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.

Background: The 2018 classification of periodontal disease characterizes the disease with a multidimensional staging and grading system. The purpose of this multicenter study was to examine variations in periodontitis classification among dental practitioners with different postgraduate educational backgrounds at the University of Maryland School of Dentistry and the Loma Linda University School of Dentistry using the 2018 classification. Methods: This cross-sectional observational study included two cohorts: dental practitioners with periodontal backgrounds (n₁ = 31) and those with other educational backgrounds (n₂ = 33). The survey instrument contained three periodontitis cases presented with the guideline of the 2018 classification and a questionnaire including closed and open-ended questions. The participants were asked to review each case and to fill out the questionnaire independently. Fisher’s exact test was conducted to examine the differences in responses between the two cohorts. Polychoric correlations were calculated to examine the relation between the level of familiarity with the 2018 classification and the accuracy of the classification. Results: The distribution of item responses was significantly different between the two cohorts regarding only one item, grading for Case 1 (p = 0.01). No significant differences in accuracy between the two cohorts were observed except for two items, grading in Case 1 (p = 0.03) and staging in Case 3 (p = 0.04). There were no significant differences in risk factor identification for each case among the two cohorts (p = 1.00, Case 1; p = 0.22, Case 2). Staging in Case 3 ( $$\widehat{\rho }$$ρ ^ = 0.52) and risk factor identification in Case 2 ( $$\widehat{\rho }$$ρ ^ = 0.32) were significantly correlated with familiarity with the 2018 classification. Conclusion: A fair level of agreement in periodontitis classification was observed among dental practitioners with different educational backgrounds when the 2018 classification was used. The periodontal cohort showed better agreement levels and partially better accuracy. Risk factor identification for periodontal disease was difficult regardless of the educational background.