Oral session: Diagnosis and risk factors ORALS Oral session: Diagnosis and risk factors 18.3 cm2). 39.3 cm2 and 36.9 cm2 are the mean values for the upper 2 2 Subgingival – in vivo – calculus detection using and lower jaw respectively (SD 9.3 cm and 8.7 cm ). The mean value for the coronal root thirds is 33.3 cm2 (SD 7.8 cm2), for the 655 nm diode laser irradiation. middle thirds 28.3 cm2 (SD 6.3 cm2) and for the apical thirds P. Purucker*, R. Bluehdorn and J.-P. Bernimoulin 14.3 cm2 (SD 3.9 cm2). On the basis of the single teeth-data it Charit, University Medicine Berlin, Germany seems to be possible to get a better estimation of the area of Background: Clinical subgingival calculus detection has a poor test attachment loss in patients with periodontal disease. It needs to be sensitivity. The aim of this in vivo study was to compare a shown whether the extent of inflamed periodontal area plays a role diagnostic laser with an explorer in their ability of subgingival for the severity of systemic response. calculus detection. Methods: Fifteen teeth with untreatable periodontitis were analysed directly before their extraction. At the mesial and distal Periodontal disease in 3-generation Brazilian surface of each tooth calculus was diagnosed either by a thin families – genetic power estimation explorer (EXD 11/12) or by a diagnostic InGaAsP diode laser G. E. Rapp*, N. P. Trujillo, P. M. Brett and M. S. Tonetti (KaVo KEY 3 laser) with a headpiece for the irradiation (655 nm UFBA, Brazil, UA, Columbia, UCL, UK, UC, USA wavelength) of the root surface. The intensity of the resulting fluorescence was analysed and a peak value >30 was counted as Linkage analysis is a powerful method to detect predisposing presence of calculus. The clinical detection was performed before gene(s), providing there is sufficient pedigree information. The aim or after laser detection. On each surface five areas were assessed was to estimate the power of 3-generation families to detect linkage separately. After extraction, digital images were taken and the for future detection of genetic effects in periodontal disease (PD). presence of calculus was determined. Three Brazilian families were selected after confirmed diagnoses of Results: The result shows that 64 out of 150 surfaces were covered generalized aggressive periodontitis in the probands. A 6 site/tooth with calculus. The explorer method discovered 24 of the 64 surfaces full-mouth probing was performed by a calibrated examiner in 58 (sensitivity 37.5%) and the laser method was positive on 52 of the family members (all non-smokers). The phenotype was dichotom- 64 areas with calculus (sensitivity 81.3%). Areas free of calculus ized based on questionnaire (edentulous cases) and clinical were detected on 64 out of 86 (explorer: specificity 74.4%) vs. 69 attachment loss of 4 mm due to pocketing in at least 4 sites of out of 86 (laser: specificity 80.2%) surfaces. different teeth. A dominant mode of inheritance (autosomal) and Conclusion: Within the limits of this study it can be concluded, that recombination fraction Q = 0 were adopted in the model. Pene- the sensitivity of subgingival calculus detection by laser induced trance values (F) of 0.98, 0.75, 0.5 and phenocopy rates (P) 0 and fluorescence (655 nm excitation wavelength) is significantly higher 0.02 were tested using the SLINK simulation method in 100 than the detection sensitivity of an explorer. replicas. A lod score of 3 is considered significant for genetic linkage analysis. The highest values were found in F = 0.98 and P = 0, followed by F = 0.98 and P = 0.02. The average/maxi- Quantification of the periodontal attachment area in mum expected lod scores were 5.90/9.67 and 4.80/8.83 respectively. Bearing in mind the heterogeneity of periodontal disease (genetic fully dentate humans by computed tomography and/or environmental contributors), the authors conclude that the P. Solar*, C. Kropf, J. Gruber and A. Gahleitner analysed pedigrees provide sufficient power for future genotyping. Bernhard-Gottlieb Dent. Univ. Clin., Vienna, Austria Current literature does not provide data of the total periodontal attachment area measured in single individuals. This presentation Genetic influences on neutrophil function as risk focuses on a study using Computed tomography (CT)-data of fully dentate, periodontal healthy subjects to determine the total root factors for aggressive periodontitis surface area of humans. CT-data of 57 patients, who underwent L. Nibali*, G. Griffiths, M. Parkar and M. Tonetti et al. CT-scanning for other than periodontal indications, were analysed. Univ. After image processing the root surface of every single tooth was Background: Neutrophils (PMN) in Aggressive Periodontitis calculated. In the next step every root area was vertically divided in (AgP) patients are hyper active especially with regards to thirds (coronal, middle, apical) and the surface area of each third superoxide production. Polymorphisms in genes influencing PMN calculated. Statistic processing of the data was performed to function have been proposed as candidate risk factors for AgP. The determine mean values and standard deviations for the root surface aim of this study was to test the association of specific gene area of single teeth, the root thirds, the upper and lower jaw polymorphisms affecting PMN functions with AgP. separately and the total of all 28 teeth. The results for the total Methods: Two hundred and twenty four patients with confirmed 2 periodontal attachment area show a mean value of 75.4 cm (SD diagnosis of AgP and 231 subjects with healthy periodontium took part in the study. A blood sample was collected from subjects and genotypes for C242T p22phox NADPH oxidase, FP, Fca and Fcc *Presenting author receptors were analysed in a blind fashion. 23 Oral session: Diagnosis and risk factors Results: The C242T p22phox NADPH oxidase T allele was marked reduction in OPG expression (66% of healthy subject significantly associated with AgP in a multiple logistic regression levels). However, the G-AgP group showed strong induction in model adjusting for confounders, both in Caucasian (P = 0.009, RANKL expression, whereas in CP patients there was no increased OR = 2.07, 95% CI = 1.20–3.59) and Black subgroups (P= RANKL expression. When RANKL/OPG ratios were calculated, 0.032, OR = 3.16, 95% CI = 1.28–7.76). The same genotype and this was markedly increased in both AgP and CP compared with FccR IIIb polymorphism were associated with the Generalised controls, there was no significant difference between CP and AgP phenotype both in all subjects and Caucasians. FccR G-AgP in RANKL/OPG ratios. haplotypes were associated with AgP in Blacks (P=0.034). Conclusion: These preliminary results suggest that the increased Discussion: The C242T p22phox NADPH oxidase and FccR RANKL/OPG ratio in CP patients may account for a down- polymorphisms may predispose to Aggressive Periodontitis, regulation of OPG expression, whereas in G-AgP patients this may probably through a modulation of neutrophil superoxide be due to up-regulation of RANKL expression. production. VDR, osteoprotegerin and IL-6 gene polymorphisms in Salivary pro-inflammatory cytokine arrays for diagnosis Turkish population with aggressive and chronic of periodontitis periodontitis C. A. Ramseier*, J. Kinney, A. Kim, A. Singh and W. Giannobile University of Michigan, Ann Arbor, USA P. Emecen*, E. Yılmaz, P. Geyik and R. M. Nohutcu H.U. Dental and Medical School, Turkey Aims: Increased levels of pro-inflammatory cytokines may be found in oral fluids of patients afflicted with chronic periodontitis. Epidemiologic studies suggest that there is a genetic component of The identification of multiple analytes from the same biological susceptibility to periodontitis. In this study, the VDR, osteopro- sample remains a challenge in the evaluation of periodontal disease tegerin (OPG) and IL-6 gene polymorphisms, which are thought to biomarkers. The aim of the present cross-sectional study was to play roles in bone metabolism, were evaluated in Turkish popu- measure salivary-derived pro-inflammatory cytokines in lation with aggressive periodontitis (AP) patients, chronic perio- periodontally healthy and diseased subjects. dontitis (CP) patients and periodontally healthy controls (HC). Materials and methods: Clinical attachment levels (CAL), probing Sixty-two AP patients, 63 CP patients and 64 HC were enrolled in depths (PPD), bleeding on probing (BOP) were assessed from a the study. A full-mouth periodontal examination including probing total of 20 patients with periodontal health or periodontitis. Whole depth (PD), clinical attachment level (CAL), plaque index (PI) and saliva (WS) was collected and analysed using protein microarray bleeding on probing (BOP) were performed. DNA’s isolated from techniques for IL-6, IL-1b, IL-2, IL-13, IL-4, IFN-c, IL-5 and peripheral blood were analysed for the polymorphisms in VDR, TNF-a. These assays are based on a miniaturized immunoassay OPG and IL-6 genes by PCR followed by restriction enzyme using microarrays of biotinylated monoclonal antibodies and digestion and gel electrophoresis. There were no significant streptavidin-conjugated fluorophores. differences between AP, CP and HC groups for VDR, OPG and Results: In WS, a > 20 fold increase of IL-1b was found in IL-6 genotype analysis or allele frequencies investigated. When the subjects with periodontal disease compared to healthy individuals patient groups (AP and CP) were classified as mild-moderate (P<0.05), while >2 fold increases in IL-4, IL-6 and IL-10 were (CAL < 4 mm) and severe (CAL > 4 mm) according to CAL, found in disease vs. health. A statistical significant correlation genotype 1/1 and allele 1 were found significantly higher in CP between PPD and CAL, was found in WS with multiple cytokines patients severe group in OPG gene polymorphism and although it evaluated (Spearman’s rank correlation rho: 0.57–0.72).