IADR Abstract Archives
Independent Proinflammatory and Anti-Inflammatory Cytokine Pathways in PISA
Objectives: Periodontal disease (PerioD) is a chronic, complex inflammatory condition resulting from the interplay between bacteria and host immune response. Since, host response is complex and multidimensional, our goal was to examine the salivary factors that would associate with clinical periodontal inflammation.
Methods: Sixty-three (63) mid-age and elderly [mean age (SD): 67 (9)], highly educated [mean (SD): 17 (2)] subjects with 59% female, 7% African American were recruited into this study. They underwent standardized periodontal exams and stimulated saliva collection. Periodontal Inflamed Surface Area (PISA), a continuous measure of clinical periodontal inflammation was calculated using periodontal measures. Salivary cytokines, chemokines and angiogenesis factors IL-1α, IL-7, IL-12p40, IL-15, IL-16, IL-17, TNF-β, VEGF-A, IL-1β, IL-6, IL-8, IL-10, IL-13, TNF-α, IP10, MIP1-A, bFGF-A, Fit1, PIGF, VEGF-A, VEGF-D were determined using electrochemiluminescence assays (MSD platform). Principal Component Analysis (PCA) was used to reduce the dimensionality of data. Regression analyses were used to determine the associations between principal components and PISA.
Results: PCA showed six components with an eigenvalue greater than unity and it explained 70% of the total variance. IL-15, IL-7, IL-8, VEGF-A, Fit1, PIGF, VEGF-D loaded on component one (T cell – angiogenic regulator component-TARC), IL-16, IL1α, IL1β, TNF-α loaded on component 2 (proinflammatory component - PIC), bFGF-A and VEGF-A loaded on component 3 (Growth factor component - GFC), IL-10, IL6, IL13 loaded on component 4 (anti-inflammatory - AIC), IL-12p40, IL-17 and TNF- β loaded on component 5 (chemokine regulators component - CRC) and MPI1-A and IP-10 loaded on component 6 (chemokine component - CC). In regression analysis with PISA as the dependent variable and PCI and AIC as independent variables, we found that after adjusting for age PISA scores significantly associated with salivary PIC and AIC (PIC: part r=0.33, p=0.01; AIC: part r=0.30, p<0.02). All the other PC were not significant.
Conclusions: These results showed that clinical periodontal inflammation associates with proinflammatory and anti-inflammatory molecules pointing to clinical periodontal inflammation resulting from either pro-inflammatory or anti-inflammatory pathways.
Methods: Sixty-three (63) mid-age and elderly [mean age (SD): 67 (9)], highly educated [mean (SD): 17 (2)] subjects with 59% female, 7% African American were recruited into this study. They underwent standardized periodontal exams and stimulated saliva collection. Periodontal Inflamed Surface Area (PISA), a continuous measure of clinical periodontal inflammation was calculated using periodontal measures. Salivary cytokines, chemokines and angiogenesis factors IL-1α, IL-7, IL-12p40, IL-15, IL-16, IL-17, TNF-β, VEGF-A, IL-1β, IL-6, IL-8, IL-10, IL-13, TNF-α, IP10, MIP1-A, bFGF-A, Fit1, PIGF, VEGF-A, VEGF-D were determined using electrochemiluminescence assays (MSD platform). Principal Component Analysis (PCA) was used to reduce the dimensionality of data. Regression analyses were used to determine the associations between principal components and PISA.
Results: PCA showed six components with an eigenvalue greater than unity and it explained 70% of the total variance. IL-15, IL-7, IL-8, VEGF-A, Fit1, PIGF, VEGF-D loaded on component one (T cell – angiogenic regulator component-TARC), IL-16, IL1α, IL1β, TNF-α loaded on component 2 (proinflammatory component - PIC), bFGF-A and VEGF-A loaded on component 3 (Growth factor component - GFC), IL-10, IL6, IL13 loaded on component 4 (anti-inflammatory - AIC), IL-12p40, IL-17 and TNF- β loaded on component 5 (chemokine regulators component - CRC) and MPI1-A and IP-10 loaded on component 6 (chemokine component - CC). In regression analysis with PISA as the dependent variable and PCI and AIC as independent variables, we found that after adjusting for age PISA scores significantly associated with salivary PIC and AIC (PIC: part r=0.33, p=0.01; AIC: part r=0.30, p<0.02). All the other PC were not significant.
Conclusions: These results showed that clinical periodontal inflammation associates with proinflammatory and anti-inflammatory molecules pointing to clinical periodontal inflammation resulting from either pro-inflammatory or anti-inflammatory pathways.