Journal of clinical periodontology · 2016
Localized aggressive periodontitis immune response to healthy and diseased subgingival plaque.
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Shaddox Luciana M, Spencer William P, Velsko Irina M, Al-Kassab Hiba, Huang Hong, Calderon Nadia, Aukhil Ikramuddin, Wallet Shannon M
Аннотация
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.
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.