RESUMO
BACKGROUND: Periprosthetic joint infection (PJI) treatment has high failure rates even after 2-stage revision. Risk factors for treatment failure (TF) after staged revision for PJI are not well defined, nor is it well established how they correlate with the risks of developing an index PJI. Identifying modifiable risk factors may allow preoperative optimization, while identifying nonmodifiable risk factors can influence surgical options or advise against further surgery. We performed a systematic review and meta-analysis to better define predictors of TF in 2-stage revision for PJI. METHODS: The PubMed, Embase, and Scopus databases were searched from their inception in December 1976 to April 15, 2023. Studies comparing patient-related variables between patients successfully treated who had 2-staged revision total hip arthroplasty (THA) and patients with persistent infections were included. Studies were screened, and 2 independent reviewers extracted data, while a third resolved discrepancies. Meta-analysis was performed on these data. There were 10,052 unique studies screened, and 21 studies met the inclusion criteria for data extraction. RESULTS: There was good-quality evidence that obesity, liver cirrhosis, and previous failed revisions for PJI are nonmodifiable risk factors, while intravenous drug use (IVDU) and smoking are modifiable risk factors for TF after 2-stage revision for hip PJI. Reoperation between revision stages was also significantly associated with an increased risk of TF. Interestingly, other risk factors for an index PJI including male gender, American Society of Anesthesiology score, diabetes mellitus, and inflammatory arthropathy did not predict TF. Evidence on Charlson Comorbidity Index was limited. CONCLUSIONS: Patients with a smoking history, obesity, IVDU, previous failed revision for PJI, reoperation between stages, and liver cirrhosis are more likely to experience TF after 2-stage revision THA for PJI. Modifiable risk factors include smoking and IVDU and these patients should be referred to services for cessation as early as possible before 2-stage revision THA.
RESUMO
OBJECTIVE: EFNB1 mutation causes craniofrontonasal dysplasia (CFND), a congenital syndrome associated with craniomaxillofacial anomalies characterised by coronal craniosynostosis, orbital hypertelorism, and midface dysplasia. The aim of this murine study was to investigate the effect of the EfnB1 conditional gene deletion in osteoprogenitor cells on the craniomaxillofacial skeletal morphology. DESIGN: The skulls of male and female mice, in which EfnB1 was deleted by Cre (a site-specific DNA recombinase) under the control of the Osterix (Osx) promoter (EfnB1OB-/-), were compared to those without EfnB1 deletion (Osx:Cre control) at two ages (4 and 8 weeks; n = 6 per group). The three-dimensional micro-computed tomography reconstructions were prepared to calculate 17 linear measurements in the cranial vault (brain box), midface and mandible. Coronal and sagittal sutures from the 8-week-old mice were also subjected to histological examination. RESULTS: EfnB1OB-/- mice displayed significantly larger cranial height, larger interorbital and nasal widths, smaller maxillary width than controls by 8 weeks (p < 0.05), but mandibular size was not significantly different (p > 0.05). Binomial testing showed significantly smaller EfnB1OB-/- skulls at 4 weeks but larger at 8 weeks (p < 0.05). Histological examination revealed increased bony fusion and fibrous connective tissue deposition at the coronal suture of EfnB1OB-/- mice compared with controls. CONCLUSIONS: Craniofacial phenotype of the murine model of EfnB1 deletion in osteoprogenitor cells partially represents the human CFND phenotype, with implications for better understanding mechanisms involved in skeletal morphogenesis and malocclusion.
