Diabetic Neuropathic Osteoarthropathy Research Articles

Bone Defect Replacement in Diabetic Neuropathic Osteoarthropathy (Charcot Foot): Review

Background. The number of patients with diabetes mellitus, including those with its severe complications such as Charcot neuropathic osteoarthropathy, is increasing worldwide. Restoration of weight bearing ability and creation of conditions for ulcer healing is challenging for trauma and orthopedic surgeons, especially because of the need to restore bone tissue defects.
 Aim of the review to compare modern methods of replacement of large bone tissue defects of the distal segment of the lower limb in patients with Charcot neuropathic osteoarthropathy.
 Methods. The articles were searched in PubMed/MEDLINE, Google Scholar, Scopus, eLIBRARY, CyberLeninka databases. The search was performed using the following keywords and word combinations: Charcot foot, diabetic neuropathic osteoarthropathy and bone grafting. Full-text articles in Russian and English were selected. The search was carried out without chronological limitations due to the small number of published studies and specific subject of research.
 Results. The possibilities of bone defect replacement in Charcot foot are poorly described in the world literature. The narrow specificity and relative infrequency of this pathology is the probable reason for the small number of publications and the lack of studies with a high level of evidence.
 Conclusion. Bone autografting for lesions of the medial or lateral midfoot column and Ilizarov tibial lengthening to compensate for limb shortening after reconstructive surgeries at the level of the hindfoot and ankle joint are the most commonly used methods of bone defect replacement in patients with Charcot foot. Free bone autografting (possibly with demineralized bone matrix) is the method of choice for small defects of the lateral or medial column of the midfoot.

Cartilage Damage Pathological Characteristics of Diabetic Neuropathic Osteoarthropathy.

Diabetic neuropathic osteoarthropathy (DNOAP) is a rare and easily missed complication for diabetes that leads to increased morbidity and mortality. DNOAP is characterized by progressive destruction of bone and joint, but its pathogenesis remains elusive. We herein aimed to investigate the pathological features and pathogenesis of the cartilages damage in DNOAP patients. The articular cartilages of eight patients with DNOAP and eight normal controls were included. Masson staining and safranine O/fixed green staining (S-O) were used to observe the histopathological characteristics of cartilage. The ultrastructure and morphology of chondrocytes were detected by electron microscopy and toluidine blue staining. Chondrocytes were isolated from DNOAP group and control group. The expression of receptor activator of nuclear factor kappaB ligand (RANKL), osteoprotegerin (OPG), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and Aggrecan protein was evaluated by western blot. Reactive oxygen species (ROS) levels were measured using a 2',7'-dichlorofluorescin diacetate (DCFH-DA) probe. The percentage of apoptotic cells was determined by flow cytometry (FCM). The chondrocytes were cultured with different glucose concentrations to observe the expression of RANKL and OPG. Compared with the control group, the DNOAP group showed fewer chondrocytes, subchondral bone hyperplasia, and structural disorder, and a large number of osteoclasts formed in the subchondral bone area. Moreover, mitochondrial and endoplasmic reticulum swellings were observed in the DNOAP chondrocytes. The chromatin was partially broken and concentrated at the edge of nuclear membrane. The ROS fluorescence intensity of chondrocyte in DNOAP group was higher than that in normal control group (28.1 ± 2.3 vs. 11.9 ± 0.7; P < 0.05). The expression of RANKL, TNF-α, IL-1β, and IL-6 protein in DNOAP group was higher than that in normal control group, whereas OPG and Aggrecan protein were lower than that in normal control group (both P < 0.05). FCM showed that the apoptotic rate of chondrocyte in DNOAP group was higher than that in normal control group (P < 0.05). The RANKL/OPG ratio showed significant upward trend when the concentration of glucose was over than 15 mM. DNOAP patients tend to have severe destruction of articular cartilage and collapse of organelle structure including mitochondrion and endoplasm reticulum. Indicators of bone metabolism (RANKL and OPG) and inflammatory cytokines (IL-1β, IL-6, and TNF-α) play an important role in promoting the pathogenesis of DNOAP. The glucose concentration higher than 15 mM made the RANKL/OPG ratio change rapidly.

Pathological Characters and Molecular Pathogenesis of Diabetic Neuropathic Osteoarthropathy Cartilages Damage

Category:Basic Sciences/BiologicsIntroduction/Purpose:The aim of current study was to investigate the pathological characters and relative molecular pathogenesis of the cartilages damage in diabetic neuropathic osteoarthropathy (DNOAP) patients.Methods:The articular cartilages of ankle joint, subtalar joint and talonavicular joint of 8 patients with DNOAP from March 2017 to June 2018 were selected as DNOAP group. And the articular cartilage of matched joints from 8 amputation patients were selected as control group. Masson staining and safranine O/fixed green staining were used to observe the histopathological characteristics of cartilage, and the ultrastructural changes of chondrocytes were observed by electron microscopy. Chondrocyte culture was carried out in DNOAP group and control group. Western blot was used to detect the expression of RANKL, OPG, IL-1ß, IL-6, TNF-a, Aggrecan protein in chondrocyte. DCFH-DA probe was used to detect the level of reactive oxygen species in chondrocyte. Flow cytometry was used to detect the apoptotic rate of chondrocyte.Results:In DNOAP group, chondrocytes decreased, subchondral bone proliferated, structure disordered and osteoclasts formed in a large number in subchondral bone area. Under transmission electron microscopy, mitochondrial and endoplasmic reticulum swelling were observed in DNOAP chondrocytes. The chromatin was partially broken and concentrated at the edge of nuclear membrane. The ROS fluorescence intensity of chondrocyte in DNOAP group was higher than that in normal control group (28.1±2.3 VS 11.9±0.7, P<0.05). The relative expression of RANKL, TNF-a, IL-1ß and IL-6 protein in DNOAP group was higher than that in normal control group, while the relative expression of OPG and Aggrecan protein was lower than that in normal control group (both P < 0.05). Flow cytometry showed that the apoptotic rate of chondrocyte in DNOAP group was 3.3%±0.2%, which was higher than that in normal control group (1.2%±0.1%, P<0.05).Conclusion:Serious destruction of chondrocytes and organelles structure was the pathological characteristics of DNOAP. Inflammation plays a role in promoting the pathogenesis of DNOAP.

Bone Mineral Density in Diabetes Mellitus Foot Patients for Prediction of Diabetic Neuropathic Osteoarthropathic Fracture.

Background Diabetic neuropathic osteoarthropathy (DNOAP) is known as debilitating diabetes complications. The aim of study is to compare bone mineral density (BMD) among diabetic foot and DNOAP, and investigate the impact of BMD proceeded from diabetic foot to DNOAP.Methods A DNOAP group (subgroup A and subgroup B) and control group were examined for this study. Subgroup A (n=21) were patients diagnosed with DNOAP with the development of new foot and ankle fractures, whereas subgroup B (n=4) were patients being managed with the diabetic foot before a diagnosis of DNOAP. BMD was also evaluated before the diagnosis. Control group (n=30) was diabetic foot patients without DNOAP. The demographic data, clinical and radiologic data, comorbidities, and BMD were compared for each group. And optimal BMD score was reviewed to predict fractures in neuropathic arthropathy.Results BMD was significantly lower in DNOAP group (group A and B) compared with control group. Also neuropathic arthropathy group showed poor radiological results. After comparisons of 2 group lumbar and femur BMD was significantly different, but logistic regression analysis revealed that low femur T-score could be risk predictors of the condition. Base on the data of group B and control group, the cut-off point for predicting foot and ankle fracture-related with DNOAP was -1.65 of femur BMD.ConclusionsLow BMD shows greater incidence in foot and ankle fracture patients associated with neuropathic arthropathy. A femur T score can be a risk predictor of diabetic neuropathic arthropathy for diabetic foot patients.

Magnetic resonance imaging of the ankle and foot.

This article reviews the magnetic resonance imaging (MRI) findings of the normal anatomy and various pathologic conditions of the ankle and foot commonly encountered in clinical practice. The spectrum of entities discussed includes osseous and osteochondral injuries, ligamentous injuries, common traumatic and degenerative tendon pathology, abnormalities of transverse tarsal joint (Chopart) and tarsometatarsal joint (Lisfranc) complexes, pathological conditions affecting capsuloligamentous structures of the great toe and lesser toes, as well as pedal infection, with a focus on diabetic osteomyelitis and neuropathic osteoarthropathy.

The Charcot foot: pathophysiology, diagnosis and classification.

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: Bone Joint J 2016;98-B:1155-9.

A specific characteristic of the diabetic foot - the diabetic-neuropathic osteoarthropathy

Der Charcot-Fus ist eine potenziell verheerende Komplikation des Diabetes mellitus, die im ungunstigen Verlauf zur Amputation fuhren kann. Daher ist es wichtig, dass Sie bei entsprechender Klinik (Schwellung, Rotung, Uberwarmung) fruhzeitig daran denken. Bei den Betroffenen selbst ist das Krankheitsempfinden bei dem nicht schmerzhaften und wenig bedrohlich erscheinenden lokalen Befund oft nur masig ausgepragt.

Diagnostic for Charcot foot

Early recognition of Charcot foot can save a long period of suffering for the patient, high doctor and hospital costs and ultimately amputation. This article aims to raise awareness of the diagnostics of Charcot foot also known as diabetic neuropathic osteoarthropathy (DNOAP) and the possible differential diagnostic options (e.g. diabetic foot, erysipelas and peripheral arterial occlusive disease). Clinical diagnostic pathways and classifications are presented and the resulting treatment options are discussed. In recent years new technologies for wound treatment and interventional radiological optimization of vessels have been developed. Many promising surgical options are available for stabilizing and reconstructimg a plantigrade foot. Treatment of Charcot foot should be based on a structured diagnosis and classification. In addition to conservative treatment new surgical options are also available.

Visualization of local cortical defects in Charcot foot using microcomputed tomography

In the pathogenesis of diabetic neuropathic osteoarthropathy (Charcot's foot) fractures cause chronic destruction of soft tissue and bone structure. To improve an early diagnosis of Charcot foot, modern diagnostic imaging is mainly based on magnetic resonance imaging (MRI), for example in relation to the detection of cortical bone fractures. In this study we investigated the cortical microstructure in cases of Charcot foot with respect to fractures and porosity in order to visualize local cortical defects. This may substantiate recent efforts in a reclassification based on MRI. Using microcomputed tomography (microCT) we investigated bone parameters, such as cortical thickness and porosity in order to quantify the local metatarsal microstructure in cases of Charcot foot. All bone samples showed a high degree of cortical porosity including pores that perforated the cortical bone. The data suggest that areas with reduced cortical thickness coincide with large cortical pores that may serve as initial points for fractures. Whether the detected microfractures are physiological or artefacts of preparation could not be determined. By means of microCT we were able to visualize and quantify the extent of cortical porosity for the first time in high resolution. The data suggest that both cortical fractures and cortical porosity play an important role in the pathogenesis in cases of Charcot foot.

Geschlossene Reposition einer akuten Mittelfußluxationsfraktur im Rahmen einer Charcot-Arthropathie mit Hilfe des Ringfixateurs

Diabetic neuropathic osteo-arthropathy (DNOAP; Charcot arthropathy) is a progressive disease characterized by joint luxation, fractures and excessive destruction of foot architecture. The operative therapy is indicated when conservative therapy fails, in progressive breakdown, in hindfoot Charcot and in spreading infections due to plantar ulcers. The complication rate of 10-20% in open surgery is high. We present a minimally invasive technique of closed reduction and application of a ring fixator for reconstruction of the foot architecture and arthrodesis of the involved joints.

Surgical Management of the Unstable Diabetic Charcot Deformity Using the Taylor Spatial Frame

The surgical repair of unstable acute and chronic Charcot foot and ankle deformities remain a challenge with little guidance available in the medical literature regarding surgical intervention with the use of external fixation devices and specifically the Taylor Spatial Frame. The authors present a brief review of the diabetic Charcot neuropathic osteoarthropathy process and a detailed review of their approach to surgical intervention using the Taylor Spatial Frame. In this regard, a detailed “step-by-step” guide through the foot specific Taylor Spatial Frame computer-based system is provided.

Erythromelia, or Mitchell's syndrome – new names for unexplained signs of inflammation in distal symmetrical neuropathy in diabetes

Two cases are described in which distal symmetrical sensorimotor neuropathy complicating diabetes was associated with episodes of subacute vasodilation of one or other lower limb, and which were otherwise unexplained. The vasodilation was associated with swelling and stiffness, but was painless and self-limiting. It is suggested that this phenomenon results from disordered vasoregulation in diabetic neuropathy, and is linked to the processes which underlie diabetic neuropathic osteoarthropathy (Charcot foot), as well as disorders such as complex regional pain syndrome-1 (CRPS-1, reflex sympathetic dystrophy) and erythromelalgia. As self-limiting vasodilation may be not uncommon in distal symmetrical neuropathies, but unrecognized because the phenomenon has not been named, the terms 'neuropathic erythromelia' or 'Mitchell's syndrome' are proposed. The adoption of either of these names may lead to earlier diagnosis and prevent inappropriate investigation and treatment.

Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot)

To determine the mortality of a population of patients diagnosed with Charcot neuropathic osteoarthropathy managed by a single specialist unit and to compare the results with a control population. We have undertaken a retrospective analysis of all cases of Charcot foot on the comprehensive database which has been maintained at the specialist diabetic foot clinic at the City Hospital, Nottingham since 1982. Survival and the incidence of amputation (major and minor) was compared with a control population referred with uncomplicated neuropathic ulceration. Controls were individually matched for gender, age (+/-2 years), disease type, disease duration (+/-2 years) and year of referral (+/-3 years). Forty-seven cases (21 female, 26 male) of Charcot foot were identified, of whom 18 (38.3%) had Type 1 diabetes. Mean age and disease duration at presentation were 59.2 +/- 13.4 (sd) and 16.2 +/- 11.2 years, compared with 59.7 +/- 12.6 and 16.3 +/- 11.2 years, respectively, in the controls. Twenty-one (44.7%) of those with Charcot had died, after a mean interval of 3.7 +/- 2.8 years. This compared with 16 (34.0%) after a mean 3.1 +/- 2.7 years in the control group. Mean duration of follow-up in the survivors was 4.7 +/- 4.9 years (Charcot) and 5.3 +/- 3.9 years (controls). A total of 11 (23.4%) Charcot patients had had a major amputation on the side of the index lesion, compared with five (10.6%) controls. There was no difference between the two groups (P > 0.05, Chi-square). The mortality in this group of patients with Charcot foot was higher than expected. Nevertheless, there was no difference between those with Charcot and those with uncomplicated neuropathic ulceration. It is possible that it is neuropathy, rather than Charcot osteoarthropathy, which is independently associated with increased mortality in diabetes. The mechanism underlying any such association is not known. There is a need for a formal, prospective, multicentre study to investigate the life expectancy and cardiovascular risk of those with Charcot osteoarthropathy.

Orthopedic aspects in diabetic neuropathic osteoarthropathy.

Orthopedic aspects in diabetic neuropathic osteoarthropathy.

Management of leg ulcers.

Introduction - management of leg ulcers. Part I Wound healing: molecular biology of chronic wounds cytokines in progressing stages of chronic venous insufficiency bacteriology of leg ulcers synthetic dressings therapy with growth factors cultured keratinocyte grafts. Part II Venous leg ulcers: epidemiology of leg ulcers postthrombbtic syndrome classification of chronic venous insufficiency venous mapping with Doppler and duplex sonography duplex ultrasound for the assessment of venous reflux phlebography magnetic resonance imaging and computed tomography in advanced chronic venous insufficiency plethysmography micoangiopathy in the pathogenesis of chronci venous insufficiency compression therapy of venous ulcers physical therapy of the ankle joint in patients with chronic venous imcompetence and arthrogenic congestive syndrome manual lymph drainage adjuvant systemic drug therapy in venous leg ulcers chronic leg ulcers and eczema complications in the treatment of leg ulcers surgical management of varicose veins in advanced chronic venous insufficiency paratibial fasciootomy and crural fasciectomy subfascial and edcoscopic perforator surgery shave therapy for recalcitrant venous ulcers. Part III Arterial leg ulcers: assessment of peripheral arterial occulsive disease management of arterial leg ulcers and of combined (mixed) venous-arterial leg ulcers percutaneous transulminal angioplasty in the mangement of arterial leg ulcers reconstructive arterial surgery. Part IV Conservative therapy of diabetic foot: orthopaedic aspects in diabetic neuropathic osteoarthropathy diabetic foot infection. Part V Leg ulcers of different origins: differential diagnosis of leg ulcers management of leg ulcers in rheumatoid arthritis and in systemic sclerosis management of vasculitic leg ulcers and pyoderma gangrenosum conclusions.

Deformity following fracture in diabetic neuropathic osteoarthropathy. Operative management of adults who have type-I diabetes.

We studied fifteen lower extremities that had a deformity following a fracture in the region of the ankle or the tarsal bones, in fourteen adults who had type-I diabetes and neuropathic osteoarthropathy. The skeletal deformities associated with these fractures were either diagnosed late (two limbs) or occurred in lower extremities that had been treated by means other than non-weight-bearing and immobilization (thirteen limbs). All deformities were severe and secondary to a non-union or malunion of the fracture; all were ultimately treated with operative reconstruction. Before the reconstruction, the limbs had had either persistent ulceration associated with an uncorrectable skeletal deformity (four) or a severe deformity that was difficult to contain with a custom-made orthosis (eleven). The most recent result was considered a success when the ulceration had healed, the involved foot was planti-grade, and the involved limb was capable of bearing weight with use of a patellar tendon-bearing orthosis. Following reconstruction, ten patients had a plantigrade foot without ulceration, three had a plantigrade foot with a persistent draining ulcer, and one had a foot that was not plantigrade. In the limbs that had an ulcer at the time of the operation, there was one successful outcome and three failures. In contrast, the outcome was successful for ten of the limbs that had not had an ulcer and a failure for one. There were three complications following sixteen operative reconstructive procedures in the fourteen patients, including one infection and two instances of accelerated bone resorption and collapse.(ABSTRACT TRUNCATED AT 250 WORDS)