Potential Activities of Synovial Immune Response Suppression as JNK Pathway Inhibitor in Osteoarthritis Management

Main Article Content

Renti Kusumaningrum Samosir
Emeraldha Theodorus
Debby Cinthya Damiri Valentina
Theodora Agverianti

Abstract

ABSTRACT


IntroductionOsteoarthritis (OA) is a degenerative joint disease affecting 10-15% population of adults above 60 years old.  Prevalence rate of the disease in Indonesia in 2013 is 8,1% over the populations. Osteoarthritis is a slow progressive erosion of cartilage components which caused decreased of physical activity level and quality of life. Treatment for osteoarthritis can prevent the progressiveness of the disease. DiscussionDegradation of cartilage joint and subchondral bonein OA patients iscaused by mechanical stress or trauma. Trauma and the overuse of jointscouldrelease oxidative stress and activate sinovial immune response,IL-1 and TNF-α specifically. Activation of immune response can cause the decreased of aggrecans, decreased synthesis of hyaluronic acid which produce lubricant of joints, and impairment of c-Jun NH 2-terminal Kinase (JNK) signalling pathway which cause cartilage degradation and may lead to significant pain. JNKpathway inhibitor potencytoprevent and treat OA can inhibit cartilage degradation. Several compounds which are used to inhibit those proinflammatory cytokines activation are melatonine, vildagliptin (DPP-4 inhibitor), epigallocathecin-3-gallate (EGCG)and Lycorine. Conclusion: Inhibition of JNK pathway which is involved in the regulation of differentiation and apoptosis after oxidative stress exposureare supposed to decrease cartilage degradation significantly, so that it could be developed as a novel therapy modality to prevent worsening the disease of patients with OA.


 


Keywords: Cytokine, JNK pathway inhibitor, Osteoarthritis, Treatment


 

Article Details

How to Cite
Samosir, R., Theodorus, E., Valentina, D., & Agverianti, T. (2020). Potential Activities of Synovial Immune Response Suppression as JNK Pathway Inhibitor in Osteoarthritis Management. JIMKI: Jurnal Ilmiah Mahasiswa Kedokteran Indonesia, 8(2), 88-94. https://doi.org/10.53366/jimki.v8i2.128
Section
Article Review

References

1. Martin AP. “Symptoms. Localizations: knee, hip, hands, spine, other localizations.” Aten Primaria. 9: Supp 1(2014):11-7.
2. Blagojevic M, Jinks C, Jeffery A, Jordan KP. “Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis.” Osteoarthritis Cartilage. 18:1(2010):24-33.
3. World Health Organization. Chronic rheumatic conditions. Geneva: Chronic Diseases and Health Promotion World Health Organization, 2016.
4. Deshpande BR, et al. “Number of persons with symptomatic knee osteoarthritis in the US: impact of race and ethnicity, age, sex, and obesity”. Arthritis Care Res. 2016; 68:12(2016):1743–50.
5. Kementerian Kesehatan Republik Indonesia. Riset kesehatan dasar tahun 2018. Jakarta: Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan Republik Indonesia, 2018.
6. Ahmad IW, Rahmawati LD, Wardhana TH. “Demographic profile, clinical and analysis of osteoarthritis patients in Surabaya.” Biomolecular and Health Science Journal. 2018; 1:1(2018):34-9.
7. Vargas NF, et al. “Treatment of patients with osteoarthritis.” Aten Primaria. 46:Supp 1(2014):39-61.
8. Buttgereit F, Burmester GR, Bijlsma JWJ. “Non-surgical management of knee osteoarthritis: where are we now and where do we need to go?” RMD Open. 1:1(2015):1-4.
9. Ge HX, et al. “JNK pathway in osteoarthritis: pathological and therapeutic aspects.” Journal of Receptors and Signal Transduction. 37:5(2017):431-6.
10. Ashkavand Z, Malekinejad H, Vishwanath BS. “The pathophysiology of osteoarthritis.” Journal of Pharmacy Research. 2013(2013):132-8.
11. Perhimpunan Reumatologi Indonesia. Diagnosis dan penatalaksanaan osteoartritis. Jakarta: Perhimpunan Reumatologi Indonesia, 2014.
12. Palazzo C, et al. “Risk factors and burden of osteoarthritis.” Ann Phys Rehabil Med. 59:3(2016):134-8.
13. Sokolove J, Lepus CM. “Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations.” Theurapeutic Advances in Muskuloskeletal Disease. 5:2(2012):77-88.
14. Destianti NA, Fatimah SN, Dewi S. “Vitamin C intake and risk factors for knee osteoarthritis.” AMJ. 4:2(2018):173-7.
15. Roughley PJ, Mort JS. “The role of aggrecan in normal and osteoarthritis cartilage.” Journal of Experimental Orthopaedics. 1:8(2014):1-11.
16. Lespasio, et al. “Knee osteoarthritis: A primer.” Perm J. 21:16(2017):1-7.
17. Pereira D, Ramos E, Branco J. “Osteoarthritis.” Acta Med Port. 28:1(2015):99-106.
18. Leung R. “Osteoarthritis of the knee.” InnovaIT. 2018(2018):1-8.
19. Kolasinski SL, et al. “2019 American college of rheumatology or arthritis foundation guideline for the management of osteoarthritis of the hand, hip and knee.” Arthritis Care and Research. 72:2(2020):149-62.
20. Hosseinzadeh, et al. “Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin.” Journal of Pineal Research. 61(2016):411–25.
21. Wang Z, et al. “Vildagliptin reduced extracellular matrix degradation in human primary chondrocytes.” Eur J of Pharmacol. 884(2019):49-55.
22. Akhtar N, Haqqi TM. “Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced inflammatory response in human chondrocytes.” Arthritis Res Ther. 13:93(2011):1-16.
23. Chen S, et al. “Lycorine protects cartilage through suppressing the expression of matrix metalloprotenases in rat chondrocytes and in a mouse osteoarthritis model.” Mol Med Rep. 14:4(2016):3389-96.