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• W1774664673 abstract "Abstract Periodontitis results from the interaction of bacteria on the tooth surfaces and the host immune response. Although periodontal pathogens are essential for the initiation and progression of the disease, the tissue damage in periodontitis is primarily mediated by the host immune response. Differences in the susceptibility to the disease and in the clinal outcome of the therapy seem to be less dependent on genetics but more on lifestyle factors, like smoking, overweight, stress and nutrition. It has been shown that these lifestyle factors may modulate the immune response and therefore influence the initiation and progression of the disease. To study the host immune response, whole blood cell cultures ( WBCC ) stimulated with lipopolysaccharide ( LPS ) have been widely used and they specifically reflect the behaviour of monocytes. It has been shown that peripheral blood monocytes in LPS ‐stimulated WBCC from non‐smoking periodontitis patients display a T ‐helper 2 ( T h2)‐promoting phenotype in comparison with controls. After periodontal therapy, this phenotype reversed and was comparable with controls. However, in smoking but treated patients, the T h2‐promoting phenotype of monocytes still remained. Therefore, the aberrant phenotype of monocytes in the peripheral blood from periodontitis patients is likely to be a systemic response to exogenous and endogenous danger molecules released or induced by the periodontal infection or by smoking. It can be concluded that periodontal therapy in non‐smoking periodontitis patients has beneficial health effects and that smoking cessation should be an integral part of the therapy as well for general health reasons as for the clinical outcome." @default.
• W1774664673 created "2016-06-24" @default.
• W1774664673 creator A5080070175 @default.
• W1774664673 date "2012-08-01" @default.
• W1774664673 modified "2023-09-26" @default.
• W1774664673 title "Peripheral blood monocyte responses in periodontitis" @default.
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• W1774664673 doi "https://doi.org/10.1111/j.1601-5037.2012.00572.x" @default.
• W1774664673 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23046009" @default.
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