Editorial: Inflammatory pain: mechanisms, assessment, and intervention
Yonghui Zhang, Daniela Adamo, Howe Liu, Quanxing Wang, Wen Wu, Yi-Li Zheng, Xue‐Qiang Wang
Abstract
Inflammatory pain refers to the increased sensitivity of perception and emotional response to noxious stimuli, that arises from an inflammatory reaction associated with tissue damage (Layne-Stuart and Carpenter, 2022). Under normal conditions, acute inflammation is a protective response by the body to tissue damage or infection, potentially leading to the perception of pain while damaged tissues are being cleared and repaired (Muley et al., 2016). Inflammatory pain can serve as a reminder of a recent injury to prevent re-injury and thereby achieve quick recovery. In general, inflammation management effectively relieves inflammatory pain due to the reduced stimulation of nerves following the resolution of inflammation. However, chronic inflammation can lead to adverse pain because inflammatory mediators act on pain-sensitive nerve endings by decreasing the thresholds of neuronal excitability, and increasing the sensitivity of firing rates, thereby causing peripheral and central sensitization (Prescott and Ratté , 2017). Under these sensitized conditions, pain perception can be abnormal, such as allodynia (perceiving innocuous stimuli as painful) and hyperalgesia (amplifying the intensity and duration of pain caused by noxious stimuli) (Laverdure-Dupont et al., 2009). In clinics, chronic pain is normally a complex of inflammatory and neuropathic components.Inflammatory mediators can result in neuronal damage, which triggers an inflammatory reaction.