Evaluation of t-PA, PAI-2, IL-1<i>β</i> and PGE<sub>2</sub> in gingival crevicular fluid of rheumatoid arthritis patients with periodontal disease


Biyikoglu B., BUDUNELİ N. G., Kardesler L., AKSU K., Oeder G., Kuetuekcueler N.

JOURNAL OF CLINICAL PERIODONTOLOGY, cilt.33, sa.9, ss.605-611, 2006 (SCI-Expanded, Scopus) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 9
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1111/j.1600-051x.2006.00961.x
  • Dergi Adı: JOURNAL OF CLINICAL PERIODONTOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.605-611
  • İstanbul Üniversitesi-Cerrahpaşa Adresli: Hayır

Özet

Aims: This study was undertaken to compare periodontal conditions, gingival crevicular fluid (GCF) levels of tissue-type plasminogen activator (t-PA), its inhibitor plasminogen activator inhibitor-2 (PAI-2), interleukin-1 beta (IL-1 beta), prostaglandin E-2 (PGE(2)) in rheumatoid arthritis (RA) patients and control groups. Methods: Twenty-three RA patients, 17 systemically healthy patients with periodontal disease (PD), and 17 systemically and periodontally healthy subjects were recruited. GCF samples were obtained from two single-rooted teeth. Full-mouth clinical periodontal measurements were recorded at six sites/tooth. GCF samples were analysed using relevant ELISA kits. Data were tested statistically by appropriate tests. Results: Total amounts of t-PA, PAI-2 and PGE(2) in GCF samples of the healthy control group were significantly lower than the other groups (p < 0.05). The RA group exhibited a higher total amount of t-PA in GCF samples than the PD group (p < 0.05). PAI-2, IL-1 beta and PGE(2) total amounts were similar in RA and PD groups (p > 0.05). Conclusion: The coexistence of RA and periodontitis does not seem to affect clinical periodontal findings or systemic markers of RA. Similar inflammatory mediator levels in RA and PD groups, despite the long-term usage of corticosteroids, non-steroidal anti-inflammatory drugs, suggest that RA patients may have a propensity to overproduce these inflammatory mediators.