The stiffness and pain that our ancestors described through 'wind, dampness, cold, heat' and 'coagulation and stagnation of qi and blood' are referred to in modern medicine as 'frozen shoulder' or technically as 'adhesive capsulitis,' explained through specific biological mechanisms.
Adhesive capsulitis occurs when the joint capsule surrounding the shoulder joint becomes inflamed, thickens, contracts, and develops adhesion. A normal shoulder joint capsule is loose, allowing a wide range of arm movement. In adhesive capsulitis, however, this joint capsule becomes thick and stiff like solid ice, severely restricting arm motion.
This condition progresses roughly through three stages. The first is the 'freezing stage,' where pain begins throughout the shoulder and worsens at night, disrupting sleep. Movement gradually becomes restricted due to pain during this phase. Next is the 'frozen stage,' where pain may subside somewhat, but joint motion restriction becomes more severe, making lifting or rotating the arm nearly impossible. The final phase is the 'thawing stage,' where the stiff joint gradually loosens, pain eases, and mobility slowly recovers. However, natural recovery takes at least one to over three years, and some patients do not recover fully.
Why do this adhesion and inflammation occur? Although no single clear cause has been identified, multiple risk factors interact. The most well-known is age, as it commonly occurs between ages 40 and 60, giving rise to its colloquial Korean name. It also tends to be slightly more common in women. Notably, patients with diabetes have more than five times higher risk of developing adhesive capsulitis compared to the general population, often with bilateral onset or more severe symptoms. In diabetes, glucose in the body binds with protein to form advanced glycation end products, which stiffen collagen fibers and reduce joint capsule elasticity. Other systemic conditions such as thyroid disease, heart disease, and Parkinson's disease can increase risk, and it easily occurs after prolonged shoulder immobilization following an injury or surgery.
Looking closer at the modern pathophysiological mechanisms, a chronic inflammatory response inside the joint capsule plays a central role. Inflammatory substances like cytokines, including interleukin-1 beta and tumor necrosis factor-alpha, and prostaglandins secreted by inflammatory cells cause tissue damage to the joint capsule and stimulate fibroblasts to induce excessive proliferation of collagen fibers. This accelerates the process of fibrosis, leaving the joint capsule thick and stiff. Moreover, excessive formation of new blood vessels and nerve proliferation accompanying the inflammatory response have been reported, pointing to causes of the severe pain felt by patients.
What Donguibogam described as 'coagulation and stagnation of qi and blood' aligns modernly with the inflammatory response and fibrosis driven by blood circulation disorders and micro-metabolite accumulation within the joint capsule. When tissues around the shoulder receive insufficient nutrients and oxygen while metabolic waste builds up, tissue damage, inflammation, and stiffness follow. Furthermore, external factors such as wind-cold-dampness can worsen inflammatory responses or disrupt blood circulation by harming the shoulder joint microenvironment. Internal factors such as liver and kidney deficiency parallel systemic metabolic imbalances like diabetes or thyroid disease that increase shoulder joint vulnerability.
Adhesive capsulitis goes beyond simple aching, interfering with daily activities such as dressing, washing hair, and sleeping, which can significantly reduce quality of life. Therefore, obtaining an accurate diagnosis early and starting proper treatment and management is crucial. Rather than enduring the pain, actively care for your shoulder.
