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Porphyromonas gingivalis has been strongly implicated in the pathogenesis of human periodontitis. Fimbriae mediate adherence and colonization of the oral cavity by this organism and may, therefore, have potential for use as antigen in an anti-P. gingivalis vaccine. The purpose of our study was to determine whether P. gingivalis fimbriae have opsonic target sites and whether they are accessible on the cell surfaces and cross-reactive among P. gingivalis fimbrial types and serotypes. Rabbits were immunized with a vaccine. The antiserum reacted with a 43-kDa fimbrillin monomer and a 43-kDa component in whole-cell sonicates of P. gingivalis 33277, but it showed only very weak reactivity in the 43-kDa region of Western blots of a whole-cell sonicate of strain DPG3, a mutant that does not express functional fimbriae. The antibody enhanced chemiluminescence approximately six-fold relative to preimmune serum values and significantly enhanced phagocytosis and killing of P. gingivalis 33277 by human polymorphonuclear leukocytes. Peak opsonic activity was observed at week 6 followed by a plateau that remained until week 16. The fimbria-deficient mutant DPG3 did not bind antifimbrial antibody and was not opsonized, whereas strain 381, the parent of the mutant, was opsonized. The specific antibody bound to and opsonized P. gingivalis strains 33277 and 381 (fimbria type I) but not W50, A7A-1-28, 9-14K-1 or FAY-19M-1 (fimbrial types II-V). Specific antibody bound to strain 2561 (fimbrial type I) but, as assessed by chemiluminescence, did not opsonize it. While fimbriae have opsonic target sites that are accessible on P. gingivalis cell surfaces, the relevant opsonic target sites do not appear to be shared across serotypes or fimbrial types. Thus, a vaccine containing, as antigen, fimbrial protein from a single P. gingivalis strain would likely be ineffective against infections by P. gingivalis strains expressing other fimbrial types.

Recent evidence has established an association between chronic periodontitis and cardiovascular disease. Periodontitis is a chronic inflammatory disease caused by a small group of gram-negative bacteria, of which Porphyromonas gingivalis is considered an important causative agent. It has been proposed that dental plaque bacteria and their products can disseminate into the bloodstream from the site of infection and promote thromboembolic events associated with atherosclerosis and myocardial infarction. In this regard, Streptococcus sanguis and P. gingivalis have been shown to induce platelet aggregation in vitro. Here we report that P. gingivalis was able to induce platelet aggregation, and that oral strains of Actinobaillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Prevotella intermedia and Trepenoma denticola failed to aggregate platelets when tested for platelet aggregation activity under similar conditions. Additionally, we show that vesicles (outer membrane evaginations that are shed into the environment by the bacteria) of P. gingivalis are potent inducers of mouse platelet aggregation in vitro. In summary, our data show that i) initial adherence of the bacterium to platelet may be facilitated by P. gingivalis fimbriae and ii) P. gingivalis vesicles possess platelet aggregation-inducing activity.

Guided bone regeneration (GBR) is a viable treatment for osseous defects surrounding dental implants. Controversy exists regarding the choice of barrier membrane used and the method of membrane fixation to achieve GBR.This study compared the efficacy of a porcine-derived bioabsorbable collagen membrane and an expanded polytetrafluoroethylene (ePTFE) membrane (non-resorbable) for GBR using a bovine bone xenograft/autograft bone composite in defects surrounding dental implants. The study also examined the effect of primary barrier fixation on GBR. Defect size was recorded at Stage 1 and 2 surgeries (performed 6 months apart). Forty-eight subjects (41% males, 59% females) requiring GBR were treated with either collagen (23) or ePTFE (25) barriers, respectively. Implants were titanium self-tapping screw-type. In 34 GBR sites, barrier fixation was achieved with polylactic acid resorbable pins. The remaining barriers were secured with the implant cover screw and/or embedded beneath the flaps.At 6 months, a decrease in defect width (collagen barrier 1.95 +/- 0.60 mm, ePTFE barrier 2.65 +/- 0.56 mm), length (collagen barrier 2.65 +/- 0.61 mm, ePTFE barrier 2.26 +/- 0.66 mm), and circumference (degrees) (collagen barrier 57.7 +/- 18.7, ePTFE barrier 80.2 +/- 19.9) was observed for both membranes. A significant number (chi2, P = 0.041) of postoperative complications occurred when barrier fixation was lacking at initial surgery. Furthermore, a significant difference (P0.05) in the success of GBR with respect to defect size was observed when barrier fixation was taken into account.In conclusion, both collagen and ePTFE barriers proved suitable for achieving GBR of osseous defects surrounding dental implants. The results of this study stress the importance of barrier fixation at the time of initial surgery.

Ultrasonic and sonic scalers appear to attain similar results as hand instruments for removing plaque, calculus, and endotoxin. Ultrasonic scalers used at medium power seem to produce less root surface damage than hand or sonic scalers. Due to instrument width, furcations may be more accessible using ultrasonic or sonic scalers than manual scalers. It is not clear whether root surface roughness is more or less pronounced following power-driven scalers or manual scalers. It is also unclear if root surface roughness affects long-term wound healing. Periodontal scaling and root planing includes thorough calculus removal, but complete cementum removal should not be a goal of periodontal therapy. Studies have established that endotoxin is weakly adsorbed to the root surface, and can be easily removed with light, overlapping strokes with an ultrasonic scaler. A significant disadvantage of power-driven scalers is the production of contaminated aerosols. Because ultrasonics and sonics produce aerosols, additional care is required to achieve and maintain good infection control when incorporating these instrumentation techniques into dental practice. Preliminary evidence suggests that the addition of certain antimicrobials to the lavage during ultrasonic instrumentation may be of minimal clinical benefit. However, more randomized controlled clinical trials need to be conducted over longer periods of time to better understand the long-term benefits of ultrasonic and sonic debridement.

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

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.

Porphyromonas gingivalis, a gram-negative oral anaerobic bacterium, has been implicated in the onset and development of periodontitis. The P. gingivalis fimbriae which mediate bacterial adherence to host oral sites and induce host inflammatory responses have been suggested as a potential antigen candidate. for vaccine development. This study was undertaken to generate Streptococcus gordonii vectors expressing the major subunit protein (FimA) of P. gingivalis fimbriae for testing as a potential live vaccine against periodontitis. We report here the expression of the C-terminal saliva-binding epitopes of P. gingivalis FimA on the surface of S. gordonii and demonstrate that domains containing free cysteine residues are poorly expressed on the surface of S. gordonii.

Bacteroides forsythus is a recently recognized human periodontopathogen associated with advanced, as well as recurrent, periodontitis. However, very little is known about the mechanism of pathogenesis of this organism. The present study was undertaken to identify the surface molecules of this bacterium that may play roles in its adherence to oral tissues or triggering of a host immune response(s). The gene ( bspA ) encoding a cell surface-associated protein of B. forsythus with an apparent molecular mass of 98 kDa was isolated by immunoscreening of a B. forsythus gene library constructed in a lambda ZAP II vector. The encoded 98-kDa protein (BspA) contains 14 complete repeats of 23 amino acid residues that show partial homology to leucine-rich repeat motifs. A recombinant protein containing the repeat region was expressed in Escherichia coli , purified, and utilized for antibody production, as well as in vitro binding studies. The purified recombinant protein bound strongly to fibronectin and fibrinogen in a dose-dependent manner and further inhibited the binding of B. forsythus cells to these extracellular matrix (ECM) components. In addition, adult patients with B. forsythus -associated periodontitis expressed specific antibodies against the BspA protein. We report here the cloning and expression of an immunogenic cell surface-associated protein (BspA) of B. forsythus and speculate that it mediates the binding of bacteria to ECM components and clotting factors (fibronectin and fibrinogen, respectively), which may be important in the colonization of the oral cavity by this bacterium and is also a target for the host immune response.

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.

This study tested the hypothesis that persons with non-insulin dependent diabetes mellitus (NIDDM) have greater risk of more severe alveolar bone loss progression over a 2-year period than those without NIDDM. Data from the longitudinal study of the oral health of residents of the Gila River Indian Community were analyzed for 362 subjects, aged 15 to 57, 338 of whom had less than 25% radiographic bone loss at baseline, and who did not develop NIDDM nor lose any teeth during the 2-year study period. The other 24 subjects had NIDDM at baseline, but met the other selection criteria. Bone scores (scale 0-4) from panoramic radiographs corresponded to bone loss of 0%, 1%-24%, 25%-49%, 50%-74%, or 75% and greater. Change in bone score category was computed as the change in worst bone score (WBS) reading after 2 years. Age, calculus, NIDDM status, time to follow-up examination, and baseline WBS were explanatory variables in regression models for ordinal categorical response variables. NIDDM was positively associated with the probability of a change in bone score when the covariates were controlled. The cumulative odds ratio for NIDDM at each threshold of the ordered response was 4.23 (95% C.I. = 1.80, 9.92). In addition to being associated with the incidence of alveolar bone loss (as demonstrated in previous studies), these results suggest an NIDDM-associated increased rate of alveolar bone loss progression.

In this field trial, the authors assess the feasibility of screening for diabetes and prediabetes in dental practices and in a community health center.Dental patients 45 years and older who were not aware of their diabetic status underwent evaluation for diabetes risk with an American Diabetes Association Diabetes Risk Test and with hemoglobin (Hb) A1c measurement. Participants with an HbA1c level of 5.7 percent or greater were referred to their physicians for diagnosis.Of the 1,022 patients screened, 416 (40.7 percent) had an HbA1c blood level of 5.7 percent or greater and were referred for diagnosis. The HbA1c and the American Diabetes Association Diabetes Risk Test were correlated (P.001). Of the 416 participants who were referred, 35.1 percent received a diagnosis from their physicians within one year; 78.8 percent of these patients were seen in the community health center and 21.4 percent were seen in private dental offices. The diagnoses were diabetes (12.3 percent of patients), high risk of developing diabetes (that is, prediabetes) (23.3 percent) and no diabetes (64.4 percent).The study results show that screening for prediabetes and diabetes is feasible in a dental office, with acceptance by the dentist and dental office staff members, patients' physicians and patients. Patients from the community health center demonstrated good compliance with referrals to physicians; however, compliance was poor among those in the private dental offices.Screening for diabetes and prediabetes in the dental office may provide an important benefit to patients and encourage interprofessional collaboration to achieve a chronic care model in which health care professionals work together to care for a panel of patients.

Please cite this article as: Borgnakke WS, Madianos PN, Chapple ILC, Murakami S, Genco RJ, Papapanou PN, Armitage G, Preshaw PM, Bartold PM, Rahman Au, D’Aiuto F, Sanz M, Eke PI, Slots J, Giannobile WV, Tonetti MS, Kornman KS, Van Dyke TE, Lang NP, WITHDRAWN: The randomized controlled trial (RCT) published by the Journal of the American Medical Association (JAMA) on the impact of periodontal therapy on glycated hemoglobin (HbA1c) has fundamental flaws, The Journal of Evidence-Based Dental Practice (2014), doi: 10.1016/j.jebdp.2014.01.011.

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.

Fimbriae are major adhesive components on the cell surface of Prophyromonas gingivalis. In this study, we evaluated the role of fimbriae in coaggregation with Streptococcus oralis. Fimbriae purified from P. gingivalis competitively inhibited the coaggregation by 100% at a concentration of 50 micrograms/mL. On the other hand, the same amount of lipopolysaccharide isolated from P. gingivalis was inhibited by only 25% of the level of the fimbriae. A fimA-inactivated mutant of P. gingivalis failed to show distinct coaggregation activity. Fimbriae added to a solution of various strains of streptococci caused their self-aggregation at a concentration of 10 to 30 micrograms/mL. The self-aggregation induced by fimbriae was inhibited by lambda-arginine (20 to 40 mM/L). Iodinated fimbriae reacted with S. oralis cells immobilized on the nitrocellulose membrane, and 100 degrees C heating of the cells diminished the binding abilities. Recombinant fimbrillin (r-Fim, corresponding to whole residues 1 to 337 of native fimbrillin) of P. gingivalis also showed 100% inhibition of the coaggregation. The r-Fim variant (residues 1 to 286) lacking the C-terminal 51 residues was as inhibitory as r-Fim. However, the variant (residues 1 to 265) without the C-terminal 72 residues lost 77% of the inhibitory activity. These findings suggested that residues 266 to 286 contain a domain involved in the coaggregation of P. gingivalis with S. oralis. Inhibition by three polypeptides corresponding to residues 266 to 286, 266 to 337, and 287 to 337 was studied. Peptides 266 to 286 and 266 to 337 inhibited by 96 and 100%, respectively, at a concentration of 1.5 nmol/mL. Peptide 287 to 337 also showed a significant inhibitory effect but to a slightly lesser extent than that of peptide 266 to 286. P. gingivalis fimbriae appear to be involved in coaggregation with streptococci, probably through an adhesive protein molecule(s) of the latter, and the fimbriae possess several domains in the C-terminal residues 266 to 337 for interaction with S. oralis.

This study examines the accuracy of self-reported periodontal disease in a cohort of older females.The study comprised 972 postmenopausal females aged 53 to 83 years who completed baseline (1997 to 2001) and follow-up (2002 to 2006) whole-mouth oral examinations. Examinations included: 1) probing depth, 2) clinical attachment level, and 3) oral radiographs for alveolar crestal height in a study ancillary to the Women's Health Initiative Observational Study (WHI-OS) conducted in Buffalo, New York, called the OsteoPerio study. Participants also self-reported any history of diagnosis of periodontal/gum disease on a WHI-OS study-wide questionnaire administered during the time interval between the two OsteoPerio examinations.Participants reporting diagnosis of periodontal/gum disease on the WHI-OS questionnaire (n = 259; 26.6%) had worse oral hygiene habits, periodontal disease risk factors, and clinical periodontal measures compared with those not reporting periodontal/gum disease. Frequency of reported periodontal/gum disease was 13.5%, 24.7%, and 56.2% across OsteoPerio baseline examination categories of none/mild, moderate, and severe periodontal disease, respectively (trend: P0.001), defined by criteria of the Centers for Disease Control and Prevention/American Academy of Periodontology (CDC/AAP). Sensitivity, specificity, and positive and negative predictive values for reported periodontal disease status were 56.2%, 78.8%, 32.8%, and 90.7%, respectively, when CDC/AAP-defined severe periodontal disease at baseline was the criterion measure (prevalence of 15%) and were 76.0%, 77.4%, 22.0%, and 97.4%, respectively, when tooth loss to periodontitis (prevalence of 7%) was the criterion.A simple question for self-reported periodontal disease characterizes periodontal disease prevalence with moderate accuracy in postmenopausal females who regularly visit their dentist, particularly in those with more severe disease.

Dental caries is the demineralization of tooth structures by lactic acid from fermentation of carbohydrates by commensal gram-positive bacteria. Cariogenic bacteria have been shown to elicit a potent Th1 cytokine polarization and a cell-mediated immune response.To test the association between dental caries and head and neck squamous cell carcinoma (HNSCC).Case-control study in a comprehensive cancer center including all patients with newly diagnosed primary HNSCC between 1999 and 2007 as cases and all patients without a cancer diagnosis as controls. Those with a history of cancer, dysplasia, or immunodeficiency or who were younger than 21 years were excluded.Dental caries, fillings, crowns, and endodontic treatments, measured by the number of affected teeth; missing teeth. We also computed an index variable: decayed, missing, and filled teeth (DMFT).Incident HNSCC.We included 620 participants (399 cases and 221 controls). Cases had a significantly lower mean (SD) number of teeth with caries (1.58 [2.52] vs 2.04 [2.15]; P = .03), crowns (1.27 [2.65] vs 2.10 [3.57]; P = .01), endodontic treatments (0.56 [1.24] vs 1.01 [2.04]; P = .01), and fillings (5.39 [4.31] vs 6.17 [4.51]; P = .04) but more missing teeth (13.71 [10.27] vs 8.50 [8.32]; P.001) than controls. There was no significant difference in mean DMFT. After adjustment for age at diagnosis, sex, marital status, smoking status, and alcohol use, those in the upper tertiles of caries (odds ratio [OR], 0.32 [95% CI, 0.19-0.55]; P for trend = .001), crowns (OR, 0.46 [95% CI, 0.26-0.84]; P for trend = .03), and endodontic treatments (OR, 0.55 [95% CI, 0.30-1.01]; P for trend = .15) were less likely to have HNSCC than those in the lower tertiles. Missing teeth was no longer associated with HNSCC after adjustment for confounding.There is an inverse association between HNSCC and dental caries. This study provides insights for future studies to assess potential beneficial effects of lactic acid bacteria and the associated immune response on HNSCC.

Smoking is associated with tooth loss. However, smoking's relationship to the specific reason for tooth loss in postmenopausal women is unknown.Postmenopausal women (n = 1,106) who joined a Women's Health Initiative ancillary study (The Buffalo OsteoPerio Study) underwent oral examinations for assessment of the number of missing teeth, and they reported the reasons for tooth loss. The authors obtained information about smoking status via a self-administered questionnaire. The authors calculated odds ratios (ORs) and 95 percent confidence intervals (CIs) by means of logistic regression to assess smoking's association with overall tooth loss, as well as with tooth loss due to periodontal disease (PD) and with tooth loss due to caries.After adjusting for age, education, income, body mass index, history of diabetes diagnosis, calcium supplement use and dental visit frequency, the authors found that heavy smokers (≥ 26 pack-years) were significantly more likely to report having experienced tooth loss compared with never smokers (OR = 1.82; 95 percent CI, 1.10-3.00). Smoking status, packs smoked per day, years of smoking, pack-years and years since quitting smoking were significantly associated with tooth loss due to PD. For pack-years, the association for heavy smokers compared with that for never smokers was OR = 6.83 (95 percent CI, 3.40 -13.72). The study results showed no significant associations between smoking and tooth loss due to caries.Smoking may be a major factor in tooth loss due to PD. However, smoking appears to be a less important factor in tooth loss due to caries. Further study is needed to explore the etiologies by which smoking is associated with different types of tooth loss. Dentists should counsel their patients about the impact of smoking on oral health, including the risk of experiencing tooth loss due to PD.

This study tested the hypothesis that severe periodontitis in persons with non-insulin-dependent diabetes mellitus (NIDDM) increases the risk of poor glycemic control. Data from the longitudinal study of residents of the Gila River Indian Community were analyzed for dentate subjects aged 18 to 67, comprising all those: 1) diagnosed at baseline with NIDDM (at least 200 mg/dL plasma glucose after a 2-hour oral glucose tolerance test); 2) with baseline glycosylated hemoglobin (HbA1 ) less than 9%; and 3) who remained dentate during the 2-year follow-up period. Medical and dental examinations were conducted at 2-year intervals. Severe periodontitis was specified two ways for separate analyses: 1) as baseline periodontal attachment loss of 6 mm or more on at least one index tooth; and 2) baseline radiographic bone loss of 50% or more on at least one tooth. Clinical data for loss of periodontal attachment were available for 80 subjects who had at least one follow-up examination, 9 of whom had two follow-up examinations at 2-year intervals after baseline. Radiographic bone loss data were available for 88 subjects who had at least one follow-up examination, 17 of whom had two follow-up examinations. Poor glycemic control was specified as the presence of HbA1 of 9% or more at follow-up. To increase the sample size, observations from baseline to second examination and from second to third examinations were combined. To control for non-independence of observations, generalized estimating equations (GEE) were used for regression modeling. Severe periodontitis at baseline was associated with increased risk of poor glycemic control at follow-up. Other statistically significant covariates in the GEE models were: 1) baseline age; 2) level of glycemic control at baseline; 3) having more severe NIDDM at baseline; 4) duration of NIDDM; and 5) smoking at baseline. These results support considering severe periodontitis as a risk factor for poor glycemic control and suggest that physicians treating patients with NIDDM should be alert to the signs of severe periodontitis in managing NIDDM. J Periodontol 1996;67:1085-1093.

We explored the association between social factors and adult periodontitis by comparing self-reported information for daily strains and symptoms of depression in 71 cases and 77 controls. Cases and controls were selected from among 1,426 participants in the Erie County Risk Factor Study. We found differences among those who scored higher than their peers on measures of social strain. The odds ratio (OR) and 95% confidence interval (95% CI) for the association between case status and Role Strain score of 2.27 or more was 2.84, 95% CI = 1.08 to 7.46. We also examined serum antibody, dichotomized at the median, for three periodontal pathogens (Bacteroides forsythus [IgG Bf], Porphyromonas gingivalis [IgG Pg], Actinobacillus actinomycetemcomitans [IgG Aa]), and assessed interaction between antibody levels and a Depression score derived from the Brief Symptom Inventory. IgG Pg and IgG Aa were both strongly associated with case status (OR = 4.52, 95% CI = 1.99 to 10.3 and OR = 5.29, 95% CI = 2.34 to 12.0, respectively). IgG Bf was associated with periodontal disease but only among individuals who had higher scores for Depression (OR = 6.75, 95% CI = 1.25 to 36.5). Smoking status was associated with case status (OR = 4.95, 95% CI = 1.86 to 13.2). We assessed these findings prospectively by examining factors associated with more extensive disease among the 71 case subjects after 1 year of follow-up. We found baseline smoking status and IgG Bf among individuals scoring high on Depression at baseline to be associated with more extensive disease (8.1% or more of the sites showing further breakdown). In this population an elevated Depression score may be a marker for social isolation, which could play a role in immune function during periods of social strain. This exploratory analysis has served to identify specific lines of inquiry concerning psychosocial measures as important environmental factors in adult periodontitis. J Periodontol 1996;67:1060-1069.

The aim of the present study was to characterize the responses of macrophages to surface antigens of Porphyromonas gingivalis. Native fimbriae, full-length recombinant fimbrillin, and a lectin-like 12-kDa antigen all stimulated BALB/c peritoneal macrophages to secrete interleukin (IL)-1 beta. The antigens induced similar patterns of tyrosine phosphorylation; proteins in approximately 35-46 kDa range of undetermined identities were phosphorylated in the macrophages. The abilities of the surface antigens to induce IL-1 beta were markedly attenuated by tyrosine kinase inhibitors. This inhibition correlated with inhibition of the induced phosphorylation of specific macrophage proteins at tyrosine. The data suggest that tyrosine kinase(s) plays an important role in the regulatory intracellular signaling mechanisms by which P. gingivalis surface antigens can mediate certain responses in macrophages.

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.

P. gingivalis fimbriae play an important role in attachment of bacteria to various salivary components as well as to host cells and matrix proteins including fibronectin. In the present study, we investigated the binding domain of P. gingivalis fimbriae to fibronectin using synthetic peptides. A series of 20 mer fimbrillin peptides were used. Binding of fibronectin to purified fimbriae and synthetic peptides was assayed using polyclonal fibronectin antibodies as well as iodinated fibronectin. Purified fimbriae and peptide 126-146 (RMAFTEIKVQMSAAYDNIYTF) showed high levels of binding to fibronectin, while peptide 318-337(HLNVQCTVAEWVLVGQNATW) showed low but statistically significant binding. Our results suggest V-Q-X-X-X-A or V-X-X-X A common domain/domains present in both peptides might be involved in protein-protein interaction between P. gingivalis fimbriae and fibronectin.

Binding of Porphyromonas gingivalis to pellicle-coated teeth is mediated to a large extent by fimbrillin, a major structural subunit of fimbriae. A simple and efficient method for purifying the major fimbrial proteins from various strains of P. gingivalis was developed. The sonic extracts of crude fimbriae were prepared from P. gingivalis strains 2561, A7A1-28, EM-3, and 9-14K-1, which are representatives of different fimbrial groups. The crude fimbriae were precipitated from the extracts with 40% saturated ammonium sulfate. The dialyzed crude fimbriae were dissolved in 8 M guanidine HCl and loaded onto a Sepharose CL-6B column equilibrated with 6 M guanidine HCl. The major fimbrial protein-enriched fractions were obtained and further purified to homogeneity by repetitive gel filtration on the same column. The purity and intactness of the purified fimbrial proteins were ascertained by SDS-polyacrylamide gel electrophoresis followed by silver nitrate staining and immunoblot analysis using rabbit antisera raised against the purified fimbrial proteins. The result demonstrates the usefulness of guanidine HCl as a reliable reagent for purifying various fimbrial proteins of P. gingivalis, which are often associated strongly with other outer membrane proteins and show different physicochemical and antigenic characteristics.

The origin of fibroblasts, their proliferative activity and roles in the early stages of periodontal repair were investigated in order to better understand the periodontal healing process in furcation defects of the beagle dog after guided tissue regenerative therapy. Newly divided cells were identified by immunolocalization of bromodeoxyuridine (BrdU) injected 1 hour prior to sacrificing the animals. At 1 and 2 weeks after creation of the defects, the lesions were occupied primarily by granulation tissue. Under this condition, periodontal ligaments (PDL) fibroblasts in a coronal portion of the remaining PDL close to wounds proliferated actively, migrated along the root surface and formed fibrous connective tissue on the surface. Similarly, the fibroblasts adjacent to the bone surface also showed proliferative activity and engaged in active formation of fibrous connective tissue on the bone surface. The majority of labeled cells in both areas were located in the extravascular area. At 3 and 4 weeks, the defects were filled with an increased amount of new connective tissue and bone. The labeled fibroblasts were preferentially found in the most coronal portion of connective tissue formed on the root surface that was in direct contact with inflamed tissue, and the collagen fibers projected into granulation tissue. In areas of active bone formation, numerous labeled fibroblasts were located in connective tissue adjacent to the newly-formed bone. However, fibroblasts in the endosteum of new bone were rarely labeled These results indicate that fibroblasts involved in periodontal repair originate primarily from both the remaining PDL and alveolar bone, and actively engage in fibrous connective tissue formation in the early stages of periodontal repair The ability of PDL fibroblasts to proliferate, migrate, and form connective tissue on the root surfaces in the early repair stages appears to play a crucial role in the formation of the PDL and cementum, and consequently, in periodontal regeneration in the absence of root resorption and ankylosis. As the formation of new connective tissue and bone continues, the precursor cells for fibroblasts and osteoblasts are supplied locally through the continued divisions of the fibroblastic cells in association with the newly-formed connective tissue. Paravascular and endosteal cells appear to be minor contributors to new cell population during furcation defect repair in the beagle dog.

Periodontal regeneration requires formation of periodontal tissues lost due to periodontal disease. To better understand the formation of new periodontal tissues during periodontal repair and regeneration, immunohistochemical expression of extracellular matrix components of normal as well as healing periodontal tissues was evaluated and compared using the avidin-biotin complex immunohistochemical technique. For this purpose, horizontal furcation defects were created around mandibular P2 and P4 of 6 dogs after extraction of P1 and P3. The root surfaces were conditioned with citric acid and expanded polytetrafluoroethylene (ePTFE) membranes were placed and retained 0.5 mm above the cemento-enamel junction. The mucoperiosteal flaps were sutured in a coronal position. Two animals were sacrificed at 2, 4, and 8 weeks, and mesio-distal tissue slices containing normal or healing periodontal tissues were demineralized, dehydrated, and embedded in paraffin. Immunohistochemical localization of type I collagen (CI), fibronectin (FN), secreted protein, acidic and rich in cysteine (SPARC), vitronectin (VN), and bone sialoprotein (BSP) was performed on 6 microns thick sections. Morphological results demonstrated that at 2 weeks after defect creation, lesions were filled primarily with granulation tissue which was gradually replaced by newly-formed fibrous connective tissue, periodontal ligament (PDL), cementum, and bone between 4 and 8 weeks. The results of immunohistochemical study revealed that at 2 weeks the granulation tissue, especially in the intercellular spaces of inflammatory cells, was intensively stained for FN and VN. At 4 and 8 weeks, staining for CI, FN, and VN was found in fibrous connective tissue, the newly-formed PDL, cementum, and osteoid. Further the attachment zone of the PDL collagen fibers to cementum showed intense staining for FN. Immunostaining for SPARC was positive in the new PDL, cementum, and bone, while staining for BSP was restricted to the new cementum and bone. Interestingly, the PDL, especially in areas adjacent to active bone formation, demonstrated intense staining for BSP. However, fibrous connective tissue and PDL proper were unstained for BSP. These results indicate that FN and VN are involved in the early stages of periodontal repair, and periodontal regeneration is achieved through formation of periodontal tissues that are composed of different matrix components specific to different types of periodontal tissues.

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)

Background: Periodontal disease and diabetes mellitus are common, chronic diseases worldwide. Epidemiologic and biologic evidence suggest periodontal disease may affect diabetes. Objective: To systematically review non-experimental, epidemiologic evidence for effects of periodontal disease on diabetes control, complications and incidence. Data sources: Electronic bibliographic databases, supplemented by hand searches of recent and future issues of relevant journals. Study eligibility criteria and participants: Longitudinal and cross-sectional epidemiologic, non-interventional studies that permit determination of directionality of observed effects were included. Study appraisal and synthesis methods: Four reviewers evaluated pair-wise each study. Review findings regarding study results and quality were summarized in tables by topic, using the PRISMA Statement for reporting and the NewcastleOttawa System for quality assessment, respectively. From 2246 citations identified and available abstracts screened, 114 full-text reports were assessed and 17 included in the review. Results: A small body of evidence supports significant, adverse effects of periodontal disease on glycaemic control, diabetes complications, and development of type 2 (and possibly gestational) diabetes. Limitations: There were only a limited number of eligible studies, several of which included small sample sizes. Exposure and outcome parameters varied, and the generalizability of their results was limited. Conclusions and implications of key findings: Current evidence suggests that periodontal disease adversely affects diabetes outcomes, and that further longitudinal studies are warranted.

A total of 506 adults participated in this study. The study population was recruited from a pool of new patients presenting to the Columbia University College of Dental Medicine over a 12-month period (April 2009 to March 2010). New patients were screened to determine potential eligibility for participation based on 2 criteria: age and knowledge of their diabetes status. Non-Hispanic white adults were required to be 40 years old or older and Hispanic or non-white adults were required to be 30 years or older. Additionally, all potential participants had to respond that a health care provider had never told them that they had diabetes or prediabetes. This screening yielded 601 individuals. From this group, 535 were selected based on having 1 of 4 self-reported risk factors (hypertension, high cholesterol, overweight, or a family history of diabetes). These 535 adults continued with a periodontal examination and an HbA1c test. Five hundred six participants returned for a follow-up visit to collect blood for a fasting plasma glucose (FPG) test.HbA1c test, and dentate and periodontal status.FPG level.Among the 535 individuals participating in the study, 161 were determined potentially to be prediabetic (FPG was 100-125 mg/dL) and 21 potentially to be diabetic (FPG ≥ 126 mg/dL). Receiver operating characteristics (ROCs) via logistic regression was used to assess model performance and calculate key findings. The area under the curve of a multivariate regression model that included oral health status indicators and all 4 self-reported risk factors had a predicted value of 0.68 (confidence interval [CI]: 0.63, 0.73) for abnormal FPG (≥100 mg/dL). A model with just the percentage of periodontal pockets ≥5 mm and the number of missing teeth had a predicted value of 0.65 (CI: 0.60, 0.70). When the test results from HbA1C were added to the simpler model, the predictive value improved to 0.79 (CI: 0.75, 0.83). The authors also determined that the presence of 4 or more missing teeth or having pocket depth of 5 mm or more involving more than 25% of the sites identified 73% of the true cases (ie, abnormal FPG).Dental care professionals have the potential to identify patients at risk for diabetes and refer them to a physician for follow-up evaluation.

Recombinant human platelet-derived growth factor (rhPDGF) is safe and effective for the treatment of periodontal defects in short-term studies up to 6 months in duration. We now provide results from a 36-month extension study of a multicenter, randomized, controlled clinical trial evaluating the effect and long-term stability of PDGF-BB treatment in patients with localized severe periodontal osseous defects.A total of 135 participants were enrolled from six clinical centers for an extension trial. Eighty-three individuals completed the study at 36 months and were included in the analysis. The study investigated the local application of β-tricalcium phosphate scaffold matrix with or without two different dose levels of PDGF (0.3 or 1.0 mg/mL PDGF-BB) in patients possessing one localized periodontal osseous defect. Composite analysis for clinical and radiographic evidence of treatment success was defined as percentage of cases with clinical attachment level (CAL) ≥2.7 mm and linear bone growth (LBG) ≥1.1 mm.The participants exceeding this composite outcome benchmark in the 0.3 mg/mL rhPDGF-BB group went from 62.2% at 12 months, 75.9% at 24 months, to 87.0% at 36 months compared with 39.5%, 48.3%, and 53.8%, respectively, in the scaffold control group at these same time points (P0.05). Although there were no significant increases in CAL and LBG at 36 months among all groups, there were continued increases in CAL gain, LBG, and percentage bone fill over time, suggesting overall stability of the regenerative response.PDGF-BB in a synthetic scaffold matrix promotes long-term stable clinical and radiographic improvements as measured by composite outcomes for CAL gain and LBG for patients possessing localized periodontal defects ( ClinicalTrials.gov no. CT01530126).

This report adds a new definition for mild periodontitis that allows for better descriptions of the overall prevalence of periodontitis in populations. In 2007, the Centers for Disease Control and Prevention in partnership with the American Academy of Periodontology developed and reported standard case definitions for surveillance of moderate and severe periodontitis based on measurements of probing depth (PD) and clinical attachment loss (AL) at interproximal sites. However, combined cases of moderate and severe periodontitis are insufficient to determine the total prevalence of periodontitis in populations.The authors proposed a definition for mild periodontitis as ≥ 2 interproximal sites with AL ≥ 3 mm and ≥ 2 interproximal sites with PD ≥ 4 mm (not on the same tooth) or one site with PD ≥ 5 mm . The effect of the proposed definition on the total burden of periodontitis was assessed in a convenience sample of 456 adults ≥ 35 years old and compared with other previously reported definitions for similar categories of periodontitis.Addition of mild periodontitis increases the total prevalence of periodontitis by ≈31% in this sample when compared with the prevalence of severe and moderate disease.Total periodontitis using the case definitions in this study should be based on the sum of mild, moderate, and severe periodontitis.

The Centers for Disease Control and Prevention (CDC) has as one of its strategic goals to support and improve surveillance of periodontal disease. In 2003, the CDC initiated the CDC Periodontal Disease Surveillance Project in collaboration with the American Academy of Periodontology to address population-based surveillance of periodontal disease at the local, state, and national levels. This initiative has made significant advancements toward the goal of improved surveillance, including developing valid self-reported measures that can be obtained from interview-based surveys to predict prevalence of periodontitis in populations. This will allow surveillance of periodontitis at the state and local levels and in countries where clinical resources for surveillance are scarce. This work has produced standard case definitions for surveillance of periodontitis that are now widely recognized and applied in population studies and research. At the national level, this initiative has evaluated the validity of previous clinical examination protocols and tested new protocols on the National Health and Nutrition Examination Survey (NHANES), recommending and supporting funding for the gold-standard full-mouth periodontal examination in NHANES 2009 to 2012. These examinations will generate accurate estimates of the prevalence of periodontitis in the US adult population and provide a superior dataset for surveillance and research. Also, this data will be used to generate the necessary coefficients for our self-report questions for use in subsets of the total US population. The impact of these findings on population-based surveillance of periodontitis and future directions of the project are discussed along with plans for dissemination and translation efforts for broader public health use.

Fimbriae are considered important in the adherence and colonization of Porphyromonas gingivalis in the oral cavity. It has been demonstrated that purified fimbriae bind to whole human saliva adsorbed to hydroxyapatite (HAP) beads, and the binding appears to be mediated by specific protein-protein interactions. Recently, we expressed the recombinant fimbrillin protein (r-Fim) of P. gingivalis corresponding to amino acid residues 10 to 337 of the native fimbrillin (A. Sharma, H.T. Sojar, J.-Y. Lee, and R.J. Genco, Infect. Immun. 61:3570-3573, 1993). We examined the ability of individual salivary components to promote the direct attachment of r-Fim to HAP beads. Purified r-Fim was radiolabeled with 125I and incubated with HAP beads which were coated with saliva or purified individual salivary components. Whole, parotid, and submandibular-sublingual salivas increased the binding of 125I-r-Fim to HAP beads. Submandibular-sublingual saliva was most effective in increasing the binding of 125I-r-Fim to HAP beads (1.8 times greater than that to uncoated HAP beads). The binding of 125I-r-Fim to HAP beads coated with acidic proline-rich protein 1 (PRP1) or statherin was four and two times greater, respectively, than that to uncoated HAP beads. PRP1 and statherin molecules were also found to bind 125I-r-Fim in an overlay assay. The binding of intact P. gingivalis cells to HAP beads coated with PRP1 or statherin was also enhanced, by 5.4 and 4.3 times, respectively, over that to uncoated HAP beads. The interactions of PRP1 and statherin with 125I-r-Fim were not inhibited by the addition of carbohydrates or amino acids. PRP1 and statherin in solution did not show inhibitory activity on 125I-r-Fim binding to HAP beads coated with PRP1 or statherin. These results suggest that P. gingivalis fimbriae bind strongly through protein-protein interactions to acidic proline-rich protein and statherin molecules which coat surfaces.

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.

Fimbrial production by Porphyromonas gingivalis was inactivated by insertion-duplication mutagenesis, using the cloned gene for the P. gingivalis major fimbrial subunit protein, fimA. by several criteria, this insertion mutation rendered P. gingivalis unable to produce fimbrilin or an intact fimbrial structure. A nonfimbriated mutant, DPG3, hemagglutinated sheep erythrocytes normally and was unimpaired in the ability to coaggregate with Streptococcus gordonii G9B. The cell surface hydrophobicity of DPG3 was also unaffected by the loss of fimbriae. However, DPG3 was significantly less able to bind to saliva-coated hydroxyapatite than wild-type P. gingivalis 381. This suggested that P. gingivalis fimbriae are important for adherence of the organism to saliva-coated oral surfaces. Further, DPG3 was significantly less able to cause periodontal bone loss in a gnotobiotic rat model of periodontal disease. These observations are consistent with other data suggesting that P. gingivalis fimbriae play an important role in the pathogenesis of human periodontal disease.

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

Nanoparticles of calcium sulfate (nCS) have potential advantages as a ceramic matrix, scaffold and/or vehicle for delivering growth factors for osseous regeneration in a variety of clinical situations. The objectives of this study were to synthesize and characterize nanoparticles of hemihydrate calcium sulfate (nCS) and to develop a nCS-based system for bone regeneration. A cryo-vacuum method was used to process dihydrate CS into dihydrate nCS, which was then subjected to oven drying to produce hemihydrate. The nCS was sterilized by glow discharge treatment for use as a synthetic graft material for the treatment of bone defects. Electron microscopy showed that the nCS powder consisted of aggregates of closely arranged acicular crystals, approximately 30-80 nm in width, 400-600 nm in length and approximately 80-100 nm in diameter, providing a surface area about ten times that of conventional CS. Thorough physico-chemical characterization confirmed the composition and phase of the material. Cell viability/metabolic activity assays and alkaline phosphate assays confirmed the safety and biocompatibility of nCS. Release kinetics for adsorbed platelet-derived growth factor and bone morphogenetic protein-2 (BMP-2) suggests that nCS may serve as an appropriate vehicle for slow release delivery of these agents. The studies presented here give evidence of the advantages of nCS as a scaffold to support osteoblastic cell activity.

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