J Oral Facial Pain Headache. 2019 Spring;33(2):227–233. doi: 10.11607/ofph.2007. Epub 2018 Oct 10.
To investigate whether acute dental pain due to pulpal or periapical inflammation is associated with increased expression of cortisol and inflammatory markers and mediators in the saliva, as well as changes in salivary flow rate.
Patients experiencing pain (n = 42) were recruited when seeking emergency dental treatment. A 0 to 10 numeric rating scale (NRS) was used as a measure of the severity of pain, and the number of days with pain sensation was also recorded. Unstimulated saliva was collected for 3 minutes (salivary flow measured in mL/minute) and stored at -80°C. Saliva was analyzed for the biomarkers cortisol, C-reactive protein (CRP), and cytokines interleukin-1β (IL-1β) and interleukin-6. In addition, the participants completed a simple questionnaire about stress-inducing factors such as insomnia, dental anxiety, or home/workplace stress. Patients received a dental examination and diagnosis (eg, symptomatic pulpitis/apical periodontitis or acute apical abscess), which was confirmed during dental treatment. The control group (n = 39) consisted of participants without any pain and no known medical or dental problems.
Patients experiencing acute pain due to pulpal or periapical inflammation had a mean NRS score of 7.0 ± 2.59. The mean duration of pain was 6.5 ± 7.9 days. There was no significant difference in pain level between male and female subjects, tooth type affected, or diagnosis. Higher levels of cortisol, IL-1β, and IL-6 and increased salivary flow were detected in patients with pain when compared to controls (P < .05). CRP was higher in patients with acute pain compared to control participants without pain, but this difference was not statistically significant. Stress at home or the workplace was reported by 79% of patients experiencing pain and by 28% of control participants.
Acute dental pain due to pulpal or periapical inflammation was associated with an increase in salivary cortisol, IL-1β, and IL-6 levels and in salivary flow rate. Stress arising from home or the workplace may aggravate a symptom-free pulpal or periapical inflammation to an acute phase. Inflammation in the pulp and periapical region can have effects in regions remote from the disease site.
探讨牙髓或根尖周炎症引起的急性牙痛是否与唾液中皮质醇和炎症标志物及介质的表达增加以及唾液流率的变化有关。
招募因急性牙痛而寻求紧急牙科治疗的患者(n=42)。采用 0-10 数字评分量表(NRS)作为疼痛严重程度的衡量标准,并记录疼痛持续天数。收集 3 分钟的非刺激性唾液(以毫升/分钟计为唾液流率),并在-80°C 下储存。分析唾液中的生物标志物皮质醇、C 反应蛋白(CRP)和细胞因子白细胞介素-1β(IL-1β)和白细胞介素-6。此外,参与者还完成了一份关于压力诱发因素的简单问卷,例如失眠、牙科焦虑或家庭/工作场所压力。患者接受牙科检查和诊断(例如,有症状性牙髓炎/根尖周炎或急性根尖脓肿),并在牙科治疗期间得到确认。对照组(n=39)由无任何疼痛且无已知医学或牙科问题的参与者组成。
因牙髓或根尖周炎症而出现急性疼痛的患者平均 NRS 评分为 7.0±2.59。疼痛持续时间平均为 6.5±7.9 天。男性和女性受试者、受影响的牙齿类型或诊断均无明显差异。与对照组相比,疼痛患者的皮质醇、IL-1β和 IL-6水平更高,唾液流率也更高(P<0.05)。与无疼痛的对照组参与者相比,急性疼痛患者的 CRP 水平更高,但差异无统计学意义。79%的疼痛患者和 28%的对照组参与者报告称存在家庭或工作场所的压力。
牙髓或根尖周炎症引起的急性牙痛与唾液皮质醇、IL-1β 和 IL-6 水平升高以及唾液流率增加有关。来自家庭或工作场所的压力可能会使无症状的牙髓或根尖周炎症加重为急性阶段。牙髓和根尖周区域的炎症可能会对远离疾病部位的区域产生影响。