The aim of this retrospective study was to compare the functional
and radiological outcomes of bridge plating, screw fixation, and
a combination of both methods for the treatment of Lisfranc fracture
dislocations. A total of 108 patients were treated for a Lisfranc fracture
dislocation over a period of nine years. Of these, 38 underwent
transarticular screw fixation, 45 dorsal bridge plating, and 25
a combination technique. Injuries were assessed preoperatively according
to the Myerson classification system. The outcome measures included
the American Orthopaedic Foot and Ankle Society (AOFAS) score, the
validated Manchester Oxford Foot Questionnaire (MOXFQ) functional
tool, and the radiological Wilppula classification of anatomical
reduction.Aims
Patients and Methods
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.
