Acute and Chronic Pain from Facial Skin and Oral Mucosa: Unique Neurobiology and Challenging Treatment

The oral cavity is a portal into the digestive system, which exhibits unique sensory properties. Like facial skin, the oral mucosa needs to be exquisitely sensitive and selective, in order to detect harmful toxins versus edible food. Chemosensation and somatosensation by multiple receptors, including transient receptor potential channels, are well-developed to meet these needs. In contrast to facial skin, however, the oral mucosa rarely exhibits itch responses. Like the gut, the oral cavity performs mechanical and chemical digestion. Therefore, the oral mucosa needs to be insensitive, to some degree, in order to endure noxious irritation. Persistent pain from the oral mucosa is often due to ulcers, involving both tissue injury and infection. Trigeminal nerve injury and trigeminal neuralgia produce intractable pain in the orofacial skin and the oral mucosa, through mechanisms distinct from those seen in the spinal area, which is particularly difficult to predict or treat. The diagnosis and treatment of idiopathic chronic pain, such as atypical odontalgia (idiopathic painful trigeminal neuropathy or post-traumatic trigeminal neuropathy) and burning mouth syndrome, remain especially challenging. The central integration of gustatory inputs might modulate chronic oral and facial pain. A lack of pain in chronic inflammation inside the oral cavity, such as chronic periodontitis, involves the specialized functioning of oral bacteria. A more detailed understanding of the unique neurobiology of pain from the orofacial skin and the oral mucosa should help us develop novel methods for better treating persistent orofacial pain.

Post-traumatic trigeminal neuropathy: correlation between objective and subjective assessments and a prediction model for neurosensory recovery

Background Post-traumatic trigeminal neuropathy (PTN) can have a substantial effect on patient well-being. However, the relation between the neuropathic symptoms and their effect on psychosocial functioning remains a matter of debate. The purpose of this study was to evaluate the association between objective and subjective assessments of neurosensory function in PTN and predict neurosensory outcome using baseline measurements. Methods This prospective observational cohort study included patients diagnosed with PTN at the Department of Oral and Maxillofacial Surgery, University Hospital Leuven, Belgium, between April 2018 and May 2020. Standardized objective and subjective neurosensory examinations were recorded simultaneously on multiple occasions during the follow-up period. Correlation analyses and principal component analysis were conducted, and a prediction model of neurosensory recovery was developed. Results Quality of life correlated significantly (P < 0.05) with percentage of affected dermatome (ρ = − 0.35), the presence of brush stroke allodynia (ρ = − 0.24), gain-of-function sensory phenotype (ρ = − 0.41), Medical Research Council Scale (ρ = 0.36), and Sunderland classification (ρ = − 0.21). Quality of life was not significantly correlated (P > 0.05) with directional discrimination, stimulus localization, two-point discrimination, or sensory loss-of-function. The prediction model showed a negative predictive value for neurosensory recovery after 6 months of 87%. Conclusions We found a strong correlation of subjective well-being with the presence of brush stroke allodynia, thermal and/or mechanical hyperesthesia, and the size of the neuropathic area. These results suggest that positive symptoms dominate the effect on affect. In patients reporting poor subjective well-being in the absence of positive symptoms or a large neuropathic area, additional attention towards psychosocial triggers might enhance treatment outcome. The prediction model could contribute to establishing realistic expectations about the likelihood of neurosensory recovery but remains to be validated in future studies.