Charcot arthropathy in the midfoot and ankle
Charcot arthropathy is a severe destructive arthropathy which can occur in any patient with a sensory deficit. It was originally described in tertiary syphilis. Nowadays most cases occur in diabetics, but about 10% of our Charcot patients have other causes, such as:
- spina bifida
- hereditary motor/sensory neuropathy
- post-traumatic sensory deficits
- alcoholic peripheral neuropathy
- sensory neuropathy of unknown origin
A recent systematic review of Charcot neuroarthropathy was authored by Rogers (2011) on behalf of the American Podiatric Medical Association and the American Diabetes Association.
Charcot arthropathy probably begins with trauma – about 30-50% of patients have a recognised injury, others probably have subclinical injuries. Injury to the joint is followed by rapid destruction of the joint surfaces and demineralisation. There appears to be osteoclast overactivity, bone vascular shunting and bone breakdown. Vascular shunting may be due to sympathetic denervation. However, osteoclast acivity is promoted by sympathetic stimulation rather than denervation, so the osteoclast activity of Charcot is likely to be a local effect, possibly part of deranged fracture repair mechanisms. Christensen (2011) did not find an assocation between sympathetic denervation and Charcot arthropathy.
Some of the metabolic features are similar to those of complex regional pain syndromes and regional osteoporosis, but in these conditions there is no joint destruction. There is some demineralisation in Type 1 (but not type 2) diabetics' feet prior to the onset of Charcot arthropathy, but in both types there is marked demineralisation with the onset of Charcot (Petrova 2004). Current attention focuses on the role of proinflammatory cytokines and the RANK-L pathway in osteoclast activation (Jeffcoate 2005, Rogers 2011) and an excellent review is provided by Larson (2012).
Charcot arthropathy is often said to be painless, but in fact there is usually pain, though this may be less than might be expected from the degree of arthropathy and deformity. The joint destruction and demineralisation may lead to deformity, skin pressure and ulceration. After a few weeks healing begins and after a few months there is usually bony union with joint incongruity and deformity.