The neuropathic joint: a neurovascular bone disorder.

The pathogenesis of the neuropathic joint has long been a subject of controversy. Two main theories have evolved: (1) the neurotraumatic theory, which states that the changes result from repeated mechanical trauma to a joint that is insensitive to pain, and (2) the neurovascular theory, which states that the changes result from a neurally initiated vascular reflex that leads to hyperemia and very active bone resorption by osteoclasts. Through clinical, radiographic, and pathologic observation, it is evident that both theories play a role. Initially, the alteration of sympathetic control triggers a persistent hyperemia, leading to active bone resorption. There may or may not be secondary pathologic fractures and subsequent repair. This depends upon whether the joint is insensitive and whether it is subjected to continued weight-bearing; if so, then the neurotraumatic mechanism comes into play, but only secondarily.