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 aim of this study was to evaluate antegrade autologous bone
grafting with the preservation of articular cartilage in the treatment
of symptomatic osteochondral lesions of the talus with subchondral
cysts. The study involved seven men and five women; their mean age was
35.9 years (14 to 70). All lesions included full-thickness articular
cartilage extending through subchondral bone and were associated
with subchondral cysts. Medial lesions were exposed through an oblique
medial malleolar osteotomy, and one lateral lesion was exposed by
expanding an anterolateral arthroscopic portal. After refreshing
the subchondral cyst, it was grafted with autologous cancellous
bone from the distal tibial metaphysis. The fragments of cartilage
were fixed with 5-0 nylon sutures to the surrounding cartilage.
Function was assessed at a mean follow-up of 25.3 months (15 to
50), using the American Orthopaedic Foot and Ankle Society (AOFAS)
ankle-hindfoot outcome score. The radiological outcome was assessed
using MRI and CT scans.Aims
Patients and Methods
Neuropathic changes in the foot are common with
a prevalence of approximately 1%. The diagnosis of neuropathic arthropathy
is often delayed in diabetic patients with harmful consequences
including amputation. The appropriate diagnosis and treatment can
avoid an extensive programme of treatment with significant morbidity
for the patient, high costs and delayed surgery. The pathogenesis
of a Charcot foot involves repetitive micro-trauma in a foot with impaired
sensation and neurovascular changes caused by pathological innervation
of the blood vessels. In most cases, changes are due to a combination
of both pathophysiological factors. The Charcot foot is triggered
by a combination of mechanical, vascular and biological factors
which can lead to late diagnosis and incorrect treatment and eventually
to destruction of the foot. This review aims to raise awareness of the diagnosis of the Charcot
foot (diabetic neuropathic osteoarthropathy and the differential
diagnosis, erysipelas, peripheral arterial occlusive disease) and
describe the ways in which the diagnosis may be made. The clinical
diagnostic pathways based on different classifications are presented. Cite this article:
We compared the clinical and radiographic results
of total ankle replacement (TAR) performed in non-diabetic and diabetic
patients. We identified 173 patients who underwent unilateral TAR
between 2004 and 2011 with a minimum of two years’ follow-up. There
were 88 male (50.9%) and 85 female (49.1%) patients with a mean
age of 66 years ( The mean AOS and AOFAS scores were significantly better in the
non-diabetic group (p = 0.018 and p = 0.038, respectively). In all,
nine TARs (21%) in the diabetic group had clinical failure at a
mean follow-up of five years (24 to 109), which was significantly
higher than the rate of failure of 15 (11.6%) in the non-diabetic
group (p = 0.004). The uncontrolled diabetic subgroup had a significantly
poorer outcome than the non-diabetic group (p = 0.02), and a higher
rate of delayed wound healing. The incidence of early-onset osteolysis was higher in the diabetic
group than in the non-diabetic group (p = 0.02). These results suggest
that diabetes mellitus, especially with poor glycaemic control,
negatively affects the short- to mid-term outcome after TAR. Cite this article:
The incidence of acute and chronic conditions
of the tendo Achillis appear to be increasing. Causation is multifactorial
but the role of inherited genetic elements and the influence of
environmental factors altering gene expression are increasingly
being recognised. Certain individuals’ tendons carry specific variations
of genetic sequence that may make them more susceptible to injury.
Alterations in the structure or relative amounts of the components
of tendon and fine control of activity within the extracellular
matrix affect the response of the tendon to loading with failure
in certain cases. This review summarises present knowledge of the influence of
genetic patterns on the pathology of the tendo Achillis, with a
focus on the possible biological mechanisms by which genetic factors
are involved in the aetiology of tendon pathology. Finally, we assess
potential future developments with both the opportunities and risks
that they may carry. Cite this article:
