This study used an experimental periodontitis model to detail the gingival transcriptome related to cell death processes of pyroptosis, necroptosis, ferroptosis, and cuproptosis. Healthy Macaca mulatta primates stratified by age, ≤3 years (young), 7-12 years (adolescent), 12-15 years (adult), and 17-23 years (aged), provided gingival tissue biopsies for microarray analysis focused on 257 genes representative of the four cell death processes and bacterial plaque samples for 16S rRNA gene analysis. Age differences in the profiles of gene expression in healthy tissues were noted for cuproptosis, ferroptosis, necroptosis, and pyroptosis. Major differences were then observed with disease initiation, progression, and resolution also related to the age of the animals. Distinct bacterial families/consortia of species were significantly related to the gene expression differences for the cell death pathways. These results emphasized age-associated differences in the gingival tissue molecular response to changes in the quality and quantity of bacteria accumulating with the disease process reflected in regulated cell death pathways that are both physiological and pathophysiological.

The splicing factor transformer-2 homolog beta (Tra2β) plays a pivotal role in various cancers. Nonetheless, its role in oral squamous cell carcinoma (OSCC) has not been comprehensively explored. This study sought to discern the influence of Tra2β on OSCC and its underlying mechanisms. We assessed Tra2β expression in OSCC utilizing immunohistochemistry, qRT-PCR, and western blotting techniques. siRNA transfection was used to silence Tra2β. Whole transcriptome RNA sequencing (RNA-seq) analysis was carried out to reveal the alternative splicing (AS) events. KEGG pathway analysis enriched the related pathways. Colony formation, transwell, wound healing, and Annexin V-FITC/PI were employed to appraise the consequences of Tra2β silencing on OSCC. Tra2β was highly expressed in both OSCC tissues and cell lines. Knockdown of Tra2β-regulated AS events with skipped exon (SE) accounts for the highest proportion. Meanwhile, downregulation of Tra2β reduced cell proliferation, migration, and invasion, however increasing cell apoptosis. Moreover, Wnt signaling pathway involved in the function of Tra2β knockdown which was demonstrated directly by a discernible reduction in the expression of GSK3/β-catenin signaling axis. These findings suggest that knockdown of Tra2β may exert anti-tumor effects through the GSK3/β-catenin signaling pathway in OSCC.

This systematic review and meta-analysis aimed to compare the occurrence of dental caries and developmental defects of enamel (DDE) in individuals with and without cerebral palsy (CP). We conducted searches across five databases and the grey literature. Data were organized using EndNote 20. Reporting followed the MOOSE checklist. A random-effects model meta-analyses were conducted using RStudio, presenting results as mean difference (MD), odds ratio (OR), and 95% confidence interval (CI). The risk of bias of studies was analyzed using the Newcastle-Ottawa Scale, and the certainty of evidence was assessed using GRADE. Among 1336 identified records, 25 studies involving 59,997 participants (mean age: 11.1 years) were included. Data of 12 were pooled into meta-analyses. No significant differences were found between CP and non-CP individuals across indices: DMFT (k = 7) (MD = 0.31; 95% CI [-0.42-1.05]), dmft (k = 4) (MD = 0.31; 95% CI [-0.50-1.14]), DMFS (k = 2) (MD = -0.61; 95% CI [-20.56-19.33]), dmfs (k = 3) (MD = 0.54; 95% CI [-1.09-2.17]), and DDE (k = 3) (OR = 0.80, 95% CI [0.09-7.31]). The certainty of evidence was very low. Individuals with CP do not appear to differ significantly from those without CP in terms of dental caries experience and DDE.

Acute and chronic orofacial pain are very common and remain a vexing health problem that has a negative effect on the quality of life. Serotonin (5-HydroxyTryptamine, 5-HT) is a kind of monoamine neurotransmitter that is involved in many physiological and pathological processes. However, its role in orofacial pain remains inconclusive. Therefore, this review aims to summarize the recent advances in understanding the effect exerted by 5-HT on the modulation of orofacial pain. An extensive search was conducted on PubMed and Web of Science for pertinent studies focusing on the effects of 5-HT on the modulation of orofacial pain. In this review, we concisely review how 5-HT mediates orofacial pain, how 5-HT is regulated and how we can translate these findings into clinical applications for the prevention and/or treatment of orofacial pain. 5-HT plays a key role in the modulation of orofacial pain, implying that 5-HT modulators may serve as effective treatment for orofacial pain. However, further research on the precise mechanisms underlying the modulation of orofacial pain is still warranted.

Circular RNAs (circRNAs) have emerged as pivotal regulators of cellular processes in human malignancies, including oral squamous cell carcinoma (OSCC). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect RNA expression levels of circXPO1, miR-524-5p and cyclin D1 (CCND1). Colony formation assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay were performed to analyze cell proliferation, while transwell assay was carried out to investigate the cell migration and invasion. Cell apoptosis was assessed by flow cytometry. Protein expression analysis was implemented by Western blot assay. Additionally, lactate production and glucose consumption were investigated using a lactate assay kit and glucose assay kit, respectively. The invivo tumorigenic potential of circXPO1 was evaluated using a xenograft mouse model assay. Elevated levels of circXPO1 and CCND1, alongside reduced miR-524-5p expression were decreased in OSCC tissues and cells. Knockdown of circXPO1 in OSCC cells inhibited their proliferative, migratory and invasive capacities, as well as glycolysis, prompting apoptosis. Moreover, circXPO1 silencing hindered tumor growth invivo. MiR-524-5p could be sequestered by circXPO1, and its inhibition could counteract the beneficial effects of circXPO1 knockdown on OSCC progression. Knockdown of circXPO1 inhibited OSCC progression by up-regulating miR-524-5p and down-regulating CCND1 expression, which might provide potential targets for OSCC treatment.

To investigate the clinical characteristics and salivary biomarkers in each type of burning mouth syndrome (BMS) patients. Ninety-eight postmenopausal female patients with BMS were included. Fifty and 21 patients were assigned to the primary and secondary groups, respectively. Twenty-seven patients with both primary and secondary characteristics were assigned to the intermediate group. Comprehensive clinical characteristics and salivary biomarkers were analyzed. Significant differences in age, proportion of hyposalivator patients based on unstimulated whole saliva (UWS), symptom distribution, severties of burning sensation and effect of oral complaints in daily life (Eff-life), and positive symptom distress index (PSDI) were observed among the three groups. The primary group had significant higher UWS flow rate, fewer UWS hyposalivator proportions, and lesser severity of Eff-life than the secondary group. The intermediate group had significantly greater intensities of burning sensation and Eff-life and higher PSDI score than did the primary group. The primary group had significantly higher cortisol and dehydroepiandrosterone (DHEA) levels in stimulated whole saliva than did the secondary group. This study's findings show that clinical characteristics differentiate each BMS type. Cortisol and DHEA levels are potential salivary biomarkers for discriminating between the primary and secondary types of BMS.

To evaluate osteoradionecrosis (ORN) incidence in a cohort of patients undergoing tooth extraction (TE) before radiotherapy (RT) for head and neck cancers. The study protocol was approved by the Ethics Committee of Università Cattolica del Sacro Cuore (ID-2132) and registered at clinicaltrials.gov (ID: NCT04009161). TE was performed in case of signs of pericoronitis, periapical lesions, restorative impossibility, severe periodontitis. ORN was defined as exposed bone at an unhealed post-extraction socket in the absence of oncological recurrence. The RT plans were reviewed, and each post-extractive socket was contoured to calculate the received radiation dose. In total, 156 patients with 610 TE were enrolled. The mean follow-up was 567 days. ORN was diagnosed in four patients (2.6% of patients and 0.7% of TE). Need for osteotomy and radiation dose at the extraction site were associated with ORN (OR for osteotomy: 21.9, 95% CI: 2.17-222.2, p = 0.009; OR for RT dose: 1.1, 95% CI: 1-1.15, p = 0.05). TE appears to be a significant risk factor for ORN, particularly when osteotomy is required, and post-extraction sockets receive a high RT dosage. This study proposes a decision-making algorithm for TE and outlines a straightforward surgical protocol.

Neutrophil response is critical in inflammatory regulation and immune response to bacterial infections. During periodontal disease, pathogenic bacteria lead to exaggerated neutrophil responses. We hypothesized that low-level laser application (LLLT), therapeutic strategy for dampening inflammatory processes, will regulate neutrophil activity in response to periodontopathogens. The impact of LLLT on neutrophil responses was measured by light delivered at wavelength of 850 nm. The direct effect of LLLT on P. gingivalis A7436 was determined by flow cytometry using LIVE/DEADTM Cell Vitality kit. The phagocytosis of P. gingivalis A7436 by human neutrophils was measured using flow cytometry. Superoxide generation was measured by cytochrome-C-reduction in the presence of N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP; 1 mM). Cytokine release by neutrophils was measured by multiplex immunoassay. The phagocytosis of P. gingivalis by primary human neutrophils was significantly reduced in response to LLLT (p < 0.05). While LLLT led to increased superoxide production in neutrophils that were not challenged by P. gingivalis, it dampened the increased superoxide and IL-6 release by the neutrophils in response to P. gingivalis. LLLT did not directly affect the viability of P. gingivalis. These results suggested that LLLT can provide therapeutic strategy in periodontal disease, regulating the neutrophil response to P. gingivalis.