Charcot Joint

Neuropathic osteoarthropathy, also known as Charcot joint (often "Charcot foot"), refers to progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity. Onset is usually insidious.

If this pathological process continues unchecked, it could result in joint deformity, ulceration and/or superinfection, loss of function, and in the worst case scenario: amputation or death. Early identification of joint changes is the best way to limit morbidity.

Pathogenesis

Basically, any condition resulting in decreased peripheral sensation, proprioception, and fine motor control:

• Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics. Related to long-term poor glucose control.
• Alcoholic neuropathy
• Cerebral palsy
• Leprosy
• Syphilis (tabes dorsalis), caused by the organism Treponema pallidum
• Congenital insensitivity to pain
• Spinal cord injury
• Myelomeningocele
• Syringomyelia
• Intra-articular steroid injections

Underlying Mechanisms

Two primary theories have been

• Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint in question; this damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. Indeed, it is a vicious cycle. In addition, poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.
• Neurovascular: Neuropathic patients have dysregulated autonomic nervous system reflexes, and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads to bony destruction.

In reality, both of these mechanisms probably play a role in the development of a Charcot joint.

Joint Involvement

Diabetes is the foremost cause in America today for neuropathic joint disease, and the foot is the most affected region. In those with foot deformity, approximately 60% are in the tarsometatarsal joints (medial joints affected more than lateral), 30% Metatarsophalangeal joints and 10% have ankle disease. Over half of diabetic patients with neuropathic joints can recall some kind of precipitating trauma, usually, minor.

Patients with neurosyphilis tend to have knee involvement, and patients with syringomyelia of the spinal cord may demonstrate shoulder deformity.

Hip joint destruction is also seen in neuropathic patients.

Treatment

Once the process is recognized, immobilization with a total contact cast will help ward off further joint destruction. Pneumatic walking braces are also used. Surgical correction of a joint is rarely successful in the long-term in these patients.

It can take 6–9 months for the edema and erythema of the affected joint to recede.