Comparison of serum amyloid A protein and C-reactive protein levels as inflammatory markers in periodontitis
2
조회
0
다운로드
2
인용
0
참고문헌
키워드
초록
Purpose: The purpose of this study was to compare serum amyloid A (SAA) protein levelswith high-sensitive C-reactive protein (hs-CRP) levels as markers of systemic inflammationin patients with chronic periodontitis. The association of serum titers of antibodies to periodontalmicrobiota and SAA/hs-CRP levels in periodontitis patients was also studied. Methods: A total of 110 individuals were included in this study. Patients were assessed forlevels of hs-CRP and SAA. Nonfasting blood samples were collected from participants atthe time of clinical examination. The diagnosis of adipose tissue disorders was made accordingto previously defined criteria. To determine SAA levels, a sandwich enzyme-linkedimmunosorbent assay was utilized. Paper points were transferred to a sterile tube to obtaina pool of samples for polymerase chain reaction processing and the identification of Porphyromonasgingivalis, Aggregatibacter actinomycetemcomitans, and Tannerella forsythia. The serum level of IgG1 and IgG2 antibodies to P. gingivalis, A. actinomycetemcomitans,and T. forsythia was also determined. Results: SAA and hs-CRP levels were higher in periodontitis patients than in controls(P<0.05). In bivariate analysis, high levels of hs-CRP (>3 mg/L) and SAA (>10 mg/L) weresignificantly associated with chronic periodontitis (P=0.004). The Spearman correlationanalysis between acute-phase proteins showed that SAA positively correlated with hs-CRP(r=0.218, P=0.02). In the adjusted model, chronic periodontitis was associated with highlevels of SAA (odds ratio [OR], 5.5; 95% confidence interval [CI], 1.6–18.2; P=0.005) andelevated hs-CRP levels (OR, 6.1, 95% CI, 1.6–23.6; P=0.008). Increased levels of serum IgG2antibodies to P. gingivalis were associated with high levels of SAA (OR, 3.6; 95% CI, 1.4–8.5;P=0.005) and high concentrations of hs-CRP (OR, 4.3; 95% CI, 1.9–9.8; P<0.001). Conclusions: SAA and hs-CRP concentrations in patients with chronic periodontitis arecomparably elevated. High serum titers of antibodies to P. gingivalis and the presence ofperiodontal disease are independently related to high SAA and hs-CRP levels.
Abstract
Purpose: The purpose of this study was to compare serum amyloid A (SAA) protein levelswith high-sensitive C-reactive protein (hs-CRP) levels as markers of systemic inflammationin patients with chronic periodontitis. The association of serum titers of antibodies to periodontalmicrobiota and SAA/hs-CRP levels in periodontitis patients was also studied. Methods: A total of 110 individuals were included in this study. Patients were assessed forlevels of hs-CRP and SAA. Nonfasting blood samples were collected from participants atthe time of clinical examination. The diagnosis of adipose tissue disorders was made accordingto previously defined criteria. To determine SAA levels, a sandwich enzyme-linkedimmunosorbent assay was utilized. Paper points were transferred to a sterile tube to obtaina pool of samples for polymerase chain reaction processing and the identification of Porphyromonasgingivalis, Aggregatibacter actinomycetemcomitans, and Tannerella forsythia. The serum level of IgG1 and IgG2 antibodies to P. gingivalis, A. actinomycetemcomitans,and T. forsythia was also determined. Results: SAA and hs-CRP levels were higher in periodontitis patients than in controls(P<0.05). In bivariate analysis, high levels of hs-CRP (>3 mg/L) and SAA (>10 mg/L) weresignificantly associated with chronic periodontitis (P=0.004). The Spearman correlationanalysis between acute-phase proteins showed that SAA positively correlated with hs-CRP(r=0.218, P=0.02). In the adjusted model, chronic periodontitis was associated with highlevels of SAA (odds ratio [OR], 5.5; 95% confidence interval [CI], 1.6–18.2; P=0.005) andelevated hs-CRP levels (OR, 6.1, 95% CI, 1.6–23.6; P=0.008). Increased levels of serum IgG2antibodies to P. gingivalis were associated with high levels of SAA (OR, 3.6; 95% CI, 1.4–8.5;P=0.005) and high concentrations of hs-CRP (OR, 4.3; 95% CI, 1.9–9.8; P<0.001). Conclusions: SAA and hs-CRP concentrations in patients with chronic periodontitis arecomparably elevated. High serum titers of antibodies to P. gingivalis and the presence ofperiodontal disease are independently related to high SAA and hs-CRP levels.
참고문헌 (36)
- Holmlund A, "Porphyromonas gingivalis (Pg) a possible link between impaired oral health and acute myocardial infarction", Int J Cardiol, 148, pp.148~153 (2011)
- Glurich I, "Systemic inflammation in cardiovascular and periodontal disease: comparative study", Clin Diagn Lab Immunol, 9, pp.425~432 (2002)
- Persson GR, "Cardiovascular disease and periodontitis: an update on the associations and risk", J Clin Periodontol, 35(8 Suppl), pp.362~379 (2008)
- Pepys MB, "C-reactive protein: a critical update", J Clin Invest, 111, pp.1805~1812 (2003)
- Pitiphat W, "C-reactive protein associated with periodontitis in a Thai population", J Clin Periodontol, 35, pp.120~125 (2008)
- Chait A, "Thematic review series:the immune system and atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?", J Lipid Res, 46, pp.389~403 (2005)
- Yamada T, "Serum amyloid A (SAA): a concise review of biology, assay methods and clinical usefulness", Clin Chem Lab Med, 37, pp.381~388 (1999)
- Cunnane G, "Serum amyloid A in the assessment of early inflammatory arthritis", J Rheumatol, 27, pp.58~63 (2000)
- Mayer JM, "Serum amyloid A is a better early predictor of severity than C-reactive protein in acute pancreatitis", Br J Surg, 89, pp.163~171 (2002)
- Rivera MF, "Polymicrobial infection with major periodontal pathogens induced periodontal disease and aortic atherosclerosis in hyperlipidemic ApoE(null) mice", PLoS One, 8, pp.e57178~ (2013)
- Lösche W, "Plasma lipid and blood glucose levels in patients with destructive periodontal disease", J Clin Periodontol, 27, pp.537~541 (2000)
- Dye BA, "Serum antibodies to periodontal pathogens and markers of systemic inflammation", J Clin Periodontol, 32, pp.1189~1199 (2005)
- Aoki-Nonaka Y, "Natural killer T cells mediate alveolar bone resorption and a systemic inflammatory response in response to oral infection of mice with Porphyromonas gingivalis", J Periodontal Res, 49, pp.69~76 (2014)
- Eke PI, "Update of the case definitions for population-based surveillance of periodontitis", J Periodontol, 83, pp.1449~1454 (2012)
- Expert Panel on Detection, Evaluation, "Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III)", JAMA, 285, pp.2486~2497 (2001)
- Gillmore JD, "Amyloid load and clinical outcome in AA amyloidosis in relation to circulating concentration of serum amyloid A protein", Lancet, 358, pp.24~29 (2001)
- Pearson TA, "Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association", Circulation, 107, pp.499~511 (2003)
- Ashimoto A, "Polymerase chain reaction detection of 8 putative periodontal pathogens in subgingival plaque of gingivitis and advanced periodontitis lesions", Oral Microbiol Immunol, 11, pp.266~273 (1996)
- Saiki RK, "Primer-directed enzymatic amplification of DNA with a thermostable DNA polymerase", Science, 239, pp.487~491 (1988)
- Bishop RF, "Estimation of rotavirus immunoglobulin G antibodies in human serum samples by enzyme-linked immunosorbent assay: expression of results as units derived from a standard curve", J Clin Microbiol, 19, pp.447~452 (1984)
- Taylor BA, "Full-mouth tooth extraction lowers systemic inflammatory and thrombotic markers of cardiovascular risk", J Dent Res, 85, pp.74~78 (2006)
- Medzhitov R, "Recognition of microorganisms and activation of the immune response", Nature, 449, pp.819~826 (2007)
- Loos BG, "Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of periodontitis patients", J Periodontol, 71, pp.1528~1534 (2000)
- Delanghe JR, "Discriminative value of serum amyloid A and other acute-phase proteins for coronary heart disease", Atherosclerosis, 160, pp.471~476 (2002)
- Graziani F, "Effects of non-surgical periodontal therapy on the glomerular filtration rate of the kidney: an exploratory trial", J Clin Periodontol, 37, pp.638~643 (2010)
- Vuletic S, "SAA and PLTP activity in plasma of periodontal patients before and after full-mouth tooth extraction", Oral Dis, 14, pp.514~519 (2008)
- Clifton PM, "Effects of serum amyloid A protein (SAA) on composition, size, and density of high density lipoproteins in subjects with myocardial infarction", J Lipid Res, 26, pp.1389~1398 (1985)
- O'Brien KD, "Serum amyloid A and lipoprotein retention in murine models of atherosclerosis", Arterioscler Thromb Vasc Biol, 25, pp.785~790 (2005)
- Barassi A, "Serum amyloid a and C-reactive protein independently predict the recurrences of atrial fibrillation after cardioversion in patients with preserved left ventricular function", Can J Cardiol, 28, pp.537~541 (2012)
- Noack B, "Periodontal infections contribute to elevated systemic C-reactive protein level", J Periodontol, 72, pp.1221~1227 (2001)
- Linden GJ, "Persistently raised C-reactive protein levels are associated with advanced periodontal disease", J Clin Periodontol, 35, pp.741~747 (2008)
- Slade GD, "Acute-phase inflammatory response to periodontal disease in the US population", J Dent Res, 79, pp.49~57 (2000)
- Unlü Y, "Comparison of levels of inflammatory markers and hemostatic factors in the patients with and without peripheral arterial disease", Thromb Res, 117, pp.357~364 (2006)
- Kosuge M, "Serum amyloid A is a better predictor of clinical outcomes than C-reactive protein in non-ST-segment elevation acute coronary syndromes", Circ J, 71, pp.186~190 (2007)
- Beck JD, "Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease", J Periodontol, 76(11 Suppl), pp.2089~2100 (2005)
- Craig RG, "Relationship of destructive periodontal disease to the acute-phase response", J Periodontol, 74, pp.1007~1016 (2003)
