Affiliations: [a] Department of Physical Medicine and Rehabilitation, Gaziler Physical Medicine and Rehabilitation Training and Research Hospital, Ankara, Turkey | [b] Department of Physical and Rehabilitation Medicine, Medical School, Hacettepe University, Ankara, Turkey | [c] Department of Biostatistics, Faculty of Medicine, Ankara University, Ankara, Turkey | [d] Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Ankara University, Ankara, Turkey
Correspondence:
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Corresponding author: Merve Örücü Atar, Department of Physical Medicine and Rehabilitation, Gaziler Physical Medicine and Rehabilitation Training and Research Hospital, Ankara, Turkey. Tel.: +90 312 291 1000; Fax: +90 0312 291 1009; E-mail: drmerveorucu@hotmail.com.
Abstract: 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 Duruöz 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.
