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ISSN 2007-8560 (Print)
Órgano Oficial de Difusión Científica de la Federación Mexicana de Colegios de Ortopedia y Traumatología, A.C. (FEMECOT)

2019, Number 3

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Ortho-tips 2019; 15 (3)

Pathophysiology of Charcot’s neuroarthropathy

Medina GR

Language: Spanish
References: 16
Page: 146-152
PDF size: 136.15 Kb.


ABSTRACT

The Charcot neuroarthropathy is a rare but extremely debilitating complication in diabetic patients and other conditions with neuropathic affection of the limbs (syphilis, leprosy, alcoholic neuropathy, syringomyelia, idiopathic peripheral neuropathy, amyloidosis, cerebral palsy, CMT). It is characterized by an inflammatory and destructive process of the foot and ankle, progressive, non-infectious, which results in bone, joint and ligament damage that determines the loss of the architecture and normal function of the foot. The pathophysiology of this disease has been disconcerting since its initial descriptions by Musgrave and Charcot, but recently the molecular mechanisms that are involved in the pathogenesis of the disease have been characterized in detail, enriching the two traditional theories of its pathophysiology: Neurotraumatic and neurovascular theory, which instead of excluding they are complementary and should be strengthened by their coincidences such as the already known prerequisite of established neuropathy and the local pro-inflammatory state. The effect of sustained hyperglycemia and increased proinflammatory mediators that can activate osteoclasts via RANKL and even by alternative pathways, as well as dysfunction of the counterregulatory mechanisms of osteoclastic activity in the acute phase of the illness, has recently been described. Knowing in detail the pathophysiology of this disease has allowed us to consider new therapeutic strategies in the treatment of Charcot Neuropathy.


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