Expression of molecules related to AKT pathway as putative regulators of ameloblastoma local invasiveness.

BACKGROUND: Ameloblastoma is an odontogenic neoplasm with local invasiveness and high recurrence. We previously suggested that growth factors, matrix metalloproteinases (MMPs), and TIMPs influence ameloblastoma invasiveness (Pathol. Res. Pract., 208, 2012, 225; Oral. Surg. Oral. Med. Oral. Pathol. Oral Radiol. Endod., 111, 2011, 474). Signals generated by this molecular network would be transduced by ERK 1/2 pathway (Oral. Surg. Oral. Med. Oral. Pathol. Oral Radiol. Endod., 111, 2011, 474). Others signaling pathways may influence ameloblastoma biology. Here, we studied expression of AKT and related molecules in ameloblastoma. METHODS: Fourteen cases of solid/multicystic ameloblastomas were examined. Immunohistochemistry was carried out to detected AKT (phospho-AKT), NF-қB (phospho-NF-қB), ß-catenin, cyclin-D1, and COX-2 in ameloblastoma samples. These molecules were evaluated in neoplastic cells and stroma. RESULTS: All proteins were detected in ameloblastoma. Expression of these markers was quantified and compared. Spearman's rank test was carried out to address positive correlations between proteins (P < 0.05). Ameloblastoma had a significant positive correlation of AKT (phospho-AKT) with ß-catenin. ß-catenin correlated with Cyclin-D1 and COX-2 in neoplastic cells. AKT (phospho-AKT) correlated with ß-catenin; ß-catenin with Cyclin-D1; AKT (phospho-AKT) with NF-қB (phospho-NF-қB); and NF-қB (phospho-NF-қB) with COX-2 in stromal cells. CONCLUSIONS: Results suggest that proteins studied are present and probably involved in a functional pathway in neoplastic cells and stroma and may therefore influence the local invasiveness of ameloblastoma.

Life-threatening expansive sublingual hematoma: a stab wound with lingual artery injury.

Vascular injuries are a constant risk in facial trauma, although bone and soft tissues of the face have provided some protection to the larger blood vessels. However, penetrating injuries usually do not have this type of protection and can damage significant vascular arteries. This article presents a case of a stab wound, which led to airway obstruction arising to a large sublingual hematoma due to lingual artery injury. A healthy 44-year-old man was stabbed in the submandibular region and admitted with an airway obstruction. He was subjected to an emergency tracheotomy and evolved with progressive sublingual edema. Computed tomography (CT) angiography showed a left lingual artery injury with the formation of an expansive hematoma. The CT angiography findings helped to identify the cause of the hematoma and guided the surgery to drain the hematoma after ligation of the lingual artery. The treatment was safely performed as planned and evolved uneventfully. The patient recovered fast and well and presented normal functions 6 months after the treatment. This surgical technique is an effective method for treating such injuries because it can be safely performed when guided by CT angiography. The authors argue that the demand for vascular lesions should be routine in patients who have facial trauma.

Matrix metalloproteinases, tissue inhibitors of metalloproteinases, and growth factors regulate the aggressiveness and proliferative activity of keratocystic odontogenic tumors.

OBJECTIVE: The objective of this preliminary study was to evaluate the expression of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and growth factors in keratocystic odontogenic tumors (KOTs). STUDY DESIGN: The expression of MMPs, TIMPs, growth factors, and the extracellular signal-regulated kinase (ERK) 1/2 signaling pathway were assessed by immunohistochemistry in 15 cases of KOT and 4 cases of calcifying cystic odontogenic tumor (CCOT). RESULTS: KOT samples expressed significantly higher amounts of MMPs, TIMPs, growth factors, epidermal growth factor receptor (EGFR), and ERK compared with CCOT samples, with the exception of MMP-2 and TIMP-1. CONCLUSIONS: MMP-9, TIMP-2, EGF and transforming growth factor α act together and likely regulate the proliferation and aggressiveness of KOT. ERK-1/2 serves as the transducer of signals generated by these proteins, which signal through the common receptor, EGFR. This process may be related to the increased proliferation and aggressiveness observed in KOT.