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Background: It is a consensus that symptomatic impacted mandibular third molars (MTMs) need to be removed. Although the prophylactic extraction of asymptomatic impacted MTMs remains controversial. This study aims to investigate the effects of MTMs on themselves and adjacent teeth pathophysiology and provide the evidence for prophylactic extraction of impacted MTMs.Methods: A retrospective study of panoramic radiographs of patients visited the Affiliated Stomatology Hospital of Guangzhou Medical University from April 2014 to May 2018 was conducted to investigate the dental and periodontal lesions in MTMs and adjacent mandibular second molars (MSMs), as well as the correlation of tooth lesion severity with patient age.Results: Among the 2650 impacted MTMs, 6.98% dental lesions and 37.81% periodontal lesions were found, as well as 24.63% dental lesions and 35.30% periodontal lesions in the distal of adjacent MSMs. 9.27%, 2.02%, 0.47%, and 13.33% dental lesions and 48.81%, 17.31%, 5.19%, and 10% periodontal lesions were observed in MTMs with mesioangular, horizontal, inverted and distoangular impaction types, respectively. For the adjacent MSMs, 31.98%, 11.82%, 1.94%, and 13.33% distal dental lesions and 45.74%, 16.95%, 2.91%, and 23.33% distal periodontal lesions were found in mesioangular, horizontal, inverted and distoangular impaction types, respectively. In mesioangular MTMs, the severity of the distal dental and periodontal lesions in the adjacent MSMs showed a high-positive correlation with patient age (P < 0.05) CONCLUSION: Early prophylactic extraction of MTMs with mesioangular-impaction and close monitoring of MTMs with horizontal/inverted-impaction could prevent impacted MTMs-associated lesions in MTMs/MSMs. [ABSTRACT FROM AUTHOR]

Oral squamous cell carcinoma (OSCC) is the most common and aggressive epithelial tumor in the head and neck region with a rising incidence. Despite the advances in basic science and clinical research, the overall survival rate of OSCC remains low. Thus finding novel effective therapeutic agents for OSCC is necessary. In this study, we investigated the effects and mechanisms of combined metformin and 4SC‐202 in OSCC. Our results showed that metformin and 4SC‐202 synergistically suppressed the proliferation and promoted the intrinsic apoptosis of OSCC cells in vitro and in vivo. Importantly, the proteasome inhibitor MG132 impeded the ΔNp63‐decreasing effects after metformin and 4SC‐202 treatment, indicating that metformin and 4SC‐202 could promote the degradation of ΔNp63 protein. Moreover, ubiquitination level of ΔNp63 increased after metformin or/and 4SC‐202 administration. Furthermore, we revealed that ΔNp63 mediated anticancer effects of metformin and 4SC‐202, as overexpression or suppression of ΔNp63 could attenuate or facilitate the apoptosis rate of OSCC under metformin or/and 4SC‐202 treatment. Collectively, metformin and 4SC‐202 synergistically promote intrinsic apoptosis through accelerating ubiquitin‐mediated degradation of ΔNp63 in OSCC, and this co‐treatment can serve as a potential therapeutic scheme for OSCC. [ABSTRACT FROM AUTHOR]

Abstract: Radiotherapy for nasopharyngeal carcinoma has been reported to cause second primary oral squamous cell carcinoma (s‐OSCC). The prognosis and pathologic characteristic of s‐OSCC are largely unknown. Bmi1 was associated with the repair of radiation‐induced DNA damage, suggesting its possible involvement in the pathologic process of s‐OSCC. Herein, we compared the prognosis between s‐OSCC and primary OSCC (p‐OSCC) and explored the involvement of Bmi1 in s‐OSCC development. In this retrospective study, s‐OSCC and p‐OSCC patients were matched by propensity scores. Their outcomes were compared by univariate and multivariate analyses. The expression of Bmi1 in s‐OSCC and p‐OSCC was detected by immunohistochemistry (IHC). Radiation‐induced Bmi1 alteration in early‐stage was explored in a rat model and HaCaT cells. After matching, 116 pairs of patients with highly balanced characteristics were included. In univariate analysis, the overall survival (OS), disease‐specific survival (DSS), and local recurrence‐free survival (LRFS) were poorer in s‐OSCC than in p‐OSCC (P < 0.05), while their regional metastasis‐free survival (RMFS) was parallel (P = 0.112). Multivariate analysis further revealed that radiotherapy history was an independent risk factor for OS, DSS, and LRFS (P < 0.05). IHC results showed that the positive rate of Bmi1 was higher in s‐OSCC (P = 0.0027). In a rat model of radiotherapy‐induced mucositis, Bmi1 upregulation was observed 8 days after irradiation. Consistently, Bmi1 was upregulated in HaCaT cells 1 h after irradiation, and its upregulation was in accord with X‐ray exposure duration. In conclusion, the prognosis of s‐OSCC is poorer as compared to p‐OSCC, which may be attributed to Bmi1 upregulation. [ABSTRACT FROM AUTHOR]

Chemokine ( CC motif) ligand 18 ( CCL18) is involved in remodeling of the tumor microenvironment and plays critical roles in oncogenesis, invasiveness, and metastasis. We previously investigated the overexpression of CCL18 in primary oral squamous cell carcinoma ( OSCC) tissues and its association with advanced clinical stage in OSCC patients. However, the underlying mechanisms of this CCL18-derived activity remains unidentified. This study showed exogenous CCL18 increased cell migration and invasion and induced cell epithelial-mesenchymal transition ( EMT), and that E-cadherin, an epithelial marker, decreased and N-cadherin, a mesenchymal marker, increased, compared to negative control in OSCC cells. Furthermore, we detected that CCL18 induced the acquisition of cancer stem(-like) cell characteristics in oral cancer cells, but also found a significantly positive correlation between the expression of CCL18 and Bmi-1 ( P < 0.001) in OSCC surgical specimens by immunohistochemistry analysis. The expression of octamer-binding transcription factor 4 and Bmi-1 were significantly upregulated, and proportions of aldehyde dehydrogenasehigh+ cells and CD133+ cells were markedly increased in CCL18-treated cells compared to untreated cells. Sphere formation ability was observably enhanced when cells were continually exposed to high levels of CCL18. Moreover, CCL18 upregulated Slug expression by stimulating the mammalian target of rapamycin ( mTOR) signaling pathway in OSCC cell lines. Inhibition of the mTOR pathway by INK128, or Slug knockdown by RNA interference, reversed CCL18-induced EMT and the stemness response at both molecular and functional levels. In conclusion, our data suggested that CCL18 upregulated Slug expression to promote EMT and stem cell-like features by activating the mTOR pathway in oral cancer. These findings provide new potential targets for the early diagnosis and treatment of OSCC. [ABSTRACT FROM AUTHOR]