Locking vs. non-locking plate fixation in comminuted talar neck fractures: a biomechanical study using cadaveric specimens.

BACKGROUND: Talar neck fractures are rare but potentially devastating injuries, with early reduction and rigid fixation essential to facilitate union and prevent avascular necrosis. Even small degrees of malunion will alter load transmission and subtalar joint kinematics. Changes in fixation techniques have led to dual plating strategies. While locked plating has perceived advantages in porotic bone and comminution, its biomechanical benefits in talar neck fractures have not been shown. AIM: To compare the strength of locking vs. non-locking plate fixation in comminuted talar neck fractures. METHOD: Seven pairs of cadaveric tali were randomised to locking or non-locking plate fixation. A standardised model of talar neck fracture with medial comminution was created, and fixation performed. The fixed specimens were mounted onto a motorised testing device, and an axial load applied. RESULTS: Peak load to failure, deformation at failure, work done to achieve failure, and stiffness of the constructs were measured. No statistically significant difference was found between locking and non-locking constructs for all parameters. CONCLUSIONS: Both constructs provide similar strength to failure in talar neck fracture fixations. Mean peak load to failure did not exceed the theoretical maximum forces generated of 1.1 kN when weight-bearing. We would advocate caution with early mobilisation in both fixations.

The 3D-printed miniplate-jig system: a new, rapid, precise, and user-friendly approach to miniplate fixation of free-tissue mandibular reconstructions.

Patient-specific, additively manufactured (printed) titanium reconstruction plates have been widely used to improve accuracy and efficiency of fibular flap reconstruction of the mandible. Miniplates possess some potential advantages over single-piece reconstruction plates, however multiple-miniplate fixation can be more technically demanding and may lengthen the duration of surgery. Furthermore, incremental angulation errors in screw placement for each miniplate could compromise overall dimensional accuracy of the neomandibular reconstruction. This preliminary article reports the first clinical use of a new patient-specific, printed titanium miniplate-jig system in a patient undergoing hemimandibulectomy for osteoradionecrosis of the mandible withfibular flap reconstruction. Our initial experience with the new deviceand technique demonstratesa quick, user friendly, and precise method for the placement and fixation of multiple miniplates in fibular-flap reconstruction of the mandible.

The Orthopedic Effects of Electronic Cigarettes: A Systematic Review and Pediatric Case Series.

Electronic cigarette (EC) use is highly prevalent, especially in the adolescent population, where 29% of Canadian adolescents have used an EC in the past thirty days per national surveys. Our pediatric orthopedic referral centre observed a cluster of delayed unions of bone fractures in adolescents using ECs and present the case series here. We then asked whether electronic cigarettes impair bone healing or influence orthopedic outcomes. A PRISMA-compliant systematic review was carried out, which revealed no human clinical studies and a general paucity of evidence around ECs and musculoskeletal health. The existing experimental evidence relevant to orthopedics is summarized. The effect of ECs on the musculoskeletal system is poorly understood and is a target for further research.

Type I but Not Type II Calreticulin Mutations Activate the IRE1α/XBP1 Pathway of the Unfolded Protein Response to Drive Myeloproliferative Neoplasms.

Approximately 20% of patients with myeloproliferative neoplasms (MPN) harbor mutations in the gene calreticulin (CALR), with 80% of those mutations classified as either type I or type II. While type II CALR-mutant proteins retain many of the Ca2+ binding sites present in the wild-type protein, type I CALR-mutant proteins lose these residues. The functional consequences of this differential loss of Ca2+ binding sites remain unexplored. Here, we show that the loss of Ca2+ binding residues in the type I mutant CALR protein directly impairs its Ca2+ binding ability, which in turn leads to depleted endoplasmic reticulum (ER) Ca2+ and subsequent activation of the IRE1α/XBP1 pathway of the unfolded protein response. Genetic or pharmacologic inhibition of IRE1α/XBP1 signaling induces cell death in type I mutant but not type II mutant or wild-type CALR-expressing cells, and abrogates type I mutant CALR-driven MPN disease progression in vivo. SIGNIFICANCE: Current targeted therapies for CALR-mutated MPNs are not curative and fail to differentiate between type I- versus type II-driven disease. To improve treatment strategies, it is critical to identify CALR mutation type-specific vulnerabilities. Here we show that IRE1α/XBP1 represents a unique, targetable dependency specific to type I CALR-mutated MPNs. This article is highlighted in the In This Issue feature, p. 265.