Local inflammatory markers and systemic endotoxin levels in aggressive periodontitis

While much research has focused on local and systemic factors which contribute to periodontal disease progression, little is known regarding mechanisms which link these factors. We have reported preliminary data on systemic hyper-inflammatory response to bacterial LPS along with elevated expression of some local cyto/chemokines in sites of localized AgP (LAgP)as well as sites of periodontal health. Objectives: 1-To further delineate cytokines associated with periodontal disease, periodontal health and those as markers for future breakdown. 2-To correlate elevated levels of local mediators with systemic release of endotoxin. Methods: GCF and peripheral blood was collected from 54 African-American children: 34 diagnosed with LAgP, 12 healthy siblings and 10 healthy unrelated controls. GCF samples were collected from one healthy and one diseased site in LAgP patients and one healthy site from healthy controls. Twenty-two cyto/chemokines were quantified in the GCF, while systemic endotoxin levels were semi-quantified in serum. Results: Nine chemical mediators were found to be elevated in the GCF of diseased sites as compared to healthy related and unrelated controls (p<0.01). Interestingly, mediators, such as INF, IL1, IL6 and MIP1, were elevated in periodontally healthy sites from LAgP participants. Higher systemic levels of endotoxin were detected in LAgP participants compared to healthy siblings and unrelated controls (p<0.0001). Conclusions: High concentrations of certain cyto/chemokines in LAgP participants are associated with periodontal destruction, while other cytokines can be found in sites of periodontal health. Whether these cytokines can be used as markers for future periodontal breakdown is yet to be determined. Higher systemic levels of endotoxin in LAgP participants are most likely due to a loss of gingival integrity, and systemic release of bacterial products, potentially stimulating a systemic hyper-inflammatory response which is then called to the oral tissues by local cyto/chemokines perpetuating an inflammatory cycle.on 10-5-2008-->