Efficacy of communicating periodontal risk on psychological outcomes and supragingival plaque control in patients undergoing first periodontal consultation: A parallel-arm, randomized trial.

AIM: To evaluate the efficacy of the PerioRisk prognostic tool in implementing the effect of motivational interviewing (MI) on psychological outcomes and supragingival plaque control. MATERIALS AND METHODS: Participants underwent MI immediately after their first periodontal visit. According to a parallel-arm, randomized study design, MI was performed with (RISK group) or without (CTR group) information on PerioRisk level and treatment goals based on PerioRisk output. Psychological outcomes were assessed using the Positive Affect Negative Affect Scale (PANAS) and Protection Motivation Theory (PMT). Plaque index (PI) was re-evaluated after 8-12 weeks. RESULTS: Significant improvements in PMT overall score and PI were observed in CTR and RISK groups, without inter-group difference in PANAS and PMT overall scores and PI. A sub-analysis showed that the overall PMT scores recorded immediately after MI in both CTR and RISK groups for subjects with no tooth loss due to periodontitis were higher than those recorded before MI in subjects with tooth loss due to periodontitis. CONCLUSIONS: At first periodontal visit, MI (implemented with without PerioRisk) has tangible effects on psychological outcomes and supragingival plaque control and seems to anticipate the awareness that is commonly generated by periodontitis-related tooth loss (ClinicalTrials.gov protocol registration ID: NCT05078411).

Functional profile of oral plaque microbiome: Further insight into the bidirectional relationship between type 2 diabetes and periodontitis.

Increasing evidence support the association between the oral microbiome and human systemic diseases. This association may be attributed to the ability of many oral microbes to influence the inflammatory microenvironment. Herein, we focused our attention on the bidirectional relationship between periodontitis and type 2 diabetes using high-resolution whole metagenomic shotgun analysis to explore the composition and functional profile of the subgingival microbiome in diabetics and non-diabetics subjects with different periodontal conditions. In the present study, the abundance of metabolic pathways encoded by oral microbes was reconstructed from the metagenome, and we identified a set of dysregulated metabolic pathways significantly enriched in the periodontitis and/or diabetic patients. These pathways were mainly involved in branched and aromatic amino acids metabolism, fatty acid biosynthesis and adipocytokine signaling pathways, ferroptosis and iron homeostasis, nucleotide metabolism, and finally in the peptidoglycan and lipopolysaccharides synthesis. Overall, the results of the present study provide evidence in favor of the hypothesis that during the primary inflammatory challenge, regardless of whether it is induced by periodontitis or diabetes, endotoxemia and/or the release of inflammatory cytokines cause a change in precursor and/or in circulating innate immune cells. Dysbiosis and inflammation, also via oral-gut microbiome axis or adipose tissue, reduce the efficacy of the host immune response, while fueling inflammation and can induce that metabolic/epigenetic reprogramming of chromatin accessibility of genes related to the immune response. Moreover, the presence of an enhanced ferroptosis and an imbalance in purine/pyrimidine metabolism provides new insights into the role of ferroptotic death in this comorbidity.

Validation of reported genetic risk factors for periodontitis in a large-scale replication study.

AIM: Many studies investigated the role of genetic variants in periodontitis, but few were established as risk factors. We aimed to validate the associations of recent candidate genes in aggressive periodontitis (AgP). MATERIAL AND METHODS: We analysed 23 genes in 600 German AgP patients and 1441 controls on the Illumina custom genotyping array Immunochip. We tested a suggestive association in a Dutch and German/Austrian AgP case-control sample, and a German chronic periodontitis (CP) case-control sample using Sequenom iPlex assays. We additionally tested the common known risk variant rs1333048 of the gene ANRIL for its association in a Turkish and Italian population. RESULTS: None of the analysed genes gave statistical evidence for association. Upon covariate adjustment for smoking and gender, in the pooled German-Austrian AgP sample, IL10 SNP rs6667202 was associated with p = 0.016, OR = 0.77 (95% CI = 0.6-0.95), and in the Dutch AgP sample, adjacent IL10 SNP rs61815643 was associated with p = 0.0009, OR = 2.31 (95% CI = 1.4-3.8). At rs61815643, binding of the transcription factor PPARG was predicted. ANRIL rs1333048 was associated in the Turkish sample (pallelic = 0.026, OR = 1.67 [95% CI = 1.11-2.60]). CONCLUSIONS: Previous candidate genes carry no susceptibility factors for AgP. Association of IL-10 rs61815643 with AgP is suggested. ANRIL is associated with periodontitis across different populations.

Age-related treatment response following non-surgical periodontal therapy.

BACKGROUND: To date, no studies have evaluated the effect of patient age on the treatment response following non-surgical periodontal therapy (NSPT). AIM: To evaluate the outcomes of NSPT in two cohorts of patients with a substantial age difference. MATERIALS AND METHODS: Two groups of periodontitis patients with a substantial age difference (younger group, Y, and older group, O) were retrospectively selected. The effectiveness of NSPT was assessed by evaluating the changes in the prevalence of sites with different pocket probing depths (PPD) as well as the changes in patient- and site-specific bleeding on probing (BoP) scores. RESULTS: Y group comprised 57 patients, mean age: 34.7 +/- 4.4 years, and O group comprised 60 patients, mean age: 58.9 +/- 5.3 years (p<0.0001). NSPT resulted in a significant improvement of PPD and BoP in both age groups. No statistically significant inter-group differences were observed in the investigated clinical parameters as well as their changes with respect to pre-treatment. However, multiple regression analysis showed a significantly higher risk of showing residual pockets following treatment in group O. CONCLUSIONS: The results of the present study seem to indicate that age has a limited effect on treatment response following NSPT in periodontitis patients.

Interleukin-1 beta levels in gingival crevicular fluid and serum under naturally occurring and experimentally induced gingivitis.

AIMS: To evaluate the interleukin-1 beta (IL-1 beta) levels in gingival crevicular fluid (GCF) and serum in either naturally occurring (N-O) or experimentally induced (E-I) plaque-associated gingivitis. MATERIAL AND METHODS: Thirty-seven periodontally healthy subjects were evaluated in real life conditions (N-O gingivitis) as well as after 21 days of experimental gingivitis trial (E-I gingivitis). During the experimental gingivitis trial, in one maxillary quadrant (test quadrant), gingival inflammation was induced by oral hygiene abstention, while in the contralateral (control) quadrant, oral hygiene was routinely continued. IL-1 beta concentrations in N-O and E-I gingivitis were investigated for IL-1B(+3954) and IL-1B(-511) gene polymorphisms. RESULTS: (i) GCF IL-1 beta concentrations in E-I gingivitis were significantly higher compared with N-O gingivitis; (ii) an intra-individual correlation between GCF concentrations of IL-1 beta detected in N-O and E-I gingivitis was observed in control quadrants, but not in test quadrants; (iii) IL-1 beta concentration in GCF was associated with IL-1B(+3954) genotype only at test quadrants; (iv) IL-1 beta was detectable in serum only at low levels in a limited number of subjects, without difference between gingivitis conditions. CONCLUSIONS: Aspects of the bacterial challenge to the gingival tissues, such as the amount of plaque deposits and plaque accumulation rate, appear to affect the IL-1 beta levels in GCF in subjects with a specific IL-1B genotype.

Whole metagenomic shotgun sequencing of the subgingival microbiome of diabetics and non-diabetics with different periodontal conditions.

OBJECTIVE: The aim of this study was to use high-resolution whole metagenomic shotgun sequencing to characterize the subgingival microbiome of patients with/without type 2 Diabetes Mellitus and with/without periodontitis. DESIGN: Twelve subjects, falling into one of the four study groups based on the presence/absence of poorly controlled type 2 Diabetes Mellitus and moderate-severe periodontitis, were selected. For each eligible subject, subgingival plaque samples were collected at 4 sites, all representative of the periodontal condition of the individual (i.e., non-bleeding sulci in subjects without a history of periodontitis, bleeding pockets in patients with moderate-severe periodontitis). The subgingival microbiome was evaluated using high-resolution whole metagenomic shotgun sequencing. RESULTS: The results showed that: (i) the presence of type 2 Diabetes Mellitus and/or periodontitis were associated with a tendency of the subgingival microbiome to decrease in richness and diversity; (ii) the presence of type 2 Diabetes Mellitus was not associated with significant differences in the relative abundance of one or more species in patients either with or without periodontitis; (iii) the presence of periodontitis was associated with a significantly higher relative abundance of Anaerolineaceae bacterium oral taxon 439 in type 2 Diabetes Mellitus patients. CONCLUSIONS: Whole metagenomic shotgun sequencing of the subgingival microbiome was extremely effective in the detection of low-abundant taxon. Our results point out a significantly higher relative abundance of Anaerolineaceae bacterium oral taxon 439 in patients with moderate to severe periodontitis vs patients without history of periodontitis, which was maintained when the comparison was restricted to type 2 diabetics.

Experimental gingivitis: reproducibility of plaque accumulation and gingival inflammation parameters in selected populations during a repeat trial.

OBJECTIVES: This study aimed to assess whether and to what extent the experimental gingivitis clinical parameters are reproducible within selected populations with different gingival inflammatory response (high or low) to plaque accumulation. In addition, the consistency in developing a high or low gingival inflammatory response within the selected populations was evaluated. MATERIAL AND METHODS: Thirty-seven subjects previously identified as high (HR, n=20) or low responders (LR, n=17) during an experimental gingivitis trial (first trial) were enrolled in a "repeat" experimental gingivitis trial. RESULTS: No significant differences in plaque accumulation parameters and bleeding index values were detected between first and repeat trial for the 37 participants. Gingival index was higher during the repeat trial but behaved consistently in terms of the temporal changes in the course of both trials in both populations. Of the 17 LR participants, 10 manifested low susceptibility to inflammation after repeat trial. Among the 20 HR, 10 manifested high susceptibility to inflammation after repeat trial. CONCLUSIONS: These results indicate that our experimental gingivitis model is reproducible to some extent in selected populations. The high reproducibility of plaque and, to a lesser extent, of inflammation parameters under the employed controlled conditions could be a valuable tool in gingivitis research.

Immediate loading of dental implants supporting fixed partial dentures in the posterior mandible: a randomized controlled split-mouth study--machined versus titanium oxide implant surface.

PURPOSE: A split-mouth study was conducted to compare dental implants with either machined or titanium oxide (TiO) surfaces immediately loaded with fixed partial dentures in the posterior mandible. MATERIALS AND METHODS: Ten patients with bilateral partial edentulism in the posterior mandible received 42 implants; 20 on the test (TiO) and 22 on the control (machined) side. The implants were loaded within 24 hours postsurgery. At implant placement the maximum insertion torque (IT) was recorded. Implant stability quotient (ISQ) was also evaluated at baseline (day 0) and 1, 2, 4, 12, 24, and 52 weeks following implant placement. The radiographic bone level (RBL) change was measured on periapical radiographs at baseline and 12 months after loading. Means for the 2 groups were compared by paired t test. RESULTS: The overall implant success rate was 95%. No implants were lost in the test group; 2 failed in the control group. The difference between the groups in RBL change after 1 year of function was not statistically significant (P = .224). However, average RBL change for machined implants in distal positions was significantly higher than for TiO surface implants in the same position (post-hoc comparison; P = .048). ISQ and peak IT values did not differ between the groups (P = .414 and P = .762, respectively). The high IT necessary to insert the implants did not seem to affect the RBL change (P = .203). CONCLUSIONS: No significant difference was observed between machined and TiO implant surface in terms of RBL change or ISQ, although TiO implants may provide a lower RBL change compared to machined implants when utilized in the distal position. Immediate loading of implants using fixed partial dentures in posterior mandible may be considered as a treatment option if implants are inserted with IT > or = 20 Ncm and ISQ > or = 60 into nonaugmented bone and loaded with light centric occlusal contact.

Modulation of clinical expression of plaque-induced gingivitis: interleukin-1 gene cluster polymorphisms.

BACKGROUND: The purpose of the present study was to determine the association of interleukin-1 (IL-1) gene polymorphisms with clinical parameters of gingivitis in a large experimental gingivitis trial and with each of two subgroups, high responders (HR) and low responders (LR), with distinct susceptibility to gingivitis. METHODS: Ninety-six systemically and periodontally healthy non-smokers, 46 males (mean age: 23.9+/-1.7) and 50 females (mean age: 23.3+/-1.6) were included in a randomized, split-mouth, localized 21-day experimental gingivitis trial. Plaque index (PI), gingival index (GI), gingival crevicular fluid volume (GCF), and angulated bleeding score (AngBS) were recorded. Two subgroups were defined from the total study population (HR, LR) characterized by substantially different severity of gingival inflammation despite similar plaque accumulation rate. The study population was typed for interleukin-1 alpha (IL-1A+4845), interleukin-1 beta (IL-1B+3953, IL-1B-511), and IL-1 receptor antagonist (IL-1RN, intron 2 variable number tandem repeats) gene polymorphisms. Gene variants were analyzed by amplifying the polymorphic region using polymerase chain reaction, followed by restriction-enzyme digestion and agarose gel electrophoresis. RESULTS: Neither IL-1A+4845, IL-1B+3953, or the combined (IL-1A+4845 x 2 - IL-1B+3953 x 2) genotype was associated with clinical parameters in the overall population. IL-1RN was significantly associated with test quadrant PI (P= 0.046), GCF (P= 0.05), and GI (P= 0.018). The genotype distribution in HR and LR subjects was significantly different for IL-1RN (P= 0.045) and for IL-1B-511 (P= 0.023). CONCLUSION: The results of the present study suggest an association between IL-1RN polymorphism and subject-based clinical behavior of the gingiva in response to de novo plaque accumulation, as well as a possible association between IL-1B-511 polymorphism and gingivitis susceptibility.

Prevalence of bleeding on probing: a cohort study in a specialist periodontal clinic.

OBJECTIVES: to assess the prevalence and distribution of bleeding on probing (BoP) in a cohort of periodontally diseased patients, evaluate the influence of patient-related predictors on BoP variability, and characterize two subgroups of patients with a significantly different BoP score. METHOD AND MATERIALS: six hundred and one patients were retrospectively included. The percentage of BoP-positive sites was calculated for the entire dentition (%BoPtotal) and within different areas of the dentition. The influence of patient-related predictors on intersubject variability in %BoPtotal was evaluated. Two subgroups of patients, belonging to the lowest (LB, low bleeding) and highest (high bleeding, HB) quartile of patient distribution according to %BoPtotal, were identified. RESULTS: median %BoPtotal was 26.4%, with 99% of the population showing at least one BoP-positive site. %BoPtotal was positively correlated with patient age and number of sites with pocket probing depth (PPD) ⋝ 5 mm, and significantly more prevalent in mandibular vs maxillary sites, posterior vs anterior sites, interproximal vs oral/buccal sites, and sites with PPD ⋝ 5 mm vs PPD ⋜ 4 mm. LB and HB patients were significantly different for %BoPtotal, as well as in sites with PPD ⋜ 4 mm and PPD ⋝ 5 mm, but not for sex, age, smoking status, daily cigarette consumption, diabetic status, and number of sites with PPD ⋝ 5 mm. CONCLUSIONS: BoP was highly prevalent and variable in both patients and different areas of the dentition; patient-related factors and site-specific characteristics (such as age, number of periodontal pockets, probing depth, tooth type, and aspects) seem to be partly responsible for the individual variation in BoP; and HB and LB were not significantly different with respect to the investigated predictors.

Role of IL-6, TNF-A and LT-A variants in the modulation of the clinical expression of plaque-induced gingivitis.

AIM: The purpose of the present study was to assess the association of interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-A) and lymphotoxin alpha (LT-A) gene polymorphisms with the clinical parameters of gingivitis in a large experimental gingivitis trial and with each of two subgroups, "high responder" (HR, n=24) and "low responder" (LR, n=24), with distinct susceptibility to gingivitis. MATERIAL AND METHODS: Ninety-six systemically and periodontally healthy non-smokers, 46 males (mean age: 23.9+/-1.7) and 50 females (mean age: 23.3+/-1.6), were included in a randomized split-mouth localized 21-day experimental gingivitis trial. Plaque index, gingival index, gingival crevicular fluid volume and angulated bleeding score were recorded. HR and LR subgroups were characterized by substantially different severities of gingival inflammation despite a similar plaque accumulation rate. All subjects were genetically characterized for IL-6(-174), IL-6(-597), TNF-A(-308) and LT-A(+252) polymorphisms. RESULTS: None of the variants analysed, either as single polymorphisms or as a combined genotype, was associated with the clinical parameters in the overall population. For the polymorphisms studied, genotypic distributions in HR and LR subjects were not significantly different. CONCLUSIONS: The present results suggest an absence of association between IL-6, TNF-A and LT-A polymorphisms and subject-based clinical behaviour of the gingiva in response to de novo plaque accumulation.

Time as a factor in the identification of subjects with different susceptibility to plaque-induced gingivitis.

OBJECTIVES: The purpose of this study was to assess whether identification of subjects with different susceptibility to plaque-induced gingival inflammation is dependent on the length of time of de novo plaque accumulation. METHODS: Retrospective analysis of data obtained from a recently reported randomized split-mouth localized experimental gingivitis trial involving 96 healthy non-smokers. Gingival and plaque index, gingival crevicular fluid volume (GCF), angulated bleeding score, and the derived parameter cumulative plaque exposure (CPE) were recorded at days 0, 7, 14, and 21. The primary outcome variable to express severity of inflammation was GCF and each subject was a statistical unit. Based on subject distribution of GCF-day 21 residuals after standardization for CPE-day 21, two sub-populations (upper and lower distribution quartiles) were selected. They were, respectively, defined as "high responders" (HR) (n=24) and "low responders" (LR) (n=24) and characterized by significantly different severity of gingivitis to similar amounts of plaque deposits. The same analysis was repeated at days 7 and 14. Prevalence of HR and LR was compared between days using the chi(2) [ML] test. RESULTS: For both day 7 and day 14, the quartile distribution of LR and HR was statistically significant (p=0.02). Fifty percent of LR and 71% of HR presented a consistent level of susceptibility to plaque-induced gingival inflammation even after only 7 and/or 14 days of plaque accumulation. CONCLUSIONS: These findings support the concept that the subject-based susceptibility to plaque-induced gingival inflammation is an individual trait, only partly related to the length of time of exposure to plaque.

Modulation of clinical expression of plaque-induced gingivitis: response in aggressive periodontitis subjects.

AIM: The aim of this study was to characterize the gingival inflammatory response to de novo plaque accumulation in subjects treated for aggressive periodontitis (AP). The gingival inflammatory response of the AP subjects was retrospectively compared with that of periodontally healthy individuals (PH) matched for exposure to plaque and of periodontally healthy subjects previously identified as "high responders" (HR) and "low responders" (LR). MATERIALS AND METHODS: 13 AP subjects and 26 matched PH subjects participated in a 21-day experimental gingivitis trial. Plaque index (PlI), Gingival index (GI), gingival crevicular fluid volume (GCF) and angulated bleeding score (AngBS) were recorded at days 0, 7, 14 and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was also calculated. RESULTS: GCF was significantly higher in AP compared with PH group at each observation interval (p< or =0.001). In addition, GCF was significantly higher in AP group compared with either LR or HR groups at each observation interval (p<0.001). CONCLUSIONS: These results suggest that susceptibility to gingival inflammation in response to de novo plaque accumulation may be related to susceptibility to periodontitis.

Modulation of clinical expression of plaque-induced gingivitis: effects of personality traits, social support and stress.

BACKGROUND: Studies have shown an association between an acute stressful event and gingivitis. However, the possible effects of personality traits associated with stress resistance/susceptibility and current level of stress on the clinical expression of plaque-induced inflammation remain to be examined. The aim of this study was to characterize the subject-based clinical behaviour of the gingiva during experimental gingivitis in relation to personality profile, psychological stress and coping behaviour. METHODS: Ninety-six systemically and periodontally healthy subjects (mean age: 23.6+/-1.7 years), 46 males and 50 females, non-smokers, participated in a randomized, split-mouth, localized experimental gingivitis trial. Prior to the trial, subjects were asked to complete self-administered questionnaires evaluating personality traits (Hardiness scale and Courtauld Emotional Control Scale), subjective stress (Visual Analogue Scale-Total Distress), social support (Multidimensional Scale of Perceived Social Support, MSPSS) and life events (Life Experiences Survey (LES)). The influence of psychosocial factors was investigated in the overall population as well as in two sub-populations with different inflammatory response to plaque accumulation. RESULTS: No significant relationships were found between gingival inflammation variables and psychological measures. No significant differences were detected between subjects with different susceptibilties to plaque-associated gingivitis for any considered psychological variable. A significant association between plaque variables and LES (negative) or MSPSS (positive) was found; however, the variance explained by the model was low. CONCLUSIONS: Differences in the current level of stress and psychosocial variables indicative of stress susceptibility do not account for variability in plaque accumulation and gingival inflammation during experimental gingivitis in young adults.

Modulation of clinical expression of plaque-induced gingivitis. II. Identification of "high-responder" and "low-responder" subjects.

AIM: The aims of this study were to validate a randomized, split-mouth, localized experimental gingivitis model and to identify subjects with different gingivitis susceptibility. MATERIAL AND METHODS: In each of 96 healthy subjects, one maxillary quadrant was randomly assigned as "test" (experimental gingivitis) and the contralateral quadrant as "control". Plaque index (PlI), gingival index (GI), gingival crevicular fluid volume (GCF), and angulated bleeding score (AngBS) were recorded in both quadrants at days 0, 7, 14, and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was calculated. Day-21 GCF was standardized according to CPE, and residuals of GCF on CPE were calculated. Two subpopulations were then defined, based on upper and lower quartiles of GCF-residual distribution and were, respectively, identified as "high-responder" (HR; n=24) and "low-responder" (LR; n=24). RESULTS: At test quadrants, all parameters significantly increased throughout the trial, while in control quadrants, PlI, GI, and AngBS remained low. Significant differences were noted between test and control quadrants on days 7, 14, and 21 for all parameters. Significant increases in GI, AngBS, and GCF were observed in test quadrants over the course of the study in both HR and LR groups. Significant differences were noted between HR and LR groups for all gingivitis parameters on day 21 in test quadrants, without any significant differences in PlI or CPE between the groups. CONCLUSIONS: We identified two subpopulations characterized by significant differences in clinical parameters of plaque-induced gingival inflammation, despite similar amounts of plaque deposits and plaque accumulation rates.

Modulation of clinical expression of plaque-induced gingivitis. III. Response of "high responders" and "low responders" to therapy.

AIM: The aim of the present study was to characterize the subject-based clinical behavior of the gingiva in response to a tooth-cleaning regimen in two subpopulations, "high-responder" (HR) and "low-responder" (LR) groups, presenting a different inflammatory response to plaque accumulation. MATERIAL AND METHODS: The study population comprised of 96 systemically and periodontally healthy subjects, 46 males and 50 females, non-smokers, enrolled in an experimental gingivitis trial. At completion of the experimental gingivitis period (day 21), all subjects were prescribed the same 21-day treatment regimen of amine/stannous fluoride (AmF/SnF(2))-containing toothpaste and mouthrinse. Plaque index (PlI), gingival index (GI), gingival crevicular fluid volume (GCF), and angulated bleeding score (AngBS) were recorded on three selected teeth. Treatment efficacy was evaluated in the overall population as well as in HR and LR groups, separately. RESULTS: A statistically significant decrease of PlI was observed after treatment (p<0.001), with PlI reversing to baseline levels. Changes in PlI revealed the same trend in both HR and LR groups, without differences between groups. Treatment also resulted in a significant decrease of all gingivitis parameters (p<0.001 for all comparisons). After treatment, GI, AngBS, and GCF were comparable with baseline condition. However, when the two groups were compared, day 42-GCF was significantly higher in the HR group than the LR group. CONCLUSIONS: A treatment regimen based on mechanical plaque control supplemented with AmF/SnF(2)-containing toothpaste and mouthrinse is effective in reducing plaque accumulation and re-establishing healthy gingival conditions after experimentally induced gingivitis, even in subjects with different inflammatory response to plaque accumulation.

Impaired healing response of periodontal furcation defects following flap debridement surgery in smokers. A controlled clinical trial.

OBJECTIVES: The purpose of the present parallel-design, controlled clinical trial was to evaluate the treatment outcome of periodontal furcation defects following flap debridement surgery (FDS) procedure in cigarette smokers compared to non-smokers. MATERIALS AND METHODS: After initial therapy, 31 systemically healthy subjects with moderate to advanced periodontitis, who presented at least one Class I or II molar furcation defect, were selected. Nineteen patients (mean age: 40.3 years, 15 males) were smokers (>or=10 cigarettes/day) and 12 patients (mean age: 44.8 years, 3 males) were non-smokers. Full-mouth plaque score (FMPS) and full-mouth bleeding score (FMBS), probing pocket depth (PPD), vertical clinical attachment level (v-CAL), and horizontal clinical attachment level (h-CAL) were assessed immediately before and 6 months following surgery. RESULTS: Overall, statistically significant v-CAL gain was observed in smokers (1.0 +/- 1.3 mm) and non-smokers (1.3+/-1.1 mm), the difference between groups being statistically significant (p=0.0003). In proximal furcation defects, v-CAL gain amounted to 2.3+/-0.7 mm in non-smokers as compared to 1.0+/-1.1 mm in smokers (p=0.0013). At 6 months postsurgery, non-smokers presented a greater h-CAL gain (1.3+/-1.1 mm) than smokers (0.6+/-1.0 mm), with a statistically significant difference between groups (p=0.0089). This trend was confirmed in both facial/lingual (1.4+/-1.0 versus 0.8+/-0.8 mm) and proximal furcation defects (1.2+/-1.3 versus 0.5+/-1.2 mm). The proportion of Class II furcations showing improvement to postsurgery Class I was 27.6% in smokers and 38.5% in non-smokers. After 6 months, 3.4% of presurgery Class I furcation defects in smokers showed complete closure, as compared to 27.8% in non-smokers. CONCLUSIONS: The results of the present study indicated that (1) FDS produced clinically and statistically significant PPD reduction, v-CAL gain, and h-CAL gain in Class I/II molar furcation defects, and (2) cigarette smokers exhibited a less favorable healing outcome following surgery in terms of both v-CAL and h-CAL gain.

Evaluation of additional amine fluoride/stannous fluoride-containing mouthrinse during supportive therapy in patients with generalized aggressive periodontitis. A randomized, crossover, double-blind, controlled trial.

OBJECTIVES: The objective of the present randomized controlled trial was to evaluate the efficacy of a mouthrinse containing a combination of AmF/SnF2 in controlling supragingival plaque accumulation and gingival inflammation during a 12-week period in patients affected by generalized aggressive periodontitis (GAP). METHODS: Eighteen subjects, six males and 12 females, mean age: 32.2 years, were evaluated. One-half of the patients was either prescribed an AmF/SnF2-containing mouthrinse (test mouthrinse) or a control mouthrinse in addition to mechanical plaque control for 12 weeks. After a 2-week wash-out period, the patients received the alternative mouthrinse. Before and after treatment plaque index (PlI), gingival index (GI), angulated bleeding index (AngBI), tooth stain (GMSI), and tongue stain were recorded. RESULTS: Test mouthrinse resulted in a statistically significant decrease in PlI (p = 0.029) and GI (p = 0.017). After treatment, PlI was significantly lower in test compared to control mouthrinse (p = 0.027). GMSI significantly increased post-treatment for both mouthrinse regimens (p < 0.001), a significantly higher score being observed for the test compared to control mouthrinse (p = 0.002). CONCLUSIONS: The 12-week use of a AmF/SnF2-containing mouthrinse as an adjunct to conventional mechanical oral hygiene procedures in GAP patients was effective in controlling the amount of supragingival plaque deposits.