The Role of Inflammatory Cytokine and Inflammatory Regulator Protein Related to Severity of Joint Effusion in Osteoarthritis
Keywords:Osteoarthritis, Joint effusion, TNF alpha, IL-1B, NFATC1, C1orf38
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.
Plum Analytics Artifact Widget Block
Ashkavand Z, Malekinejad H, Vishwanath BS. The pathophysiology of osteoarthritis. JOPR J Pharm Res. 2013;7(1):132-8. PMid:29280010
Wojdasiewicz P, Poniatowski AA, Szukiewicz D. The role of inflammatory and anti-inflammatory cytokines in the pathogenesis of osteoarthritis. Mediators Inflamm. 2014;2014:561459. https:// doi.org/10.1155/2014/561459 PMid:24876674
Maricar N, Callaghan MJ, Parkes MJ, Felson DT, O’Neill TW. Clinical assessment of effusion in knee osteoarthritis a systematic review. Semin Arthritis Rheum. 2016;45(5):556-63. https://doi.org/10.1016/j.semarthrit.2015.10.004 PMid:26581486
Mabey T, Honsawek S. Cytokines as biochemical markers for knee osteoarthritis. World J Orthop. 2015;6(1):95-105. https:// doi.org/10.5312/wjo.v6.i1.95 PMid:25621214
Partan RU, Hidayat R. The relationship between TNF-α gene polymorphism, pro-inflammatory cytokines and bone turnover markers in COPD patients with osteoporosis. J Phys: Conf Ser. 2019;1246(2019):012035. https://doi. org/10.1088/1742-6596/1246/1/012035
Saito T. Molecular mechanisms underlying osteoarthritis development: Notch and NF- κ-B. Arthritis Res Ther. 2017;19(1):94. https://doi.org/10.1186/s13075-017-1296-y PMid:28506315
Peters MJ, Ramos YF, den Hollander W, Schiphof D, Hofman A, Uitterlinden AG. Associations between joint effusion in the knee and gene expression levels in the circulation: A meta-analysis. F1000Res. 2016;5:109. https://doi.org/10.12688/ f1000research.7763.1 PMid:27134727
Peirce MJ, Brook M, Morrice N, Snelgrove R, Begum S, Lanfrancotti A, et al. Themis2/ICB1 is a signaling scaffold that selectively regulates macrophage toll-like receptor signaling and cytokine production. PLoS One. 2010;5(7):e11465. https:// doi.org/10.1371/journal.pone.0011465 PMid:20644716
Hartweger H, Schweighoffer E, Davidson S, Peirce MJ, Wack A, Tybulewicz VL. Themis2 is not required for B cell development, activation, and antibody responses. J Immunol. 2014;193(2):700-7. https://doi.org/10.4049/jimmunol.1400943 PMid:24907343
Lawrence MC, Naziruddin B, Levy MF, Jackson A, Mcglynn K. Calcineurin/NFAT and MAP kinase signaling induce TNF-α gene expression in pancreatic islet endocrine cells. J Biol Chem. 2011;286:1025-36. https://doi.org/10.1074/jbc.m110.158675
Li C, Zheng Z, Zhang X, Asatrian G, Chen E, Song R, et al. Nfatc1 Is a functional transcriptional factor mediating nell-1- induced runx3 upregulation in chondrocytes. Int J Mol Sci. 2018;19(1):E168. https://doi.org/10.3390/ijms19010168 PMid:29316655
Greenblatt MB, Ritter SY, Wright J, Tsang K, Hu D, Glimcher LH, et al. NFATc1 and NFATc2 repress spontaneous osteoarthritis. Proc Natl Acad Sci U S A. 2013;110(49):19914-9. https://doi. org/10.1073/pnas.1320036110 PMid:24248346
Singh MM, Devi R. Identification, assessment, and management of overweight and obesity: Summary of updated NICE guidance. BMJ. 2014;349:g6608. https://doi.org/10.1136/bmj.g6608 PMid:25430558
Guarner J, Dolan HK, Cole L. Erythrocyte sedimentation rate: Journey verifying a new method for an imperfect test. Am J Clin Pathol. 2015;144(4):536-8. https://doi.org/10.1309/ ajcpqo81bgtktvjj PMid:26386074
Salehi-Abari I. 2016 ACR revised criteria for early diagnosis of knee osteoarthritis. Autoimmune Dis Ther Approaches. 2016;3(1):118.
Tegner Y, Lysholm J. Rating systems in the evaluation of knee ligament injuries. Clin Orthop Relat Res. 1985;(198):43-9. PMid:4028566
Ghosh P, Smith M. Osteoarthritis, genetic and molecular mechanisms. Biogerontology. 2002;3(1-2):85-8. PMid:12014849
Uhalte EC, Wilkinson JM, Southam L, Zeggini E. Pathways to understanding the genomic aetiology of osteoarthritis. Hum Mol Genet. 2017;26(R2):R193-201. https://doi.org/10.1093/hmg/ ddx302 PMid:28977450
Haywood L, McWilliams DF, Pearson CI, Gill SE, Ganesan A, Wilson D, et al. Inflammation and angiogenesis in osteoarthritis. Arthritis Rheum. 2003;48(8):2173-7. https://doi.org/10.1002/ art.11094 PMid:12905470
Livshits G, Ermakov S, Vilker A. Outlines of the biochemistry of osteoarthritis. Curr Rheumatol Rev. 2010;6(4):234-50. PMid:25693037
Oza P, Reginato AM. Calcium-containing crystal-associated arthropathies in the elderly. Fed Pract. 2016;33(4):14-20.
Lambert C, Dubuc JE, Montell E, Vergés J, Munaut C, Noël A, et al. Gene expression pattern of cells from inflamed and normal areas of osteoarthritis synovial membrane. Arthritis Rheumatol. 2014;66(4):960-8. https://doi.org/10.1002/art.38315 PMid:24757147
Xu Y, Barter MJ, Swan DC, Rankin KS, Rowan AD, Santibanez- Koref M, et al. Identification of the pathogenic pathways in osteoarthritic hip cartilage: commonality and discord between hip and knee OA. Osteoarthritis Cartilage. 2012;20(9):1029-38. https://doi.org/10.1016/j.joca.2012.05.006 PMid:22659600
Liu YM, Chen JW, Chen LX, Xie X, Mao N. Overexpression of P-glycoprotein on fibroblast-like synoviocytes in refractory rheumatoid arthritis patients: A potential mechanism for multidrug resistance in rheumatoid arthritis treatment. Genet Mol Res. 2016;15(2):gmr7927. https://doi.org/10.4238/gmr.15027927 PMid:27323187
Najeeb Q, Aziz R, Hamid S, Khan AH, Najeeb Q. An analysis of different types of arthritis with joint effusions among Kashmiri population in a tertiary care hospital. Int J Biomed Res. 2015;6(4):274-8. https://doi.org/10.7439/ijbr.v6i4.1932
How to Cite
Copyright (c) 2020 Radiyati Umi Partan, Rachmat Hidayat, Muhammad Reagan, Putri Muthia (Author)
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
All rights reserved.