Objectives To evaluate national trends in opioid prescribing patterns by otolaryngologists for postoperative pain control after common otolaryngologic procedures. Study Design Cross-sectional; survey. Subjects and Methods A survey to determine opioid prescribing patterns for the treatment of postoperative pain following common otolaryngologic procedures was distributed to all members of the American Academy of Otolaryngology-Head and Neck Surgery. Results The most common pain medication prescribed for adults postoperatively was hydrocodone-acetaminophen (73%), followed by oxycodone-acetaminophen (39%). The most common pain medication prescribed postoperatively for children was acetaminophen (67%), followed by nonsteroidal anti-inflammatory drugs (65%). Overall, there was a wide variation in quantity of opioids prescribed for each surgery, ranging from 0 to more than 60 doses. Mean opioid prescriptions were greatest for tonsillectomy (37 tablets) and least for direct laryngoscopy (5.3 tablets). Conclusion This study identifies nationwide variations in opioid prescribing patterns among otolaryngologists. While otolaryngology is a relatively small specialty, we still have an obligation to work with all physicians to help combat the current opioid epidemic. By evaluating nationwide postoperative pain regimens, we are moving closer toward understanding how to reduce the opioid burden.
The cell surface receptor low-density lipoprotein receptor-related protein 5 (LRP5) is a key regulator of bone mass and bone strength. Heterozygous missense mutations in LRP5 cause autosomal dominant high bone mass (HBM) in humans by reducing binding to LRP5 by endogenous inhibitors, such as sclerostin (SOST). Mice heterozygous for a knockin allele (Lrp5p.A214V) that is orthologous to a human HBM-causing mutation have increased bone mass and strength. Osteogenesis Imperfecta (OI) is a skeletal fragility disorder predominantly caused by mutations that affect type I collagen. We tested whether the LRP5 pathway can be used to improve bone properties in animal models of OI. First, we mated Lrp5+/p.A214V mice to Col1a2+/p.G610C mice, which model human type IV OI. We found that Col1a2+/p.G610C;Lrp5+/p.A214V offspring had significantly increased bone mass and strength compared to Col1a2+/p.G610C;Lrp5+/+ littermates. The improved bone properties were not due to altered mRNA expression of type I collagen or its chaperones, nor were they due to changes in mutant type I collagen secretion. Second, we treated Col1a2+/p.G610C mice with a monoclonal antibody that inhibits sclerostin activity (Scl-Ab). We found that antibody treated mice had significantly increased bone mass and strength compared to vehicle treated littermates. These findings indicate increasing bone formation, even without altering bone collagen composition, may benefit patients with OI.
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