Neuropathic arthropathy, also known as Charcot joint, is a condition characterized by progressive joint destruction and deformity caused by loss of sensation in the joints. It was first described in detail by Jean-Martin Charcot in 1868. The major theories for its pathophysiology are neurotrauma from repetitive micro-injuries without pain sensation, and neurovascular dysregulation leading to hyperemia and bone resorption. Diabetes is the most common cause. Imaging shows bone fragmentation, joint dislocation, and deformity. Treatment involves prolonged casting or bracing to immobilize joints during the acute inflammatory phase, followed by bracing and accommodative footwear. Later stages may require surgery.

1. Neuropathic Arthropathy
Charcot joint

2. Jean-Martin Charcot
Jean-Martin Charcot
29 November 1825 – 16
August 1893)
was a
French neurologist and
professor of anatomical
pathology. He is known as
"the founder of modern
neurology"

3. Definition
● Neuropathic arthropathy , neuropathic
osteoarthropathy, Charcot joint refers
to noninfectious progressive condition of
the musculoskeletal system that is
characterized by joint dislocations,
pathologic fractures, and debilitating
deformities.

4. History
● The first description of neuropathic arthropathy
was by Musgrave in 1703, in his book De
Arthritide Symptomatica.He described a
neuropathic joint as an athralgia.
● 1868 Jean-Martin Charcot gave the first detailed
description of this disease.
● In 1892, Sokoloff --upper extremity with
syringomyelia.

5. ● In 1927 Leriche stated that a lesion of
sympathetic led to Hyperaemia and bone
resorption.
● In 1936, Jordan -diabetes mellitus ---neuropathic
changes in the foot and ankle.
● Associated with intra-articular corticosteroid
injections by Chandler and Wright in 1958.
● A.C Brower—Neurovascular theory

6. Etiology
● Any condition that causes sensory or
autonomic neuropathy
● Diabetes mellitus neuropathy
● Multiple Sclerosis
● Alcoholic Neuropathy
● Syringomyelia
● Cerebral palsy
● Leprosy

7. ● Tabes Dorsalis
● Spinal cord injury
● Myelomeningocele
● Intra-articular steroid injections
● Congenital insensitivity to pain
● Familial interstial Polyneuropathy
● Amyloidosis
● Pernicious Anemia

8. ● Vitamin B12 Deficiency
● Phenylbutazone ,Indomethacin
● Ethyl Alcohol.

9. ● Diabetes mellitus is currently the most
common cause of neuropathic arthropathy.
● Neuropathic joint destruction develops in
approximately 0.1% of patients with diabetes
and 5% of those with peripheral neuropathy

10. ● Neuroarthropathy among all pts with tabes
dorsalis ranges b/w 5 to 10%
● 75% of this 5-10% involve lower extremities
and 25% upper extremities.

11. Pathophysiology
● Major theories
– Neurotraumatic theory
– Neurovascular theory
– Most probably both

12. Neurotraumatic Theory
● Loss of peripheral sensation and proprioception
leads to repetitive micro trauma 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.
● Poor fine motor control generates unnatural
pressure on certain joints, leading to additional
microtrauma.

13. ● More recent theories implicate the role of
inflammatory cytokines such as TNF-αand
IL-1 in the pathogenesis of Charcot
neuroarthropathy.
● On the molecular level, these factors lead to
increased expression of nuclear transcription
factor-κB,which in turn stimulates osteoclast
formation.

14. ● Joint destruction in the neuropathic joint is
probably brought on by a combination of
factors that include damage to the
nociceptors of the joint and the periarticular
tissues.

15. ● The activity of peptides such as substance P,
calcium gene related peptide, and vasoactive
intestinal peptide (VIP) could result in increased
vascularity and inflammation, contributing to
further joint destruction.
● Substance P can enhance the cellular synthesis
of collagenase and prostaglandin-E; activate T
lymphocytes, monocytes, and neutrophils; and
take an active part in inflammation

16. ● The initial pathologic changes occur in the
underlying bone and cartilage. Recurrent
effusions occur due to hyperplasia of the
synovium.
● The articular cartilage is slowly destroyed by
a pannus, which helps distinguish Charcot's
joints from other forms of osteoarthritis.

17. Neurovascular theory
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.

18. Clinical History
● A careful history may reveal an unrecognized
traumatic event.
● Charcot neuroarthropathy most frequently
presents in the fifth decade, after an average
duration of diabetes of 20 to 24 years; in
those with type 2 diabetes.

19. Presentation
● DEPENDS OF DURATION OF DISEASE
● Mild swelling w/o deformity-Moderate
deformity with extreme swelling.
● Signs of inflammation.
● Profound unilateral swelling. WBC and
ESR may
be normal

20. Deformity - a) rocker bottom deformity
🞭
🞭
🞭
🞭
🞭
b) medial tarsal subluxation
c) digital subluxation
d) rearfoot equinovarus
e) rearfoot subluxation
f) hypermobility
🞭 cutaneous- a) neuropathic ulcer
🞭
🞭 b) hyperkeratosis
c) infection

21. ● Increase in localized
temp
● Erythema,
● Joint effusion.
● 75% pt. have pain.
● The deep tendon
reflexes at the knee are
absent in a majority of
patients.

22. Marked Irregularities identified as bony
projections.
Bone formation in soft tissues.
Bag of Bones:
Joint can be passively and painlessly moved in
all Directions

23. Acute Charcot neuropathy

24. Diagnosis

25. IMAGING

26. ● Early Changes similar to OA
● Nontraumatic dislocations may be an early
sign.
● Later Radiographic evidence of joint
distention caused by fluid, hypertrophic
synovitis, osteophytes, and subluxation.

27. Atrophic Stage:
● Rapid joint destruction
● Loose bodies
● Subchondral bone erosions
● Subluxation
● Pathological#

28. Hypertrophic Stage
● Reduced jt space.
● Subchondral bone sclerosis
● Pathological # healing with callus
● Multiple osteophyte formation with exoxtosis
formation.
● Dislocations of joints

29. Radiographic features
6D’s Yochum and Rowe
● Dense bones (subchondral sclerosis)
● Degeneration
● Destruction of articular cartilage
● Deformity (pencil-point deformity of
metatarsal heads)
● Debris (loose bodies)
● Dislocation

31. Commonly Affected Joints
● Foot Involvment
● Knee involvement
● Hip involvement
● Shoulder
● Elbow

32. Anatomic Classification
(Sanders and Frykberg, 1991)
● I - forefoot, 10-30%
● II - Lisfranc’s joint, most
common (tarsometatarsal)
● III - midtarsal joint, often
including naviculocuneiform joint
● IV - ankle and subtalar joints, 8-
10%
● V - (“posterior pillar”) fractures of
calcaneus, 2%

33. Classification ( Brodsky and
Rouse)
● Type 1 Midfoot
● Type 2 Hindfoot
● Type 3a Ankle
3b Calcis tubercle
● Type4 Combination
● Type 5 Forefoot

35. Neuropathic Joints
Hyperr
tt
ophic
ic
or
Productiv
iv
e
MIXED
Atrophic
or
Resorptive

36. Radiographic Staging
(Eichenholtz, 1966)
●I Developmental (acute) stage
● II Coalescence (quiescent) stage
● III Consolidation (resolution) stage

37. Modified Eichenholtz Classification for the
Progression of Charcot Neuroarthropathy

38. Stage 0(Shibata and Schon)
● Swelling and erythema
● No Radiographic Changes

39. Eichenholtz Classification
● Stage I - Developmental (acute)
–
–
Hyperemia due to autonomic neuropathy weakens
bone and ligaments
Diffuse swelling, joint laxity, subluxation, frank
dislocation, fine periarticular fragmentation, debris
formation

40. Radiographs
● Stage I

41. Charcot Neuroarthropathy
Eichenholtz Classification
● Stage II - Coalescence (quiescent)
–
–
–
–
Absorption of osseous debris, fusion of larger
fragments
Dramatic sclerosis
Joints become less mobile and more stable
Aka the “hypertrophic”, or “subacute” phase of
Charcot

42. Radiographs
● Stage II

43. Radiographs
● Stage II

44. Eichenholtz Classification
● Stage III - Consolidation (resolution)
–
–
Osseous remodeling
for clinical purposes, stage I is regarded as the
acute phase, while stages II and III are regarded
as the chronic or quiescent phase

45. Radiographs
● Stage III

46. Charcot Arthropathy

47. Rocker bottom deformity

50. HIP
● Charcot neuroarthropathy in the hip is rare.
● Try conservative management - total hip
replacement.
● 50% of fractures of the femoral neck in
diabetics developed Charcot's joints.
● Late manifestation of tabes dorsalis

52. KNEE
● Most Commonly secondary to Syphilis.
● Results in Gross Instability
● Total knee arthroplasty

53. Shoulder

54. Treatment

55. MEDICAL MANAGEMENT
🞭 Control of sugar in diabetic patient
🞭 Management of infection with antibiotics
🞭 In the setting of altered bone mineral density
(BMD) in patients with diabetes,
bisphosphonates can be use to prevent
further osteoporosis in charcot arthropathy.

56. Treatment
● Primarily nonoperative.
● Consists of Acute and Postacute phases.
–
–
Acute (unloading)
Casting along with crutches and walkers.
–
–
Postacute
Include bracing, ankle-foot orthotics(AFO),
specialized shoes.

57. OFF-LOADING OR IMMOBILIZATION DEVICES
USED IN THE MANAGEMENT OF CHARCOT FEET.
🞭 -wheelchair
🞭 -crutches
🞭 -walker
🞭 -Elastic bandage or jones dressing
🞭 -total contact cast
🞭 -fixed ankle walking brace
🞭 -Posterior splint
🞭 -patellar tendon-bearing brace
🞭 -charcot restraint orthotic walker (CROW)

58. Treatment
● Casting- changed every 1-2weeks, if
ulcerations are present changed every week
for wound care, duration from 3-6 months.
● Shoes, bracing, and orthotics- duration
from 6-24 months.
● Typical total healing time 1-2 years.
When the patient enters quiescence phase, management is
directed at a gradual resumption of weight bearing with
prolonged bracing.

60. Early stage (unloading)
● Total Contact cast.

61. CROW boots

62. Surgical options
● Arthrodesis
● Exostosectomy of bony prominences
● Osteotomies
● Reconstructive Surgeries
● Autologous bone Grafting
● Amputations

64. Complication
● Ulcers
● Osteomyelitis
● Gross Deformity of the foot
● Gangrene.

65. THANK
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