Midfoot and hindfoot arthrodeses in diabetic Charcot arthropathy. (1/83)

OBJECTIVES: To review the clinical outcome of arthrodesis of the foot in patients with diabetic Charcot arthropathy and to review the pathophysiology, clinical and radiographic features of Charcot arthropathy. DESIGN: A retrospective review and clinical follow-up of a series of patients. SETTING: St. Michael's Hospital, Toronto, a tertiary care teaching hospital. PATIENTS: Ten diabetic patients treated between 1996 and 1998 who required an arthrodesis of the midfoot or hindfoot secondary to deformity of diabetic neuropathic joints. INTERVENTIONS: Three midfoot (Lisfranc) and 7 hindfoot arthrodeses with autogenous iliac-crest bone grafting and internal fixation. OUTCOME MEASURES: Patient satisfaction, maintenance of the correction of the deformity and avoidance of amputation. Western Ontario/McMaster University score and midfoot/hindfoot American Orthopaedic Foot and Ankle Society foot ratios. Clinical examination including E-MED pedographic examination. Correction and evidence of bony or fibrous union assessed radiologically. RESULTS: The postoperative correction was maintained, no further skin ulceration occurred and amputation was avoided in 9 of 10 patients. Because this is a salvage procedure and there was often significant concomitant illness, the results of clinical rating systems were poor. Five of 9 patients had clinical and radiographic evidence of a solid bony arthrodesis; 4 had a stable fibrous union. CONCLUSIONS: With careful surgical technique, a reasonable number of feet can be salvaged by an arthrodesis of a diabetic neuropathic joint when nonoperative measures fail. Patient selection is important because there is a significant complication rate.  (+info)

Charcot foot: the diagnostic dilemma. (2/83)

Primary care physicians involved in the management of patients with diabetes are likely to encounter the diagnostic and treatment challenges of pedal neuropathic joint disease, also known as Charcot foot. The acute Charcot foot is characterized by erythema, edema and elevated temperature of the foot that can clinically mimic cellulitis or gout. Plain film radiographic findings can be normal in the acute phase of Charcot foot. A diagnosis of Charcot syndrome should be considered in any neuropathic patient, even those with a minor increase of heat and swelling of the foot or ankle, especially after any injury. Early recognition of Charcot syndrome and immobilization (often with a total contact cast), even in the presence of normal radiographs, can minimize potential foot deformity, ulceration and loss of function. Orthopedic or podiatric foot and ankle specialists should be consulted when the disease process does not respond to treatment.  (+info)

Total knee arthroplasty in neuropathic arthropathy. (3/83)

We describe the results of total knee arthroplasty (TKA) undertaken for severe, neurosyphilitic Charcot arthropathy in ten patients (19 knees). A cemented condylar, constrained prosthesis was implanted in all but two knees. The mean follow-up was 5.2 years (5 to 6). The mean knee score before operation was 36.5 points (30 to 42) which improved to 76 points (58 to 90) after operation as judged by the Hospital for Special Surgery score. At final follow-up three knees (16%) had aseptic loosening which required salvage by an arthrodesis, six (31%) were functioning poorly and ten (53%) were satisfactory. We conclude that although Charcot arthropathy is not an absolute contraindication to total knee replacement, there is a high incidence of serious complications.  (+info)

A practical guide for examining and treating the diabetic foot. (4/83)

Physicians can perform a quick, complete examination of the feet of patients with diabetes to prevent serious complications. The examination should focus on circulation, nerve function, musculoskeletal problems, and the skin. All patients should be urged to wear supportive, comfortable shoes, and to wash, moisturize, and examine their feet every day.  (+info)

Tabes dorsalis with sudden onset of paraplegia. (5/83)

A case is presented of tabes dorsalis with spinal gumma producing collapse of the L5 vertebra followed by paraplegia.  (+info)

Musculoskeletal manifestations of diabetes mellitus. (6/83)

Rheumatic complaints are common in patients with diabetes. Maintaining good glycaemic control by exercise, diet, and medication improves or prevents the development of rheumatic conditions.  (+info)

Neuroarthropathy. Clinico-radiologic analysis of 115 cases. (7/83)

115 patients (163 joints) with neuroarthropathy (Charcot joint) were observed clinically and radiologically. In Charcot joint of the shoulder, the entire scapula was disintegrated. After debridement and arthrodesis, fragmentation of bone reappeared at both ends of the affected long bone and even on the lateral surface of diaphysis. Fragmentation of the articular surface and the subchondral bone was seen in the non-weight-bearing surface. 32 patients in this series sustained spontaneous fractures without a history of trauma or undue strain. Follow-up for short periods (2 to 6 weeks) showed rapid progressive destruction. These results indicated that neurotrophic theory seems to furnish an explanation for the pathogenesis of the Charcot joint, and that bone resorption should be the primary change while bone hypertrophy and proliferation, the secondary.  (+info)

Synoviolin/Hrd1, an E3 ubiquitin ligase, as a novel pathogenic factor for arthropathy. (8/83)

Rheumatoid arthritis (RA) is one of the most critical articular diseases with synovial hyperplasia followed by impairment of quality of life. However, the mechanism(s) that regulates synovial cell outgrowth is not fully understood. To clarify its mechanism(s), we carried out immunoscreening by using antirheumatoid synovial cell antibody and identified and cloned "Synoviolin/Hrd1", an E3 ubiquitin ligase. Synoviolin/Hrd1 was highly expressed in the rheumatoid synovium, and mice overexpressing this enzyme developed spontaneous arthropathy. Conversely, synoviolin/hrd1(+/-) mice were resistant to collagen-induced arthritis by enhanced apoptosis of synovial cells. We conclude that Synoviolin/Hrd1 is a novel causative factor for arthropathy by triggering synovial cell outgrowth through its antiapoptotic effects. Our findings provide a new pathogenetic model of RA and suggest that Synoviolin/Hrd1 could be targeted as a therapeutic strategy for RA.  (+info)