Abstract
Mechanisms of endogenous pain control are significant. Increasing studies have clearly produced evidence for the clinical usefulness of opioids in peripheral analgesia. The immune system uses mechanisms of cell migration not only to fight pathogens but also to control pain and inflammation within injured tissue. It has been demonstrated that peripheral inflammatory pain can be effectively controlled by an interaction of immune cell-derived opioid peptides with opioid receptors on peripheral sensory nerve terminals. Experimental and clinical studies have clearly shown that activation of peripheral opioid receptors with exogenous opioid agonists and endogenous opioid peptides are able to produce significant analgesic and anti-inflammatory effects, without central opioid mediated side effects (e.g., respiratory depression, sedation, tolerance, dependence). This article will focus on the role of opioids in peripheral inflammatory conditions and the clinical implications of targeting peripheral opioid receptors.
Highlights
Inflammation is the series of highly coordinated events that is the response of vascular tissues to detrimental stimuli which results in heat, swelling, redness, and pain (Machelska et al, 2003)
Whilst the exact mechanisms of these interactions are not yet understood, they may play a necessary role in the development of effective endogenous analgesia by ensuring delivery of opioids to peripheral sensory neurons before they are degraded by the extracellular environment within inflamed tissues (Figure 1)
Philippe et al (2003) noted that naxolone was able to reverse the muopioid receptor mediated reduction in inflammation in two in vivo models of colitis. These results suggest that a variety of complex regulatory activities may be performed by opioid agonists in various tissues of the body that may be naloxone-sensitive or naloxone insensitive and these pathways may directly or indirectly inhibit the release of cytokines and mediators involved in inflammation (Gavalas et al, 1994)
Summary
Inflammation is the series of highly coordinated events that is the response of vascular tissues to detrimental stimuli which results in heat, swelling, redness, and pain (Machelska et al, 2003). Inflammatory mediators that are released and tissue acidification activate nociceptive primary afferent neurons as well as lower their signaling threshold in order to stimulate the sensation of pain and cause hyperalgesia (Hua and Cabot, 2010). Immune cells have been demonstrated to contain and release the opioid peptide β-endorphin in inflamed tissues which acts upon opioid receptors present on primary afferent neurons to block pain transmission and provide analgesia (Mousa et al, 2000; Vetter et al, 2006).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
