Neuropathic joint disease 2394162 222090652 2008-06-27T14:45:28Z SmackBot 433328 Date the maintenance tags or general fixes {{Infobox_Disease | Name = Neuropathic joint disease | Image = | Caption = | DiseasesDB = 2344 | ICD10 = | ICD9 = | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = orthoped | eMedicineTopic = 381 | eMedicine_mult = {{eMedicine2|radio|476}} | MeshID = }} '''Neuropathic osteoarthropathy''' refers to progressive degeneration of a [[weight bearing]] [[joint]], a process marked by bony destruction, [[bone resorption]], and eventual [[deformity]]. Onset is usually insidious. It is also known as '''Charcot joint'''. If this pathological process continues unchecked, it could result in joint deformity, [[ulcer]]ation and/or [[superinfection]], loss of function, and in the worst case scenario: [[amputation]]. 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 advanced: **''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,{{Fact|2008-06-26|date=June 2008}} and the foot is the most affected region. In those with foot deformity, approximately 60% are in the [[Tarsometatarsal articulations| tarsometatarsal joints]] (medial joints affected more than lateral), 30% [[Metatarsophalangeal articulations| 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 [[Syphilis#Neurosyphilis|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. ==Clinical Findings== Clinical findings include [[erythema]], [[edema]] and increased temperature in the affected joint. In neuropathic foot joints, plantar ulcers may be present. Note that it is often difficult to differentiate [[osteomyelitis]] from a Charcot joint, as they may have similar tagged WBC scan and [[MRI]] features (joint destruction, dislocation, edema). Definitive diagnosis may require bone or [[Synovial membrane| synovial]] biopsy. ==Radiologic Findings== First, it is important to recognize that two types of abnormality may be detected. One is termed "atrophic," in which there is [[osteolysis]] of the distal metatarsals in the forefoot. The more common form of destruction is "hypertrophic" joint disease, characterized by acute peri-articular fracture and joint dislocation. The natural history of the joint destruction process has a classification scheme of its own, offered by Eichenholtz decades ago: '''Stage 0:''' Clinically, there is joint edema, but radiographs are negative. Note that a bone scan may be positive before a radiograph is, making it a sensitive but not very specific modality. '''Stage 1:''' Osseous fragmentation with joint dislocation seen on radiograph ("acute Charcot"). '''Stage 2:''' Decreased local edema, with coalescence of fragments and absorption of fine bone debris '''Stage 3:''' No local edema, with consolidation and remodeling (albeit deformed) of fracture fragments. The foot is now stable. Destroyed TMT joints in the medial left foot, with fracture and dislocation of fragments; these are classic findings. Also note loss of the foot arch and acquired [[flat foot]] (pes planus) deformity. ==Treatment== Once the process is recognized, immobilization with a total contact [[Orthopedic cast|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. ==References== *[http://uwmsk.org/residentprojects/charcot.html Neuropathic osteoarthropathy] by Monica Bhargava, M.D., University of Washington Department of Radiology *Canale: ''Campbell's Orthopaedics'', 10th edition, 2003 Mosby, Inc. *Gupta, R. 1993. A short history of neuropathic arthropathy. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8222448&dopt=Abstract Clinical Orthopaedics], 296, pp. 43-49. *Sommer, Todd C., and Lee, Thomas H. Charcot Foot: The Diagnostic Dilemma. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11730314&dopt=Abstract American Family Physician. Vol. 64, No. 9, Nov. 1, 2001]. [[Category:Rheumatology]]