Knee OA Pathophysiologic Rationale: Synovial Neovascularization and Neurogenic Inflammation

Abstract

Knee osteoarthritis is increasingly recognized as a disorder driven not only by mechanical cartilage wear but also by a chronic, low-grade inflammatory state. Synovial neovascularization and accompanying neoinnervation appear to play a central role in amplifying and maintaining nociceptive signaling. Newly formed, immature vessels facilitate leukocyte trafficking and the delivery of pro-inflammatory cytokines, chemokines, and neuropeptides, while parallel ingrowth of pain-sensitive nerve fibers increases pain sensitivity and central sensitization. Genicular artery embolization (GAE) has emerged as a targeted, endovascular treatment for knee pain. GAE is hypothesized to reduce blood flow to inflamed synovium to diminish the influx of inflammatory mediators, attenuate angiogenesis and neoinnervation, and thereby interrupt the feed-forward cycle that sustains chronic nociceptive input.