Does Arthrodesis of the First Metatarso-Phalangeal Joint Correct the Intermetatarsal M1M2 Angle? Analysis of Continuous Series of 208 Arthrodesis Plate-Osteosyntheses

Category: Midfoot/Forefoot Introduction/Purpose: MTP-1 arthrodesis allows effective correction of both inter-metatarsal M1M2 and M1P1 angles. Undercorrection of wide M1M2 angle after MTP-1 arthrodesis causes persistently wide forefoot, metatarsalgia and unaesthetic gap between first and second toes. In severe deformities, Rippstein recommended supplementary first metatarsal osteotomy or cuneo-metatarsal arthrodesis. The present study sought to investigate correction of inter-metatarsal M1M2 angle after MTP-1 arthrodesis according to aetiology and pre-operative deformity severity. Methods: A prospective continuous series (June 2007- March 2011) included 208 patients: 48% severe hallux valgus and/or osteoarthritis, 18% hallux rigidus, 16% rheumatoid osteoarthritis, 13% revision, 5% hallux varus; mean age, 62.4±9.9 years (19-87 years). All patients were operated on by a single senior surgeon with the same technique: articular surface reaming (cup-ball), osteosynthesis with titanium anatomical plate (Fyxis-Biotech) and the same rehabilitation procedure. Pre- and post-operative hallux positions were analysed on antero-posterior and lateral weightbearing views. M1M2 and M1P1 were measured according to American Orthopaedic Foot and Ankle Society guidelines. Results: Mean follow-up was 18.6±12.4 months; fusion rate, 97%; 5% plate removal. Mean M1P1 angle was 33.8±19.7° (-45° to 67°) preoperatively, and 13.4±5.3° (0-32°) at follow-up; M1M2, 14.2±5.4° (0° to 26°) and 6.5± 2.3° (0-12°) respectively. M1M2 angle was 10° in only 2 patients (0.9%) associated with cuneometatarsal osteoarthritis. Improvement increased with severity of preoperative M1M2 angle (p 10°. Pydah correlated preoperative and postoperative intermetatarsal angle with a regression line, without recommending any secondary procedure to improve M1M2 angle. In severe increased preoperative M1M2 angle, we do not recommend associating systematic C1M1 arthrodesis or basal metatarsal osteotomy to MTP-1 arthrodesis, but suggest that additional basal metatarsal osteotomy or C1M1 fusion might be required only in exceptional associated degenerative C1M1 joint

Skeletal Ryanodine Receptors Are Involved in Impaired Myogenic Differentiation in Duchenne Muscular Dystrophy Patients

International audienceDuchenne muscular dystrophy (DMD) is characterized by progressive muscle wasting following repeated muscle damage and inadequate regeneration. Impaired myogenesis and differentiation play a major role in DMD as well as intracellular calcium (Ca2+) mishandling. Ca2+ release from the sarcoplasmic reticulum is mostly mediated by the type 1 ryanodine receptor (RYR1) that is required for skeletal muscle differentiation in animals. The study objective was to determine whether altered RYR1-mediated Ca2+ release contributes to myogenic differentiation impairment in DMD patients. The comparison of primary cultured myoblasts from six boys with DMD and five healthy controls highlighted delayed myoblast differentiation in DMD. Silencing RYR1 expression using specific si-RNA in a healthy control induced a similar delayed differentiation. In DMD myotubes, resting intracellular Ca2+ concentration was increased, but RYR1-mediated Ca2+ release was not changed compared with control myotubes. Incubation with the RYR-calstabin interaction stabilizer S107 decreased resting Ca2+ concentration in DMD myotubes to control values and improved calstabin1 binding to the RYR1 complex. S107 also improved myogenic differentiation in DMD. Furthermore, intracellular Ca2+ concentration was correlated with endomysial fibrosis, which is the only myopathologic parameter associated with poor motor outcome in patients with DMD. This suggested a potential relationship between RYR1 dysfunction and motor impairment. Our study highlights RYR1-mediated Ca2+ leakage in human DMD myotubes and its key role in myogenic differentiation impairment. RYR1 stabilization may be an interesting adjunctive therapeutic strategy in DMD

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