Charcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration. Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy. It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis. Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14). Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process. An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking.
Limited forefoot amputation in diabetic patients
with osteomyelitis is frequently required. We retrospectively reviewed
diabetic patients with osteomyelitis, an unhealed ulcer and blood
pressure in the toe of >
45 mmHg who underwent limited amputation
of the foot with primary wound closure. Between 2006 and 2012, 74
consecutive patients with a mean age of 67 years (29 to 93), and
a median follow-up of 31 months, were included. All the wounds healed
primarily at a median of 37 days (13 to 210; mean 48). At a median
of 6 months (1.5 to 18; mean 353 days), 23 patients (31%) suffered
a further ulceration. Of these, 12 patients (16% of the total) required
a further amputation. We conclude that primary wound closure following limited amputation
of the foot in patients with diabetes is a safe and effective technique
when associated with appropriate antibiotic treatment. Cite this article:
