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Background Emergency department (ED) visits associated with prescription opioids have increased in the last ten years. This study describes the opioid utilization of patients discharged from the ED with an opioid prescription for pain, 14 to 21 days post discharge. Methods This is a prospective, single-centered, survey-based observational descriptive study conducted from December 2017 to February 2018 in the ED at a tertiary level 1 trauma center. The primary outcomes were the percentage of patients with unused opioids and the quantity of opioids remaining 14 to 21 days post ED discharge. A sample of ED patients who received an oral opioid prescription were approached for informed consent and received a telephone survey 14 to 21 days post discharge. Results Of 178 patients approached for consent, 122 were enrolled. Among them, 98 were successfully surveyed (80.3%). The median number of pills prescribed was 8 (IQR:8–12). Nearly half (49%) of patients had unused opioids 14 to 21 days post ED discharge, not including 9.2% of patients who never filled their prescriptions. Of the total 980 pills prescribed, 327 pills remained unused (33.4%). Only 55.1% of patients reported receiving counseling on side effect of opioids and 21.4% of patients reported they received counseling on storage and disposal. Conclusion The majority of patients in this study had unused or unfilled opioids 14 to 21 days post ED discharge, and approximately one third of the opioids prescribed remained unused. Most patients did not recall receiving opioid related education including proper disposal of medication.

Recently, several plexins and semaphorins have been associated with osteoclastogenesis, a vital process for bone remodeling. Plexin-A2 is implicated in bone homeostasis, however, whether it plays a role in osteoclastogenesis and the underlying mechanism remain unknown. We show that plexin-A2 expression is upregulated during RANKL-induced osteoclastogenesis. In addition, the soluble Sema6A fused with IgG1 Fc region (Fc-Sema6A) interacts with plexin-A2 from cell lysates of osteoclasts, suggesting that plexin-A2 acts as a receptor of Sema6A in osteoclasts. Moreover, Sema6A treatment stimulates RANKL-induced osteoclastogenesis, and this effect is abolished when plexin-A2 is neutralized, which illustrates an indispensable role of plexin-A2 in mediating Sema6A effect on osteoclastogenesis. Mechanistically, Sema6A-plexin-A2 axis enhances RANKL-induced activation of PLCγ as well as downstream target NFATc1, one master transcriptional factor of osteoclastogenesis. Lastly, inhibition of PLCγ by pharmacological inhibitor U73122 abrogates Sema6A-stimulated NFATc1 activation and RANKL-induced osteoclastogenesis, thus demonstrating that the PLCγ-mediated NFATc1 activation accounts for the promotive role of Sema6A-plexin-A2 axis in RANKL-induced osteoclastogenesis. Taken together, this study uncovers a novel role of Sema6A and plexin-A2 in osteoclastogenesis, and also offers them as possible therapeutic targets in the intervention of osteolytic diseases.