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.
The purpose of this study was to compare the clinical and radiographic
outcomes of total ankle arthroplasty (TAA) in patients with pre-operatively
moderate and severe arthritic varus ankles to those achieved for
patients with neutral ankles. A total of 105 patients (105 ankles), matched for age, gender,
body mass index, and follow-up duration, were divided into three
groups by pre-operative coronal plane tibiotalar angle; neutral
(<
5°), moderate (5° to 15°) and severe (>
15°) varus deformity.
American Orthopaedic Foot and Ankle Society (AOFAS) ankle-hindfoot
score, a visual analogue scale (VAS), and Short Form (SF)-36 score
were used to compare the clinical outcomes after a mean follow-up period
of 51 months (24 to 147).Aims
Patients and Methods
The goals of this study were: 1) to determine if high-fat diet
(HFD) feeding in female mice would negatively impact biomechanical
and histologic consequences on the Achilles tendon and quadriceps
muscle; and 2) to investigate whether exercise and branched-chain
amino acid (BCAA) supplementation would affect these parameters
or attenuate any negative consequences resulting from HFD consumption. We examined the effects of 16 weeks of 60% HFD feeding, voluntary
exercise (free choice wheel running) and BCAA administration in
female C57BL/6 mice. The Achilles tendons and quadriceps muscles
were removed at the end of the experiment and assessed histologically
and biomechanically.Objectives
Methods
