Single-Dose, Preoperative Vitamin-D Supplementation Decreases Infection in a Mouse Model of Periprosthetic Joint Infection.

BACKGROUND: Despite recent advances, infection remains the most common etiology of arthroplasty failure. Recent work suggests that 25-hydroxyvitamin D (25D) deficiency correlates with the frequency of periprosthetic joint infection (PJI). We endeavored to examine whether 25D3 deficiency leads to increased bacterial burden in vivo in an established mouse model of PJI and, if so, whether this effect can be reversed by preoperative 25D3 supplementation. METHODS: Mice (lys-EGFP) possessing fluorescent neutrophils were fed a vitamin D3-sufficient (n = 20) or deficient (n = 40) diet for 6 weeks. A group of 25D3-deficient mice (n = 20) were "rescued" with 1 intraperitoneal dose of 25D3 at 3 days before surgery. A stainless steel implant was inserted into the knee joint and the joint space was inoculated with bioluminescent Staphylococcus aureus (1 × 10 colony forming units [CFUs]). In vivo imaging was used to monitor bacterial burden and neutrophil infiltration. Blood was drawn to confirm 25D3 levels 3 days before surgery and on postoperative days (PODs) 0 and 14. Mice were killed at POD 21, and CFUs were quantified after culture. Myeloperoxidase (MPO) and ß-N-acetylglucosaminidase (NAG) were assayed to look at neutrophil infiltration and activated tissue macrophage recruitment, respectively. RESULTS: Serum values confirmed 25D3 deficiency and repletion of the 25D3-rescued group. Bacterial bioluminescence and neutrophil fluorescence were significantly greater (p < 0.05) in the 25D3-deficient group. CFU counts from the joint tissue and implant were also significantly greater in this group (p < 0.05). Rescue treatment significantly decreased bacterial burden and neutrophil infiltration (p < 0.05). Compared with the 25D3-sufficient and 25D3-rescued groups, MPO activity was higher (p < 0.02) and NAG activity was lower (p < 0.03) in the 25D3-deficient group. CONCLUSIONS: This study demonstrated in vivo in a mouse model of PJI that (1) 25D3 deficiency results in increased bacterial burden and neutrophil infiltration, and (2) this effect can be reversed with preoperative repletion of 25D3. CLINICAL RELEVANCE: Considering that >65% of patients undergoing arthroplasty have insufficient or low levels of total 25D and that 25D levels can be replenished with ease using a U.S. Food and Drug Administration (FDA)-approved, oral 25D3 product, 25D deficiency may be an important modifiable risk factor in humans undergoing joint replacement.

The role of chairman and research director in influencing scholarly productivity and research funding in academic orthopaedic surgery.

The purpose of this study was to determine what orthopaedic surgery department leadership characteristics are most closely correlated with securing NIH funding and increasing scholarly productivity. Scopus database was used to identify number of publications/h-index for 4,328 faculty, department chairs (DC), and research directors (RD), listed on departmental websites from 138 academic orthopaedic departments in the United States. NIH funding data was obtained for the 2013 fiscal year. While all programs had a DC, only 46% had a RD. Of $54,925,833 in NIH funding allocated to orthopaedic surgery faculty in 2013, 3% of faculty and 31% of departments were funded. 16% of funded institutions had a funded DC whereas 65% had a funded RD. Department productivity and funding were highly correlated to leadership productivity and funding(p< 0.05). Mean funding was $1,700,000 for departments with a NIH-funded RD, $104,000 for departments with an unfunded RD, and $72,000 for departments with no RD. These findings suggest that orthopaedic department academic success is directly associated with scholarly productivity and funding of both DC and RD. The findings further highlight the correlation between a funded RD and a well-funded department. This does not hold for an unfunded RD.