Int J Stomatol

Int J Stomatol ›› 2026, Vol. 53 ›› Issue (6): 895-905.doi: 10.7518/gjkq.2026130

• Review • Previous Articles     Next Articles

Staged management strategies for pain in radiation-induced oral mucositis from a neuro-immune perspective

Chaoyu Wang1,2(),Jiao Luo2,Xueke Li1,2,Yifang Jiang1,Xi Fu1,2,Chuan Zheng1,2,Qixuan Kuang1,2,Fengming You1,2()   

  1. 1.Hospital of Chengdu University of Traditional Chinese Medicine, Sichuan Provincial Key Laboratory of Traditional Chinese Medicine for Metabolic Diseases, Chengdu 610072, China
    2.School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610035, China
  • Received:2025-09-29 Revised:2026-04-30 Online:2026-11-01 Published:2026-10-29
  • Contact: Fengming You E-mail:wcystyle@foxmail.com;yfmdoc@163.com
  • Supported by:
    Noncommunicable Chronic Diseases-National Science and Technology Major Project(2023ZD0503000);Joint Innovation Fund of Health Commission of Chengdu and Chengdu University of Traditional Chinese Medicine(WXLH202402007)

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Abstract:

The persistent severe pain caused by radiation-induced oral mucositis (RIOM) may lead to interruption of antitumor therapy, induction of mental disorders, and systemic complications. Recent studies have gradually untangled the pivotal role of neuro-immune interactions in the dynamic perception of RIOM pain and inflammatory resolution. On the basis of the structural damage characteristics of RIOM, this review categorizes its pain progression into three phases: erythema-phase pain, ulcerative-phase pain, and healing-phase pain. The innervation patterns of oral nociceptive nerves and the pathophysiological alterations at each stage were systematically summarized. A staged management strategy aligned with disease progression and microstructural changes was proposed, discussing therapeutic interventions and rehabilitation approaches for RIOM pain. The potential applications of emerging technologies in this field were explored. This review aims to advance the clinical management of RIOM pain from mere symptomatic relief to precision etiology-targeted therapy, emphasizing the cri-tical role of neuro-immune crosstalk in improving patient prognosis and quality of life.

Key words: radiation-induced oral mucositis pain, neuro-immune interaction, staged management, erythema phase, ulcerative phase, healing phase

CLC Number: 

  • R781.5

TrendMD: 

Tab 1

Commonly used clinical evaluation scale of oral mucositis/radiation injury"

分级标准0级1级2级3级4级5级
WHO标准无口腔黏膜炎酸痛、红斑溃疡但进食固体食物溃疡仅能进流食无法进食—
NCI-CTCAE—黏膜红斑小溃疡或假膜融合性溃疡/假膜、轻微出血组织坏死、明显的自发性出血、危及生命死亡
RTOG标准—红斑、充血、轻度疼痛（无需镇痛）片状黏膜炎、炎性血清血液分泌物、中度疼痛融合的纤维性黏膜炎，重度疼痛溃疡、出血、坏死—
RID评分正常轻微发红红斑伴中度水肿融合性伪膜伴渗出，磨损出血真皮坏死、溃疡、出血—

Tab 2

Tissue damage characteristics of RIOM pain in erythema, ulcer and healing stages, and corresponding to relevant reference standards"

疼痛分期结构标志疼痛特征参考标准关联
红斑期充血、红斑，无溃疡灼痛/刺痛，刺激诱发WHO 1级、NCI-CTCAE 1级、RTOG 1级、RID 1~2级、视觉口腔溃疡性黏膜炎评分0.5~3分
溃疡期溃疡形成，伪膜覆盖持续锐痛，机械敏感WHO 2~4级、NCI-CTCAE 2~4级、RTOG 2~4级、RID 3~4级、视觉口腔溃疡性黏膜炎评分4~6分
愈合期肉芽组织形成，上皮再生隐痛/痒痛，偶发刺痛—

Fig 1

Sensory nerve regulation of oral cavity and schematic diagram of five stage pathogenesis theory of RIOM"

Fig 2

Three stage structural characteristics of RIOM pain"

Tab 3

Related studies on the inhibition of epithelial junction protein disassembly by erythema-phase pain"

治疗方式研究类型研究对象研究结论参考文献

上皮紧密连接调控

细胞实验Gie-3B11细胞系锌、维甲酸、槲皮素和乳香酸衍生物AKBA都能增强Gie-3b11屏障功能，表现为紧密连接蛋白表达上升、跨上皮电阻的浓度依赖性增加和上皮通透性的降低[37]
临床试验化学治疗儿童（83名）使用蜂蜜进行口腔护理可以预防正在接受化学治疗儿童的黏膜炎发展并治愈口腔黏膜炎[38]
临床试验晚期头颈癌患者（78名）蜂蜜可用于减轻癌症患者与辐射引起的黏膜炎相关的疼痛[39]
神经调控动物实验大鼠RhoA-ROCK信号通路介导TRPV1诱导的ZO-1和ZO-2的再分布以及细胞旁通透性的增加[40]
免疫调控细胞实验永生化人牙龈角质形成细胞IL-1β导致牙龈角质形成细胞的紧密连接蛋白表达增加并导致黏膜上皮屏障加强[41]

Tab 4

Related studies on targeted immunotherapy and neurotherapy for the relief of pain during the ulcerative phase"

调控对象研究类型研究对象研究结论参考文献

神经

临床试验患者含有可乐定的黏膜颊片剂Validive，通过调节α-2肾上腺素能受体活性调节NF-κB 通路抑制细胞因子产生缓解黏膜炎进展和疼痛[49]
动物实验小鼠丝氨酸蛋白酶抑制剂可以抑制创伤性组织中T细胞和中性粒细胞表达的弹性蛋白酶以减轻神经性疼痛症状[43]
动物实验仓鼠木贼提取物可抑制伤口区域的炎性细胞因子（TNF-α、IL-6、COX-2）表达，并抑制初级感觉神经元释放SP来减轻口腔炎模型中的疼痛[50]

免疫

临床试验患者防御素模拟物Brilacidin通过调节环状腺苷酸通路和抑制下游的PDE4和PDE3来调节免疫反应和炎症，以减轻促炎反应并激活抗炎活性，缓解溃疡和疼痛[49]
动物实验小鼠和仓鼠先天免疫调节剂Dusquetide通过促进抗感染和组织愈合将小鼠和仓鼠模型中口腔溃疡的持续时间缩短了约50%，2期临床试验中严重口腔黏膜炎减少了50%[51]
动物实验小鼠Toll样受体5激动剂CBLB502通过NF-κB信号传导，导致超氧化物歧化酶2诱导和粒细胞集落刺激因子的产生，抑制NLRP3炎性小体激活，从而减少RIOM、缓解疼痛[52]
临床试验患者PDE4抑制剂（如阿普斯特、罗氟司特）抑制TNF-α、干扰素γ和IL-2、IL-10、IL-12、IL-17和IL-23来升高细胞内环磷酸腺苷表达，抑制炎症反应[53]

Tab 5

Partial studies on pain relief during the healing period"

研究类型研究对象研究结论参考文献

动物实验

大鼠

乳香提取物主要通过过氧化物酶体增殖物激活受体γ激活增强M2巨噬细胞相关基因表达并减少促炎因子释放，增加M2巨噬细胞极化并减少M1巨噬细胞浸润，促进口腔溃疡愈合

[59]

动物实验大鼠凝胶口腔敷料中的压电材料在应力刺激下产生微电流，通过提高黏膜抗菌能力并增加黏膜细胞的增殖能力，促进黏膜伤口愈合[60]
动物实验大鼠电刺激促进轴突生长和神经元激活并导致驻留在受伤区域内的成纤维细胞和肌成纤维细胞加速胶原蛋白合成，促进角质形成细胞显著增殖[61]
细胞实验人牙龈角质形成细胞、人牙龈成纤维细胞、人真皮微血管内皮细胞重组人角质形成细胞生长因子调节IL-8和TNF-α等细胞因子水平以保护角质形成细胞和上皮细胞，减轻口腔黏膜炎损伤的严重程度并加速组织功能的恢复[62]

动物实验

小鼠

高分子量透明质酸通过抑制氧化应激和细胞凋亡导致空肠绒毛长度和舌上皮厚度的恢复，减少炎症介质，促进基底角质形成细胞增殖并减少胶原蛋白形成瘢痕，促进再上皮化而加速组织愈合

[63]

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