A POSSIBLE ASSOCIATION BETWEEN GINGIVAL CREVICULAR FLUID INFLAMMATORY CYTOKINES AND RHEUMATOID ARTHRITIS DISEASE ACTIVITY

Authors

1 Assistant Professor of Oral Medicine, Periodontology, Oral Diagnosis and Radiology, Faculty of Dentistry, Alexandria University

2 Lecturer of Oral Medicine, Peiodontology, Oral Diagnosis and Radiology, Faculty of Dentistry, Alexandria University

3 Internal Medicine Specialist, Rheumatology Department, Faculty of Medicine, Alexandria University

Abstract

Backgroud: Rheumatoid arthritis (RA) and chronic periodontitis are the most common chronic inflammatory diseases with remarkable pathological and clinical similarities
Aim: This study was performed to determine a possible relation between the severity of chronic periodontitis together with increased local inflammation of the periodontium and RA disease activity.
Methods: This study was conducted on 20 patients with Rheumatoid Arthritis fulfilling the 2010 ACR/EULAR classification criteria for RA. All subjects were recruited from those attending the Rheumatology Unit and Rheumatology outpatient clinic at the Alexandria main University Hospital. Rheumatoid disease activity was assessed by DAS-28 score system. The periodontal status was assessed by measuring PD, CAL, PI and GI. Local proinflammatory cytokines from the gingival crevicular fluid (GCF) were quantified including Il-6 and TNF-α. Correlations between different parameters were assessed using Spearman coefficient
Results: A positive correlation was found between DAS28 and both GCF IL-6 and TNF-α (p=0.694- r=0.001 ) and (p=0.604- r=0.005) for IL-6 and TNF- α respectively and the values were statistically significant. A positive correlation was also found between DAS28 and each of PD (p=0.246, r=0.297), CAL (p= 0.244, r=0.300), PI (p= 0.406, r= 0.076)and GI (p= 0.340,r= 0.142) however the correlation was not statistically significant.
Conclusion: The findings provide evidence of a possible relation between Rheumatoid Arthritis and chronic periodontitis through sharing the same inflammatory mechanism.