Association of oral health-related quality of life measures with aggressive and chronic periodontitis.

BACKGROUND AND OBJECTIVE: Evidence suggests that periodontitis has a negative effect on the quality of life of an individual, with increased impacts by greater disease severity. The aim of this study was to assess the association between quality of life and the presence of different severity and forms of periodontitis (aggressive and chronic), compared to a disease-free control group. MATERIALS AND METHODS: Four hundred and seventy one study participants were classified according to periodontal diagnosis using the 1999 Consensus Classification into chronic periodontitis (CP), aggressive periodontitis (AgP) and periodontally healthy. Oral health-related quality of life was assessed using the OHIP-14 questionnaire. Outcomes consisted of the prevalence of oral impacts reported occasionally, fairly often or very often (OFOVO) as well as fairly often or very often (FOVO), OHIP-14 total and domain scores. Logistic and linear regression analyses were carried out to test associations between periodontal diagnosis and quality of life outcomes, adjusted for smoking, age, ethnicity and body mass index. RESULTS: Over 90% of periodontitis patients reported at least one oral impact experienced occasionally, fairly often or very often (OFOVO) compared with 53.8% of periodontally healthy controls (P < .001). After adjustment for covariates, significant differences were found between the periodontitis groups and healthy controls for OHIP-14 outcome scores (P < .001) and across all of the OHIP-14 domains (P < .005). These differences were clinically meaningful as they were higher than the measurement errors. No significant differences were identified between AgP and CP in adjusted analysis when comparing OHIP-14 scores. CONCLUSION: Patients with periodontitis have worse quality of life than periodontally healthy individuals, with differences being clinically meaningful. AgP patients reported worse OHRQoL overall compared to CP patients, but these moderate and meaningful differences were explained through the adjustment process.

Tooth loss in aggressive periodontitis: Results 25 years after active periodontal therapy in a private practice.

AIM: To assess tooth loss in patients with aggressive periodontitis (AgP) 10-35 years after active periodontal therapy (APT) in a private practice and to detect possible factors influencing tooth loss. MATERIAL AND METHODS: In 100 patients with AgP, tooth loss was recorded over a median follow-up period of 25.5 years after APT, retrospectively. Patient- and tooth-level factors were assessed with a Cox frailty regression model. RESULTS: Of 2,380 teeth, 227 were lost during a median follow-up time of 25.5 years (2.3 ± 3.6 teeth/patient, range 0-17 teeth), resulting in a mean tooth loss rate of 0.09 teeth/patient/year. At patient-level, statistically significant factors for tooth loss were smoking (p = .039) and the baseline diagnosis generalized AgP (p < .001). Influencing factors at tooth-level were location in the maxilla (p = .003), baseline bone loss (p < .001), molars (p < .001) and premolars (p < .001) as well as abutment teeth (p = .009). CONCLUSION: Tooth loss occurred rarely in patients with AgP treated in a private practice over a long-time period. Annual tooth loss rates are comparable with those described in university settings. Smoking, generalized form of AgP, location/type of tooth, baseline bone loss and abutment status could be detected as factors impacting upon tooth loss.

Vitamin D deficiency in patients with aggressive periodontitis.

OBJECTIVES: Vitamin D deficiency is a frequent health problem worldwide, especially as fewer people spend much time in the sun. Vitamin D deficiency is linked to several infectious and inflammatory conditions, including periodontal disease. However, its role in aggressive periodontitis (AgP) has not been well studied. We evaluated the association between vitamin D concentration and periodontal disease, both AgP and chronic (CP) periodontitis. METHOD AND MATERIALS: Forty-seven AgP 55 CP and 27 control subjects participated. All patients were tested for serum vitamin D concentration (25(OH)D), parathyroid hormone, and serum bone-related biomarkers (alkaline phosphatases, calcium, and phosphorus) regulated by vitamin D. RESULTS: The patients with AgP had lower serum 25(OH)D concentration (11.22 ± 4.8 ng/ml) than controls (16.9 ± 6.4 ng/ml) and patients with CP (16.13 ± 8.3 ng/ml; overall p value 0.0002). These associations remained significant after adjustment for age and gender (p = 0.002). No significant differences were observed in any bone-related biomarker among the three groups, and no association was observed with periodontal disease indices. CONCLUSIONS: Our results suggest that vitamin D deficiency may be a potential risk factor for AgP. Given the high prevalence of vitamin D deficiency in AgP patients, routine screening for vitamin D status may be advisable in these subjects.

Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

OBJECTIVE: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP). SUBJECTS AND METHODS: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR. RESULTS: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29. CONCLUSION: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals.

Orthodontic treatment in patients with aggressive periodontitis.

INTRODUCTION: Aggressive periodontitis (AP) is a condition that promotes breakdown of the periodontal tissues in a short time. In severe cases, pathologic migration of teeth and tooth loss can occur, producing esthetic and functional problems for the patient. Orthodontic treatment may be recommended to restore esthetics and masticatory function. We assessed the effects of orthodontic movement in the periodontal tissues of treated patients with AP. METHODS: Ten subjects (ages 25.0 ± 5.22 years) with AP received periodontal treatment followed by orthodontic treatment. Maintenance sessions were performed monthly under a strict dental biofilm control. They were compared with 10 periodontally healthy subjects (ages 22.9 ± 5.23 years) who received orthodontic treatment. Probing pocket depth, clinical attachment level, bleeding on probing, and dental plaque index were measured at baseline, after orthodontic treatment, and after 4 months. RESULTS: Statistical analysis showed improvement in all clinical parameters between baseline and 4 months after orthodontic treatment: probing pocket depth (0.29 mm), clinical attachment level (0.38 mm), bleeding on probing (4.0%), and dental plaque index (11%). CONCLUSIONS: The periodontal parameters of the AP patients remained stable during orthodontic treatment under strict biofilm control.

Tooth loss in generalized aggressive periodontitis: Prognostic factors after 17 years of supportive periodontal treatment.

AIM: This retrospective longitudinal study assessed the risk of and prognostic factors for tooth loss in patients with generalized aggressive periodontitis (GAgP) after periodontal treatment in a university setting. METHODS: Fifty-seven patients (1,505 teeth) were examined before (T0) and after active periodontal therapy (APT, T1) as well as after 17.4 ± 4.8 [range: 9-28] years of supportive periodontal therapy (SPT, T2). Descriptive statistics and a Cox-proportional-hazards shared-frailty model were applied. RESULTS: Overall, 98 and 134 teeth were lost during APT and SPT, respectively, with 0.14 ± 0.18 teeth being lost per patient and year. During SPT, three patients (5%) lost ≥10 teeth, 14 (25%) lost 4-9 teeth, 40 lost 0-3 (70%) teeth, respectively. One-third (n = 19) of all patients lost no teeth. Mean PPD of the teeth surviving SPT was stable from T1 (3.5 ± 1.1 mm) to T2 (3.4 ± 1.1 mm). Nearly, 84% of all survived teeth showed stable or improved bone level at T2. Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III). CONCLUSION: Within the provided conservative treatment regimen, GAgP patients lost only few teeth.

Predictors of long-term outcomes in patients undergoing periodontal maintenance.

AIM: This retrospective study aimed to characterize the baseline status of patients following periodontal maintenance, analysing the association between the long-term outcome of these patients, smoking, bruxism, and the main clinical and radiographic variables. MATERIAL AND METHODS: A sample of 174 patients with moderate to severe periodontitis was refined into homogeneous subsamples according to smoking and bruxism and the rate of tooth loss due to periodontal disease (TLPD): 0, 1-2, and >2 teeth. The association and the distribution (χ² test) of the variables within the subsamples were analysed. RESULTS: Smoking and bruxism were significantly associated with higher TLPD rates. Vertical and circumferential bone defects (p < .0001), and abfractions (p < .0001) were associated with bruxism and particularly with bruxism and TLPD >2. Furcation defects (p = .0002), fewer radio-opaque subgingival calculus (χ² p < .0001), a lower mean Gingival index (χ² p = .027), and increased mean recessions >1.5 mm (χ² p = .0026) were associated with smoking and higher TLPD rates. The mean baseline mobility, abfractions, and recessions characterized two basic types of TLPD. CONCLUSIONS: Smoking, bruxism, and routine clinical and radiological parameters can be used to characterize the baseline status of patients with worse outcomes.

High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis.

Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola or Fusobacterium nucleatum There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease.

Outcomes of implant therapy in patients with a history of aggressive periodontitis. A systematic review and meta-analysis.

OBJECTIVE: To investigate the outcomes of implant therapy in partially dentate patients treated for aggressive periodontitis (GAgP) in comparison to periodontally healthy (HP) and patients treated for chronic periodontitis (CP) utilizing radiographic and clinical parameters. MATERIAL AND METHODS: An electronic search of databases, supplemented by hand searching, was conducted to identify relevant clinical studies. Sequential screenings at the title, abstract and full-text levels were performed independently and in duplicate. A random effects meta-analysis was conducted and bias corrected bootstrap 95 % confidence intervals were estimated for group comparisons. RESULTS: The search strategy revealed a total of 899 results. After title screening, abstract scanning, and full-text reading, seven articles fulfilled the inclusion criteria. The 3-year survival rate for CP and HP patients was 100 % while in GAgP subjects, the respective value was 97.98 %; this difference being statistically significant. The 3-year mean marginal bone loss (MBL) was 1.07 mm for the GAgP group, 0.47 mm for the CP group, and 0.69 mm for the HP group. A significant difference between the GAgP and CP groups was identified (p < 0.05). The weighted mean differences of MBL concerning the above groups were also calculated and examined for statistical significance in both 1 and 3 years. CONCLUSIONS: The 3-year survival rate and peri-implant marginal bone loss was found statistically significantly lower in GAgP subjects (SR 97.98 % vs 100 %) in comparison to HP and CP individuals. CLINICAL RELEVANCE: The outcome of implant therapy in terms of survival rate and marginal bone loss is considered very important for the clinician in decision making when placing implants in patients with a history of aggressive periodontitis.

[Clinical evaluation of periodontal-orthodontic treatment in patients with aggressive periodontitis and malocclusion].

OBJECTIVE: To evaluate the clinical effect and safety of periodontal-orthodontic treatment in patients with aggressive periodontitis (AgP) and malocclusion. METHODS: A retrospective analysis was conducted in 25 AgP patients, who had received periodontal-orthodontic treatment in Peking University School and Hospital of Stomatology. Clinical indexes, including probing depth (PD), bleeding index (BI) and percentage of sites with bleeding on probing (BOP%) were evaluated at three time points: Baseline (T0); active periodontal treatment finished and before orthodontic treatment (T1); and after orthodontic treatment (T2). Also changes of ratio of the residual alveolar bone height (RBH) and the occurrence of root resorption were evaluated by periapical radiographs. RESULTS: (1) Compared with T0, all the clinical parameters including PD, BI, BOP% and percentage of sites with PD>3 mm were significantly improved (P<0.001). (2) Significant difference was observed in the average RBH between T0 (68.37%±15.60% and T2 (70.27%±14.23%). RBH in upper incisors [(58.79%±16.71% at T0, 65.54% (55.74%, 78.13%) at T2], upper canines [77.62% (66.06%, 87.17%) at T0, 79.57% (69.75%, 86.52%) at T2] and upper molars [74.30% (61.69%, 84.45%) at T0, 76.76% (68.12%, 85.09%) at T2] showed significant increase (P<0.05). (3) After orthodontic treatment, varying degrees of root resorption occurred in (23.94%±13.45%) of teeth per capita, among which the lower and upper incisors showed the highest incidence (68.48% and 65.31% in homogeneous teeth, respectively). CONCLUSION: After active periodontal treatment, orthodontic treatment in AgP patients had not aggravated inflammation and alveolar bone resorption; root resorption occurred in two-thirds of incisors approximately.

Oro-dental characteristics of three siblings with Papillon-Lefevre syndrome.

Papillon-Lefevre syndrome (PLS) is a rare autosomal recessive disorder, showing oral and dermatological manifestations in the form of aggressive periodontitis, leading to the premature loss of both primary and permanent teeth at a very young age and palmar-plantar hyperkeratosis. It was first described by two French physicians, Papillon and Lefevre in 1924. Immunologic, genetic, or possible bacterial etiologies have been thought to account for etiopathogenesis of PLS. Severe gingival inflammation and periodontal destruction occurred after the eruption of primary teeth. This condition should warn the physicians and dentists as a one of the important sign for the diagnosis of PLS. There have been over 250 cases reported in literature about PLS, but a few of these were in the same family. This study presents oro-dental characteristics, dental treatments, and follow-up of three siblings (age of sisters are 13, 6, and 4 years) with PLS, which is rarely seen in the same family.

[CAUSES AND WAYS OF THE NECK PHLEGMON SPREADING ON MEDIASTINUM WITH A DESCENDING PURULENT MEDIASTINITIS OCCURRENCE].

Results of treatment in 2000-2016 yrs of 183 patients for the neck phlegmon were analyzed. In 60 (32.8%) of them a descending purulent mediastinitis (DPM) was diagnosed. The main causes of the DPM occurrence were tonsilogenic and odontogenous factors. Postoperative lethality in DPM have constituted 25%.

Adjunct Antimicrobial Therapy and Periodontal Surgery to Treat Generalized Aggressive Periodontitis: A Case Report.

Here we report a case of generalized aggressive periodontitis treated with periodontal therapy including adjunct antimicrobial therapy and periodontal surgery. The patient was a 22-year-old woman who presented with the chief complaint of gingival recession. Baseline examination revealed generalized plaque deposition and gingival inflammation. Thirty-nine percent of the sites had a probing depth (PD) of 4-6 mm and 2% a PD of ≥7 mm; 63% exhibited bleeding on probing (BOP). Radiographic examination revealed vertical bone loss in the molars and horizontal bone loss in other teeth. Microbiological examination of subgingival plaque revealed the presence of Aggregatibacter actinomycetemcomitans and Tannerella forsythia. Oral health-related quality of life was assessed as a measure of patient-reported outcome. Based on a clinical diagnosis of generalized aggressive periodontitis, initial periodontal therapy and adjunct antimicrobial therapy were implemented. After reducing inflammation and subgingival bacteria, open flap debridement was performed for teeth with a PD of ≥4 mm. Reevaluation showed no sites with a PD of ≥5 mm, a minimal level of BOP, and a marked reduction in the level of the targeted periodontal pathogens. The patient's oral health-related quality of life was slightly worsened during supportive periodontal therapy (SPT). Implementation of adjunct antimicrobial therapy targeting periodontal pathogens and subsequent periodontal surgery resulted in improvement in periodontal and microbiological parameters. This improvement has been adequately maintained over a 2-year period. However, additional care is necessary to further improve the patient's oral health-related quality of life during SPT.

Association of levels of antibodies against citrullinated cyclic peptides and citrullinated α-enolase in chronic and aggressive periodontitis as a risk factor of Rheumatoid arthritis: a case control study.

BACKGROUND: Periodontal disease could be a risk factor for rheumatoid arthritis (RA). It is assumed that the bacterial strain Porphyromonas gingivalis mediates citrullination of host peptides and thereby the generation of RA-associated autoantibodies in genetically predisposed individuals. For that reason non-RA individuals who suffered from generalized aggressive (GAgP, N = 51) and generalized chronic periodontitis (GChP, N = 50) were investigated regarding the occurrence of antibodies against citrullinated cyclic peptides (anti-CCP) and citrullinated α-enolase peptide-1 (anti-CEP-1) in comparison to non-RA non-periodontitis controls (N = 89). Furthermore, putative associations between infections with five periodontopathic bacteria or expression of certain human leucocyte antigens (HLA) to these autoantibodies were investigated. METHODS: The presence of anti-CCP and anti-CEP-1 in plasma samples was conducted with enzyme linked immunosorbent assay. Subgingival plaque specimens were taken from the deepest pocket of each quadrant and pooled. For detection of DNA of five periodontopathic bacteria PCR with sequence specific oligonucleotides was carried out. Low resolution HLA typing was carried out with PCR with sequence specific primers. Differences between patients and controls were assessed using Chi square test with Yates correction or Fisher`s exact test if the expected number n in one group was <5. RESULTS: Two patients with GAgP (3.9%), no patient with GChP and two controls (2.2%, pFisher = 0.662) were positive for anti-CEP-1 whereas no study participant was anti-CCP positive. Individuals with P. gingivalis were slightly more often anti-CEP-1 positive in comparison to individuals without P. gingivalis (3.2 vs. 1.1%, pFisher = 0.366). Carrier of HLA-DQB1*06 or the HLA combination DRB1*13; DRB3*; DQB1*06 were slightly more anti-CEP-1 positive (6.1 and 4.3%) than no carriers (0.7 and 0%, pFisher 0.053). CONCLUSIONS: GAgP and GChP and the presence of periodontopathic bacteria are not associated with an increased risk for occurrence of anti-CCP and anti-CEP-1 autoantibodies. The putative relationship between periodontitis and RA should be investigated in further studies.

Limited Evidence Suggests High Risk of Implant Failure Rates Among People With Generalized Aggressive Periodontitis.

ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION: Generalized aggressive periodontitis as a risk factor for dental implant failure: a systematic review and meta-analysis. Monje A, Alcoforado G, Padial-Molina M, Suarez F, Lin GH, Wang HL.J Periodontol 2014;85(10):1398-1407. REVIEWERS: Ahmed Yaseen Alqutaibi, BDS, MDSc, PhD(c), Radhwan saleh Algabri, BDS, MDSc, PhD(c) PURPOSE/QUESTION: In patients with dental implants, what are the differences in implant survival rate (SR), and marginal bone loss (MBL) between people with or without generalized aggressive periodontitis (AgP)? SOURCE OF FUNDING: University of Michigan Periodontal Graduate Student Research Fund and the Talentia Scholarship Program, Junta de Andalucia, Spain TYPE OF STUDY/DESIGN: Systematic review and meta-analysis LEVEL OF EVIDENCE: Level 2: Limited-quality, patient-oriented evidence STRENGTH OF RECOMMENDATION GRADE: Grade B: Inconsistent, limited quality patient-oriented evidence.

Collaborative management of a young patient with generalized aggressive periodontitis.

What are the orthodontic treatment possibilities, limitations and risks inherent in patients with periodontal disorders, particularly active periodontal disease? This case report describes the interface between orthodontics, periodontics and restorative dentistry in the management of a 25-year-old young man with generalized aggressive periodontitis.

A consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis is present in sites prior to bone loss in a longitudinal study of localized aggressive periodontitis.

Aggregatibacter actinomycetemcomitans-induced localized aggressive periodontitis (LAP) in African-American adolescents has been documented but is poorly understood. Two thousand fifty-eight adolescents aged 11 to 17 years were screened for their periodontal status and the presence of A. actinomycetemcomitans in their oral cavity. Seventy-one A. actinomycetemcomitans-negative and 63 A. actinomycetemcomitans-positive periodontally healthy subjects were enrolled, sampled, examined, and radiographed yearly for 3 years. Gingival and periodontal pocket depth and attachment levels were recorded. Disease presentation was characterized by bone loss (BL). Subgingival sites were sampled every 6 months to assess (i) the role of A. actinomycetemcomitans in BL and (ii) the association of A. actinomycetemcomitans and other microbes in their relationships to BL. Sixteen of 63 subjects with A. actinomycetemcomitans developed BL (the other 47 subjects with A. actinomycetemcomitans had no BL). No A. actinomycetemcomitans-negative subjects developed BL. Human oral microbe identification microarray (HOMIM) was used for subgingival microbial assessment. On a subject level, pooled data from A. actinomycetemcomitans-positive subjects who remained healthy had higher prevalences of Streptococcus and Actinomyces species, while A. actinomycetemcomitans-positive subjects with BL had higher prevalences of Parvimonas micra, Filifactor alocis, A. actinomycetemcomitans, and Peptostreptococcus sp. human oral taxon 113 (HOT-113). At vulnerable sites, A. actinomycetemcomitans, Streptococcus parasanguinis, and F. alocis levels were elevated prior to BL. In cases where the three-organism consortium (versus A. actinomycetemcomitans alone) was detected, the specificity for detecting sites of future BL increased from 62% to 99%, with a sensitivity of 89%. We conclude that detecting the presence of A. actinomycetemcomitans, S. parasanguinis, and F. alocis together indicates sites of future BL in LAP. A synergistic interaction of this consortium in LAP causation is possible and is the subject of ongoing research.

[Predictive model for post-treatment tooth loss of patients with aggressive periodontitis].

OBJECTIVE: To establish a predictive model for long-term tooth loss of patients with aggressive periodontitis (AgP) after periodontal treatment. METHODS: Patients diagnosed as AgP in Department of Periodontology, Peking University School and Hospital of Stomatology, who were re-evaluated 3 to 11 years after periodontal treatment were enrolled (n=85). Logistic regression was performed to select background, periodontal and radiographic factors which were related to long-term post-treatment tooth loss. A predictive model was built and analyzed by receiver operator characteristic (ROC) curve. RESULTS: After periodontal treatment, 55 teeth from 22 patients lost further. High prevalence of baseline bone loss, root abnormality, and residual severe bleeding sites, as well as poor compliance to maintenance were detected as risk factors in the predictive model. ROC analysis found the sensitivity and specificity of the model could reach up to 80% simultaneously. CONCLUSION: Predictive model for post-treatment tooth loss of patients with AgP is an important adjunct in clinical practice.

Prognostic value of the periodontal risk assessment in patients with aggressive periodontitis.

OBJECTIVES: Aim of the study was to evaluate the predictive value of the modified periodontal risk assessment (PRA) in patients with aggressive periodontitis (AgP) for the first time. MATERIAL AND METHODS: A total of 86 Patients with AgP were re-examined 5-17 years after active periodontal treatment. Risk profile according to the modified PRA was assigned and regularity of maintenance monitored. Tooth loss, bone loss and recurrence of periodontitis were analysed in association with gender, diagnosis, compliance and risk profile using uni- and multivariate parametric regression and Cox proportional hazards models. RESULTS: A total of 14 patients showed a localized AgP, 60 a high-risk-profile and 19 were compliant with the proposed maintenance-interval. Of 2202 teeth 98 were lost. Multivariate analysis could not assign a statistically significant impact to risk-profile. By excluding Interleukin-1 composite genotype from the modified PRA a significant influence (p = 0.003, HR 2.74) was detected. The impact of compliance was shown to be nearly significant (p = 0.059, HR 2.0). In patients with generalized AgP a tendency for increased tooth loss was found. CONCLUSION: The prognostic value of the modified PRA could not be confirmed in patients with AgP. However, exclusion of Interleukin-1 composite genotype led to a model with significant influence on tooth loss.

CDKN2BAS is associated with periodontitis in different European populations and is activated by bacterial infection.

Epidemiological studies have indicated a relationship between coronary heart disease (CHD) and periodontitis. Recently, CDKN2BAS was reported as a shared genetic risk factor of CHD and aggressive periodontitis (AgP), but the causative variant has remained unknown. To identify and validate risk variants in different European populations, we first explored 150 kb of the genetic region of CDKN2BAS including the adjacent genes CDKN2A and CDKN2B, covering 51 tagging single nucleotide polymorphisms (tagSNPs) in AgP and chronic periodontitis (CP) in individuals of Dutch origin (n=313). In a second step, we tested the significant SNP associations in an independent AgP and CP population of German origin (n=1264). For the tagSNPs rs1360590, rs3217992, and rs518394, we could validate the associations with AgP before and after adjustment for the covariates smoking, gender and diabetes, with SNP rs3217992 being the most significant (OR 1.48, 95% CI 1.19 to 1.85; p=0.0004). We further showed in vivo gene expression of CDKN2BAS, CDKN2A, CDKN2B, and CDK4 in healthy and inflamed gingival epithelium (GE) and connective tissue (CT), and detected a significantly higher expression of CDKN2BAS in healthy CT compared to GE (p=0.004). After 24 h of stimulation with Porphyromonas gingivalis in Streptococcus gordonii pre-treated gingival fibroblast (HGF) and cultured gingival epithelial cells (GECs), we observed a 25-fold and fourfold increase of CDKN2BAS gene expression in HGFs (p=0.003) and GECs (p=0.004), respectively. Considering the global importance of CDKN2BAS in the disease risk of CHD, this observation supports the theory of inflammatory components in the disease physiology of CHD.