“Platelet-rich plasma holds promise in management of rheumatoid arthritis”—systematic review

The treatment of rheumatoid arthritis (RA) has been closely evolving with an understanding of disease pathogenesis with disease modifying anti-rheumatoid drugs (DMARDS) and Biologic DMARDS being the main stay. platelet rich plasma (PRP) has been the center of research in many specialties in the past decade. Its ability to stop and reverse inflammation have attracted researchers to try PRP in RA. A systematic review of studies on PRP in RA is lacking. The study protocol was prospectively registered in PROSPERO. Detailed search of Cochrane, Scopus, Medline, Embase, and Web of science databases were made to identify the relevant articles till Sep 2020 following Cochrane and PRISMA guidelines. Number of subjects, Animal model used, cell lines used for the study, method of induction of arthritis, PRP dose, concentration used, frequency of administration and clinical, histologic, and molecular changes from baseline following PRP use were extracted and analysed. Eight studies were included for the review. Four of these were in-vitro studies. Two were exclusive animal studies. One study analysed the effects of PRP in RA in both animal models (mice) and Hela cell lines. One study was a report of a series of patients of resistant RA treated with PRP. In the in vitro studies while platelets increase the migration and invasion of RA-FLS, they suppressed the inflammation on the whole. Available animal studies and the Human study have shown encouraging results. There has been no evidence of exacerbation of inflammation in these studies. The quantity and quality of literature on the effects of PRP in treating joint pathologies in RA is limited. Preclinical studies show decrease in disease activity with good safety profile. Invitro studies show suppression of inflammation. Thus, the available literature is encouraging towards the use of PRP in RA. Larger trials and molecular studies to understand the exact role of platelets in disease pathogenesis and treatment mechanisms are needed to decide the future course of PRP in RA.