Platelet-rich plasma in discogenic pain: therapeutic potential of multifactorial action

Abstract

Intervertebral disc degeneration (IVDD) is one of the leading causes of chronic low back pain and disability. The key pathogenetic mechanism of IVDD is chronic inflammation, which leads to extracellular matrix catabolism and the death of disc cells. It has been established that these changes are based on the activation of pro-inflammatory signaling cascades, particularly NF-κB, MAPK, and JAK/STAT pathways, as well as the induction of caspase-dependent apoptosis.

Objective: To summarize current understanding of the molecular signaling pathways involved in degenerative processes within the intervertebral disc, and to elucidate the mechanisms of action of platelet-rich plasma (PRP) components capable of modulating these pathways.

Materials and methods: A comprehensive analysis of contemporary experimental and clinical studies was performed to evaluate the effects of the main growth factors present in PRP (TGF-β, PDGF, IGF-1, FGF, CTGF, EGF, HGF) on signaling pathways in intervertebral disc cells associated with catabolism, apoptosis, and inflammation.

Results: PRP-derived factors exert their effects through activation of the Smad, PI3K/AKT, MAPK, and JAK/STAT pathways while attenuating NF-κB activity, leading to decreased levels of pro-inflammatory cytokines (IL-1β, TNF-α) and metalloproteinases (MMPs, ADAMTS). These effects are accompanied by enhanced expression of type II collagen and aggrecan, stabilization of the extracellular matrix, restoration of tissue homeostasis and increased cell proliferation.

Conclusions: PRP therapy demonstrates considerable potential as a pathogenetically oriented regenerative strategy for the treatment of IVDD. Its efficacy arises from a multimodal influence on inflammatory, catabolic, and apoptotic pathways. Further clinical research is warranted to standardize treatment protocols and confirm the long-term therapeutic effectiveness of PRP.