The Charcot Joint: A Modern Neurologic Perspective

Chisholm, Kara A.; Gilchrist, James M.

doi:10.1097/cnd.0b013e3181c6f55b

Cited by 61 publications

(50 citation statements)

References 46 publications

(67 reference statements)

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“…But none of these theories can explain this pathogenesis by themselves. Nevertheless, as the research advanced, neither the neurotrophic theory which was represented by Charcot himself (22) nor the neurotraumatic theory which was supported mainly by German scientists, have lost value. On the contrary, as complex biochemical processes revealed, the pathways of the two theories became more and more intertwined (22, 27).…”

Section: Pathophysiologymentioning

confidence: 99%

“…Monocytes and osteoclasts storm the affected site and this accelerates the bone resorption rate resulting in osteopenia. Lower structural resistance cause minor traumas to end up in fractures, dislocations, and joint collapses (22). Volkman and Virchow confronted this theory, suggesting an insensate foot is prone to repetitive unrecognized traumas (38).…”

Section: Pathophysiologymentioning

confidence: 99%

“…The prevalence of diagnosed Charcot arthropathy in patients with diabetes is reported to be 0.08–7.5% (3). However, some studies suggest higher prevalence with as many as 13% of all diabetic patients and 29% of the neuropathic patients affected (22, 27). Due to the lack of specific markers or diagnostic criteria and Charcot artropathy's clinical resemblance to relatively more common disorders such as osteomyelitis, the diagnosis is missed or delayed in 25% of the cases (28).…”

mentioning

confidence: 99%

“…Moreover, after prospective computerized tomography examinations, bilateral neuroarthropathic changes are demonstrated in 75% of Charcot patients (17). Chisholm and colleagues suggest that obesity is also a predisposing factor for Charcot arthropathy since at least two thirds of Charcot patients are obese (22, 32). …”

mentioning

confidence: 99%

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An overview of the Charcot foot pathophysiology

Kaynak¹,

Birsel²,

Güven³

et al. 2013

Diabetic Foot & Ankle

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Charcot arthropathy of the foot is a rare but devastating complication of diabetes that remains to be a challenging issue for the foot and ankle surgeons. Charcot foot fails to be an obvious diagnostic option that comes to mind, even in a pathognomonic clinical appearance. The rarity of the disorder, more common pathologies that mimic the condition, and the self-limiting prognosis deviate the clinician from the right diagnosis. The clinical challenges in the diagnosis of Charcot foot require in-depth investigations of its enigmatic nature to establish useful guidelines. Yet, this goal seems to be beyond reach, without a holistic view of the immense literature concerning the pathophysiology of the disorder. The primary objective of this article is to put together and review the recent advancements about the etiology and intrinsic mechanisms of diabetic Charcot foot.

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Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

An overview of the Charcot foot pathophysiology

Kaynak¹,

Birsel²,

Güven³

et al. 2013

Diabetic Foot & Ankle

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“…The patient then presented with painless left foot swelling and was found to have an atraumatic, posterior calcaneal fracture suspicious for a Charcot joint about 2 years after treatment was initiated (Figure 2). Sensory neuropathy, autonomic dysfunction, and loss of protective pain and proprioceptive sensation are thought to predispose a joint to Charcot arthropathy 2,3 . Charcot arthropathy is associated with diabetes mellitus, syringomyelia, spinal cord lesions, cerebral palsy, polio, leprosy, tabes dorsalis, and chronic alcoholism 3 .…”

Section: To the Editormentioning

confidence: 99%

Severe Sensory Neuronopathy in Primary Sjögren Syndrome Resulting in Charcot Arthropathy

Nguyen

Peschken

2016

J Rheumatol

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When Is Osteonecrosis Not Osteonecrosis?: Adjudication of Reported Serious Adverse Joint Events in the Tanezumab Clinical Development Program

Hochberg

Tive

Abramson

et al. 2016

Arthritis & Rheumatology

136

141

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Objective. Tanezumab, a monoclonal antibody against nerve growth factor, has demonstrated efficacy in clinical trials of chronic pain in osteoarthritis (OA) and chronic low back pain. Unexpected adverse events (AEs) described as osteonecrosis (ON) occurred during tanezumab development, leading the US Food and Drug Administration to impose a partial clinical hold for all indications except cancer pain. A blinded Adjudication Committee (AC) including orthopedic surgeons, rheumatologists, and an orthopedic pathologist reviewed and adjudicated jointrelated AEs in the tanezumab clinical program.Methods. The AC adjudicated all reported cases of ON as well as cases of total joint replacements (TJRs) not reported as ON for which radiographs obtained within 9 months of the surgery were available. The AC prespecified categories for joint safety events including primary ON, worsening OA (rapid progression of OA [RPOA], normal progression of OA, insufficient information to distinguish between rapid and normal progression of OA), other, or insufficient information to distinguish between primary ON and worsening OA or another diagnosis.Results. The AC reviewed events in 249 of 386 patients with an investigator-reported AE of ON and/or a TJR. Two events were adjudicated as primary ON, 200 events were adjudicated as worsening OA (68 of which were classified as RPOA), 29 events had another diagnosis, 11 had insufficient information to distinguish primary ON from worsening OA, and 7 did not have committee member consensus.Conclusion. Despite initial reports, tanezumab treatment was not associated with an increase in ON but was associated with an increase in RPOA. Higher doses of tanezumab, tanezumab administered with nonsteroidal antiinflammatory drugs, and preexisting subchondral insufficiency fractures were risk factors for RPOA in this cohort.Tanezumab, a humanized monoclonal antibody, specifically targets and inhibits, with high affinity, interaction of nerve growth factor (NGF) with its receptors, TrkA (neurotrophic tyrosine kinase receptor type 1) and p75 (a low-affinity NGF receptor) (1-11). Tanezumab has been shown to reduce pain and improve function and patient's global assessment in patients with osteoarthritis (OA) of the knee and hip and those with chronic low back pain in phase II and III randomized controlled cliniClinicalTrials.gov identifiers:

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The Charcot Joint: A Modern Neurologic Perspective

Cited by 61 publications

References 46 publications

An overview of the Charcot foot pathophysiology

An overview of the Charcot foot pathophysiology

Severe Sensory Neuronopathy in Primary Sjögren Syndrome Resulting in Charcot Arthropathy

When Is Osteonecrosis Not Osteonecrosis?: Adjudication of Reported Serious Adverse Joint Events in the Tanezumab Clinical Development Program

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