TY - JOUR
T1 - Systemic manifestations of periodontitis in the non-human primate
AU - Ebersole, J. L.
AU - Cappelli, D.
AU - Mott, G.
AU - Kesavalu, L.
AU - Holt, S. C.
AU - Singer, R. E.
PY - 1999/10
Y1 - 1999/10
N2 - This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis: and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, α1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.
AB - This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis: and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, α1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.
KW - Acute phase reactants
KW - Lipids/lipoproteins
KW - Non-human primates
KW - Periodontitis
KW - Serum
UR - http://www.scopus.com/inward/record.url?scp=0033201896&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033201896&partnerID=8YFLogxK
U2 - 10.1111/j.1600-0765.1999.tb02266.x
DO - 10.1111/j.1600-0765.1999.tb02266.x
M3 - Article
C2 - 10685361
AN - SCOPUS:0033201896
VL - 34
SP - 358
EP - 362
JO - Journal of Periodontal Research
JF - Journal of Periodontal Research
SN - 0022-3484
IS - 7
ER -