These results indicate that LPS derived from P. gingivalis may cause DNA hypermethylation of some ECM-related genes followed by downregulated expression of their transcriptional levels.

BackgroundOsseous choristoma is a very rare, benign lesion in the maxillofacial region. It appears as a benign mass of normally matured bony tissue covered by the normal epithelium of the tongue. It is usually seen in front of the foramen cecum of the tongue. Surgical excision is the treatment of choice with an excellent prognosis and there have been very few cases of recurrence.Case presentationHere we present two cases of osseous choristoma on the dorsum of the tongue. Case 1 was a 15-year-old Japanese girl who presented with a painless but gradually growing swelling on the dorsum of her tongue approximately 1 year before her admission. Case 2 was a 21-year-old Japanese woman with a complaint of pain in the lower left, posterior side of her mouth. Histological findings showed that both lesions were composed of well-organized, mature, compact bone beneath the oral mucosal membrane. Subsequent to simple surgical excision, no recurrence of the lesions was observed after the follow-up period. Previous literatures have proposed both malformation and trauma hypotheses as the etiopathologies of osseous choristoma. However, the histopathological findings of the two cases in the present study do not support the trauma hypothesis.ConclusionsAlthough osseous choristoma is clinically a benign condition, the underlying histopathological processes are important. The outcome of aberrant formation of calcified tissue in the vicinity of vital structures such as nerves and blood vessels may be of clinical significance.

Carcinoma follows a course of multiple changes that are affected by several important factors, with epigenetic silencing of the promoter gene being one of them. A series of studies have suggested that epigenetic changes in the anti-aging gene Klotho may be one of the emerging areas of concern in the study of carcinogenesis. We hypothesized that epigenetic silencing of Klotho due to hypermethylation of DNMT3a may be one of the causes of carcinoma in the oral and maxillofacial region. In this study, we analyzed the immunohistochemical expressions of Klotho and DNMT3a in tissues obtained from oral dysplasia and oral squamous cell carcinoma. Our results showed increased immune expression of DNMT3a, and decreased expression of Klotho in cells of the cancer tissues when compared with those in the dysplasia and healthy control samples. Chi-square tests complemented by adjusted residual analysis revealed significantly higher number of Klotho-positive and DNMT3a-negative cases in healthy controls, Klotho-negative and DNMT3a-negative cases in ODL, and Klotho-negative and DNMT3a-positive cases in OSCC when compared with the other types among the three groups (X = 46.66, p< 0.001). Thus, downregulation of Klotho may be associated with the overexpression of DNMT3a in cancer tissues.

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Objectives Epigenetic phenomena are changes in gene expression not involving the DNA sequence. DNA methylation is a major occurrence underlying epigenetic changes in human cells. Although aberrant DNA methylation is well documented in malignant lesions, limited information has been shown on the involvement of DNA methylation in oral lichen planus and oral lichenoid lesions (OLP). The present study aimed to investigate DNA methylation of E‐cadherin and p16 in OLP, and compare the findings with those in non‐inflamed gingiva (Non), radicular cyst (RC), and oral squamous cell carcinoma (SCC). Materials and methods Paraffin‐embedded surgical biopsy specimens were sliced, DNA was extracted, bisulfite treatment was applied, and methylation‐specific polymerase chain reaction was performed. Immunohistochemistry was performed to observe the relative expression patterns of these genes. Results E‐cadherin was hypermethylated in OLP (p < 0.01), SCC (p < 0.01), and RC (p < 0.05), when compared with Non; DNA hypermethylation was confirmed in OLP and SCC when compared to Non and RC. Hypermethylation of p16ink4a was observed only in SCC (p < 0.01). Conclusion DNA methylation levels of E‐cadherin and p16ink4a were significantly higher in OLP than in normal tissues, and may be associated with the pathogenesis and progression of the disease.