Objective
Burning mouth syndrome (BMS) and atypical odontalgia (AO) are examples of somatic symptom disorders with predominant pain around the orofacial region. Neuroinflammation is thought to play a role in the mechanisms, but few studies have been conducted. We aimed to better understand the role of neuroinflammation in the pathophysiology and treatment of BMS/AO.
Methods
Plasma levels of 28 neuroinflammation‐related molecules were determined in 44 controls and 48 BMS/AO patients both pretreatment and 12‐week post‐treatment with duloxetine.
Results
Baseline plasma levels of interleukin (IL)‐1β (p < .0001), IL‐1 receptor antagonist (p < .001), IL‐6 (p < .0001), macrophage inflammatory protein‐1β (p < .0001), and platelet‐derived growth factor‐bb (.04) were significantly higher in patients than in controls. Plasma levels of granulocyte macrophage colony stimulating factor were significantly higher in patients than in controls (p < .001) and decreased with treatment (.009). Plasma levels of eotaxin, monocyte chemoattractant protein‐1, and vascular endothelial growth factor decreased significantly with treatment (p < .001, .022, and .029, respectively).
Conclusions
Inflammatory mechanisms may be involved in the pathophysiology and/or treatment response of somatic symptom disorders with predominant pain around the orofacial region.