The Effect of Platelet-Rich Plasma on Synovial Fibrosis and Cartilage Degeneration in Knee Osteoarthritis

Abstract

Background:

Synovial fibrosis is a prevalent pathological feature of osteoarthritis and a primary contributor to joint pain and stiffness. Studies indicate that platelet-rich plasma (PRP) is rich in growth factors and cytokines, exhibiting anti-inflammatory, anti-apoptotic, chemotactic, and proliferative properties that can facilitate tissue repair. However, little is known about its effect on synovial fibrosis in knee osteoarthritis (KOA).

Purpose:

To determine the effect of PRP on synovial fibrosis and cartilage degeneration in KOA.

Study Design:

Controlled laboratory study.

Method:

Anterior cruciate ligament transection was performed to induce KOA in male Sprague-Dawley rats, and then rats were randomly assigned to 4 different groups: sham operation, KOA only, KOA treated with phosphate-buffered saline (PBS), and KOA treated with PRP. Synovial collagen fiber deposition was observed using Masson and Sirius red staining, and synovial inflammation was assessed using hematoxylin and eosin (H&E) staining. Moreover, immunohistochemistry was conducted to analyze the expression of synovial fibrosis–related factors including PLOD2, COL1A1, TIMP1, TGF-β1, and α-SMA. KOA severity and articular cartilage degradation were assessed using micro–computed tomography (micro-CT), safranin O–fast green staining, H&E staining, immunohistochemistry, and the Osteoarthritis Research Society International (OARSI) criteria. A quantitative analysis of growth factors (platelet-derived growth factor, IGF-1, epidermal growth factor, TGF-β1, fibroblast growth factor, and endothelial growth factor) in activated PRP was performed using enzyme-linked immunosorbent assay.

Results:

Micro-CT imaging and histological staining showed that the KOA model had been successfully established. Compared with the KOA and PBS groups, Masson staining and Sirius red staining results showed that PRP aggravated the degree of synovial fibrosis, which was consistent with the results of immunohistochemistry analysis. Immunohistochemistry analysis showed that PRP promoted the protein expression of PLOD2, COL1A1, TIMP1, TGF-β1, and α-SMA, indicating that the degree of fibrosis was aggravated. However, the PRP group showed lower OARSI and synovitis scores, as well as attenuated abnormal tibial subchondral bone remodeling, suggesting that PRP inhibited further cartilage degeneration and synovial inflammation and improved the subchondral bone microarchitecture.

Conclusion:

PRP may aggravate KOA synovial fibrosis, but it still has an inhibitory effect on cartilage degeneration and abnormal subchondral bone remodeling.

Clinical Relevance:

Synovial fibrosis is a significant pathological feature in KOA that is closely linked to clinical symptoms like joint pain and stiffness. This study offers insights into enhancing the effectiveness of PRP therapy for patients with KOA.