Opercula of permanent first and second molars delayed in eruption were investigated histologically to detect possible causes of eruption failure. The material comprised operation specimens from exposure of 74 non-erupted molars in 63 young individuals (34 boys, 29 girls). Eighteen of the 74 specimens (or 24.3%) were diagnosed as "classical" odontogenic tumors belonging to the following entities: ameloblastic fibroma (seven), ameloblastic fibrodentinoma (six), ameloblastic fibro-odontoma (four) and complex odontoma (one). Twenty-two specimens (or 29.7%) showed a hitherto unrecognized odontogenic lesion of hamartomatous character, termed odontogenic giant cell fibromatosis (OGCF). Thus, 54.1% of the specimens could be diagnosed as odontogenic tumors or hamartomas. Histomorphologic changes could not be detected in the remaining 34 specimens (45.9%). Odontogenic tumors were associated with unerupted first molars much more frequently than with second molars (ratio 8:1). The OGCF had a strong association with unerupted mandibular molars. Further, opercula of mandibular first molars frequently revealed odontogenic lesions whereas tissue overlying the crown of unerupted maxillary second molars often was reported as normal operculum.

The results of the present study indicated that OLP in certain patients was significantly associated with HCV. This could warrant screening for HCV-infected patients with OLP in Thailand.

Ameloblastoma is one of the most common odontogenic tumors in Asia. In the past decade, many studies have shown gene mutations in the mitogen-activated protein kinase (MAPK) signaling pathway, especially on an extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Mutations of fibroblast growth factor receptor 2 (FGFR2), rat sarcoma virus (RAS), and B-rapidly accelerated fibrosarcoma (BRAF) are able to cause a continuous activation of the ERK1/2 signaling pathway, hence uncontrolled tumor cell proliferation. Due to the ERK1/2 signaling pathway role in cell growth and cell survival, upregulation of this pathway can cause approximately one-third of human tumors including ameloblastoma. After the discovery of gene mutations in several cancers, many inhibitors have been designed to target these mutations. We, here, reviewed the alteration of the FGF-MAPK signaling pathway in ameloblastoma and targeted treatment used as an adjuvant or neoadjuvant therapy for ameloblastoma especially in cases where wide surgical resection is needed. Keywords: Genetic, Growth factor, Mutation, Targeted therapy

Background: Several studies have reported an association between high expression of CD44 in different types of cancer. However, no study has reported a link among CD44 expression, other biomarkers, and the aggressiveness of salivary gland tumors. Methods: A total of 38 specimens were obtained from non-tumorous salivary glands, benign and malignant tumors in salivary glands. Immunohistochemical analyses of CD44s, CD44v6, IL-1β, CXCL1, and CXCR2 were performed, and the area of positive cells was assessed. Results: We found that both CD44s and CXCR2 expression were increased in the benign and malignant groups. CD44v6 was also increased in both groups, but it had the highest level in the malignant group. IL-1β was the only biomarker that increased significantly in the malignant group in comparison to the other two groups. Conclusions: CD44s, CD44v6, CXCR2, and IL-1β expressions were found to be higher in salivary gland tumors. However, IL-1β alone may play a crucial role in the aggressiveness of salivary gland tumors as this cytokine was expressed only in the malignant group with high expression associated with high-grade malignancy.