Healthy joints rely on articular cartilage—a smooth, resilient tissue that cushions bone surfaces during movement. After age 30, cartilage loses approximately 1-2% of its volume per year as chondrocyte activity declines and the balance between tissue repair and breakdown shifts toward degradation, a process known as osteoarthritis progression.
As cartilage thins, exposed bone surfaces generate friction and trigger inflammatory cytokines such as interleukin-1 and TNF-alpha. This inflammatory cascade not only accelerates further cartilage loss but also irritates surrounding nerves, converting localized joint wear into radiating pain patterns that patients describe as burning, tingling, or shooting sensations.
Peripheral nerves depend on intact myelin sheaths for proper signal transmission. Chronic inflammation, metabolic dysfunction, and mechanical compression gradually damage these protective coverings, resulting in neuropathy—a condition where nerve signals misfire, causing pain, numbness, or weakness in areas far from the original injury site.
