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PGY-1
The Brooklyn Hospital Center
A Non-infective bone and
joint destructive process
that occurs in association
with peripheral
neuropathy.
DM Type 1& 2 leading
cause in developed world.
First described by
Musgrave 1703
named for Jean Martin
Charcot- 1868 I.D. in
patients with tertiary
syphilis
Diabetes
Hansen’s Disease
Tabes Dorsalis (and Tertiary
Syphilis)
Spinal Cord Tumor
Charcot Marie Tooth Disease
Pernicious Anemia
Chronic Alcoholism
Cerebral Palsy
Hereditary Insensitivity to pain
Myelodysplasia
Meningomyelocele
Poliomyelitis
Syringomyelia
Medications:
• Steroids, phenylbutazone,
indomethacin, vincristine
Sensory-Motor Other Factors
Neuropathy • Metabolic
Autonomic Abnormalities
Neuropathy • Renal Transplant
Minor Trauma • Immunosuppressive
treatment
• Steroid induced
osteoporosis
• Glycosylation of
collagen
Secondary Trauma
overactive vasomotor autonomic
neuropathy AV shunting
regional hyperemia increase
osteoclast activity bone
resorption and ligamentous
weakening mechanical
breakdown/fractures and
deformity
Increased blood flow Warm
Foot & dilated veins
Volkman and Virchow
• “ Peripheral neuropathy
leading to loss of protective
sensation may render the
foot susceptible to injury
from either repeated or
acute trauma “
Insensitivity to
proprioception and pain
repetitive mechanical
macro and micro trauma
spontaneous
fragmentation, subluxation
and dislocation of bone
Minor trauma
Sudden onset
edema/erythema
Increased TG (warm –
hot)
Pain: increased or
decreased.
X-rays unremarkable
Tc-99 Scan uptake all 3
phases.
Edema, hyperemia,
increased
temperature, joint
laxity
Radiological:
• Caspular distention
• Fragementation
• Debris
• Subluxation
Decrease in erythema,
temperature, edema
X-Ray :
• absorption of fine
debris
• new bone formation
• larger fragments
coalesce
• sclerosis of bone
Decrease joint mobility
No edema, erythema
Ulcers may develop at
site of deformity
X-rays:
• bony remodeling,
• decreased sclerosis
CONSERVATIVE SURGICAL