The pathogenesis of the neuropathic joint has been a subject of controversy for many years. Two main theories of pathophysiologic pathways have evolved: (1) the neurotraumatic, which states that the changes result from mechanical trauma and repetitive injuries to an insensitive extremity or joint and (2) the neurovascular, which states that the changes result from a neurally initiated vascular reflex that leads to hyperemia, angiogenesis, and very active bone resorption by osteoclasts. Through clinical, radiographic, and pathologic observation, it appears evident that both pathways contribute to neuropathic bone and joint disease. Initially, the alteration of sympathetic control triggers a persistent hyperemia, leading to active bone resorption. There may or may not be associated pathologic fractures and subsequent repair. This depends upon the degree of joint insensitivity and whether or not it is subjected to continued weightbearing. If so, the neurotraumatic mechanisms come into play, but only secondarily.