Hospital type is an indicator for structures and processes of care. The effect of hospital type on hip fracture in-hospital mortality is unknown. We determine whether hip fracture in-hospital mortality differs according to hospital type.

We retrieved records of hip fracture for 167,816 patients aged 65 years and older, who were admitted to a Canadian acute hospital between 2004 and 2012. For each hospital type we measured and compared the cumulative incidence of in-hospital death by in-patient day, accounting for discharge as a competing event.

The cumulative incidence of in-hospital death at in-patient day 30 was lowest for teaching hospital admissions (7.3%) and highest for small community hospital admissions (11.5%). The adjusted odds of in-hospital death were 12% (95% CI 1.06–1.19), 25% (95% CI 1.17–1.34), and 64% (95% CI 1.50–1.79) higher for large, medium, and small community hospital versus teaching hospital admissions. The adjusted odds of nonoperative death were 1.6 times (95% CI 1.42–1.86), and 3.4 times (95% CI 2.96–3.94) higher for medium and small community hospital versus teaching hospital admissions. The adjusted odds of postoperative death were 14% (95% CI 1.07–1.22) and 20% (95% CI 1.10–1.31) higher at large and medium community hospitals versus teaching hospitals. The adjusted odds of postoperative death were largest at small community hospitals but the confidence interval crossed 1 (OR = 1.25, 95% CI 0.92–1.70).

A higher proportion of hip fracture patients die at non-teaching compared to teaching hospitals accounting for length of stay. Higher mortality at small community hospitals may reflect disparities in access to resources and delay to treatment.

Summary Statement

The modulation of both quantity and quality of peri-implant bone with either PTH or loading may be viable options to improve implant fixation and patient outcomes.

A strong bone-implant interface is essential for successful joint replacement surgery. This study investigated the differences in bone surrounding and within a porous titanium implant after single or combined treatment with two anabolic bone therapies: intermittent parathyroid hormone (teriparatide) and mechanical loading. Porous titanium implants were inserted bilaterally on the distal lateral femurs of rabbits. The right implant was loaded daily (1 MPa, 50 cycles/day) while the left implant was not. Rabbits received daily PTH injections (20 ug/kg) or saline vehicle. Periprosthetic cancellous bone 0.5, 1.0, and 2.0 mm below the implant surface, bone at the 0.25 mm bone-implant interface and total bone within each implant were examined using tissue-level analyses (quantitative backscattered electron microscopy), cellular analyses (immunohistochemistry staining of osteoblasts with procollagen-1 and TRAP staining of osteoclasts), and shear testing (implant-bone interface).

Statistical significance was determined using GEE models (p<0.05). For tissue located 0.5 mm below the implant, significant increases in bone area per total area (BA/TA) were observed with PTH treatment (56%) and with loading (27%). Further, an 18% increase in mineralization density with PTH treatment and a 20% increase in mineralization density with loading was found. Loading effects were not present beyond the 0.5 mm periprosthetic region, but PTH significantly increased BA/TA 2.0 mm below and mineralization density 1.0 mm below the implant. Tissue-level changes were supported by increases in osteoblast activity 0.5 mm below the implant with PTH (79%) and loading (34%), as well as by minimal osteoclast changes. At the 0.25 mm implant-bone interface PTH and loading increased BA/TA (16% and 23%, respectively), but only loading increased mineralization density (7%). Further, total integrated bone area was increased 35% with PTH.

Both PTH and loading enhanced the mechanical integrity of the implant-bone; shear strength increased 34% and 60%, respectively. Although combined treatment was not synergistic, both PTH and loading individually enhanced the amount and mineralization density of bone at the implant interface and immediately below the interface, thereby increasing the mechanical strength of the metal-bone interface. This research suggests that modulation of both quantity and quality of peri-implant bone may be viable options to improve implant fixation and patient outcomes.

Improving periprosthetic bone is essential for implant fixation and reducing peri-implant fracture risk. This studied examined the individual and combined effects of iPTH and mechanical loading at the cellular, molecular, and tissue level for periprosthetic cancellous bone. Adult rabbits had a porous titanium implant inserted bilaterally on the cancellous bone beneath a mechanical loading device on the distal lateral femur. The right femur was loaded daily, the left femur received a sham loading device, and half of the rabbits received daily PTH. Periprosthetic bone was processed up to 28 days for qPCR, histology, and uCT analysis. We observed an increase in cellular and molecular markers of osteoblast activity and decrease in adipocytic markers for both treatments, with small additional effects in the combined group. Loading and iPTH led to a decrease and increase, respectively, in osteoclast number, acting through changes in RANKL/OPG expression. Changes in SOST and beta-catenin mRNA levels suggested an integral role for the Wnt pathway. We observed strong singular effects on BV/TV of both loading (1.53 fold) and iPTH (1.54 fold). Combined treatment showed a small additive effect on bone volume. In conclusion, loading and iPTH act through a pro-osteoblastic/anti-adipocytic response and through control of bone turnover via changes in the RANKL/OPG pathway. These changes led to a small additional, but not synergistic, increase in bone volume with the combined therapy.