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Inflammatory osteolysis is sine-qua-non of active Charcot neuroarthropathy (CN) causing decreased foot bone mineral density (BMD) and fractures. We aimed to explore the effect of anti-inflammatory or anti-resorptive agents for effect on foot bone mineral content (BMC) and consequent long-term outcomes of foot deformities, fractures and amputation. Forty-three patients with active CN (temperature difference >2°C from normal foot) were evaluated. Patients were off-loaded with total contact cast and randomized to receive either methylprednisolone (1gm) (group A), zoledronate (5mg) (group B) or placebo (100ml normal saline) (group C) once monthly infusion for three consecutive months. Change in foot BMC was assessed at 6 months or at remission and followed subsequently up to 4 years for the incidence of new-onset fracture, deformities, or CN recurrence. Thirty-six participants (24 male, 12 female) were randomized (11 in group A, 12 group B, 13 group C). The mean age was 57.7± 9.9 years, duration of diabetes 12.3± 5.8 years and symptom duration 6.5± 2.8 weeks. BMC increased by 36% with zoledronate (p = 0.02) but reduced by 13% with methylprednisolone (p = 0.03) and 9% (p = 0.09) with placebo at remission. There were no incident foot fractures, however, two patients sustained ulcers, and 3 had new-onset or worsening deformities and none required amputation during 3.36 ± 0.89 years of follow-up. Bisphosphonate for active CN is associated with an increase in foot bone mineral content as compared to decrease with steroids or total contact cast but long-term outcomes of foot deformities, ulceration and amputation are similar. ClinicalTrials.gov: NCT03289338.

The aim of the study was to determine the degree of neuropathy (autonomic and somatic) in patients with diabetes mellitus with or without Charcot osteoarthropathy (CA). Forty-nine patients with diabetes mellitus type 1 or 2 were investigated. The patient population of interest was the patients with acute Charcot foot ( n=17) or chronic Charcot foot ( n=7). The inclusion criterion for an acute Charcot foot was a temperature difference of more than 2° between the two feet, oedema of the affected foot, typical hotspots in a bone scintigram and a typical clinical course. In addition, patients with first toe amputation ( n=5), a high-risk group for development of CA, and two control groups consisting of diabetes patients with ( n=9) or without somatic neuropathy ( n=11) were investigated. Regional blood flow in the feet was measured by venous occlusion plethysmography. Quantitation of somatic neuropathy was done by the Neuropathy Disability Score and modified Neuropathy Symptom Score. Quantitation of autonomic neuropathy was done by measurements of local venoarteriolar sympathetic axon reflex in the feet and of heart rate variability during deep breathing and orthostatic challenge. The patients with acute Charcot foot and first toe amputation had an increased blood flow in the affected foot and weakened but not absent venoarteriolar sympathetic axon reflex. In the other patient groups, a normal venoarteriolar sympathetic axon reflex in the feet was found. Peripheral sympathetic neuropathy is not likely to be the pathophysiologic mechanism behind the hyperemia in the foot during an acute attack of CA. The hyperemia is more likely secondary to local inflammatory events.

Background Charcot neuroarthropathy (CN) is a rare musculoskeletal disorder caused by peripheral neuropathy, predominantly affecting the forefoot and ankle joints in diabetic patients. While more common in type 2 diabetes, type 1 diabetes-associated CN carries high risks of disability and mortality due to delayed diagnosis and nonspecific pathophysiology. Knee joint CN in type 1 diabetes remains exceptionally rare, with limited reports on standardized management—particularly regarding knee arthroplasty outcomes. Case Presentation We report two female type 1 diabetes patients with knee joint CN. Both presented with poorly controlled hyperglycemia (blood glucose > 20 mmol/L) and elevated HbA1c. Each underwent total knee arthroplasty (TKA); one patient additionally received autologous bone grafting with titanium mesh screw fixation for severe bone defects, Intraoperative pathological examination was performed in all cases to rule out infection. Conclusion These cases highlight the complexity of managing knee CN in type 1 diabetes. TKA represents a viable intervention, though outcomes may vary based on surgical adjuncts like bone grafting. This report, contextualized with a literature review, underscores the need for individualized approaches in this high-risk population.

BackgroundNeuropathic arthropathy (NA) of the shoulder is a chronic progressive process characterized by joint destruction in the presence of a neurosensory deficit. Syringomyelia, a spinal cord disease, is the leading cause of NA in the upper extremity. ObjectiveWe present a systematic review of NA with syringomyelia cases alongside a case report of an adult with NA of the shoulder that occurs a few 4 years after a revelation and surgical management of a Chiari malformation with syringomyelia.MethodsA systematic review was conducted following PRISMA guidelines. A PubMed, Scopus, Isiknowledge, and manual search through references of relevant publications were used to identify all published case reports of NA. Data were collected from each case report on patient characteristics.ResultsThe systematic review identified 56 publications and 85 patients (including ours): nearly the same number of males (n = 41) and females (n = 44). The mean age was 50,69. Presentations included reduction of mobility (n = 66), swelling (n = 61) and sensory disorder (n = 63). The pain was absent in 41 cases. In the majority of reported cases 56 (65.1%), syringomyelia was revealed by neuropathic arthropathy, and eleven patients (12.9%) had a history of syringomyelia. Treatment was categorized into non-operative management (37[43.5%]), operative management (27[31.7%]). Following-up was non-reported in 31 (36%) cases. Improvement was reported more with patients who underwent a surgical approach than medical one 28.5% versus 8.1%.ConclusionPhysicians need to be more aware of this destructive joint disease, rare, and often misdiagnosed. Also, it is imperative to integrate clinical, pathological, and imaging findings for accurate diagnosis and for delivering appropriate therapy.

Acute Charcot neuroarthropathy of the foot and ankle is often difficult to diagnose because of limited findings in the patient history, physical examination, imaging, and laboratory studies. Delay in treatment results in the development of rigid foot and ankle deformities, increasing the risk of ulceration, infection, and major lower extremity amputation. Acute Charcot neuroarthropathy should be suspected in any patient 40 years or older with obesity and peripheral neuropathy who presents with an acutely swollen foot following minimal or no recalled trauma and who reports minimal to no pain, particularly if radiography and laboratory markers of infection are normal. Magnetic resonance imaging or computed tomography should be performed in these cases. If changes consistent with acute Charcot neuroarthropathy are observed, prompt immobilization and/or referral to a foot and ankle subspecialist is needed to minimize sequelae. Immobilization should continue until lower extremity edema and warmth resolve, and serial radiography shows evidence of osseous consolidation. Intranasal calcitonin salmon may have a role as adjunctive therapy. Although controversial, surgery may be indicated if there is severe dislocation or instability, concern for skin breakdown, or failure of conservative treatment to obtain a stable, plantigrade foot.

Aim: To describe the demographic and clinical characteristics of patients with Charcot neuro‐osteoarthropathy (CNO) and to examine for differences between participants with Type 1 diabetes mellitus (DM) (T1DM) and Type 2 diabetes mellitus (T2DM). Materials and Methods: Multicenter observational study in eight diabetic foot clinics in six countries between January 1, 1996, and December 31, 2022. Demographic, clinical, and laboratory parameters were obtained from the medical records. Analyses were performed using parametric or nonparametric statistical tests for variables with normally or nonnormally distributed values, respectively. Comparisons of the qualitative data were performed using the chi‐square test. Results: Seven hundred seventy‐four patients with DM and CNO were included. The mean age at diagnosis of CNO was 54.5 ± 11.7 years, and the median (interquartile range (IQR)) diabetes duration at diagnosis of CNO was 15 (10–22) years. Among participants, 71.8% ( n = 546) were male and 83.2% ( n = 634) had T2DM. Neuropathy was present in 91.7% ( n = 688), retinopathy in 60.2% ( n = 452), and nephropathy in 45.2% ( n = 337). Subjects with T1DM, compared to T2DM, were diagnosed with CNO at a younger age (46.9 ± 11.0 vs. 57.9 ± 10.2 years, p < 0.001), had longer diabetes duration (median value (IQR): 29.0 (21.0–38.0) vs. 14.0 (8.0–20.0) years, p < 0.001), and had more often microvascular complications (neuropathy, 95.2% in T1DM vs. 87.4% in T2DM, p = 0.006; retinopathy, 83.3% vs. 55.4%, p < 0.001; and nephropathy 67.5% vs. 40.5%, p < 0.001). Conclusions: CNO is predominant in males, occurs in long‐standing DM, and is often accompanied by microvascular complications. People with T1DM, compared to those with T2DM, are affected at a younger age, have longer diabetes duration, and have more often microvascular complications.

Neuropathic arthropathy (NA) is a long-term progressive disorder that causes joint destruction in the existence of a neurologic deficit. Minor injuries and fractures are commonly overlooked until the visible joint deterioration becomes persistent. Syringomyelia is one of the important causes of NA. The appearance of clinical signs in syringomyelia is caused by longitudinal cysts formed in the cervical and cervicothoracic regions of the spinal cord. Depending on the existence of the underlying disorder, the number and localization of the syrinxes, a range of symptoms, involving pain, sensation deficit, loss of motor function, and deep tendon reflex abnormality, emerge. The case is here described of a 68-year-old female patient with shoulder NA following syringomyelia, who partially responded to the rehabilitation program. Furthermore, the available case reports were comprehensively reviewed on Web of Science, Scopus, and PubMed/Medline. Furthermore, the available case reports were comprehensively evaluated on Web of Science, Scopus, and PubMed/Medline. Thus, we aimed to present the demographic characteristics, symptoms, physical examination signs, treatment, and follow-up parameters of syringomyelia-related shoulder NA cases.

Aims/hypothesis We studied factors associated with the development and resolution of acute Charcot foot using a web-based observational study. Methods Clinicians managing cases of acute Charcot foot in the UK and Ireland between June 2005 and February 2007 were invited to register anonymised details on a secure website. Results A total of 288 cases (age 57.0 ± 11.3 years [mean ± SD]; 71.2% male) were registered from 76 centres. Of these, 36% of patients recalled an episode of relevant trauma in the preceding 6 months, while 12% had had surgery to the affected foot. In 101 (35%) cases, ulceration was present at registration and 20% of these had osteomyelitis. Non-removable off-loading devices were used at presentation in 35.4% of cases, with removable off-loading used in 50%. Data on resolution were available for 219 patients. The median time to resolution was 9 months in patients whose initial management included the use of non-removable off-loading, compared with 12 months in the remainder ( p  = 0.001). Bisphosphonates were administered intravenously in 25.4% and orally in 19.4% of cases. The median time to resolution in patients who received bisphosphonates was 12 months and was longer than in those who did not (10 months, p  = 0.005). Conclusions/interpretation The median time to resolution was longer than in earlier series. Although limited by being observational and non-randomised, these data suggest that the use of non-removable off-loading at presentation may shorten the time to resolution. They provide no evidence to indicate that the use of bisphosphonates is beneficial.

Background Rheumatoid arthritis (RA) is an autoimmune disease.However, there are few cases of Charcot Neuro-osteoarthropathy (CN) caused by rheumatoid diseases in clinical reports. It is not easy to pay attention to the diagnosis of CN in the complications of rheumatoid disease, which greatly increases the probability of misdiagnosis and missed diagnosis. This case reported a rare complication of rheumatoid arthritis, Charcot arthritis, and the molecular mechanism and diagnosis and treatment of CN caused by RA were systematically discussed. Case presentation The patient, a 79-year-old woman, was hospitalized due to bilateral shoulder pain, limited activity for half a year, aggravated for 4 months to the hospital. During this period, the symptoms did not improve after treatment with acupuncture and Chinese medicine. The patient was previously diagnosed with rheumatoid arthritis for more than 3 years and intermittent irregular use of methylprednisolone and methotrexate for 2 years. She had a history of osteoporosis. Physical examination: symmetrical malformed swelling of the finger joints of both hands; Bilateral supraspinatus and deltoid muscle atrophy, tenderness at the acromion, and attachment of the long head tendon of the biceps brachii were observed. The left Dugas test and the right Dugas test were positive.Blood test: anti-cyclic citrullinated peptide antibody (A-CCP) 33.10U/ml (normal range: 0-5RU/ml); antinuclear antibody quantification (ANA) 47.40AU/ml (normal range: Negative or < 32); anti-double stranded DNA IgG antibody quantification (dsDNA) 31.00 IU/ml (normal range: 0-100 IU/ml); D-Dimer 6.43 µg/ml (normal range: 0–0.5 mg/L); erythrocyte sedimentation rate (ESR) was 27 mm/h (normal range: < 20 mm/60 min). C-reactive protein (CRP) 39.06 mg/L(0.068-8 mg/L).MRI 3.0 T enhancement of bilateral shoulder joints, cervical spine and thoracic spine showed: 1.Large bone destruction, cartilage injury, multiple effusion, synovitis, obvious on the right side. 2.Intervertebral disc degeneration, cervical 3/4, 4/5, 5/6, 6/7 disc herniation, with cervical 3/4 obvious, posterior central herniation; Conclusions Rheumatoid arthritis complicated with Charcot's joint is rare. Clinically, patients with rheumatoid diseases should not ignore Charcot's joint complications because of rareness. Early blood inflammatory markers, neuro electrophysiology, and imaging MRI of rheumatoid CN are of great significance for the diagnosis of this mild or early neurovascular inflammation. Early diagnosis and treatment are helpful to prevent further joint injury. The clinical diagnosis, treatment, and molecular mechanism of osteolysis in RA and peripheral sensory nerve injury remain to be further revealed.

Bone in diabetes mellitus is characterized by an altered microarchitecture caused by abnormal metabolism of bone cells. Together with diabetic neuropathy, this is associated with serious complications including impaired bone healing culminating in complicated fractures and dislocations, especially in the lower extremities, so-called Charcot neuroarthropathy (CN). The underlying mechanisms are not yet fully understood, and treatment of CN is challenging. Several in vitro and in vivo investigations have suggested positive effects on bone regeneration by modifying biomaterials with sulfated glycosaminoglycans (sGAG). Recent findings described a beneficial effect of sGAG for bone healing in diabetic animal models compared to healthy animals. We therefore aimed at studying the effects of low- and high-sulfated hyaluronan derivatives on osteoclast markers as well as gene expression patterns of osteoclasts and osteoblasts from patients with diabetic CN compared to non-diabetic patients with arthritis at the foot and ankle. Exposure to sulfated hyaluronan (sHA) derivatives reduced the exaggerated calcium phosphate resorption as well as the expression of genes associated with bone resorption in both groups, but more pronounced in patients with CN. Moreover, sHA derivatives reduced the release of pro-inflammatory cytokines in osteoclasts of patients with CN. The effects of sHA on osteoblasts differed only marginally between patients with CN and non-diabetic patients with arthritis. These results suggest balancing effects of sHA on osteoclastic bone resorption parameters in diabetes.