Tumor necrosis factor-α and oral inflammation in patients with Crohn disease.

Background: Crohn disease (CD) is a chronic inflammatory bowel disease often accompanied by periodontal symptoms. Based on its function in immune response, tumor necrosis factor (TNF)-α and its genetic variants have been discussed as risk indicators in inflammatory processes. Therefore, the aim of the present study is to investigate the impact of TNF-α polymorphisms on periodontal parameters and inflammatory lesions of oral mucosa as a characteristic of CD.

The genetic impact of the Q551R interleukin-4 receptor alpha polymorphism for aggressive or chronic periodontitis and the occurrence of periodontopathic bacteria.

Objective: The Q551R polymorphism of the gene encoded for the α chain of the interleukin-4 receptor (IL-4RA) could influence both IL-4 and IL-13 signalling. Since both cytokines could be important in the pathogenesis of periodontitis the aim of this study was to evaluate putative associations of the Q551R polymorphism to generalized aggressive or chronic periodontitis and five periodontopathogens.

Design: 154 patients with severe generalized periodontitis (chronic: n=68, mean age=48.

Single nucleotide polymorphisms in interleukin-1gene cluster and subgingival colonization with Aggregatibacter actinomycetemcomitans in patients with aggressive periodontitis.

Periodontitis is initiated by the subgingival occurrence of periodontopathogens. It is triggered by a specific host-dependent immune response that is influenced by genetic predisposition. Polymorphisms in the interleukin-1 (IL-1) gene cluster have been suggested to influence the pathogenesis of periodontitis.

Interferon-gamma and interleukin-12 gene polymorphisms and their relation to aggressive and chronic periodontitis and key periodontal pathogens.

Background: The gene polymorphisms interferon-gamma (IFN-gamma) 874 T/A and interleukin (IL)-12 1188 A/C have been associated with the altered production of cytokines. Therefore, they might be indicative of the occurrence of chronic periodontitis (CP) or aggressive periodontitis (AgP) and the prevalence of key periodontal pathogens. For this purpose, we analyzed these polymorphisms in subjects with generalized AgP or generalized CP.