View clinical trials related to Arthropathy, Neurogenic.
Filter by:This study's goal was to determine how denosumab 60 mg, combined with total contact casting and restricted weightbearing status, would affect the treatment of acute CN with CKD. METHODS Participants in the research were those who visited the outpatient foot clinic at PGIMER, CHD in India. During the study period, 446 persons with CN were identified, 102 of whom met the criteria for the first screening, and 78 of whom were ultimately enrolled in the study. Aim: To assess the clinico-radiological remission of Acute Charcot-neuroarthropathy in patients of CKD.
The aim of this study is to evaluate the outcome of healing rate of ankle fusion using modified retrograde IM femoral nail with plate in charcot ankle
Charcot foot, characterized by progressive destructive damage to bone, soft tissue and tendons, involving joint dislocation in the ankle and foot, is a complication of diabetes that is still poorly understood by patients and caregivers. The clinical signs are non-specific and it is therefore largely underestimated due to a delay in diagnosis/lack of diagnosis.This study will be on a prospective multicenter cohort of patients with chronic Charcot's foot in France to evaluate the evolution of quality of life at 2 years, as well as predictive factors in order to better identify subjects with the worst outcome among this population. Our hypothesis is that, in patients with chronic Charcot foot, the deterioration in quality of life over time is primarily related to loss of foot and ankle functionality, foot and ankle deformity and the presence of foot wounds/comorbidities/severe diabetic complications.
The purpose of the study is to evaluate the therapeutic effect of the Charcot Restraint Orthotic Walker three-dimensional printed sole on Charcot foot ulcer healing.
The surgical techniques described in the literature for surgical management of diabetic charcot arthropathy of the foot and ankle include simple exostectomy, open reduction and internal fixation of neuropathic fractures, external fixation, arthrodesis, Achilles tendon lengthening. Patients are followed up at 1 year postoperative by an x-ray of the foot and ankle anteroposterior , lateral and oblique views to assess rate of union ,the correction of deformity by measuring the foot angles . The functional outcome is assessed by the AOFAS scoring system and the diabetic foot ulcer scaoeuulcer scale(18).
Charcot neuropathic osteoarthropathy (CNO) is a progressively destructive process resulting from significant peripheral neuropathy of almost any aetiology. Diabetes mellitus has emerged as the commonest cause of CNO. The Charcot foot in diabetes poses many clinical challenges in its diagnosis and management. The lacuna primarily lies in delineation of its etio-pathogenesis and consequently in targeted treatment modalities. Although traditional approaches focus on neurotraumatic and neurovascular theories, these fail to explain all the features of CNO, hence, other hypotheses have been put forward.The current belief is that once the disease is triggered in a susceptible individual, it is mediated through a process of uncontrolled inflammation which, in turn, leads to osteolysis, fractures and joint destruction. Of these processes, the involvement of the receptor activator of nuclear factor- кB (RANK) ligand /RANK/osteoprotegerin (OPG) system in the process of acute CNO is particularly appealing and suggests new pharmacological approaches. Standard modalities of treatment include offloading and casting. Although various trials have analysed the impact of medical agents including bisphosphonates, teriparatide and bone stimulation techniques, the results have been either inconclusive or not translated into clinical practice. Hence, there is no efficacious treatment of active CNO apart from the traditional offloading. In view of recent advances in understanding of the disease process, the target of intervention should, logically, be interruption of the inflammatory cascade and subsequent osteoclast resorption. Zoledronic acid is the most potent bisphosphonate that has been studied in clinical trials to date and has the distinctive profile of strong inhibitory activity on the enzyme farnesyl pyrophosphate synthase, essential for osteoclast function. Methylprednisolone conceivably has a potential benefit by offsetting the RANKL/OPG system involved. There have been conflicting reports with bisphophosphonates in active CNO and Zoledronic acid has been infrequently used despite being the most potent. Glucocorticoids including methylprednisolone have also not been systematically tried in this condition. We hypothesise that targeting the inflammatory cascade with Methylprednisolone and osteoclast mediated damage by Zoledronic acid will address the basic etiopathogenesis of active CNO and may result in earlier resolution of the disease activity. The above mentioned hypothesis is hence, planned to be tested in a randomised, double-blind, placebo-controlled study.
Charcot neuroarthropathy (CN) is a debilitating disease primarily affecting poorly controlled diabetic patients with peripheral neuropathy. The consequences of CN include ulcerations of the foot and ankle, osteomyelitis, and severe musculoskeletal deformity. These consequences frequently lead to below-knee amputation of the affected limb. Currently treatment options are limited, and no pharmaceutical treatment has been efficacious in the medical literature. The purpose of this pilot study is to investigate the potential of the medication denosumab for acute stage Charcot neuroarthropathy.
The study is designed to investigate biomarkers related to bone turnover in diabetics with charcot foot. This is done by measuring local blood samples in the feet, and systemically in a vene and an artery. Measurements are done before and after cooling the feet in icewater to lower the bloodflow. Patients will be compared with healthy diabetic controls.
The project concerns a type of very debilitating diabetic foot complications called Charcots osteoarthropathy (COA). This disease is characterized by a rapidly progressing destruction of the load bearing joints, primarily in the feet, resulting in loss of structure and remodeling. Untreated this cascade leads to the collapse of the bones, meaning severe pain and walking disability for the patient. Reconstruction is often very difficult or impossible, and furthermore the collapse can lead to chronic foot ulcers and infections, which in the worst case can be fatal. Treatment options are currently limited to early diagnosis and physical offloading (immobilisation), assisted wound healing and surgical intervention. The purpose of this project is to investigate and describe the bone-related factors, which separate COA from other, less acute, diabetic foot changes. The investigators wish to describe the long term consequences of COA - both anatomically, physiologically and biochemically. The investigators will be doing this in a follow-up investigations on a group of COA patients tested 8 years ago. Little is known of the long term changes to the bone structure after acute COA, and the investigators want to visualize to what extend the bone damage is permanent. To do this the investigators will be using DXA-scans, x-ray, blood tests including bone markers, neurophysiological tests and occlusion plethysmography.
To assess the hypothesis that Charcot foot is associated with more vascular complications compared to matched diabetic patients without Charcot foot and to classify patients with Charcot foot according to the human genetic classification of the Qatari population.