Recent studies indicate that platelet-rich plasma (PRP) is receiving growing attention as a biologically based intervention for cartilage damage and osteoarthritis. Its proposed therapeutic potential is attributed to its capacity to modulate multiple molecular pathways involved in cartilage metabolism and inflammatory responses. Evidence from in vitro and animal studies suggests that PRP may affect signaling pathways, including PI3K/AKT/mTOR, NF-κB, Wnt/β-catenin, and TGF-β/Smad, all of which are implicated in autophagy regulation, inflammatory modulation, and extracellular matrix homeostasis. Nevertheless, most of the mechanistic evidence currently comes from preclinical models, whereas high-quality clinical data validating these biological effects in patients remain scarce. Consequently, the translational relevance of these mechanisms to clinical outcomes requires further clarification. Standardized PRP preparation methods, well-defined dosing strategies, and robust long-term studies evaluating clinical safety and efficacy are essential before PRP can be reliably incorporated into routine regenerative orthopedic practice.
Li et al. (Wed,) studied this question.