Background: As the popularity of total ankle arthroplasty (TAA) increases and indications expand, surgeons require a better understanding of which patient factors are associated with implant failure. In this study, we aimed to use a large total ankle database to identify independent risk factors for implant failure at mid- to long-term follow-up. Methods: A prospectively collected database was used to identify all patients who underwent primary TAA with a minimum 5 years’ follow-up. The primary outcome was revision, defined as removal of one or both metal components; failures due to infection were excluded. Patient and clinical factors analyzed included age, sex, body mass index (BMI), smoking status, presence of diabetes, indication for TAA, implant, tourniquet time, and presence of ipsilateral hindfoot fusion. Preoperative coronal deformity and sagittal talar translation were assessed, as were postoperative coronal and sagittal tibial component alignment. Univariable and multivariable analyses were performed to identify predictors of implant failure. After excluding 5 ankles that failed because of deep infection, 533 ankles with a mean 7 (range, 5-11) years of follow-up met the inclusion criteria. Four implants were used: INBONE I, INBONE II, STAR, and Salto-Talaris. Results: Thirty-four ankles (6.4%) were revised or removed a mean 4 (range, 1-9) years postoperatively. The only independent predictors of failure were the INBONE I prosthesis and ipsilateral hindfoot fusion ( P = .006 and P = .023, respectively). Conclusions: This is among the largest studies to analyze the relationship between TAA failure rates and multiple different patient, operative, and radiographic factors. Of note, age, BMI, and amount of deformity were not associated with higher failure rates. Only patients with ipsilateral hindfoot fusion or who received the INBONE I prosthesis were at significantly higher risk of implant failure. Level of Evidence: Level III, retrospective cohort study.

BackgroundObesity-related diseases, including type 2 diabetes and cardiovascular disease, have reached epidemic proportions in industrialized nations, and dietary interventions for their prevention are therefore important. Resistant starches (RS) improve insulin sensitivity in clinical trials, but the mechanisms underlying this health benefit remain poorly understood. Because RS fermentation by the gut microbiota results in the formation of physiologically active metabolites, we chose to specifically determine the role of the gut microbiota in mediating the metabolic benefits of RS. To achieve this goal, we determined the effects of RS when added to a Western diet on host metabolism in mice with and without a microbiota.ResultsRS feeding of conventionalized mice improved insulin sensitivity and redressed some of the Western diet-induced changes in microbiome composition. However, parallel experiments in germ-free littermates revealed that RS-mediated improvements in insulin levels also occurred in the absence of a microbiota. RS reduced gene expression of adipose tissue macrophage markers and altered cecal concentrations of several bile acids in both germ-free and conventionalized mice; these effects were strongly correlated with the metabolic benefits, providing a potential microbiota-independent mechanism to explain the physiological effects of RS.ConclusionsThis study demonstrated that some metabolic benefits exerted by dietary RS, especially improvements in insulin levels, occur independently of the microbiota and could involve alterations in the bile acid cycle and adipose tissue immune modulation. This work also sets a precedent for future mechanistic studies aimed at establishing the causative role of the gut microbiota in mediating the benefits of bioactive compounds and functional foods.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-017-0230-5) contains supplementary material, which is available to authorized users.

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