AIM: The objective of this case-control study was to compare the inflammatory response of peripheral blood from localized aggressive periodontitis (LAP) patients when stimulated with healthy or diseased plaque samples. MATERIALS AND METHODS: Whole blood and subgingival plaque samples were collected from 13 LAP subjects, 14 siblings of LAP subjects and six periodontally healthy individuals. Whole blood was stimulated for 24 h with plaque samples generated from healthy or diseased sites. The levels of 14 cyto/chemokines were detected using multiplex technology. RESULTS: Localized aggressive periodontitis-derived cultures displayed higher levels of G-CSF, INFγ, IL10, IL12p40, IL1β, IL-6, IL-8, MCP-1, MIP-1α, and TNFα, than control cultures regardless of stimulus used. Whole blood from healthy siblings displayed higher levels of IL-6 compared to control subjects, but lower levels than those observed in cultures from LAP participants. CONCLUSIONS: This study suggests that although bacteria is an important factor in eliciting the hyper-inflammatory response observed in LAP patients, the predisposition of host's response to bacterial presence may play a more significant role than the components of the stimulatory plaque.
AIM: The objective of this case-control study was to compare the inflammatory response of peripheral blood from localized aggressive periodontitis (LAP) patients when stimulated with healthy or diseased plaque samples. MATERIALS AND METHODS: Whole blood and subgingival plaque samples were collected from 13 LAP subjects, 14 siblings of LAP subjects and six periodontally healthy individuals. Whole blood was stimulated for 24 h with plaque samples generated from healthy or diseased sites. The levels of 14 cyto/chemokines were detected using multiplex technology. RESULTS:Localized aggressive periodontitis-derived cultures displayed higher levels of G-CSF, INFγ, IL10, IL12p40, IL1β, IL-6, IL-8, MCP-1, MIP-1α, and TNFα, than control cultures regardless of stimulus used. Whole blood from healthy siblings displayed higher levels of IL-6 compared to control subjects, but lower levels than those observed in cultures from LAP participants. CONCLUSIONS: This study suggests that although bacteria is an important factor in eliciting the hyper-inflammatory response observed in LAP patients, the predisposition of host's response to bacterial presence may play a more significant role than the components of the stimulatory plaque.
Authors: Scott R Diehl; Tianxia Wu; Bryan S Michalowicz; Carol N Brooks; Joseph V Califano; John A Burmeister; Harvey A Schenkein Journal: J Periodontol Date: 2005-02 Impact factor: 6.993
Authors: L M Shaddox; H Huang; T Lin; W Hou; P L Harrison; I Aukhil; C B Walker; V Klepac-Ceraj; B J Paster Journal: J Dent Res Date: 2012-08-03 Impact factor: 6.116
Authors: Karina A F S Miller; Luciana S Branco-de-Almeida; Sandra Wolf; Nicole Hovencamp; Tina Treloar; Peter Harrison; Ikramuddin Aukhil; Yan Gong; Luciana M Shaddox Journal: J Clin Periodontol Date: 2016-12-27 Impact factor: 8.728