Pathophysiology and Drivers of Knee Arthrofibrosis

Arthrofibrosis is fibrosis within and around the joint, including the capsule and ligaments. Inflammation is needed for healing, but here it becomes a loop: fibroblasts turn into myofibroblasts and keep laying down scar tissue and extracellular matrix. The knee stays warm, swollen and stiff for months, patellar mobility drops and patients describe the knee as caged. Loss of extension is the main concern, and the psychological impact is large. Drivers include immobilization, bleeding without drainage, hypoxia from tourniquet use or packed scar tissue, persistent inflammation, infection and genetic predisposition. Unlike frozen shoulder, knee arthrofibrosis needs an insult such as surgery and does not start on its own. Substance P can sensitize the infrapatellar fat pad, which then limits extension. Aggressive physiotherapy that forces flexion triggers arthrofibrosis and central sensitization. Myofibroblasts can persist for years, so the knee stays reactive. Blood flow restriction training should be avoided early because of its hypoxic effect. The speaker suggests treating every slow, stiff knee as possible arthrofibrosis from the start.