Association Between Patient Factors and Outcome of Synthetic Cartilage Implant Hemiarthroplasty vs First Metatarsophalangeal Joint Arthrodesis in Advanced Hallux Rigidus

BACKGROUND: We evaluated data from a clinical trial of first metatarsophalangeal joint (MTPJ1) implant hemiarthroplasty and arthrodesis to determine the association between patient factors and clinical outcomes. METHODS: Patients ≥18 years with hallux rigidus grade 2, 3, or 4 were treated with synthetic cartilage implant MTPJ1 hemiarthroplasty or arthrodesis. Pain visual analog scale (VAS), Foot and Ankle Ability Measure (FAAM) sports and activities of daily living (ADL) scores, and Short Form-36 Physical Function (SF-36 PF) subscore were obtained preoperatively, and at 2, 6, 12, 24, 52, and 104 weeks postoperatively. Final outcome data, great toe active dorsiflexion motion, secondary procedures, radiographs, and safety parameters were evaluated for 129 implant hemiarthroplasties and 47 arthrodeses. The composite primary endpoint criteria for clinical success included VAS pain reduction ≥30%, maintenance/improvement in function, no radiographic complications, and no secondary surgical intervention at 24 months. Predictor variables included hallux rigidus grade; gender; age; body mass index (BMI); symptom duration; prior MTPJ1 surgery; preoperative hallux valgus angle, range of motion (ROM), and pain. Two-sided Fisher exact test was used ( P .05) when stratified by hallux rigidus grade, gender, age, BMI, symptom duration, prior MTPJ1 surgery status, and preoperative VAS pain, hallux valgus, and ROM. CONCLUSION: Synthetic cartilage implant hemiarthroplasty was appropriate for patients with grade 2, 3, or 4 hallux rigidus. Its results in those with associated mild hallux valgus (≤20 degrees) or substantial preoperative stiffness were equivalent to MTPJ1 fusion, irrespective of gender, age, BMI, hallux rigidus grade, preoperative pain or symptom duration. LEVEL OF EVIDENCE: Level II, randomized clinical trial

The pathogenesis of Charcot neuroarthropathy: current concepts

The pathogenesis of Charcot neuroarthropathy (CN) has been poorly understood by clinicians and scientists alike. Current researchers have made progress toward understanding the cause of CN and possible treatment options. The authors review the current literature on the pathogenesis of this debilitating disorder and attempt to explain the roles of inflammation, bone metabolism, and advanced glycation end products

Increased osteoclastic activity in acute Charcot’s osteoarthopathy: the role of receptor activator of nuclear factor-kappaB ligand

Aims/hypothesis: Our aims were to compare osteoclastic activity between patients with acute Charcot's osteoarthropathy and diabetic and healthy controls, and to determine the effect of the receptor activator of nuclear factor-kappaB ligand (RANKL) and its decoy receptor osteoprotegerin (OPG). Methods: Peripheral blood monocytes isolated from nine diabetic Charcot patients, eight diabetic control and eight healthy control participants were cultured in the presence of macrophage-colony stimulating factor (M-CSF) alone, M-CSF and RANKL, and also M-CSF and RANKL with excess concentrations of OPG. Osteoclast formation was assessed by expression of tartrate-resistant acid phosphatase on glass coverslips and resorption on dentine slices. Results: In cultures with M-CSF, there was a significant increase in osteoclast formation in Charcot patients compared with healthy and diabetic control participants (p=0.008). A significant increase in bone resorption was also seen in the former, compared with healthy and diabetic control participants (p<0.0001). The addition of RANKL to the cultures with M-CSF led to marked increase in osteoclastic resorption in Charcot (from 0.264±0.06% to 41.6±8.1%, p<0.0001) and diabetic control (0.000±0.00% to 14.2±16.5%, p<0.0001) patients, and also in healthy control participants (0.004±0.01% to 10.5±1.9%, p0.0001). Although the addition of OPG to cultures with M-CSF and RANKL led to a marked reduction of resorption in Charcot patients (41.6±8.1% to 5.9±2.4%, p=0.001), this suppression was not as complete as in diabetic control patients (14.2±16.5% to 0.45±0.31%, p=0.001) and in healthy control participants (from 10.5±1/9% to 0.00±0.00%, p<0.0001). Conclusions/interpretation: These results indicate that RANKL-mediated osteoclastic resorption occurs in acute Charcot's osteoarthropathy. However, the incomplete inhibition of RANKL after addition of OPG also suggests the existence of a RANKL-independent pathway

Hemi-Castaing ligamentoplasty for the treatment of chronic lateral ankle instability: a retrospective assessment of outcome

Purpose: In the treatment of chronic ankle instability, most non-anatomical reconstructions use the peroneus brevis tendon. This, however, sacrifices the natural ankle stabilising properties of the peroneus brevis muscle. The aim of this study was to evaluate the functional outcome of patients treated with a hemi-Castaing procedure, which uses only half the peroneus brevis tendon. Methods: We performed a retrospective cohort study of patients who underwent hemi-Castaing ligamentoplasty for chronic lateral ankle instability between 1993 and 2010, with a minimum of one year follow-up. Patients were sent a postal questionnaire comprising five validated outcome measures: Olerud-Molander Ankle Score (OMAS), Karlsson Ankle Functional Score (KAFS), Tegner Activity Level Score (pre-injury, prior to surgery, at follow-up), visual analog scale on pain (VAS) and the Short Form 36 (SF-36). Results: Twenty patients completed the questionnaire on functional outcome. The OMAS showed good to excellent outcome in 80% and the KAFS in 65%, the Tegner Score improved from surgery but did not reach pre-injury levels, the VAS on pain was 1 of 10 and the SF-36 returned to normal compared with the average population. Conclusions: Even though most patients were satisfied with the results, outcome at long-term follow-up was less favourable compared with the literature on anatomical reconstructions. In accordance with the literature, we therefore conclude that the initial surgical treatment of chronic lateral ankle instability should be an anatomical repair with augmentation (i.e. the Broström-Gould technique) and the non-anatomical repair should be reserved for unsuccessful cases after anatomical repair or in cases where no adequate ligament remnants are available for reconstruction