Hind foot Charcot deformity is a disastrous complication of diabetic neuropathy and can lead to instability, ulceration and major amputation. The treatment of these patients is controversial. Internal stabilization and/or external fixation have demonstrated variable results of limb salvage and some authorities thus advise patients to undergo elective major amputation. However, we report a series of 9 diabetic patients with severe hind foot deformity complicated by ulceration in 5/9, who underwent acute corrective internal fixation with successful correction of deformity, healing of ulceration in 4/5 patients and limb salvage in all cases. We treated 9 diabetic patients attending a multidisciplinary diabetic/orthopaedic foot clinic with progressive severe Charcot hind foot deformity despite treatment with total contact casting, 5 with predominant varus deformity and 2 with valgus deformity and 2 with unstable ankle joints. Five patients had developed secondary ulceration. All patients underwent corrective hind foot fusion with tibiotalo-calcaneal arthrodesis using a retrograde intra-medullary nail fixation and screws and bone grafting. One patient also with fixed plano-valgus deformity of the foot underwent a corrective mid-foot reconstruction.Introduction
Methods
Tightrope fixation is known method for reconstructing acromioclavicular joint and the presence of good bone stock around the two drillholes is the most important determining factor for preventing failure. Arthroscopic-assisted tightrope stabilisation involve drilling clavicle and coracoids in a straight line. This leads to eccentric drillholes with inadequate bone around it. Open tightrope fixation involves drilling holes under direct vision, independently and leading to centric hole with adequate bone around it. Our study assesses the hypothesis of tightrope fixation in relation to location of drillholes using CT-scan and cadaveric models for arthroscopic and open technique for ACJ fixation. CT-scans of 20 shoulders performed. Special software used to draw straight line from distal end of clavicle to coracoid. Bone volume around coracoid drillhole was calculated. Cadaveric shoulder specimens were dissected. The arthroscopic technique was performed under vision by drilling both clavicle and base of coracoid holes in one direction. Same specimens were used for open technique. Base of coracoid crossectioned and volume calculated.Aim
Methods
Parathyroid hormone-related peptide (PTHrP) has been shown to be an important regulator of bone remodelling1. The aim of this study was to investigate the effect of the N-terminal domain of PTHrP (1–36) on osteogenic and angiogenic gene expression in human osteoblasts (HOB) and human bone marrow stromal cells (hBMSCs). Primary hBMSC's and HOBs were cultured in standard or osteogenic media with different concentrations of PTHrP, either continuously for 8, 24, 48 h and 9 days, or with 3 cycles of intermittent exposure (24 h with PTHrP, 24 h without) over 6 days. Cell lysates were then processed for analysis of gene expression. Expression of the osteogenic markers runt-related transcription factor 2 (RUNX-2), alkaline phosphatase (ALP) and Collagen 1, and the angiogenic marker; vascular endothelial growth factor (VEGF), were measured.Introduction
Materials and Methods
