Charcot joint
Updates to Article Attributes
Charcot joint, also known as a neuropathic or neurotrophic joint, refers to a progressive degenerative/destructive joint disorder in patients with abnormal pain sensation and proprioception.
Epidemiology
In modern Western societies by far the most common cause of Charcot joints is diabetes, and therefore, the demographics of patients matches those of older diabetics. Prevalence differs depending on the severity of diabetes 10:
- ~0.1% in general diabetic population
- ~15% in high-risk diabetic population
- ~30% in patients with peripheral neuropathy
Clinical presentation
Patients present insidiously or are identified incidentally, or as a result of investigation for deformities. Unlike septic arthritis, Charcot joints although swollen are normal temperature without elevated inflammatory markers. Importantly they are painless.
Pathology
There are two forms of Charcot joint: atrophic and hypertrophic. Charcot joints are typically unilateral but are bilateral in ~20% (range 5.9-39.3%) of cases 10.
The pathogenesis of a Charcot joint is thought to be an inflammatory response from a minor injury that results in osteolysis. In the setting of peripheral neuropathy both the initial insult and inflammatory response is not well appreciated, allowing ongoing inflammation and injury 10.
Atrophic form
- most common form 1
- occurs earlier 2
- has an acute progression
- characterised by reabsorption of the ends of the affected bone
- joint destruction with resorption of fragments
- absence of osteosclerosis and osteophytes
- mainly occurs in non-weight bearing joints of the upper limb 1
Hypertrophic form
- only sensory nerves affected
- slow progression
- joint destruction with periarticular debris/bone fragmentation
- initially widened then narrowed joint space
- presence of osteosclerosis and osteophytes 1
- absence of osteoporosis (unless joint is infected) 3
Aetiology
- diabetes (most common)
- leprosy
- multiple sclerosis
- poliomyelitis
- rheumatoid arthritis
- tertiary syphilis
- steroid use
- syringomyelia
- spinal cord injury
- spina bifida
- scleroderma
These can be recalled with the "S" mnemonic.
Location
The involved joint is highly suggestive of the aetiology:
- wrist: diabetes, syringomyelia
- hip: alcohol, tabes dorsalis
- knee: tabes dorsalis, congenital insensitivity to pain
- ankle and foot: diabetes
- spine: spinal cord injury, diabetes, tabes dorsalis
Radiographic features
RadiographPlain radiograph and CT
General characteristics include (six Ds mnemonic) 1:
- dense bones (subchondral sclerosis)
- degeneration
- destruction of articular cartilage
- deformity (pencil-point deformity of metatarsal heads)
- debris (loose bodies)
- dislocation
MRI
T1:-
Involved joints appear diffusely swollen, showing decreased signal intensity. Fat planes adjacent to ulcerated skin show decreased signal intensity.If infected (with a gas-producing organism), there will be a loss of signal intensity.
-
-
T1 Gd-enhancement:-
Inflammatory areas show enhancement, with central non-enhancing necrotic areas.
-
-
STIR:-
Early infection: increased signal intensity due to marrow edema. Later stages: loss of demarcation of cortical outline and cortical destruction.
-
-
In the spine:It is important to differentiate between spinal neuropathy and disc infection.-
Features favoring spinal neuropathy over disc infection:Joint disorganisationFacet involvement.DebrisDiffuse signal intensity in the vertebral body.Spondylolisthesis.Rim enhancement of disc after Gadolinium.
-
Features that are common between spinal neuropathy and disc infection (non-discriminating features):Endplate sclerosis.Erosions.Osteophytes.Decreased disc height.Paraspinal soft tissue masses.
-
MRI plays an important role in diagnosing complications, assessing the extent of the disease, and presence of osteomyelitis.
-
T1:
- involved joints appear diffusely swollen, showing decreased signal intensity
-
Bone marrow edema is a nonspecific sign, but closenessfat planes adjacent totheulcerated skin show decreased signal intensity - if superinfected with a gas-producing organism, there will be a loss of signal intensity.
- T1C+:inflammatory areas show enhancement, with central non-enhancing necrotic areas
-
STIR:
- early infection: increased signal intensity due to marrow oedema
-
later stages: loss of demarcation of cortical outline and
farness from the affected joint favour infection over Charcot joint.cortical destruction
Differential diagnosis
Imaging differential considerations include:
- advanced osteomyelitis: can co-exist (especially in the foot) 4-5
- tuberculous spondylitis / Pott's disease (in the spine)
- chondrosarcoma (shoulder): chondroid matrix instead of bony debris
- inflammatory osteoarthritis/arthritis: early stages can resemble Charcot joint
History and etymology
Jean-Martin Charcot was the first person to give a detailed description of the neuropathic aspect of this condition in 1868 in a patient suffering syphilis.
Practical points
Useful MRI features that support superimposed osteomyelitis on a Charcot joint include 4:
- sinus tract
- diffuse marrow signal abnormality
- replacement of soft tissue fat
- thick rim enhancement
- joint erosion
-
T1:
-</ul><h4>Radiographic features</h4><h5>Radiograph and CT</h5><p>General characteristics include (<a href="/articles/features-of-a-charcot-joint-mnemonic">six Ds mnemonic</a>) <sup>1</sup>:</p><ul>- +</ul><h4>Radiographic features</h4><h5>Plain radiograph and CT</h5><p>General characteristics include (<a href="/articles/features-of-a-charcot-joint-mnemonic">six Ds mnemonic</a>) <sup>1</sup>:</p><ul>
-</ul><h5>MRI</h5><ul>- +</ul><h5>MRI</h5><p>MRI plays an important role in diagnosing complications, assessing the extent of the disease, and presence of osteomyelitis.</p><ul>
-<li>-<strong></strong>Involved joints appear diffusely swollen, showing decreased signal intensity. </li>-<li>Fat planes adjacent to ulcerated skin show decreased signal intensity. </li>-<li>If infected (with a gas-producing organism), there will be a loss of signal intensity. </li>- +<li>involved joints appear diffusely swollen, showing decreased signal intensity</li>
- +<li>fat planes adjacent to ulcerated skin show decreased signal intensity</li>
- +<li>if superinfected with a gas-producing organism, there will be a loss of signal intensity. </li>
-<strong>T1 Gd-enhancement:</strong><ul><li>-<strong></strong>Inflammatory areas show enhancement, with central non-enhancing necrotic areas.</li></ul>-</li>- +<strong>T1C+:</strong><strong> </strong>inflammatory areas show enhancement, with central non-enhancing necrotic areas</li>
-<li>-<strong></strong>Early infection: increased signal intensity due to marrow edema.</li>-<li>Later stages: loss of demarcation of cortical outline and cortical destruction. </li>-</ul>-</li>-<li>-<strong>In the spine:</strong><ul>-<li>It is important to differentiate between spinal neuropathy and disc infection.</li>-<li>Features favoring spinal neuropathy over disc infection:<ol>-<li>Joint disorganisation </li>-<li>Facet involvement. </li>-<li>Debris </li>-<li>Diffuse signal intensity in the vertebral body. </li>-<li>Spondylolisthesis. </li>-<li>Rim enhancement of disc after Gadolinium.</li>-</ol>-</li>-<li>Features that are common between spinal neuropathy and disc infection (non-discriminating features):<ol>-<li>Endplate sclerosis. </li>-<li>Erosions. </li>-<li>Osteophytes. </li>-<li>Decreased disc height. </li>-<li>Paraspinal soft tissue masses. </li>-</ol>-</li>- +<li>early infection: increased signal intensity due to marrow oedema</li>
- +<li>later stages: loss of demarcation of cortical outline and cortical destruction</li>
-<li>MRI plays an important role in diagnosing complications, assessing the extent of the disease, and presence of osteomyelitis.</li>-<li>Bone marrow edema is a nonspecific sign, but closeness to the ulcerated skin and farness from the affected joint favour infection over Charcot joint.</li>
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