Assessment, Quantification, and Management of Fracture Pain: from Animals to the Clinic

Abstract

Purpose of review: Fractures are painful and disabling injuries that can occur due to trauma, especially when compounded with pathologic conditions, such as osteoporosis in older adults. It is well documented that acute pain management plays an integral role in the treatment of orthopedic patients. There is no current therapy available to completely control post-fracture pain that does not interfere with bone healing or have major adverse effects. In this review, we focus on recent advances in the understanding of pain behaviors post-fracture.

Recent findings: We review animal models of bone fracture and the assays that have been developed to assess and quantify spontaneous and evoked pain behaviors, including the two most commonly used assays: dynamic weight bearing and von Frey testing to assess withdrawal from a cutaneous (hindpaw) stimulus. Additionally, we discuss the assessment and quantification of fracture pain in the clinical setting, including the use of numeric pain rating scales, satisfaction with pain relief, and other biopsychosocial factor measurements. We review how pain behaviors in animal models and clinical cases can change with the use of current pain management therapies. We conclude by discussing the use of pain behavioral analyses in assessing potential therapeutic treatment options for addressing acute and chronic fracture pain without compromising fracture healing. There currently is a lack of effective treatment options for fracture pain that reliably relieve pain without potentially interfering with bone healing. Continued development and verification of reliable measurements of fracture pain in both pre-clinical and clinical settings is an essential aspect of continued research into novel analgesic treatments for fracture pain.

Keywords: Animal fracture model; Fracture pain; Nociceptive behaviors; Opioids; Pain management.

Figure 1.

Anatomic levels of nociceptive processing following bone fracture. Upon injury, inflammatory mediators, including prostaglandins, are released locally by a variety of non-neural cells and the nervous system. Biosynthesis of prostaglandins are attributed to two different enzymes, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and are blocked by nonsteroidal anti-inflammatory drugs (NSAIDs). Opioid receptors are critical in the modulation of pain following fracture. Opioid receptors are expressed throughout the nociceptive neural circuitry in the peripheral nervous system, spinal cord, and critical regions of the brain involved in reward and emotion-related brain structures