Pain is a subjective experience with significant individual differences. Laboratory studies investigating pain thresholds and experimental acute pain have identified structural and functional neural correlates. However, these types of pain stimuli have limited ecological validity to real-life pain experiences. Here, we use an orthodontic procedure—the insertion of an elastomeric separator between teeth—which typically induces mild to moderate pain that peaks within 2 days and lasts several days. We aimed to determine whether the baseline structure and resting-state functional connectivity of key regions along the trigeminal nociceptive and pain modulatory pathways correlate with subsequent peak pain ratings. Twenty-six healthy individuals underwent structural and resting-state functional MRI scanning before the placement of a separator between the first molar and second premolar, which was kept in place for 5 days. Participants recorded pain ratings 3 times daily on a 100-mm visual analogue scale. Peak pain was not significantly correlated with diffusion metrics of the trigeminal nerve or gray matter volume of any brain region. Peak pain did, however, positively correlate with baseline resting-state functional connectivity between the thalamus contralateral to the separator and bilateral insula, and negatively correlated with connectivity between the periaqueductal gray (PAG) and core nodes of the default mode network (medial prefrontal and posterior cingulate cortices). The ascending (thalamic) nociceptive and the descending (PAG) pain modulatory pathways at baseline each explained unique variation in peak pain intensity ratings. In sum, preinterventional functional neural architecture of both systems determined the individual pain experience to a subsequent ecologically valid pain stimulus.

Summary Background Whether precise orthodontic detailing of occlusion impacts masticatory function is unknown. In this study, we aimed to assess the impact of post-orthodontic dental occlusion on masticatory performance and chewing efficiency. Materials and methods Fifty-four adults who completed orthodontic treatment were categorized into two groups using the American Board of Orthodontics (ABO) model grading system: one meeting ABO standards (ABO, N = 29), the other failing to meet them (non-ABO, N = 25). The electromyographic (EMG) signals of the anterior temporalis (AT) and superficial masseter muscles were recorded bilaterally during static (clenching) and dynamic (gum chewing) tests. Chewing efficiency was measured by calculating the median particle size (MPS) and broadness of particle distribution (BPD) after five chewing trials of experimental silicone food at a standardized chewing rate. Results Participants of the ABO group had a slightly more symmetric activation of the AT muscles during clenching (P = 0.016) and chewed a gum at a slower rate (P = 0.030). During the standardized chewing test with silicone food, ABO subjects had slightly greater EMG potentials at all muscle locations than non-ABO individuals (all P < 0.05). MPS and BDP did not differ significantly between groups (all P > 0.05). Limitations The severity of the initial malocclusion of the study participants was not in the statistical model as a potential confounder on the outcome measures. Conclusions Meeting ABO standards contributes to a slightly more balanced activation of the temporalis muscles during clenching and more efficient muscle recruitment during chewing but does not improve chewing efficiency.

Background: The diagnosis of temporomandibular disorders (TMD) is based on patient history and physical examination, and may require medical imaging. Masticatory muscle palpation is essential to make a diagnosis of TMD. However, the response of masticatory muscles to mechanical pressure stimuli depends on many physical and psychological factors. Objective: This study aimed at determining the impact of somatosensory amplification (SSA)-an estimate of somatic awareness and bodily hypervigilance-on pressure pain thresholds (PPTs) measured at both trigeminal and extra-trigeminal locations in healthy individuals. Methods: PPTs were measured at the right anterior temporalis and superficial masseter, and the thenar eminence of the right hand in one hundred healhty individuals (69F, 31M), divided in three groups based on their SSA scores: low (N = 32), intermediate (N = 34) and high (N = 34). General linear models were used to test betweengroup differences in PPTs including sex as a covariate. The level of significance was set at P < .05. Results: Individuals with high SSA had lower PPTs at the anterior temporalis than individuals with low (P = .006) and intermediate (P = .001) SSA. No significant betweengroup differences were found in PPTs measured at the masseter (P = .372). PPTs measured at the thenar eminence were significantly lower in the high than the low SSA group (P = .009). Females had lower PPTs at the masseter than males (P = .021) but not at other muscle locations (all P > .05). Conclusion: Increased somatosensory amplification is associated with decreased pressure pain thresholds at both trigeminal and extra-trigeminal locations in healthy individuals. SSA could be a potential confounder while diagnosing TMD and evaluating treatment outcomes.

Pain is a subjective experience with significant individual differences. Laboratory studies investigating pain thresholds and acute pain have identified structural and functional neural correlates. However, these types of pain stimuli have limited ecological validity to real-life pain experience. Here, we use an orthodontic procedure which typically induces pain lasting several days. We aimed to determine whether the baseline structure and resting-state functional connectivity (rsFC) of key regions along the trigeminal nociceptive and pain modulatory pathways correlate with subsequent peak pain ratings. Twenty-six healthy individuals underwent structural (T1, diffusion-weighted MRI) and resting-state functional (rs-fMRI) scanning prior to the orthodontic procedure, the insertion of an elastomeric separator between teeth, for five days. Participants recorded pain ratings three times, daily. Peak pain was not correlated with structural measures for the trigeminal nerve or any brain region. However, peak pain correlated with rsFC between the contralateral thalamus and bilateral insula, and negatively correlated with connectivity between the periaqueductal gray and core nodes of the default mode network (medial prefrontal and posterior cingulate cortices). In this ecologically valid model, we demonstrate that both ascending nociceptive and descending pain modulatory pathways shape the individual pain experience.

No abstract