Reduced Incidence of Intraoperative Femur Fracture With a Second-Generation Tapered Wedge Stem.

BACKGROUND: Intraoperative fractures during total hip arthroplasty (THA) are more common when using cementless stems. The purpose of this study was to investigate the impact of a new shorter second-generation cementless, tapered wedge stem with improved proximal femoral fit in reducing the incidence of intraoperative fracture. METHODS: A retrospective study was conducted on primary THA cases performed at a single institution using a first-generation or second-generation cementless stem from 2006-2016. All intraoperative femur fractures were identified, as well as early 30-day postoperative periprosthetic femur fractures, which could represent nondisplaced intraoperative fractures that were initially missed. Risk for intraoperative femur fracture was analyzed using logistic regression, accounting for demographic covariates and surgeon. RESULTS: Of 6473 primary THA performed with a cementless, tapered wedge stem during the study period, 3126 used a first-generation stem and 3347 used a second-generation stem. The incidence of intraoperative fracture was 1.79% for first-generation stems and 0.24% for second-generation stems, representing a 7.5-fold reduction of risk for fracture. After accounting for covariates, the odds of intraoperative fracture were 0.33 using the second-generation stem relative to the first-generation stem (P = .01). However, there was no significant difference in the odds of early 30-day postoperative fractures using the second-generation stem (odds ratio 0.93, P = .56). CONCLUSION: A new second-generation cementless stem resulted in a 7.5-fold decrease in the incidence of intraoperative femur fracture compared with the preceding stem.

Context-specific interactions between Notch and ALK1 cannot explain ALK1-associated arteriovenous malformations.

AIMS: Notch and activin receptor-like kinase 1 (ALK1) have been implicated in arterial specification, angiogenic tip/stalk cell differentiation, and development of arteriovenous malformations (AVMs), and ALK1 can cooperate with Notch to up-regulate expression of Notch target genes in cultured endothelial cells. These findings suggest that Notch and ALK1 might collaboratively program arterial identity and prevent AVMs. We therefore sought to investigate the interaction between Notch and Alk1 signalling in the developing vertebrate vasculature. METHODS AND RESULTS: We modulated Notch and Alk1 activities in zebrafish embryos and examined effects on Notch target gene expression and vascular morphology. Although Alk1 is not necessary for expression of Notch target genes in arterial endothelium, loss of Notch signalling unmasks a role for Alk1 in supporting hey2 and ephrinb2a expression in the dorsal aorta. In contrast, Notch and Alk1 play opposing roles in hey2 expression in cranial arteries and dll4 expression in all arterial endothelium, with Notch inducing and Alk1 repressing these genes. Although alk1 loss increases expression of dll4, AVMs in alk1 mutants could neither be phenocopied by Notch activation nor rescued by Dll4/Notch inhibition. CONCLUSION: Control of Notch targets in arterial endothelium is context-dependent, with gene-specific and region-specific requirements for Notch and Alk1. Alk1 is not required for arterial identity, and perturbations in Notch signalling cannot account for alk1 mutant-associated AVMs. These data suggest that AVMs associated with ALK1 mutation are not caused by defective arterial specification or altered Notch signalling.