Platelet-Rich Plasma and Cartilage Repair

Abstract

Purpose of review: To assess the utilization and efficacy of platelet-rich plasma (PRP), for the treatment of articular cartilage injury, most commonly characterized by progressive pain and loss of joint function in the setting of osteoarthritis (OA).

Recent findings: PRP modulates the inflammatory and catabolic environment through a locally applied concentrate of platelets, leukocytes, and growth factors. Clinically, PRP has been shown to be possibly a viable treatment adjuvant for a variety of inflammatory and degenerative conditions. Recent efforts have focused on optimizing delivery methods that enable platelets to slowly degranulate their biological constituents, which may promote healing and improve OA symptoms for a longer duration. There are various factors that affect the progression of OA within joints, including inhibition of inflammatory cytokines and altering the level of enzymatic expression. PRP therapy aims to mediate inflammatory and catabolic factors in a degenerative environment through the secretion of anti-inflammatory factors and chemotaxic effects. There are a growing number of studies that have demonstrated the clinical benefit of PRP for non-operative management of OA. Additional randomized controlled trials with long-term follow-up are needed in order to validate PRP's therapeutic efficacy in this setting. Additionally, continued basic research along with well-designed pre-clinical studies and reporting standards are necessary in order to clarify the effectiveness of PRP for cartilage repair and regeneration for future clinical applications.

Keywords: Anti-inflammatory; Cartilage; Cytokines; Inflammatory; Osteoarthritis; Platelet-rich plasma.

Fig. 1

(1a) Catabolic factors interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) stimulate MMP synthesis. (1b) Matrix metalloproteinases (MMPs) cause degradation of the collagenous framework and induce collagen Type X expression. (1c) Degradation of the cartilage and chondrocytes promotes catabolic activation. (2a) NF-κΒ receptor activator ligand (RANKL) activates in the presence of pro-inflammatory factors and (2b) results in the downregulation of SRY-box 9 (SOX-9) and upregulation of cyclooxygenase (COX-2) and nitric oxide synthesis (NOS). (2c) Inhibition of SOX-9 downregulates collagen Type II. (3a) Pro-inflammatory factors stimulate reactive oxygen species (ROS) and activates catabolic factors. (3b) ROS causes chondrocyte apoptosis and release of catabolic and degenerative factors [, –54]