Resection of Calcaneonavicular and Talocalcaneal Coalitions With Surgical Correction of the Hindfoot Valgus Deformity in One Step.

Background: Calcaneonavicular (CNC) and talocalcaneal (TCC) coalitions are the most common cause of rigid flatfoot in children. After resection, correction of the most frequent valgus-hindfoot deformity usually requires a second-step surgery. We report results of a retrospective study of patients treated with a one-step correction. Methods: Between 2008 and 2019, data were collected on 26 patients (19 male, 7 female) affected by CNC (n = 18) and TCC (n = 13), all with rigid symptomatic flatfeet. Average age at surgery was 12.5 ± 1.1 (SD) years (range, 9.8-15.2). All patients (26/26) underwent resection, 20 of 26 underwent at the same time subtalar extraarticular screw arthroereisis (SESA) for correction of residual hindfoot valgus deformity. Pre- and postoperative talocalcaneal angle according to Costa Bartani and Talar inclination angle in weightbearing were measured. Twenty-five of 26 patients had postoperative American Orthopaedic Foot & Ankle Society (AOFAS) ankle-hindfoot score. Results: Pre- and postoperative talocalcaneal average angle for CNC was respectively 141.5 ± 7.7 degrees and 130.5 ± 5.2 degrees (P < .0001) and 143.7 ± 7.7 degrees and 129.7 ± 7.0 degrees (P < .0001) for TCC. Talar inclination average angle for CNC was 29.2 ± 5.3 degrees and 19.3 ± 1.6 degrees (P < .0001) and 31.2 ± 6.4 degrees and 21.4 ± 3.4 degrees (P < .0001) for TCC. Average follow-up (FU) was 4.7 ± 3.0 years (range, 6 months-11.9 years, median 4.9 years), with a mean age at FU of 17.2 ± 5.8 (SD) years (min 12.1, max 25.3, median 16.8 years). The mean AOFAS ankle-hindfoot score for CNC and for TCC was 96.6 (range 83-100) for resection and valgus correction as one-step procedure with no statistical difference (P = .5) between CNC and TCC. No patients had additional surgery for complications or recurrence. Conclusion: Symptomatic rigid flatfeet affected by CNC and TCC treated with coalition resection and minimally invasive subtalar arthroereisis (SESA) for residual hindfoot valgus correction in one step in adolescent age achieved good to excellent results in all cases. Further surgery to correct malalignment was avoided. Level of Evidence: Level IV, retrospective study.

The role of the extracellular matrix in the reduction of lateral force transmission in muscle bundles: A finite element analysis.

BACKGROUND AND OBJECTIVE: Aging is associated with a reduction in muscle performance, but muscle weakness is characterized by a much greater loss of force loss compared to mass loss. The aim of this work is to assess the contribution of the extracellular matrix (ECM) to the lateral transmission of force in humans and the loss of transmitted force due to age-related modifications. METHODS: Finite element models of muscle bundles are developed for young and elderly human subjects, by considering a few fibers connected through an ECM layer. Bundles of young and elderly subjects are assumed to differ in terms of ECM thickness, as observed experimentally. A three-element-based Hill model is adopted to describe the active behavior of muscle fibers, while the ECM is modeled assuming an isotropic hyperelastic neo-Hookean constitutive formulation. Numerical analyses are carried out by mimicking, at the scale of a bundle, two experimental protocols from the literature. RESULTS: When comparing numerical results obtained for bundles of young and elderly subjects, a greater reduction in the total transmitted force is observed in the latter. The loss of transmitted force is 22 % for the elderly subjects, while it is limited to 7.5 % for the young subjects. The result for the elderly subjects is in line with literature studies on animal models, showing a reduction in the range of 20-34 %. This can be explained by an alteration in the mechanism of lateral force transmission due to the lower shear stiffness of the ECM in elderly subjects, related to its higher thickness. CONCLUSIONS: Computational modeling allows to evaluate at the bundle level how the age-related increase of the ECM amount between fibers affects the lateral transmission of force. The results suggest that the observed increase in ECM thickness in aging alone can explain the reduction of the total transmitted force, due to the impaired lateral transmission of force of each fiber.

Mitochondria can substitute for parvalbumin to lower cytosolic calcium levels in the murine fast skeletal muscle.

AIM: Parvalbumin (PV) is a primary calcium buffer in mouse fast skeletal muscle fibers. Previous work showed that PV ablation has a limited impact on cytosolic Ca2+ ([Ca2+]cyto) transients and contractile response, while it enhances mitochondrial density and mitochondrial matrix-free calcium concentration ([Ca2+]mito). Here, we aimed to quantitatively test the hypothesis that mitochondria act to compensate for PV deficiency. METHODS: We determined the free Ca2+ redistribution during a 2 s 60 Hz tetanic stimulation in the sarcoplasmic reticulum, cytosol, and mitochondria. Via a reaction-diffusion Ca2+ model, we quantitatively evaluated mitochondrial uptake and storage capacity requirements to compensate for PV lack and analyzed possible extracellular export. RESULTS: [Ca2+]mito during tetanic stimulation is greater in knock-out (KO) (1362 ± 392 nM) than in wild-type (WT) (855 ± 392 nM), p < 0.05. Under the assumption of a non-linear intramitochondrial buffering, the model predicts an accumulation of 725 µmoles/L fiber (buffering ratio 1:11 000) in KO, much higher than in WT (137 µmoles/L fiber, ratio 1:4500). The required transport rate via mitochondrial calcium uniporter (MCU) reaches 3 mM/s, compatible with available literature. TEM images of calcium entry units and Mn2+ quenching showed a greater capacity of store-operated calcium entry in KO compared to WT. However, levels of [Ca2+]cyto during tetanic stimulation were not modulated to variations of extracellular calcium. CONCLUSIONS: The model-based analysis of experimentally determined calcium distribution during tetanic stimulation showed that mitochondria can act as a buffer to compensate for the lack of PV. This result contributes to a better understanding of mitochondria's role in modulating [Ca2+]cyto in skeletal muscle fibers.