Anatomic and Patient Risk Factors for Postoperative Periprosthetic Hip Fractures: A Case-Control Study.

BACKGROUND: Periprosthetic fracture remains a major source of reoperation following total hip arthroplasty (THA). Within 90 days of surgery, fractures may occur spontaneously or with minor injury and are therefore more likely related to patient factors including anatomic variation. METHODS: From 2008 to 2018, 16,254 primary THAs were performed at our institution; of those, 48 were revised for periprosthetic fracture within 90 days of surgery. A control group of 193 patients undergoing THA for hip osteoarthritis (OA) was randomly selected from the source population. We excluded patients with genetic bone disease and THA performed for hip fracture. We used logistic regression to analyze associations between patient factors (demographics, anatomical factors, comorbidities, surgical technique, and implants) and odds of 90-day periprosthetic fracture. RESULTS: Increased age was significantly associated with fracture (P = .002), as was female gender (P = .046). After adjusting for age and gender, absence of contralateral OA was associated with increased odds of fracture relative to patients with contralateral OA (odds ratio [OR] 3.85, 95% confidence interval [CI] 1.60-9.29), as was having a contralateral THA in place (OR 3.70, 95% CI 1.59-8.60). The neck-shaft angle, femoral offset, and the Dorr classification were not associated with increased odds of fracture. Additionally, the distance from the tip of the trochanter to the top of the femoral head was associated with increased odds of fracture per half centimeter (OR 1.48, 95% CI 1.14-1.93). CONCLUSION: Risk of early postoperative periprosthetic fracture following THA is increased with age, female gender, and increasing distance from the greater trochanter to the top of the femoral head; and decreased in the setting of contralateral hip OA. The trochanter-head distance correlation with periprosthetic hip fracture indicates that the preoperative anatomy may influence PPF, particularly regarding how that anatomy is reconstructed.

Pathogenic features associated with increased virulence upon Simian immunodeficiency virus cross-species transmission from natural hosts.

UNLABELLED: While simian immunodeficiency viruses (SIVs) are generally nonpathogenic in their natural hosts, dramatic increases in pathogenicity may occur upon cross-species transmission to new hosts. Deciphering the drivers of these increases in virulence is of major interest for understanding the emergence of new human immunodeficiency viruses (HIVs). We transmitted SIVsab from the sabaeus species of African green monkeys (AGMs) to pigtailed macaques (PTMs). High acute viral replication occurred in all SIVsab-infected PTMs, yet the outcome of chronic infection was highly variable, ranging from rapid progression to controlled infection, which was independent of the dynamics of acute viral replication, CD4(+) T cell depletion, or preinfection levels of microbial translocation. Infection of seven PTMs with plasma collected at necropsy from a rapid-progressor PTM was consistently highly pathogenic, with high acute and chronic viral replication, massive depletion of memory CD4(+) T cells, and disease progression in all PTMs. The plasma inoculum used for the serial passage did not contain adventitious bacterial or viral contaminants. Single-genome amplification showed that this inoculum was significantly more homogenous than the inoculum directly derived from AGMs, pointing to a strain selection in PTMs. In spite of similar peak plasma viral loads between the monkeys in the two passages, immune activation/inflammation levels dramatically increased in PTMs infected with the passaged virus. These results suggest that strain selection and a massive cytokine storm are major factors behind increased pathogenicity of SIV upon serial passage and adaptation of SIVs to new hosts following cross-species transmission. IMPORTANCE: We report here that upon cross-species transmission and serial passage of SIVsab from its natural host, the sabaeus African green monkey (AGM), to a new host, the pigtailed macaque (PTM), viral adaptation and increased pathogenicity involve strain selection and a massive cytokine storm. These results permit the design of strategies aimed at preventing cross-species transmission from natural hosts of SIVs to humans in areas of endemicity. Furthermore, our study describes a new animal model for SIV infection. As the outcomes of SIVsab infection in PTMs, African green monkeys, and rhesus macaques are different, the use of these systems enables comparative studies between pathogenic, nonpathogenic, and elite-controlled infections, to gain insight into the mechanisms of SIV immunodeficiency and comorbidities.