in the highest quartile of BMI. A positive correlation of TNFalpha levels with periodontal disease was found only in those in the lowest quartile of BMI.Obesity is a significant predictor of periodontal disease and insulin resistance appears to mediate this relationship. Furthermore, obesity is associated with high plasma levels of TNFalpha and its soluble receptors, which in turn may lead to a hyperinflammatory state increasing the risk for periodontal disease and also accounting in part for insulin resistance. Further studies of the molecular basis of insulin resistance and its relationship to diabetes, periodontal disease, and obesity are necessary to fully test the hypothesis that adipocyte production of proinflammatory cytokines is a pathogenic factor linking obesity to diabetes and periodontal infections.

Infections have been suggested in the etiology of oral cancer. This study was carried out to evaluate the effect of periodontal disease on oral soft tissue lesions.A total of 13,798 subjects aged 20 years and older with at least six natural teeth and who participated in the Third National Health and Nutrition Examination Survey (NHANES III) constituted the study population. Severity of periodontal disease was represented by clinical attachment loss (CAL) and was dichotomized asor =1.5 mm versus1.5 mm according to its distributions in the NHANES III population. Three separate dependent variables were employed: 1) tumor (non-specific); 2) precancerous lesions; and 3) any oral soft tissue lesion. The independent effect of CAL on those three dependent variables was assessed by weighted multiple logistic regression analyses adjusting for the effects of number of filled teeth, number of decayed teeth, presence of prosthesis, age, gender, race/ethnicity, education, tobacco, alcohol, occupational hazard, and interaction term "tobacco*occupational hazard." Odds ratios (OR) and their 95% confidence intervals (CI) were calculated.CAL was not related to the presence of any soft tissue lesion (OR = 1.09, 95% CI: 0.91 to 1.31), but was specifically related to the presence of tumor (OR = 4.57, 95% CI: 2.25 to 9.30) and precancerous lesions (OR = 1.55, 95% CI: 1.06 to 2.27).This study suggests associations between periodontal disease and the risk for precancerous lesions and tumors generating a hypothesis about a possible relationship between periodontal disease and oral neoplasms. Prospective or well-designed case-control studies with histologically confirmed incident oral cancer cases are necessary to confirm this relationship.

Evidence supporting an association between osteoporosis and loss of alveolar crestal bone is limited. This study investigated that association in a large cohort of postmenopausal women.A cohort of 1,341 postmenopausal women aged 53 to 85 were assessed for alveolar crestal height (ACH) and bone density. ACH was determined from oral radiographs with subjects dichotomized by disease severity. Bone density was assessed by dual energy x-ray absorptiometry, with severity determined by worst T score measured (normal-1.00; low -1.00 to -2.00; moderate -2.01 to -2.49; osteoporotic-2.5).Compared to subjects in the normal T-score group, the odds of worse ACH increased by 39%, 59%, and 230% for those in the low, moderate, and osteoporotic groups, respectively. Adjustment for weight, education, hormone use, calcium or vitamin D supplementation, and smoking did not appreciably change the findings. Further adjustment for age attenuated the association, with osteoporotic subjects having a 1.9-fold increase of being in the worst ACH group (95% confidence interval [CI] 1.19 to 3.05). After age stratification, in women younger than 70 there was a significant trend by decreasing T-score category (P0.02). Osteoporotic subjects had worse ACH (odds ratio [OR] = 1.95; 95% CI 1.20 to 3.17). In women aged 70 and older, worse ACH was 2.5- to 4.6-fold increased for decreasing T-score category. After adjustment, the OR (95% CI) for the low, moderate, and osteoporotic groups were 2.66 (1.12 to 6.29), 2.31 (0.89 to 6.01), and 3.57 (1.42 to 8.97), respectively (P trend = 0.026).This study found a strong and consistent association between T score and ACH in postmenopausal women. Increasing age is an important modifier of that association.

Objective: This study was carried out to evaluate the effect of alcohol consumption on the severity of periodontal disease. Material and Methods: This cross-sectional study employed 13,198 subjects of the Third National Health and Nutrition Examination Survey (NHANES III) aged 20 and older who have at least six natural teeth. Alcohol intake was represented both as a continuous variable and dichotomized using 5, 10, 15, and 20 drinks/week as cut-points. Periodontal disease was represented by clinical attachment loss (CAL) and was assessed both as a continuous variable and dichotomized as

Functional polymorphisms of immunoglobulin G (IgG) Fc receptors IIIa and IIIb (FcgammaRIIIa and FcgammaRIIIb) have been shown as risk factors for periodontitis. The aim of this study is to examine whether FcgammaRIIa polymorphism is associated with a disease risk as well.Baseline periodontal and general health examinations were carried out on 1,221 Caucasian adults. From these, 422 subjects with moderate to severe, or little or no periodontal disease were assigned to two groups according to their mean clinical attachment loss (CAL). Subjects with mean CALor = 2.94 mm were diagnosed with chronic periodontitis (n = 213, 62 never-smokers and 151 smokers). Subjects with mean CALor = 1.77 mm were considered as having little or no periodontal disease and designated as controls (n = 209, 125 never-smokers and 84 smokers). The FcgammaRIIa genotype for three bi-allelic polymorphisms (FcgammaRIIa-R/ R131, R/H131, and H/H131) was determined by means of allele-specific polymerase chain reactions.The distribution of FcgammaRIIa genotype between the patient and control groups was significantly different, with enrichment of the high ligand-binding genotype FcgammaRIIa-H/H131 in the patients (patients versus controls: 36.6% versus 25.4%; P = 0.04). Multivariate logistic regression model demonstrated that subject age and gender, smoking, and the FcgammaRIIa genotype were significantly associated with severity of chronic periodontitis. For smokers, a significant over-representation of FcgammaRIIa-H/H131 in the patient group compared to the control group (patients versus controls: 35.1% versus 19.0%; P = 0.03). Additionally, smokers with FcgammaRIIa-H/H131 exhibited significantly greater mean CAL (mean +/- SE: 3.44 +/- 0.16 mm) than those with FcgammaRIIa-R/H131 (2.91 +/- 0.14 mm) and R/R131 (2.82 +/- 0.16 mm) (P = 0.04). There was no association between FcgammaRIIa genotype and the disease susceptibility or severity in subjects who had never smoked.Our results suggest that the FcgammaRIIa-H/H131 genotype may be associated with chronic periodontitis risk (and disease severity) in Caucasian smokers. Further studies with families and studies of mechanisms are necessary to help establish the extent to which this is a genetic determinant of periodontal diseases.

Probing depth (PD) is a commonly used method to determine periodontal disease severity in both treating and evaluating disease progression. Agreement among examiners collecting data in scientific investigations is necessary to establish reliable criteria for determining levels of periodontal attachment loss. The objective of our study was to evaluate inter- and intraexaminer variability of PD measurements among study examiners using a constant force periodontal probe, and to compare the variability of tooth-mean and quadrant-mean.Three examiners, who had been previously trained and calibrated, performed measurements on 20 volunteers. Intraand interexaminer variability of sites was determined by means of standard error of measurement (SE). Data analysis included determination of error for both quadrant mean and tooth mean.PD measurements for the quadrant-mean were used to calculate the intraexaminer variability, resulting in a mean (SD) value for an SE of 0.40 mm (± 0.02). Interexaminer variability for quadrant mean was 0.16 mm (± 0.02). For tooth-mean SE, the intraexaminer variability values were equal to 0.38 mm (± 0.07), and interexaminer variability equal to 0.24 mm (± 0.05).All three examiners participating in our study were able to obtain reliable measurements for PD, using the constant force electronic probe. Reproducibility did not vary appreciably when using the whole quadrant mean compared to the tooth mean. These trained examiners were able to provide reproducible measures under 0.5 mm. J Periodontol 2003;74:1736-1740.

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions.

Epidemiological studies have implicated periodontal disease (PD) as a risk factor for the development of cardiovascular disease (CVD). These studies addressed the premise that local infection may perturb the levels of systemic inflammatory mediators, thereby promoting mechanisms of atherosclerosis. Levels of inflammatory mediators in the sera of subjects with only PD, only CVD, both diseases, or neither condition were compared. Subjects were assessed for levels of C-reactive protein (CRP), serum amyloid A (SAA), ceruloplasmin, α1-acid-glycoprotein (AAG), α1-antichymotrypsin (ACT), and the soluble cellular adhesion molecules sICAM-1 and sVCAM by enzyme-linked immunoabsorbent and/or radial immunodiffusion assays. CRP levels in subjects with either condition alone were elevated twofold above subjects with neither disease, whereas a threefold increase was noted in subjects with both diseases (P= 0.0389). Statistically significant increases in SAA and ACT were noted in subjects with both conditions compared to those with one or neither condition (P= 0.0162 and 0.0408, respectively). Ceruloplasmin levels were increased in subjects with only CVD (P= 0.0001). Increases in sVCAM levels were noted in all subjects with CVD (P= 0.0054). No differences in sICAM levels were noted among subject groups. A trend toward higher levels of AAG was noted in subjects with both conditions and for ACT in subjects with only PD. Immunohistochemical examination of endarterectomy specimens of carotid arteries from subjects with atherosclerosis documented SAA and CRP deposition in association with atheromatous lesions. The data support the hypothesis that localized persistent infection may influence systemic levels of inflammatory mediators. Changes in inflammatory mediator levels potentially impact inflammation-associated atherosclerotic processes.

Alcohol consumption, like smoking, may be related to periodontal disease independently of oral hygiene status. This study assessed the relationship between alcohol consumption and severity of periodontal disease.A cross-sectional study of 1,371 subjects ages 25 to 74 in the Erie County, NY population was performed. Alcohol intake was assessed by means of previously validated self-reported questionnaires. Outcome variables were gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorganisms.Logistic regression analyses adjusting for age, gender, race, education, income, smoking, diabetes mellitus, dental plaque, and presence of any of 8 subgingival microorganisms showed that those consumingor =5 drinks/week had an odds ratio (OR) of 1.65 (95% CI: 1.22 to 2.23) of having higher gingival bleeding, and OR of 1.36 (95% CI: 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming5 drinks/week. Those consumingor =10 drinks/week had an odds ratio (OR) of 1.62 (95% CI: 1.12 to 2.33) of having higher gingival bleeding and OR of 1.44 (95% CI: 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming10 drinks/week. Alcohol consumption was not significantly related to alveolar bone loss nor to any of the subgingival microorganisms.The results suggest that alcohol consumption is associated with moderately increased severity of periodontal disease. Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease.

Dietary calcium has long been a candidate to modulate periodontal disease. Animal as well as human studies of calcium intake, bone mineral density, and tooth loss provide a rationale for hypothesizing that low dietary intake of calcium is a risk factor for periodontal disease.We evaluated the role of dietary calcium intake as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III), which is representative of the U.S. civilian non-institutionalized population. Dietary calcium intake was determined from a 24-hour dietary recall. The U.S. Department of Agriculture Nutrient Database was used as a source of nutrient composition data. Periodontal disease was measured by attachment loss. In addition, serum calcium was assessed using venous blood samples. Logistic regression analysis was used to examine the association between periodontal disease and dietary calcium intake or serum calcium levels after adjusting for covariants including age, gender, tobacco consumption, and gingival bleeding.The association of lower dietary calcium intake with periodontal disease was found for young males and females (20 to 39 years of age), and for older males (40 to 59 years of age). The relationship between low dietary calcium intake and increased levels of periodontal disease showed an estimated odds ratio (OR) of 1.84 (95% CI: 1.36 to 2.48) for young males, 1.99 (95% CI: 1.34 to 2.97) for young females, and 1.90 (95% CI: 1.41 to 2.55) for the older group of males. These odds ratios were adjusted for gingival bleeding and tobacco consumption. The dose response was also seen in females, where there was 54% greater risk of periodontal disease for the lowest level of dietary calcium intake (2 to 499 mg) and 27% greater risk in females who took moderate levels of dietary calcium (500 to 799 mg) as compared to those who took 800 mg or more dietary calcium per day. A statistically significant association between low total serum calcium and periodontal disease was found in younger females aged 20 to 39 with OR = 6.11 (95% CI: 2.36 to 15.84) but not for males or older females, after adjusting for tobacco use, gingival bleeding, and dietary calcium intake.These results suggest that low dietary intake of calcium results in more severe periodontal disease. Further studies will be needed to better define the role of calcium in periodontal disease and to determine the extent to which calcium supplementation will modulate periodontal disease and tooth loss.

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.

We evaluated the association of stress,distress, and coping behaviors with periodontal disease in 1,426 subjects, aged 25 to 74, in Erie County, NY, Demographic characteristics, medical and dental history, and tobacco and alcohol consumption, as well as clinical assessments of supragingival plaque, subgingival flora, gingival bleeding, calculus, probing depth, clinical attachment level (CAL), and radiographic alveolar bone loss (ABL) were obtained for each subject. Subjects also completed a set of 5 psychosocial instruments that measured life events, daily strains, hassles and uplifts, distress, and coping behaviors. Internal consistencies of all subscales on the instruments were high, with Cronbach's alpha ranging from 0.88 to 0.99. Logistic regression indicated that financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.70; 95% CI, 1.09-2.65; and 1.68; 95% CI, 1.20-2.37, respectively) after adjusting for age, gender, and smoking. When those with financial strain were stratified with respect to coping behaviors, it was found that those who exhibited high emotion-focused coping (inadequate coping) had and even higher risk of having more severe attachment loss (OR 2.24; 95% CI, 1.15-4.38) and alveolar bone loss (OR 1.91; 95% CI, 1.15-3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. After further adjusting for number of visits to the dentist, those with financial strain who were high emotion-focused copers still had higher levels of periodontal disease based on CAL (OR 2.12; 95% CI, 1.07-4.18). In contrast, subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain. Salivary cortisol levels were higher in a test group exhibiting severe periodontitis, a high level of financial strain, and high emotion-focused coping, as compared to a control group consisting of those with little or no periodontal disease, low financial strain, and low levels of emotion-focused coping (11.04 +/-4.4 vs/ 8.6 +/- 4.1 nmol/L salivary cortisol, respectively). These findings suggest that psychosocial measures of stress associated with financial strain are significant risk indicators for periodontal disease in adults. Further prospective studies are needed to help establish the time course of stress, distress, and inadequate coping on the onset and progression of periodontal disease, as well as to evaluate the mechanisms by which stress exerts its effects on periodontal infections.

Severe periodontal disease often coexists with severe diabetes mellitus. Diabetes is a risk factor for severe periodontal disease. A model is presented whereby severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. We propose that an infection-mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from lipopolysaccharide (LPS) and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response operative in diabetes mellitus. In this model, the combination of these 2 pathways, infection and AGE-mediated cytokine upregulation, helps explain the increase in tissue destruction seen in diabetic periodontitis, and how periodontal infection may complicate the severity of diabetes and the degree of metabolic control, resulting in a 2-way relationship between diabetes mellitus and periodontal disease/infection. This proposed dual pathway of tissue destruction suggests that control of chronic periodontal infection is essential for achieving long-term control of diabetes mellitus. Evidence is presented to support the hypothesis that elimination of periodontal infection by using systemic antibiotics improves metabolic control of diabetes, defined by reduction in glycated hemoglobin or reduction in insulin requirements.

This study assesses the reliability of a self-reported health questionnaire completed by 413 subjects aged 25-74 yr in the Erie County Periodontal Disease (ECPD) Study. Specific questions on general and oral health conditions were completed by each subject during a first visit and at a follow-up examination 2 yr later, and the two compared. Results showed that the overall measure of agreement between the two visits is substantial (average kappa, kappa = 0.80). Variation by gender and age were minimal. Questions regarding allergy to medications, oral treatment, reason for tooth extraction, health symptoms and history of systemic diseases exhibited high levels of agreement (kappa ranged from 0.71-0.90). Information on vitamin and mineral intake yielded kappa = 0.63. Oral conditions scored the lowest but were still acceptable (kappa = 0.57). These findings indicate that there were no significant discrepancies in self-reported responses to the health questionnaire used in the ECPD Study. Although the information provided by the subject may not be as accurate as compared to laboratory testing, it is nevertheless a reliable source of information which can be utilized cost-effectively in research studies.

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.

Osteoporosis and periodontitis are diseases which affect a large number of women and men, with incidence increasing with advancing age. Osteopenia is a reduction in bone mass due to an imbalance between bone resorption and formation, favoring resorption, resulting in demineralization and leading to osteoporosis. Osteoporosis is a disease characterized by low bone mass and fragility and a consequent increase in fracture risk. Periodontitis is characterized by inflammation of the supporting tissues of the teeth, resulting in resorption of the alveolar bone as well as loss of the soft tissue attachment to the tooth and is a major cause of tooth loss and edentulousness in adults. The relationship of osteopenia to oral bone loss and periodontal disease has been addressed in a limited number of studies. A review of current knowledge regarding this relationship is presented. Interpretation of the literature is complicated by the variety of methods used to assess osteopenia, oral bone mass, and periodontitis, as well as varying definitions of outcomes of interest. Results of a previously unpublished study are presented which suggest that severity of osteopenia is related to loss of alveolar crestal height and tooth loss in post-menopausal women. The literature on the relationship among these disorders is limited and points to the need for additional studies which thoroughly evaluate the influence of potential confounding factors to further define the relationship between low bone mineral density and periodontal disease in larger populations. Clearer understanding of this relationship may aid health care providers in their efforts to detect and prevent osteoporosis and periodontal disease. Increased dialogue among medical and dental professionals will be increasingly important in achieving and maintaining patients' optimal health. J Periodontol 1996;67:1076-1084.

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.