GCF Levels of MMP-8, -13, TIMP-1 in Rheumatoid Arthritis Patients

Objectives: Rheumatoid arthritis (RA) and periodontal disease are chronic destructive inflammatory diseases with many pathologic features in common. This study was conducted to compare the gingival crevicular fluid (GCF) levels of matrixmetalloproteinase-8 (MMP-8), MMP-13, tissue inhibitor of matrixmetalloproteinases -1 (TIMP-1) in RA patients having gingivitis or periodontitis with those of the control groups.

Methods: Subjects (n=74) were divided into 5 groups according to their systemic and periodontal status. Study groups were as follows: 12 RA patients with gingivitis (RA-G), 13 RA patients with periodontitis (RA-P), 12 systemically healthy patients with gingivitis (H-G), 13 systemically healthy patients with periodontitis (H-P), and 24 periodontally and systemically healthy volunteer subjects (H-C). Full-mouth clinical periodontal measurements were performed by Williams periodontal probe at 6 sites/tooth. GCF samples were obtained from two sites representing the clinical periodontal diagnosis in single rooted teeth and analyzed by ELISA. Data were tested statistically by parametric tests.

Results: Total amounts of MMP-8 in GCF samples were statistically lower in the H-C group than the RA-G, RA-P, and H-P groups (p<0.05). TIMP-1 total amount was higher in the H-C group than the RA-G, H-G, and H-P groups (p<0.05). There were no differences between the study groups in MMP-13 levels (p>0.05). RA patients with gingivitis or periodontitis exhibited similar levels of MMP-8, MMP-13 and TIMP-1 with the systemically healthy periodontal disease groups (p>0.05).

Conclusions: Coexistence of RA and periodontal disease does not seem to affect the investigated clinical and biochemical parameters. Our data indicate that GCF level of MMP-8 is increased in the presence of periodontal inflammation. Since, similar levels of MMP-8, MMP-13, and TIMP-1 were seen in the GCF of RA patients, despite the long-term usage of corticosteroids and non-steroidal anti-inflammatory drugs; it is suggested that RA patients may have a tendency to overproduce these inflammation-associated molecules.