Effective pain management during labor must balance adequate maternal pain relief with preservation of maternal participation and fetal safety. Epidural anesthesia remains the gold standard for labor analgesia. However, commonly used local anesthetics and opioid adjuvants are associated with adverse effects that include nausea, pruritus, urinary retention, and prolonged labor. Dexmedetomidine, a highly selective α₂ agonist, does not carry the same risks for misuse and abuse as opioids do and may be a promising non-opioid adjuvant for epidural labor analgesia due to its analgesic, anxiolytic, and opioid-sparing properties. Furthermore, dexmedetomidine has unique pharmacodynamic effects, including preserving maternal consciousness while providing adequate analgesia. This combination of consciousness preservation and sufficient analgesia suggests dexmedetomidine may be a promising pharmaceutic for epidural anesthesia. In addition to preserving maternal consciousness, dexmedetomidine does not appear to cause a clinically significant increase in the motor blockade. Although epidural analgesia is known to prolong labor in nulliparous and multiparous patients, the use of dexmedetomidine as an epidural adjuvant does not have a significant effect on labor duration in available trials. Across studies, dexmedetomidine does not have deleterious outcomes for neonates, measured using the neonatal Apgar score. Although dexmedetomidine is not currently FDA-approved for epidural labor analgesia, existing evidence from available trials suggests its safety and efficacy as an opioid-sparing adjuvant. This narrative review aims to highlight the current state of knowledge of dexmedetomidine’s pharmacology, efficacy, analgesic ability, and side effects.

Musculoskeletal pain is driven by degenerative conditions such as osteoarthritis or intervertebral disk degeneration. This creates a major burden on health systems and patient quality of life. Platelet-rich plasma (PRP) is an orthobiologic that contains platelets and growth factors which promote angiogenesis, modulate inflammation, and support tissue repair. Mechanobiology is central in the healing process, where mechanical loading regulates cellular behavior through mechanotransduction pathways including integrin/FAK and RhoA/ROCK. This use of signaling pathways allows for regeneration along multiple different tissue types. Evidence suggests that PRP and mechanical loading may act together to promote tissue repair, with PRP-derived signals interacting with biomechanical cues to enhance fibroblast activation, remodeling, and regenerative responses. There is variability in PRP preparation, rehabilitation protocols, and tissue-specific responses, which all highlight the need for a more standardized and guided treatment strategy. Understanding the interplay between PRP-derived biologic signaling and mechanobiologic pathways may help inform the development of more standardized, tissue-specific regenerative treatment strategies and could potentially contribute to improved clinical outcomes in patients with musculoskeletal pain.

Purpose of Review: Hidradenitis suppurativa (HS) is an extremely painful skin condition with both nociceptive and neuropathic components. Biologics may offer superior neuropathic pain relief and impede worsening of this disease compared to other treatments. Recent Findings: Of the three currently FDA-approved biologics (adalimumab, bimekizumab, and secukinumab), bimekizumab shows the largest absolute reduction in skin pain and the earliest onset of pain improvement. Summary: This review explores the pathophysiology and causes of neuropathic pain development in HS, highlights current FDA-approved and emerging biologics for its management, and raises awareness of neuropathic pain in HS. Clinical trial data assessing pain are unstandardized, and further elucidation of pain outcomes using standardized assessments of neuropathic pain is crucial for determining whether biologics targeting mediators that drive neuropathic pain development are effective in treating this aspect of HS.