Genetic susceptibility to chronic periodontal disease

Baker, Pamela J.; Roopenian, Derry C.

doi:10.1016/s1286-4579(02)01642-8

Cited by 38 publications

(41 citation statements)

References 93 publications

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“…18 Recently, some comprehensive and detailed reviews have presented convincing evidence for heritable components of both susceptibility and progression (or severity) of periodontal diseases. [19][20][21][22][23] Many studies have focused on the potential role of several cytokines involved in the inflammatory response, among which some of the most investigated are the IL-1a, IL-1b and IL-1Ra, [24][25][26][27][28] genes which are all located on the long arm of chromosome 2 (region 2q13-14).…”

Section: Introductionmentioning

confidence: 99%

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

et al. 2004

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Several studies have shown a role for the involvement of interleukin (IL)-1 gene cluster polymorphisms in the risk of periodontal diseases. In the present study, we tested polymorphisms, derived from genes of the IL-1 cluster, for association with generalized aggressive periodontitis (GAP) through both allelic association and by constructing a linkage disequilibrium (LD) map of the 2q13-14 disease candidate region. The IL-1RN (VNTR) genotype distribution observed was significantly different in GAP and control subjects (P ¼ 0.019). We also observed some evidence for an association between GAP and the IL-1B þ 3953 polymorphism (P ¼ 0.039). The pattern of association in the region, represented as an LD map, identifies a recombination hot area between the IL-1B þ 3953 and IL-1B À511 polymorphisms. Multilocus modelling of association with disease gives a location for the peak association at the IL-1B þ 3953 marker, although support for the peak is not significant. Haplotype analysis identifies a IL-1B þ 3953 -IL-1B À511 haplotype as having the lowest P-value in the region. Recognition of the presence of a recombination hot area between the IL-1B þ 3953 and IL-1B À511 polymorphisms will have an important bearing on future efforts to develop higher resolution SNP analysis in this region for both this and other diseases for which this cluster is implicated.

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Section: Introductionmentioning

confidence: 99%

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

et al. 2004

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“…The recent years has seen enormous research attempts in the study for genetic factors that may predispose individuals to periodontitis, as one of the most common chronic infectious disease in humans (1)(2)(3). The most frequently occurring form of periodontitis is chronic periodontitis (CP) that is caused by periodontopathic bacteria.…”

Section: Introductionmentioning

confidence: 99%

“…To date, studies have shown that all normal cells such as inflammatory cells, vascular endothelial cells, gingival fibroblasts, and epithelial cells can synthesize TGF-β, yet for research purposes this cytokine has been extracted from human placenta, platelets and bovine kidney (5,6). Transforming growth factor β inhibits growth of epithelial cells, fibroblasts, endothelial cells, hepatocytes, neuronal cells and lymphocytes (3,5). It acts as a stimulating factor for mesenchymal cells differentiation (3).…”

Section: Introductionmentioning

confidence: 99%

“…These isotypes are encoded by different genes and share many biological activities that are qualitatively similar in most cases (5). Transforming Growth Factor β is a regulator cytokine that induces growth and differentiation in many types of cells and is able to inhibit immune response by suppression of lymphocytes (3,12). It potentially has immunosuppressive function and down-regulatory role in transcription of some cytokines such as tumor necrosis factor alpha, metalloproteinases and interleukin-1 (17).…”

Section: Introductionmentioning

confidence: 99%

“…Allelic variation in host genes causes genetic components that induce disease processes. Rate of host response is a result of interaction between environment and genotype (3,20). Many studies have indicated that genetic background has an important role in susceptibility to periodontal disease.…”

Section: Introductionmentioning

confidence: 99%

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Association between TGF-Beta1 (-509) C/T Gene Polymorphism and Tissue Degradation Level In Chronic Periodontitis: A Stereological Study

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Efficient protocols and methods for high‐throughput utilization of the Collaborative Cross mouse model for dissecting the genetic basis of complex traits

Atamni

Iraqi

2019

Anim Models and Exp Med

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The Collaborative Cross (CC) mouse model is a next‐generation mouse genetic reference population (GRP) designated for a high‐resolution quantitative trait loci (QTL) mapping of complex traits during health and disease. The CC lines were generated from reciprocal crosses of eight divergent mouse founder strains composed of five classical and three wild‐derived strains. Complex traits are defined to be controlled by variations within multiple genes and the gene/environment interactions. In this article, we introduce and present variety of protocols and results of studying the host response to infectious and chronic diseases, including type 2 diabetes and metabolic diseases, body composition, immune response, colorectal cancer, susceptibility to Aspergillus fumigatus, Klebsiella pneumoniae, Pseudomonas aeruginosa, sepsis, and mixed infections of Porphyromonas gingivalis and Fusobacterium nucleatum, which were conducted at our laboratory using the CC mouse population. These traits are observed at multiple levels of the body systems, including metabolism, body weight, immune profile, susceptibility or resistance to the development and progress of infectious or chronic diseases. Herein, we present full protocols and step‐by‐step methods, implemented in our laboratory for the phenotypic and genotypic characterization of the different CC lines, mapping the gene underlying the host response to these infections and chronic diseases. The CC mouse model is a unique and powerful GRP for dissecting the host genetic architectures underlying complex traits, including chronic and infectious diseases.

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Genetic susceptibility to chronic periodontal disease

Cited by 38 publications

References 93 publications

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

Association between TGF-Beta1 (-509) C/T Gene Polymorphism and Tissue Degradation Level In Chronic Periodontitis: A Stereological Study

Efficient protocols and methods for high‐throughput utilization of the Collaborative Cross mouse model for dissecting the genetic basis of complex traits

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