Serum endothelin-1 levels, radiographic and ultrasonographic evaluations, and clinical parameters in patients with knee and/or hand osteoarthritis
Journal of Back and Musculoskeletal Rehabilitation, cilt.32, sa.4, ss.549-554, 2019 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 32 Sayı: 4
- Basım Tarihi: 2019
- Doi Numarası: 10.3233/bmr-181326
- Dergi Adı: Journal of Back and Musculoskeletal Rehabilitation
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.549-554
- Anahtar Kelimeler: Osteoarthritis, knee, hand, endothelin-1, ultrasound, cartilage
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
BACKGROUND: Endothelin-1 (ET-1) is one of the probable inflammatory factors stimulating cartilage degradation in osteoarthritis (OA) pathogenesis. OBJECTIVE: To assess ET-1 level in OA and its correlation with radiographic findings, cartilage morphology and clinical parameters. METHODS: One hundred and thirty-nine subjects (89 OA, 50 controls) were included in this cross-sectional study. Both knee and hand joints of the participants were examined using plain radiography and ultrasound imaging by which distal femoral cartilage thickness/grading and second metacarpophalangeal cartilage thickness were assessed. Subjects were evaluated for pain and functional status using visual analogue scale, Western Ontario and McMaster Universities Arthritis Index and Duruoz Hand Index. RESULTS: Serum ET-1 levels were higher in the OA group than the control group. Serum ET-1 levels were not correlated with cartilage thickness in patients with OA. Serum ET-1 levels were not correlated with either pain or other clinical parameters in the knee OA group and in the hand OA group. CONCLUSION: This is the first study evaluating the relationship between serum ET-1 levels and cartilage morphology and clinical parameters, which did not show any conclusive result. Future studies, overcoming the limitations of this study, might provide a better understanding of the role of ET-1 in the pathogenesis of OA.