Publications (9) View all
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Article: The relationship of periodontal disease severity to serum and GCF substance P levels in diabetics.
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ABSTRACT: To compare circulating and gingival crevicular fluid (GCF) substance P concentrations in well- and poorly controlled type 2 diabetic patients with chronic periodontitis. Forty-five serum and 90 GCF samples were collected from diabetic patients with periodontal disease, and the concentrations of substance P were quantified by radioimmunoassay. Serum substance P levels were higher in the poorly controlled diabetic group than in patients with good glycemic control (P = .01); within the poorly controlled group, patients with severe attachment levels had the highest circulating substance P levels (P = .02). Additionally, the diseased sites showed higher substance P levels than control sites (P = .0016). The GCF substance P concentrations in diseased sites correlated significantly with clinical findings such as Plaque Index (r = 0.51, P = .001) and bleeding on probing (r = 0.35, P = .029). Within the limits of this study, our preliminary findings indicate that periodontal inflammation may influence circulating and GCF substance P levels in poorly controlled diabetic subjects.Quintessence international (Berlin, Germany: 1985) 06/2012; 43(7):587-96. · 0.64 Impact Factor -
Article: Position and course of the mandibular canal in skulls.
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ABSTRACT: The aim of this study was to examine and describe the topography of the mandibular canal (MC) in both vertical and occlusal dimensions. Fifty-two adult skulls deposited in the University of Pittsburgh School of Dental Medicine skull collection were evaluated in this study. Cone-beam computerized tomographic scans of each skull were obtained. The vertical course of MC was classified into 3 types: straight projection (12.2%), catenary-like configuration (51.1%), and progressive descent from posterior to anterior (36.7%). The evaluation of the buccolingual dimension showed that the mandibular canal was located either in contact with or close to the lingual cortical plate (≤2 mm) in the molar region of the majority of the cases. As it proceeds anteriorly it moves toward the buccal aspect of the mandible, where it finally emerges through the mental foramen. Three emerging patterns of mandibular canal were observed: sharp turn (53.2%), soft curved exit (28.8%), and straight path (17.4%). The examination of the vertical dimension showed that the canal was located almost 1 cm above the inferior border of the mandible and then ascended to reach the mental foramen, which is located ∼16 mm (range 13.4-20.3 mm) above the inferior border of the mandible. We found a strong correlation between height of the mandible and location of the mental foramen (r = 0.64; P < .0001). The course of mandibular canal described in vertical and axial dimensions and variation in its path have been classified. In addition to variation in location of MC, it has different anatomic configurations which clinicians should be familiar with in any surgical procedures involving the posterior mandible.Oral surgery, oral medicine, oral pathology and oral radiology. 04/2012; 113(4):453-8. -
Article: The antimicrobial peptide DEFB1 is associated with caries.
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ABSTRACT: Genetics is an important component in the determination of individual susceptibility to caries and periodontal diseases. Since beta defensin 1 (DEFB1) localizes in the oral cavity, we tested if variation in DEFB1 is associated with caries and periodontitis. We analyzed 3 single-nucleotide polymorphisms in DEFB1 in DNA samples from unrelated individuals. Carrying a copy of the variant allele of the DEFB1 marker rs11362 (G-20A) increased the DMFT and DMFS scores more than five-fold. Also, carrying a copy of the variant allele of the DEFB1 marker rs179946 (G-52A) correlated with low DMFT scores. We found a high-caries-experience haplotype (GCA), which increased DMFT scores two-fold, and a low- caries-experience haplotype (ACG), which decreased DMFT scores two-fold, in the DEFB1 promoter. No association between DEFB1 genetic markers and periodontal disease was found. Our results suggest that functional polymorphisms of DEFB1 are potential markers for caries.Journal of dental research 04/2010; 89(6):631-6. · 3.46 Impact Factor -
Article: TLR4 as a risk factor for periodontal disease: a reappraisal.
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ABSTRACT: To determine whether genetic variants of the TLR4 gene are associated with either chronic or aggressive periodontitis. A systematic electronic search of literature was conducted to identify all published studies without any language restriction on the association between TLR4 and periodontal diseases, including chronic periodontitis and aggressive periodontitis. All case-control studies evaluating the TLR4 Asp299Gly and Thr399Ile polymorphisms in chronic or aggressive periodontitis were identified. A meta-analysis of the studies that fulfilled the inclusion criteria was performed. Seven studies comprising 744 chronic periodontitis cases and 855 controls and four studies consisting of a total of 295 aggressive periodontitis cases and 456 controls were included in the meta-analysis. In the pooled analysis, the TLR4 299Gly allele (TLR4+896 A>G) appeared to be a genetic risk factor for susceptibility to chronic periodontitis with a random effects and fixed effects odds ratio (OR) of 1.43 [95% confidence interval (CI):1.04-1.97; p=0.03]. On the other hand, the TLR4 399Ile polymorphism (TLR4+1196 C>T) showed a protective effect against aggressive periodontitis with a random effects OR of 0.29 (95% CI: 0.13-0.61; p=0.001). Our results suggest that the alleles 299Gly and 399Ile in TLR4 can be a potential genetic marker for periodontal disease.Journal Of Clinical Periodontology 04/2009; 36(4):279-86. · 3.00 Impact Factor -
Article: Association of tagSNPs in the urokinase-plasminogen activator (PLAU) gene with Alzheimer's disease and associated quantitative traits.
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ABSTRACT: The gene coding for urokinase-plasminogen activator (PLAU) is a strong biological and positional candidate gene for Alzheimer's disease (AD). Previously some studies have examined the role of common variation in the PLAU gene with AD risk but the results have been inconsistent and this inconsistency could have been due to the use of relatively small sample sizes. In this study we evaluated the distribution of four tagSNPs (rs2227562 in intron 5, rs2227564 in exon 6, rs2227571 in intron 9, and rs4065 in 3'UTR) in the PLAU gene in a large case-control study consisting of up to 1,000 AD patients and 697 white control subjects. We examined the role of these tagSNPs with AD risk and quantitative traits of AD, including age-at-onset (AAO), disease duration, and mini-mental state examination (MMSE) scores. The 3'UTR SNP revealed modest significant association with risk (OR = 0.71, 95% CI: 0.53-0.95; P = 0.02), AAO (P = 0.036) and disease duration (P = 0.04) of AD. In addition, the intron 9 SNP also revealed a significant association with AAO (P = 0.01) and disease duration (P = 0.006). Our data on a large number of AD cases and controls suggest that genetic variation in PLAU may affect the risk and AAO of AD.American Journal of Medical Genetics Part B Neuropsychiatric Genetics 02/2007; 144B(1):79-82. · 3.70 Impact Factor
