TY - JOUR ID - TI - Quantitative analysis of IgG antinuclear antibody in chronic periodontitis patients AU - Batool H. Al-Ghurabei بتول الغرابي AU - Hind Wael Al-Alousi هند وائل الالوسي AU - Ahmed A. Al-Hassan احمد الحسن PY - 2012 VL - 24 IS - 3 SP - 145 EP - 148 JO - Journal of baghdad college of dentistry مجلة كلية طب الاسنان بغداد SN - 18171869 23115270 AB - Background: Periodontitis is a bacterial infection of tooth-supporting tissues; the immunopathologic mechanismsinclude inflammatory cells and chemical mediators, which persist inflammation and develop a local autoimmune.The presence of autoantibodies against extracellular matrix components, anti-neutrophil cytoplasmic antibodies(ANCA) and anti-DNA was detected. This study aimed to provide evidence of altered humoral immune response inchronic periodontitis, as well as to determine the presence of auto-antibodies in this disease.Subjects and Methods: Blood samples were collected from 35 patients with chronic periodontitis (20 with severperiodontitis and 15 with moderate periodontitis) and from 30 healthy age and sex matched individuals served ascontrols. Clinical periodontal parameters used in this study were plaque index, gingival index, probing pocket depth,clinical attachment level and bleeding on probing. The levels of serum IgG-antinuclear antibody were determinedusing enzyme-linked immunosorbent assays, whereas serum immunoglobulin (IgG, IgM and IgA) were estimated bysingle radial immune diffusion method.Results: Serum levels of IgG-antinuclear antibody and IgG were significantly higher in sever chronic periodontitis thanin moderate chronic periodontitis and healthy controls (p<0.05). On the other hand, the serum levels of IgM and IgAshowed no significant differences among three studied groups (p>0.05). Concerning the correlation between serumIgG-antinuclear antibody and clinical periodontal parameters, the level of this autoantibody did not show anycorrelation with clinical parameters of periodontitis (p>0.05).Conclusion: The production of antibodies against self structures could be involved in the pathogenic mechanism ofchronic periodontitis

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