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      Cytokine Gene Polymorphisms Associate with Microbiogical Agents in Periodontal Disease: Our Experience

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          Abstract

          Periodontics has evolved from a simplistic model to a more complex interplay between infection and host response. Genetic factors have been a new addition to the list of risk factors for periodontal diseases. The processes leading to destruction and regeneration of the destroyed tissues are of great interest to both researchers and clinicians.

          The selective susceptibility of subjects for periodontitis has remained an enigma and wide varieties of risk factors have been implicated for the manifestation and progression of periodontitis. Emerging pathway models suggest that gene-environment interactions are etiologically important in disease pathogenesis. The current practical utility of genetic knowledge in periodontitis is limited.

          Allelic variants at multiple gene loci probably influence periodontitis susceptibility. The pro-inflammatory cytokine interleukin-1 (IL-1) is a key modulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption, and polymorphisms in the IL-1 gene cluster have been associated with an increased risk of developing severe adult periodontitis.

          The aim of this study was to test if polymorphisms of genes of IL-1α +4845 and IL-1β +3954 were linked with periodontitis, in a case-control study population, delimited to a specific geographic area, in association with microbiological findings.

          The polymorphisms observed in IL-1α +4845 and IL-1β +3954 single nucleotide polymorphisms (SNPs), was significantly different among the study groups (healthy controls, mild, moderate and severe periodontitis with p<0.05, d.f.=1.

          We found a significant correlation between the severe form of periodontitis and the presence of composite genotype (p < 0.05, d.f.=1, calculated among healthy vs. severe). Furthermore a statistically significant association between the presence of bacteria and periodontitis was detected (p<0.05, d.f.=1). In the current investigation findings were concordant with literature observations.

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          Most cited references36

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          Searching for genetic determinants in the new millennium.

          N Risch (2000)
          Human genetics is now at a critical juncture. The molecular methods used successfully to identify the genes underlying rare mendelian syndromes are failing to find the numerous genes causing more common, familial, non-mendelian diseases. With the human genome sequence nearing completion, new opportunities are being presented for unravelling the complex genetic basis of non-mendelian disorders based on large-scale genome-wide studies. Considerable debate has arisen regarding the best approach to take. In this review I discuss these issues, together with suggestions for optimal post-genome strategies.
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            Association study designs for complex diseases.

            Assessing the association between DNA variants and disease has been used widely to identify regions of the genome and candidate genes that contribute to disease. However, there are numerous examples of associations that cannot be replicated, which has led to skepticism about the utility of the approach for common conditions. With the discovery of massive numbers of genetic markers and the development of better tools for genotyping, association studies will inevitably proliferate. Now is the time to consider critically the design of such studies, to avoid the mistakes of the past and to maximize their potential to identify new components of disease.
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              The clinician's illusion.

              There are several diseases, including schizophrenia, alcoholism, and opiate addiction, for which the long-term prognosis is subject to disagreement between clinicians and researchers and also among researchers. Part of this disagreement may be attributable to a difference in the populations they sample. The clinician samples the population currently suffering from the disease (a "prevalence" or census sample), while research samples tend to more nearly represent the population ever contracting the disease (an "incidence" sample). The clinician's sample is biased toward cases of long duration, since the probability that a case will appear in a prevalence sample is proportional to its duration, hence "the clinician's illusion." The statistical mechanism of this bias is illustrated and its consequences detailed. Other sources of sampling bias in clinical and research samples are briefly described and partial remedies are suggested.
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                Author and article information

                Journal
                Int J Med Sci
                Int J Med Sci
                ijms
                International Journal of Medical Sciences
                Ivyspring International Publisher (Sydney )
                1449-1907
                2014
                1 May 2014
                : 11
                : 7
                : 674-679
                Affiliations
                1. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari “Aldo Moro”, Piazza Giulio Cesare 11, 70124, Bari, Italy.
                2. Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, Piazza Giulio Cesare 11, 70124, Bari, Italy.
                Author notes
                ✉ Corresponding author: e-mail andrea.ballini@ 123456me.com .

                Competing Interests: The Authors declared that no competing interest exists. None of the funding sources had any role in the design and conduct of the study. All Authors reviewed the paper, and read and approved the final manuscript.

                Article
                ijmsv11p0674
                10.7150/ijms.6962
                4025165
                24843315
                1fb00aaa-912c-43a2-a2bd-210cbbaf5a6d
                © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                History
                : 20 June 2013
                : 11 March 2014
                Categories
                Research Paper

                Medicine
                periodontal disease,single nucleotide polymorphisms,interleukin-1,genetic factors,oral microbiology.

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