Abstract
BACKGROUND: Osteoarthritis (OA) is an inflammatory degenerative articular disease characterized by damage narrowing the joint gap, pain, and loss of joint function. Joint effusion is a clinical feature often found in OA patients and believed to be directly proportional to the levels of pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, and interleukin 1B (IL-1B), and various other regulatory proteins such as transcription factor proteins, nuclear factor of activated T-cells 1 (NFATC1), and chromosome 1 open reading frame 38 (C1orf38).
 AIM: The aim of the study was to explore the role of pro-inflammatory cytokine expression (TNF-alpha and IL-1B) and transcription regulatory proteins (NFATC1 and C1orf38) with the severity of joint effusion in OA patients.
 METHODS: This study was an observational study with a case series study approach. A total of 80 study subjects with OA joint effusions were included in the study. The diagnosis of OA was based on clinical and radiologic assessment from American College of Rheumatology. Data of clinical severity were assessed with Kellgren-Lawrence criteria, stroke test score, and Tegner Lysholm Knee Scoring Scale. Random blood examination was performed to obtain erythrocyte sedimentation rate (ESR) and qualitative C-reactive protein to evaluate the level of inflammation in the body. TNF-alpha, IL-1B, NFATC1, and C1orf38 levels were assessed in joint fluid using the enzyme-linked immunosorbent assay method. The correlation was analyzed with the Pearson correlation test (p = 0.05).
 RESULTS: The severity of OA joint effusion was not correlated to ESR (p adjusted = 0.169; r = 0.078), TNF-alpha (p adjusted = 0.112; r = −0.087), IL-1B (p adjusted = 0.136, r = −0.078), C1orf38 (p adjusted = 0.121; r = −0.088), and NFATC1 (p adjusted = 0.102; r = −0.081).
 CONCLUSION: Pro-inflammatory cytokines of TNF-alpha and IL-1B, and the transcription factors of pro-inflammatory cytokines gene expression, NFATC1, and C1orf38, did not correlate with the severity of joint effusion in OA.
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