Platelet-rich Plasma-induced Inhibition of Chondrocyte Apoptosis Directly Affects Cartilage Thickness in Osteoarthritis.

Rafia Asjid,Saleem Ahmed Khan,Khadija Qamar,Aamna Khalil,Muhammad Sarwar Zia,Tayyaba Faisal

doi:10.7759/cureus.6050

Abstract

The search for minimally invasive treatment of osteoarthritis has led to the development of biological options such as platelet-rich plasma (PRP), mesenchymal stem cells (MSCs), and bone marrow aspirate concentrates. This research was conducted to study the outcomes of PRP administration in the chemical-induced model of osteoarthritis in rat knee.Methods and resultsTwo milligrams of monoiodoacetate (MIA) was used for the induction of arthritis in the right knee of 16 rats. Autologous PRP was prepared by double centrifugation, which was then administered in the arthritic knee of eight rats. This group was labeled as the treated group (A) while the rest were counted as the non-treated group (B). Chondrocyte count and uncalcified cartilage thickness were morphometrically assessed on hematoxylin and eosin (H&E) stained slides, and it was noted that treated group A had a higher chondrocyte count and more cartilage height as compared to non-treated group B. Intergroup comparison was done between the treated group (A) and non-treated group (B) using the independent t-test. P-values were found to be statistically significant for these parameters.ConclusionThis study thus concluded that PRP had induced an inhibitory effect on the apoptosis of chondrocytes, which, in turn, prevented the loss of cartilage height by inhibiting matrix loss.

Highlights

Osteoarthritis (OA) is a major source of disability, pain, and economic burden worldwide
The catabolic effects of interleukins secreted by chondrocytes, mononuclear cells, osteoblasts, and synovial cells interfere with the activity of growth factors and reduce the synthesis of aggrecan, which is the key constituent of the matrix providing resilience to cartilage [4]
We studied the effect of platelet-rich plasma (PRP) on chondrocyte count in the arthritic rat knee cartilage and noted a decrease in the chondrocyte apoptosis in the PRP-treated group as evident by the higher chondrocyte number in the treated group A in comparison to the non-treated group B

Summary

Introduction

Osteoarthritis (OA) is a major source of disability, pain, and economic burden worldwide. Biochemical, and mechanical factors are responsible for the complex multifactorial epidemiology of the disease. OA was believed to be caused by the mechanical degradation of cartilage but recent advances in understanding the pathophysiology have led to the conclusion that it is a complex process in which matrix proteases play a fundamental role [2]. The catabolic effects of interleukins secreted by chondrocytes, mononuclear cells, osteoblasts, and synovial cells interfere with the activity of growth factors and reduce the synthesis of aggrecan, which is the key constituent of the matrix providing resilience to cartilage [4]. Interleukin-1β (IL-1β), the proinflammatory cytokine, is a major protagonist in inducing arthritic changes, as evident by its increased levels in the synovial fluid of affected joints [5,6]

Methods

Discussion

Conclusion