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.
To evaluate the applicability of MRI for the quantitative assessment
of anterior talofibular ligaments (ATFLs) in symptomatic chronic
ankle instability (CAI). Between 1997 and 2010, 39 patients with symptomatic CAI underwent
surgical treatment (22 male, 17 female, mean age 25.4 years (15
to 40)). In all patients, the maximum diameters of the ATFLs were
measured on pre-operative T2-weighted MR images in planes parallel
to the path of the ATFL. They were classified into three groups based
on a previously published method with modifications: ‘normal’, diameter
= 1.0 - 3.2 mm; ‘thickened’, diameter >
3.2 mm; ‘thin or absent’,
diameter <
1.0 mm. Stress radiography was performed with the
maximum manual force in inversion under general anaesthesia immediately
prior to surgery. In surgery, ATFLs were macroscopically divided
into two categories: ‘thickened’, an obvious thickened ligament
and ‘thin or absent’. The imaging results were compared with the
macroscopic results that are considered to be of a gold standard.Objectives
Methods
