%0 Journal Article
%T Lymphotoxin-Alpha Gene Polymorphism +252A/G (rs909253, A/G) Is Associated with Susceptibility to Chronic Periodontitis: A Pilot Study
%A Daniel Fernando Pereira Vasconcelos
%A Marco Ant£¿nio Dias da Silva
%A Marcelo Rocha Marques
%A Rui Barbosa de Brito J¨²nior
%A Any Carolina Cardoso Guimar£¿es Vasconcelos
%A Silvana Pereira Barros
%J ISRN Dentistry
%D 2012
%R 10.5402/2012/617245
%X Background. Periodontal disease leading to clinical findings such as increased periodontal probing depth involves a complex interaction between invading pathogenic microorganisms and the patient's immune system. Lymphotoxin alpha (LT-¦Á) is a potent multifunctional immune modulator that contributes toward susceptibility to immune regulation disorders, including periodontal disease. Objective. In this study, we tested the hypothesis that chronic periodontitis (CP) is associated with polymorphisms of the LT-¦Á gene. Materials and Methods. A total of 126 subjects, 44 healthy subjects, and 82 subjects with CP, were evaluated for periodontal disease by measuring clinical attachment loss and separation. Samples of epithelial cells were obtained for DNA analysis by scraping of the buccal mucosa. The LT-¦Á gene was analyzed by polymerase chain reaction followed by endonuclease digestion with NcoI to analyze restriction fragment length polymorphisms. Results. The LT-¦Á gene (+252A/G) polymorphism was associated with CP. LT-¦Á allele frequencies were significantly different ( ) between patients with CP and healthy individuals, with an odds ratio of 2.67 for patients with CP with the G allele. Conclusions. These findings suggest the LT-¦Á gene genotype is a risk indicator for susceptibility to chronic periodontal disease in the Brazilian population studied. 1. Introduction Periodontal disease is characterized by inflammatory destruction of tissues that support the tooth, leading to loss of epithelial attachment and destruction of the periodontal ligament, cementum, and alveolar bone, and eventually tooth loss [1]. Etiological studies show that although bacterial infection causes periodontitis, a subset of individuals show severe disease in the absence of a large bacterial load, suggesting that these individuals mount an exaggerated response to a modest microbial challenge. Thus, the patient¡¯s immune response may play a critical role in periodontal disease pathogenesis and expression [1, 2]. This observation has led to interest in finding potential genetic markers of disease susceptibility, including polymorphisms in genes encoding key molecules of the host defense system, such as cytokines [3¨C5]. Lymphotoxin- (LT- ), previously known as tumor necrosis factor (TNF)- , is a proinflammatory cytokine encoded by the LT-¦Á gene (HUGO Gene Nomenclature Committee, http://www.genenames.org/). LT- plays a key role in orchestrating the inflammatory and immune responses involved in tissue destruction and bone resorption and has been suggested to be an important participant in the
%U http://www.hindawi.com/journals/isrn.dentistry/2012/617245/