Treatment for delayed wound healing resulting from peripheral vascular diseases and diabetic foot ulcers remains a challenge. A novel surgical technique named ‘tibial cortex transverse transport’ (TTT) has been developed for treating peripheral ischaemia, with encouraging clinical effects. However, its underlying mechanisms remain unclear. In the present study, we explored the potential biological mechanisms of TTT surgery using various techniques in a rat TTT animal model. A novel rat model of TTT was established with a designed external fixator, and effects on wound healing were investigated. Laser speckle perfusion imaging, vessel perfusion, histology, and immunohistochemistry were used to evaluate the wound healing processes.Aims
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:
