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To assess the speed and accuracy of a checklist user interface for the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD).A diagnostic tool formatted as a checklist was developed and compared to an existing diagnostic tool, the DC/TMD diagnsostic decision trees. Both types of tools use the DC/TMD and were tested by dental students, interns, and residents in the USA and Japan for diagnosis of hypothetical patients. The comparisons were done in a randomized, crossover, controlled, double-blinded trial.Overall, subjects using the experimental tool answered 25% more correct diagnoses (P.001) and missed 27% fewer diagnoses (P.01). They were also able to finalize their diagnoses faster than those using the control tool, in 16% less time (P.05). The difference in accuracy was more pronounced in complex cases, while the difference in speed was more pronounced in simple cases.This checklist is an alternative user interface for the DC/TMD.

The outbreak of novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide. Nasopharyngeal swabs are widely used in polymerase chain reaction (PCR) test to detect SARS-CoV-2. However, the collection of nasopharyngeal swabs has a series of drawbacks concerning exposure of healthcare staff, difficulty in collection, and discomfort of patients. Therefore, an alternative noninvasive sample for diagnostic of emerging viral diseases is required. The usefulness of saliva screening tests is compared to conventional swab tests in this report. The results suggest that saliva could be a reliable sample for detecting SARS-CoV-2.

Neuropathic pain is absent from the early stages of periodontal disease possibly due to neurite retraction. Butyric acid (BA) is a periodontopathic metabolite that activates several stress-related signals and, likewise, induce neurite retraction. Neuronal cell death is associated to neurite retraction which would suggest that BA-induced neurite retraction is ascribable to neuronal cell death. However, the underlying mechanism of BA-related cell death signaling remains unknown. In this study, we exposed NGF-treated PC12 cells to varying BA concentrations [0 (control), 0.5, 1.0, 5.0 mM] and determined selected stress-related (H2O2, glutathione reductase, calcium (Ca(2+)), plasma membrane Ca(2+) ATPase (PMCA), and GADD153/CHOPS) and cell death-associated (extrinsic: FasL, TNF-α, TWEAK, and TRAIL; intrinsic: cytochrome C (CytC), NF-kB, CASP8, CASP9, CASP10, and CASP3) signals. Similarly, we confirmed cell death execution by chromatin condensation. Our results showed that low (0.5 mM) and high (1.0 and 5.0 mM) BA levels differ in stress and cell death signaling. Moreover, at periodontal disease-level BA concentration (5 mM), we observed that only FasL amounts were affected and occurred concurrently with chromatin condensation insinuating that cells have fully committed to neurodegeneration. Thus, we believe that both stress and cell death signaling in NGF-treated PC12 cells are affected differently depending on BA concentration. In a periodontal disease scenario, we hypothesize that during the early stages, low BA amounts accumulate resulting to both stress- and cell death-related signals that favor neurite non-proliferation, whereas, during the later stages, high BA amounts accumulate resulting to both stress- and cell death-related signals that favor neurodegeneration. More importantly, we propose that neuropathic pain absence at any stage of periodontal disease progression is ascribable to BA accumulation regardless of amount.

The pathophysiology and pathology of peri-implantitis remain unclear; however, its similarity to periodontitis has been described. The evaluation of peri-implant tissue and the diagnostic criteria of peri-implant disease are not currently standardized as they are for periodontitis. In this study, we evaluated clinical parameters during the implant maintenance period to determine significant correlations between these parameters. We examined 55 implant patients at the time of maintenance visits between April and September 2016 and classified patients into a healthy group (H) and a history-of-periodontitis group (HP). For each implant, we evaluated the modified plaque index, probing pocket depth, and bleeding on probing as clinical parameters. Statistical analyses were performed with Spearman’s rank correlation coefficient. A total of 130 implants were assessed. The mean time since implant placement was 6 years and 6 months. The prevalence of implant-based peri-implantitis was 10.8% of all the implants. All cases of implant-based peri-implantitis came from the HP group, and many were present in patients with a history of severe periodontitis. The probing pocket depth around the implant was significantly greater in the HP group than in the H group. We found weak positive correlations between the probing pocket depth and bleeding on probing (r s = 0.401, p

Objective The engagement of the receptor for advanced glycation end products (RAGE) by AGE or S100 perturbs homeostatic mechanisms and provides a basis for cellular dysfunction in pathological situations. To assess the mechanism of vascular immune reactions in chronic periapical periodontitis, we analysed co-expression of RAGE and AGE or S100 in periapical granulomas. Methods Surgically removed periapical lesions, which had been diagnosed as chronic periodontitis, were inspected histologically using paraffin-embedded sections stained with haematoxylin and eosin. Cryostat sections of the tissues, which were identified histologically as periapical granulomas, were then examined by double immunohistochemistry using polyclonal antibodies raised against human CD34 and monoclonal antibodies specific for human RAGE, AGE or S100. Dual-colour immunofluorescence image analysis was also performed to assess the co-expression of RAGE and AGE or RAGE and S100 by endothelial cells. Results Marked expression of RAGE, AGE, and S100 by CD34 + endothelial cells was noted. Dual-colour immunofluorescence image analysis revealed that the RAGE-expressing endothelial cells co-expressed AGE and S100; however, the number of RAGE–AGE-expressing endothelial cells was significantly higher than that of RAGE–S100-expressing endothelial cells. Conclusions Co-expression of RAGE and AGE by endothelial cells in periapical granulomas is more relevant than that of RAGE and S100. The possible engagement of RAGE and AGE may trigger cellular activation and mediate tissue injury.