Periodontal therapy for primary or secondary prevention of cardiovascular disease in people with periodontitis.

BACKGROUND: There may be an association between periodontitis and cardiovascular disease (CVD); however, the evidence so far has been uncertain about whether periodontal therapy can help prevent CVD in people diagnosed with chronic periodontitis. This is the second update of a review originally published in 2014, and first updated in 2017. Although there is a new multidimensional staging and grading system for periodontitis, we have retained the label 'chronic periodontitis' in this version of the review since available studies are based on the previous classification system. OBJECTIVES: To investigate the effects of periodontal therapy for primary or secondary prevention of CVD in people with chronic periodontitis. SEARCH METHODS: Cochrane Oral Health's Information Specialist searched the Cochrane Oral Health's Trials Register, CENTRAL, MEDLINE, Embase, and CINAHL, two trials registries, and the grey literature to September 2019. We placed no restrictions on the language or date of publication. We also searched the Chinese BioMedical Literature Database, the China National Knowledge Infrastructure, the VIP database, and Sciencepaper Online to August 2019. SELECTION CRITERIA: We included randomised controlled trials (RCTs) that compared active periodontal therapy to no periodontal treatment or a different periodontal treatment. We included studies of participants with a diagnosis of chronic periodontitis, either with CVD (secondary prevention studies) or without CVD (primary prevention studies). DATA COLLECTION AND ANALYSIS: Two review authors carried out the study identification, data extraction, and 'Risk of bias' assessment independently and in duplicate. They resolved any discrepancies by discussion, or with a third review author. We adopted a formal pilot-tested data extraction form, and used the Cochrane tool to assess the risk of bias in the studies. We used GRADE criteria to assess the certainty of the evidence. MAIN RESULTS: We included two RCTs in the review. One study focused on the primary prevention of CVD, and the other addressed secondary prevention. We evaluated both as being at high risk of bias. Our primary outcomes of interest were death (all-cause and CVD-related) and all cardiovascular events, measured at one-year follow-up or longer. For primary prevention of CVD in participants with periodontitis and metabolic syndrome, one study (165 participants) provided very low-certainty evidence. There was only one death in the study; we were unable to determine whether scaling and root planning plus amoxicillin and metronidazole could reduce incidence of all-cause death (Peto odds ratio (OR) 7.48, 95% confidence interval (CI) 0.15 to 376.98), or all CVD-related death (Peto OR 7.48, 95% CI 0.15 to 376.98). We could not exclude the possibility that scaling and root planning plus amoxicillin and metronidazole could increase cardiovascular events (Peto OR 7.77, 95% CI 1.07 to 56.1) compared with supragingival scaling measured at 12-month follow-up. For secondary prevention of CVD, one pilot study randomised 303 participants to receive scaling and root planning plus oral hygiene instruction (periodontal treatment) or oral hygiene instruction plus a copy of radiographs and recommendation to follow-up with a dentist (community care). As cardiovascular events had been measured for different time periods of between 6 and 25 months, and only 37 participants were available with at least one-year follow-up, we did not consider the data to be sufficiently robust for inclusion in this review. The study did not evaluate all-cause death and all CVD-related death. We are unable to draw any conclusions about the effects of periodontal therapy on secondary prevention of CVD. AUTHORS' CONCLUSIONS: For primary prevention of cardiovascular disease (CVD) in people diagnosed with periodontitis and metabolic syndrome, very low-certainty evidence was inconclusive about the effects of scaling and root planning plus antibiotics compared to supragingival scaling. There is no reliable evidence available regarding secondary prevention of CVD in people diagnosed with chronic periodontitis and CVD. Further trials are needed to reach conclusions about whether treatment for periodontal disease can help prevent occurrence or recurrence of CVD.

The combined and individual impact of diabetes and smoking on key subgingival periodontal pathogens in patients with chronic periodontitis.

BACKGROUND AND OBJECTIVE: Comprehension of the similarities and differences in the composition of the subgingival microbiota of patients with diabetes mellitus (DM), smokers or smokers with DM is an important step in developing therapies specific for these groups at risk for periodontitis. Therefore, the aim of this study was to compare the combined and individual effects of DM and smoking on the levels and prevalence of key subgingival periodontal pathogens in patients with chronic periodontitis. MATERIAL AND METHODS: One hundred patients with generalized chronic periodontitis were allocated into one of the following groups: DM (n = 25, non-smokers with type 2 DM); S (n = 25, non-diabetic smokers); SDM (n = 25, smokers with type 2 DM); and control (n = 25, non-diabetic non-smokers). Two subgingival biofilm samples from healthy sites (probing depth and clinical attachment level ≤3 mm and no bleeding) and 2 from diseased sites (probing depth and clinical attachment level ≥5 mm and bleeding on probing) were analyzed by quantitative polymerase chain reaction for Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Eubacterium nodatum, Parvimonas micra, Fusobacterium nucleatum ssp. and Prevotella intermedia. RESULTS: There were no differences among groups in the mean counts of the bacterial species studied, considering all sampled sites (healthy plus diseased sites). There were also no differences among groups regarding the prevalence of any bacteria species in healthy and diseased sites (P > .05). The mean P. micra count was significantly higher in the healthy sites of both smoking groups, than in those of the control group (P < .05). CONCLUSION: The subgingival levels and prevalence of the bacterial species studied are not significantly different in subjects with chronic periodontitis presenting DM, smokers or smokers with DM. In addition, DM and smoking, jointly and individually, do not considerably affect the subgingival levels of target periodontal pathogens in patients with chronic periodontitis.

What exactly distinguishes aggressive from chronic periodontitis: is it mainly a difference in the degree of bacterial invasiveness?

At the International Workshop for Classification of Periodontal Diseases and Conditions in 1999, the classification of aggressive and chronic periodontitis that is presently used was introduced. A literature review of papers published in 2015 and having aggressive periodontitis in the title revealed that most studies use this terminology but it is questionable whether all established criteria were really applied correctly. Review of the literature showed no qualitative differences between aggressive and chronic periodontitis regarding bacterial and viral aspects. It is also unlikely that that there are major immunologic differences between aggressive and chronic periodontitis. Neutrophil function can be compromised in both conditions but may be more genetically related in aggressive periodontitis and be associated more with lifestyle factors in chronic periodontitis. In general, genetics plays a more important role in aggressive periodontitis than in chronic periodontitis. It is likely that periodontitis progresses by recurrent acute episodes during which invasion of bacteria into the connective tissue may occur. Two cases are presented for which invasive periodontitis is treated with systemic antibiotics, showing remarkable periodontal healing in terms of probing attachment gain, as well as radiographic bone gain. Periodontitis in an active state with bacterial invasion is probably accompanied with a significant increase in subgingival temperature. It is hypothesized that elevated subgingival temperature may help to distinguish between bacterial and nonbacterial invasive periodontitis. Scaling and root planing during a burst of disease activity may result in removal of connective tissue fiber attachment and down-growth of epithelium, thereby preventing the reattachment of connective tissue. Because the burst of disease is accompanied by an increase of temperature, assessment of the temperature may help in deciding whether or not to prescribe systemic antibiotics. When the use of systemic antibiotics is indicated, the antibiotic therapy may help to maintain the connective tissue attachment at the most possible coronal level. The above implies that the ability to diagnose bacterial invasive periodontitis is quite important, and future research is needed to determine if assessment of subgingival temperature may help in diagnosing invasive periodontitis. In addition, it is suggested that future classification systems of periodontitis include the item of bacterial invasive periodontitis.

A root canal filling per se does not have a significant negative effect on the marginal periodontium.

AIM: To evaluate the periodontal status of single-rooted endodontically treated teeth (ET), correcting for patient- and tooth-related factors. METHODS: Clinical parameters (BoP,PD,CAL) of 240 ET and 240 contralateral vital teeth (VT), before and after non-surgical periodontal treatment, were extracted retrospectively from the journals of 175 patients. Possible patient-related (age, gender, smoking status) and tooth-related (interproximal restoration, root canal filling's extent, post, tooth type) confounders were tested. RESULTS: At baseline, frequency of BoP at an interproximal site at ET versus VT was 70.4% versus 65.0%, respectively. The frequency of teeth with interproximal PD ≥ 5 mm and CAL ≥ 5 mm was 47.9% versus 42.9% and 54.6% versus 49.6% at ET and VT, respectively. Interproximal PD and CAL at ET versus VT were 3.86 versus 3.61 mm and 4.11 versus 3.95 mm. After correcting for tooth-related factors, no significant differences were observed between ET and VT. An improper restoration had a significant (p < 0.001) negative effect on BoP [OR 3.49 (95%CI: 1.95-6.27)], PD [36.81% (95%CI: 18.52-57.92)] and CAL [27.01% (95%CI: 12.67-43.18)]. No significant differences between ET and VT were observed regarding clinical outcome of non-surgical periodontal therapy. CONCLUSIONS: Presence of a root canal filling per se does not have a significant negative influence on the marginal periodontium, when correcting for the quality of the interproximal restoration.

Differential expression of Toll-like receptor 4 in healthy and diseased human gingiva.

BACKGROUND AND OBJECTIVE: Lipopolysaccharide (LPS)-mediated signaling in host cells involves Toll-like receptor 4 (TLR4) accessory molecules, including LPS-binding protein (LBP), cluster of differentiation 14 (CD14) and lymphocyte antigen 96 (MD-2). However, expression of these innate defense molecules in various compartments of the human periodontium is unclear. The aim of this study was to investigate the expression profile of TLR4 in human gingiva. MATERIAL AND METHODS: Human gingival biopsies were collected from healthy gingival or chronic periodontitis tissue. Primary gingival keratinocytes and fibroblasts were cultured. Immunohistochemical analysis for TLR4 was performed. Transcripts of TLR4, MD-2, CD14 and LBP, and their protein products, were examined using RT-PCR, immunoprecipitation and immunoblotting. The interactions between these molecules in keratinocytes and fibroblasts were investigated by co-immunoprecipitation. RESULTS: TLR4 immunoreactivity was found in healthy gingival epithelium and periodontitis tissue, and appeared to be lower in junctional epithelium ( p ≤ 0.01). Fibroblasts and inflammatory cells stained more strongly for TLR4 in diseased periodontal tissues (p < 0.001). Three TLR4 splicing variants, two MD-2 splicing variants and one CD14 mRNA were expressed by gingival keratinocytes and fibroblasts. Expression of TLR4, CD14 and MD-2 proteins was detected in keratinocytes and fibroblasts in vitro. TLR4 protein from gingival keratinocytes and fibroblasts could be co-immunoprecipitated with CD14 or MD-2, suggesting an association between the related molecules in vivo. LBP transcript was detected in gingival biopsies, but not in primary cultures of gingival keratinocytes or fibroblasts. CONCLUSION: TLR4, CD14 and MD-2, but not LBP, are expressed in human gingival keratinocytes and fibroblasts. The TLR4 expression level in the junctional epithelium appeared to be lowest within the periodontal epithelial barrier.

Evaluation of periodontitis in hospital outpatients with major depressive disorder.

BACKGROUND AND OBJECTIVE: Major depressive disorder (MDD) has been associated with alterations in the neuroendocrine system and immune function and may be associated with an increased susceptibility to cardiovascular disease, cancer and autoimmune/inflammatory disease. This study was conducted to investigate the relationship between periodontitis and MDD in a convenience sample of hospital outpatients. MATERIAL AND METHODS: The sample consisted of 72 physically healthy subjects (36 outpatients with MDD and 36 age-matched controls [± 3 years]). Patients with bipolar disorder, eating disorders and psychotic disorders were excluded. Probing pocket depth and clinical attachment level were recorded at six sites per tooth. Depression was assessed by means of Structured Clinical Interview for DSM-IV. RESULTS: Extent of clinical attachment level and probing pocket depth were not different between controls and subjects with depression for the following thresholds: ≥ 3 mm (Mann-Whitney, p = 0.927 and 0.756); ≥ 4 mm (Mann-Whitney, p = 0.656 and 0.373); ≥ 5 mm (Mann-Whitney, p = 0.518 and 0.870);, and ≥ 6 mm (Mann-Whitney, p = 0.994 and 0.879). Depression parameters were not associated with clinical attachment level ≥ 5 mm in this sample. Smoking was associated with loss of attachment ≥ 5 mm in the multivariable logistic regression model (odds ratio = 6.99, 95% confidence interval = 2.00-24.43). CONCLUSIONS: In this sample, periodontal clinical parameters were not different between patients with MDD and control subjects. There was no association between depression and periodontitis.

One-stage full-mouth disinfection combined with a periodontal dressing: a randomized controlled clinical trial.

AIM: To compare the clinical benefit of a periodontal dressing applied after a one-stage full-mouth disinfection (OSFMD) in patients with chronic periodontitis up to 3 months after therapy. MATERIAL AND METHODS: This randomized, controlled split-mouth study included 24 patients. After OSFMD, a test and a control side were selected by means of a computer-generated randomization list. Test sides received a periodontal dressing (Coepak(®) ) for 7 days and the control sides received no periodontal dressing. After 7 days the periodontal dressing was removed and the pain experience was recorded. After 3 months, the clinical periodontal parameters were recorded. RESULTS: The periodontal dressing group showed a significant (p < 0.05) additional pocket depth reduction and additional clinical attachment gain for the moderate pockets of single- and multi-rooted teeth compared with the control group. A significant (p < 0.05) lower percentage of sites with probing pocket depth ≥5 mm were shown for the periodontal dressing group compared with the control group (2.7 ± 16.3% versus 4.8 ± 21.4%). The pain intensity was significantly reduced when using a periodontal dressing (5.13 ± 0.89 versus 3.42 ± 1.27). CONCLUSION: The use of a periodontal dressing for 7 days after a OSFMD offers an additional short-term clinical improvement and lowers the pain intensity.

Comparing clinical attachment level and pocket depth for predicting periodontal disease progression in healthy sites of patients with chronic periodontitis using multi-state Markov models.

AIM: To understand degeneration of healthy sites and identify factors associated with disease progression in patients with chronic periodontitis. MATERIAL AND METHODS: Data on healthy sites from 163 American and Swedish subjects were analysed using two-three-state (health, gingivitis, chronic periodontitis) Markov models based on bleeding on probing (BOP), and either clinical attachment level (CAL) + BOP or pocket depth (PD) + BOP. RESULTS: In 2 years, 10% (CAL + BOP) and 3% (PD + BOP) of healthy sites developed chronic periodontitis. On average, healthy sites remained healthy for 32 months before transiting in both models. Most transitions (87-97%) from health were to the gingivitis state. The expected duration of the gingivitis lesion was 4-5 months and sites recovered with a high probability (96-98%). Disease severity as measured by number of sites with CAL/PD > 4 mm at baseline and smoking, were associated with fast progression from health to chronic periodontitis within 6 months as were gingival redness in the PD + BOP model only. With age, the rate of disease progression to gingivitis decreased. CONCLUSION: Transition probabilities for gingivitis and chronic periodontitis were higher with CAL + BOP than with PD + BOP. Smoking and disease severity were significant predictors for fast progression.

Levels of HIV-1 in subgingival biofilm of HIV-infected patients.

AIM: The aims of the current study were to compare the levels of HIV-1 in the subgingival biofilm (SHVL) between detectable and undetectable plasmatic HIV-1 viral load (PHVL) in HIV-infected patients as well as to determine the association of SHVL with PHVL and clinical periodontal parameters. MATERIAL AND METHODS: Forty-one HIV-infected individuals were divided into two groups: detectable (21) and undetectable (20) PHVL. Subgingival biofilm samples were obtained for detection and quantification of HIV-1 by real-time RT-PCR. To estimate the effect of co-variables on the outcome undetectable SHVL, the Generalized Estimation Equation (GEE) was employed. RESULTS: Detectable SHVL was observed only in the detectable PHVL group and the detection of the HIV-1 was observed in 40% of these individuals. In the bivariate analysis between co-variables from the individual level and the outcome SHVL, significant difference was observed only for the CD4+ T lymphocytes levels (p = 0.017). The multiple logistic model demonstrated that only CD4+ T lymphocytes levels had a significant effect on the outcome undetectable SHVL [OR 8.85 (CI 3.6-9.2), p = 0.002]. CONCLUSION: HIV-1 can be detected and quantified in the subgingival biofilm of HIV-infected individuals, but these findings are not associated with PHVL and periodontal clinical parameters.

Is gingival bleeding a symptom of patients with type 1 von Willebrand disease? A case-control study.

BACKGROUND: Von Willebrand disease (VWD) is the most common inherent bleeding disorder resulting in prolonged bleeding time. Gingival bleeding is a frequently reported symptom of VWD. However, gingival bleeding is also known as a leading symptom of plaque-induced gingivitis and untreated periodontal disease. Gingival bleeding in VWD patients (VWD) may be triggered by gingival inflammation and not a genuine symptom. Thus, this study evaluated whether type 1 VWD determines an increased susceptibility to gingival bleeding in response to the oral biofilm. METHODS: Fifty cases and 40 controls were examined haematologically (VWF antigen, VWF Ristocetin cofactor, factor VIII activity) and periodontally [Gingival Bleeding Index (GBI), bleeding on probing (BOP), Plaque Control Record (PCR), periodontal inflamed surface area (PISA), vertical probing attachment level]. RESULTS: GBI was significantly higher in controls (12.2%) than in VWD (10%). The study failed to find a significant difference regarding BOP between VWD (17%) and controls (17.2%). Multiple regressions identified PCR and PISA to be associated with GBI and BOP. VWD was negatively associated with GBI. Smoking and number of remaining teeth was negatively associated with BOP. CONCLUSION: VWD is not associated with a more pronounced inflammatory response to the oral biofilm in terms of GBI and BOP.

IPLA2 mRNA expression by human neutrophils in type 2 diabetes and chronic periodontitis.

Type 2 diabetes mellitus (T2D) is becoming increasingly prevalent worldwide and complications of T2D cause significant systemic and dental morbidity in the susceptible individual. Although T2D has been linked as a significant risk factor for chronic periodontitis (CP), molecular mechanisms explaining the pathogenesis and inflammatory impact of CP in T2D are lacking. iPLA2 is the calcium-independent form of phospholipase A2. In previous studies, we demonstrated that iPLA2 enzyme activity is altered in T2D. The purpose of this study was to elucidate the level of the iPLA2 abnormality in T2D by measuring messenger RNA levels in T2D-associated CP. A total of 53 healthy and T2D subjects with CP were recruited for this study. The clinical periodontal exam included probing pocket depth, clinical attachment levels and bleeding on probing. Peripheral venous blood was collected and neutrophils were isolated. Real time polymerase chain reaction was used to quantify iPLA2 mRNA in neutrophils from healthy controls and people with diabetes. Results revealed that the prevalence of moderate to severe CP was increased in people with T2D. The iPLA, mRNA levels in diabetics with different severity of CP were not significantly different compared to healthy controls; 1.07 vs 0.97 (mild CP), 1.07 vs 0.85 (moderate CP) and 1.07 vs 1.05 (severe CP). Collectively, the data suggest that levels of iPLA2 mRNA in T2D are not different than in health and are not directly influenced by periodontal disease status. The impact of inflammation on iPLA2 regulation is at the level of activation of the enzyme rather than expression at the mRNA level.

Comparisons between two biochemical markers in evaluating periodontal disease severity: a cross-sectional study.

BACKGROUND: The purpose of this study was to compare two biochemical markers, which have been previously used to determine the degrees of alveolar bone destruction, in evaluating periodontal disease severity. METHODS: The WF6 epitope of chondroitin sulfate (CS) and the alkaline phosphatase (ALP) levels were determined in gingival crevicular fluid (GCF) samples collected from patients with various degrees of disease severity, including ten patients with gingivitis (50 gingivitis sites) and 33 patients with chronic periodontitis (including gingivitis, slight, moderate, and severe periodontitis sites; n = 50 each), as well as from ten healthy volunteers (50 healthy sites) by Periopaper strips. The levels of CS and ALP were measured by an ELISA and a fluorometric assay, respectively. RESULTS: The results demonstrated low levels of CS and ALP in non-destructive and slightly destructive periodontitis sites, whereas significantly high levels of these two biomolecules were shown in moderately and severely destructive sites (p < 0.05). Although a significant difference in CS levels was found between moderate and severe periodontitis sites, no difference in ALP levels was found. Stronger correlations were found between CS levels and periodontal parameters, including probing depth, loss of clinical attachment levels, gingival index and plaque index, than between ALP levels and these parameters. CONCLUSIONS: It is suggested that the CS level is a better diagnostic marker than the ALP level for evaluating distinct severity of chronic periodontitis.

Association of subgingival colonization of Candida albicans and other yeasts with severity of chronic periodontitis.

BACKGROUND AND OBJECTIVE: The aim of this study is to analyze the relationship between the subgingival colonization by Candida albicans and other yeasts with the severity of chronic periodontitis (CP). MATERIAL AND METHODS: After sample size calculation, 40 patients with CP and 20 healthy subjects (HS) were included in the study. Cases of slight-moderate (MCP, n = 23) and severe CP (SCP, n = 17) were defined according to the Centers for Disease Control/American Association of Periodontology classification. Subgingival samples were acquired using sterile paper-points from the sulcus or the deepest periodontal pocket of each healthy and subject with CP, respectively, and were cultured aerobically on three selective media. Yeast colonies that grew on the surface of plates were later identified by biochemical reactions. Statistical tests were used to analyze the association between subgingival yeast colonization (number of yeast-positive individuals and colony forming units (CFU) per subject) and periodontal disease status, considering statistical significance when P < 0.05. RESULTS: Although several yeast species were found (C. parapisilosis, Rhodotorula sp., C. dubliniensis and C. tropicalis), only C. albicans was present in all the patients with yeast-positive CP. Twelve patients (30%) with CP presented yeasts in the subgingival biofilm while only three patients (15%) in the HS group were positive for these microorganisms. No statistical difference was found between the CP and HS groups (P = 0.084). However, when the CP group was divided on the basis of severity, statistical differences were observed between the SCP and MCP groups (47% vs. 17%, P = 0.043), and between the SCP and HS groups (47% vs. 15%, P = 0.033). No statistical difference was observed between the MCP and HS groups (17% vs. 15%, P = 0.832). High densities of yeasts were found only in patients with MCP and SCP (mean and range 61.25 (0-100) CFU/plate and mean and range 51 (0-101) CFU/plate, respectively). CONCLUSION: In this group of patients, subgingival colonization of some yeasts, especially C. albicans, was associated with the severity of CP.

Subgingival biodiversity in subjects with uncontrolled type-2 diabetes and chronic periodontitis.

BACKGROUND AND OBJECTIVE: There is a bidirectional relationship between periodontal disease and type-2 diabetes mellitus (DM). Inflammatory mediators may negatively affect glycemic control, and increased glucose levels and resultant glycation end-products may alter the host response against bacterial infection. However, no agreement has been reached regarding the effect of DM on periodontal subgingival microbiota. Therefore, the purpose of the present study was to compare the subgingival biodiversity in deep periodontal pockets of subjects with chronic periodontitis and either uncontrolled type-2 diabetes or no diabetes using 16S rRNA gene cloning and sequencing. MATERIAL AND METHODS: Twelve subjects with uncontrolled type-2 diabetes (glycated hemoglobin > 8%) and eleven nondiabetic subjects presenting severe and generalized chronic periodontitis were selected. Subgingival biofilm from periodontal pockets > 5 mm were assessed using the 16S rRNA gene cloning and sequencing technique. RESULTS: Significant differences were observed in subgingival microbiota between diabetic and nondiabetic subjects. Diabetic subjects presented higher percentages of total clones of TM7, Aggregatibacter, Neisseria, Gemella, Eikenella, Selenomonas, Actinomyces, Capnocytophaga, Fusobacterium, Veillonella and Streptococcus genera, and lower percentages of Porphyromonas, Filifactor, Eubacterium, Synergistetes, Tannerella and Treponema genera than nondiabetic individuals (p < 0.05). Moreover, some phylotypes, such as Fusobacterium nucleatum, Veillonella parvula, V. dispar and Eikenella corrodens were detected significantly more often in diabetic subjects than in nondiabetic subjects (p < 0.05). CONCLUSION: Subjects with uncontrolled type-2 diabetes and chronic periodontitis presented significant dissimilarities in subgingival biodiversity compared with nondiabetic subjects.

The effects of stress on periodontal treatment: a longitudinal investigation using clinical and biological markers.

AIM: To investigate the effects of psychosocial stress on the outcome of non-surgical periodontal treatment (NPT). METHODS: Patients were categorized as stressed or unstressed, and the degree of stress was measured. One deep bleeding and one deep non-bleeding site ≥6 mm were selected in each patient for detailed investigation, and the clinical parameters were recorded before and at 6 months after NPT. Elastase and C-terminal teleopeptide of type I collagen (ICTP) were measured in gingival crevicular fluid (GCF) samples at both intervals. RESULTS: The baseline, clinical parameters and biological markers were similar in both stressed and unstressed groups, other than for GCF elastase levels, which were significantly higher in the stressed group of patients (p < 0.05). The effect of stress on the changes for clinical measurements and elastase levels in GCF was statistically significant for deep bleeding sites, with the response to treatment being poorer in the stressed group. The effects of smoking and the degree of stress were not statistically significant for any of the clinical or biological parameters (p > 0.05). CONCLUSIONS: Patients under psychosocial stress had a poorer outcome following NPT. The assessment of psychosocial stress may be valuable in the holistic management of periodontal disease.

Association between obesity and chronic periodontitis: a cross-sectional study.

AIM: Chronic periodontitis is multifactorial and numerous risk factors have been identified to contribute in the disease progression. Current study aimed to conduct a cross-sectional study in a population of patients with cardiovascular diseases in order to correlate the association between obesity [body mass index (BMI) and waist circumference (WC)] and periodontal disease parameters. MATERIALS AND METHODS: The study was of a cross-sectional design and a total of 201 patients were examined after obtaining their informed consent. Subjects who had a history of cardiovascular diseases and under treatment were included in the study. Two indicators of obesity were used: BMI and WC. The following periodontal parameters were assessed: Probing depth, clinical attachment level. The oral hygiene status of the subjects was assessed by the oral hygiene index (OHI, simplified) given by John C Greene and Jack R Vermillion. The influence of the BMI and other confounding variables on periodontitis severity was assessed by multivariate logistic regression analysis. Data were analyzed using SPSS. RESULTS: Significant association was seen with low density lipoproteins (LDL) and severity of periodontitis (p < 0.005), triglyceride levels (TGL) and severity of periodontitis (p < 0.005), cholesterol and severity of periodontitis (p < 0.005), BMI and severity of periodontitis (p < 0.001), OHI and severity of periodontitis (p < 0.001). Significant association was seen with smoking and severity of periodontitis (p < 0.005), BMI and severity of periodontitis (p < 0.001), WC and severity of periodontitis (p < 0.001), cholesterol and severity of periodontitis (p < 0.001), OHI and severity of periodontitis (p < 0.001). CONCLUSION: Obesity has been implicated as a risk factor for several conditions including cardiovascular disease, diabetes, etc. In our study the relation between measures of overall and abdominal obesity (BMI and WC) and periodontal disease showed significant association in the multivariate logistic regression analysis independent of other confounding factors. CLINICAL SIGNIFICANCE: Obesity can act as a significant risk factor in progression of periodontitis.

Outcomes of non-surgical periodontal treatment by dental hygienists in training: impact of site- and patient-level factors.

OBJECTIVES: To investigate the site- and patient-level factors that impact on the response to non-surgical periodontal therapy in patients with chronic periodontitis. METHODS: A retrospective evaluation of clinical outcomes following non-surgical periodontal therapy delivered by dental hygienists in training was undertaken. Case notes from 195 patients with chronic periodontitis were reviewed and clinical data pre- and post-treatment abstracted. Patients were categorized as 'responders' or 'non-responders' according to defined outcome criteria, and the relationship between clinical and demographic variables and treatment outcomes was assessed. RESULTS: Overall, there was a good response to the periodontal treatment. At deep sites (those with pretreatment probing depth ≥5 mm), the mean probing depth reduction was 1.6 ± 0.9 mm. Seventy-one (36%) patients were classified as non-responders (indicating that at least 30% of their deep sites did not improve by at least 2 mm following treatment). The non-responding group contained a significantly greater proportion of smokers (28%) than the responding group (16%). Plaque scores did not differ significantly between responders or non-responders either pre- or post-treatment. Regression analyses indicated that smoking status (odds ratio, OR: 2.04), mean pretreatment probing depth (OR: 1.49) and percentage of deep sites ≥5 mm at pretreatment (OR: 1.02) were significantly associated with response to treatment. CONCLUSION: This study supports the benefits of non-surgical therapy in the treatment of chronic periodontitis by dental hygienists in training. Better responses to treatment tend to be observed in non-smokers and in those with less advanced periodontitis at baseline.

Full-mouth profile of active MMP-8 in periodontitis patients.

BACKGROUND AND OBJECTIVE: MMP-8 in gingival crevicular fluid is considered as a protease with high destructive potential because of its ability to degrade collagen in periodontitis-affected patients. The aim of this study was to investigate whether there was a relationship between clinical diagnostic parameters and the concentration of active MMP-8 (aMMP-8) in gingival crevicular fluid in a site-level full-mouth analysis. Based on these data, the prognostic value of aMMP-8 levels in relation to pocket depth may be evaluated. MATERIAL AND METHODS: Clinical measurements of pocket depth, bleeding on probing (BOP), plaque index (PlI) and gingival index (GI), as well as samples of gingival crevicular fluid, were obtained from four sites of each tooth of nine healthy female patients with chronic generalized periodontitis. The aMMP-8 concentration in gingival crevicular fluid was quantified by ELISA using specific monoclonal antibodies. Multiple linear regression models for the single measures of aMMP-8 and pocket depth were calculated with GI and BOP as additional variables. RESULTS: Between 92 and 112 recordings were obtained for each parameter in each patient. Mean values of between 31.5 and 88.8% were calculated for pocket depths of ≥ 4 mm. Mean pocket depths ranged from 3.11 to 4.73 mm, the mean BOP values ranged from 34.0 to 96.7% and the mean full-mouth gingival crevicular fluid aMMP-8 concentration ranged from 3.2 to 23.7 ng/mL. CONCLUSION: In this sample of female periodontitis patients, a broad range of intra-individual and interindividual aMMP-8 values was found. Although the explained variance was rather weak, a statistically significant relationship between aMMP-8 and pocket depth was proven.

Association of the FcγRIIB-nt645+25A/G polymorphism with the expression level of the FcγRIIb receptor, the antibody response to Porphyromonas gingivalis and the severity of periodontitis.

BACKGROUND AND OBJECTIVE: Human FcγRIIb is an immunoglobulin G (IgG) receptor that inhibits the activation of B lymphocytes through cross-linking with the B-cell receptor via immune complexes. This function acts as a negative regulator of antibody production. Our previous studies have demonstrated the gene polymorphisms in FcγRIIb to be associated with periodontitis. In this study, we presented a polymorphism--FcγRIIB-nt645+25A/G (rs2125685)--in intron 4 and analyzed its functional relevance to periodontitis. We examined whether the FcγRIIB-nt645+25A/G polymorphism is associated with periodontal parameters, the IgG response to the periodontopathic bacterium Porphyromonas gingivalis and/or the expression level of FcγRIIb on peripheral B lymphocytes. MATERIAL AND METHODS: Thirty-two patients with chronic periodontitis were genotyped with nested PCR and by direct sequencing of genome DNA. The levels of serum IgG and of specific IgG subclasses for P. gingivalis sonicate and for the recombinant 40-kDa outer membrane protein (OMP) were determined. The expression levels of FcγRIIb on peripheral B lymphocytes from 19 healthy donors were measured by flow cytometry. RESULTS: Patients with the FcγRIIB-nt645+25AA genotype showed significantly higher mean clinical attachment levels compared to patients with the FcγRIIB-nt645+25GG genotype (p = 0.003) and a significantly lower IgG response to P. gingivalis sonicate and to the 40-kDa OMP. The expression levels of FcγRIIb protein on the cell surface in peripheral B lymphocytes were higher in healthy donors with the FcγRIIB-nt645+25AA genotype than in those with the FcγRIIB-nt645+25GG genotype (p = 0.03). CONCLUSION: The higher expression levels of FcγRIIb in subjects with the FcγRIIB-nt645+25AA genotype may induce a lower level of production of IgG against P. gingivalis and therefore more severe periodontitis.

The relationship between osteoporosis and periodontitis in women aged 45-70 years.

OBJECTIVE: To explore the possible relationship between the osteoporotic condition and the severity of periodontitis in women aged 45-70 years. MATERIALS AND METHODS: Ninety women with generalized chronic periodontitis, aged 45-70 years, were studied. Areal bone mineral density (BMDa) was assessed using standardized dual energy X-ray absorptiometry (normal: T-score ≥ -1, osteopenic: -2.5 ≤ T-score <-1, osteoporotic: T-score < -2.5). Gingival index (GI), bleeding on probing, clinical attachment loss (CAL), probing pocket depth and gingival recession (GR) were recorded. Periodontitis severity was represented by CAL. Menopausal condition and smoking were documented. RESULTS: Mean GI, bleeding on probing, CAL and GR were significantly greater for osteoporotic women than women with normal BMDa (P = 0.002, P = 0.01, P = 0.04, respectively). Osteopenic women and women with normal BMDa significantly differed in mean GI (P = 0.02). The associations found between osteoporotic women and women with normal BMDa and the associations found between osteopenic women and women with normal BMDa existed even after adjusting for smoking and menopausal status. CONCLUSION: Subjects with osteoporosis (OPR) presented with greater CAL than the subjects with normal BMDa, which suggests a greater severity of periodontitis. Subjects with OPR had greater GR than the subjects with normal BMDa. Subjects with osteopenia and subjects with normal BMDa did not differ in CAL, which might suggest that the early diagnosis of reduced BMDa, prior to the establishment of a significant negative impact on the periodontal tissues, might be important. Smoking and menopausal status did not alter these associations.