Central giant cell granuloma: A clinicopathological and immunohistochemical study of macrophages, blood vessels, lymphatic vessels and regulatory proteins.

OBJECTIVE: This study seeks to investigate immunohistochemical parameters that could distinguish non-aggressive Central giant cell granuloma (CGCG) from aggressive CGCG, two groups of lesions which differ in their clinical and radiographic features and prognosis. MATERIAL AND METHODS: 12 cases of non-aggressive CGCG and 11 cases of aggressive CGCG were investigated and associated the immunohistochemical expression of macrophages (CD68 and CD163), blood vessels (CD34 and CD105), lymphatic vessels (D2-40) and regulator proteins (p63 and Ki-67). Clinical and radiographic features were also studied. RESULTS: Associations between all proteins in non-aggressive and aggressive CGCG were not significant (p > 0.05). With respect to non-aggressive CGCG, there were no significant correlations, while in aggressive CGCG there was a significant positive correlation between CD68 and CD163 (p = 0.031), between CD34 and D2-40 proteins (p = 0.04), whereas a significant negative correlation was observed between CD105 and CD68 (p = 0.040). However, regardless of aggressiveness of CGCG, there was a significant positive correlation between CD68 and CD163 (p = 0,04). Among the clinical and immunohistochemical aspects, only the symptomatology was a significant risk factor for the occurrence of aggressive CGCG (OR = 12.00/p = 0.016). CONCLUSION: Macrophages and angiogenesis contribute to their maintenance and development of CGCG. In addition, immunohistochemistry used here was not able to differentiate their aggressiveness. However, symptomatology was proved to be a risk factor for the occurrence of aggressive CGCG. It is possible that clinical features, particularly symptomatology, represent the most appropriate parameter to attempt to distinguish GCCG.

Branch of the canalis sinuosus: a rare anatomical variation--a case report.

The canalis sinuosus (CS) is a neurovascular canal, a branch of the infraorbital canal through which the anterior superior alveolar nerve passes. There are no studies or case reports of anatomical variations related to this canal. A rare case of anatomical variation in the CS is reported that was detected by cone beam computed tomography done in a 47-year-old female as a pre-operative workup before dental implants. In this case, in the region slightly medial to tooth 23, a wide accessory branch from the CS was observed, running an intraosseous course in the inferior and posterior direction up to a foramen located in the hard palate, slightly medial in relation to tooth 23. The location of this branching, as well as its neurovascular component, is important for dental implant planning because of its proximity to the upper teeth. Identification of neurovascular bundles is fundamental to avoid complications for the patient.

Transcriptional profiles of SHH pathway genes in keratocystic odontogenic tumor and ameloblastoma.

BACKGROUND: Sonic hedgehog (SHH) pathway activation has been identified as a key factor in the development of many types of tumors, including odontogenic tumors. Our study examined the expression of genes in the SHH pathway to characterize their roles in the pathogenesis of keratocystic odontogenic tumors (KOT) and ameloblastomas (AB). METHODS: We quantified the expression of SHH, SMO, PTCH1, SUFU, GLI1, CCND1, and BCL2 genes by qPCR in a total of 23 KOT, 11 AB, and three non-neoplastic oral mucosa (NNM). We also measured the expression of proteins related to this pathway (CCND1 and BCL2) by immunohistochemistry. RESULTS: We observed overexpression of SMO, PTCH1, GLI1, and CCND1 genes in both KOT (23/23) and AB (11/11). However, we did not detect expression of the SHH gene in 21/23 KOT and 10/11 AB tumors. Low levels of the SUFU gene were expressed in KOT (P = 0.0199) and AB (P = 0.0127) relative to the NNM. Recurrent KOT exhibited high levels of SMO (P = 0.035), PTCH1 (P = 0.048), CCND1 (P = 0.048), and BCL2 (P = 0.045) transcripts. Using immunolabeling of CCND1, we observed no statistical difference between primary and recurrent KOT (P = 0.8815), sporadic and NBCCS-KOT (P = 0.7688), and unicystic and solid AB (P = 0.7521). CONCLUSIONS: Overexpression of upstream (PTCH1 and SMO) and downstream (GLI1, CCND1 and BCL2) genes in the SHH pathway leads to the constitutive activation of this pathway in KOT and AB and may suggest a mechanism for the development of these types of tumors.

Trifid nasopalatine canal: case report of a rare anatomical variation and its surgical implications / Conducto nasopalatino Trifid: presentación de caso de una variación anatómica rara y sus implicaciones quirúrgicas

The nasopalatine canal is a long slender structure present in the midline of the anterior maxilla that connects the palate to the floor of the nasal cavity. The nasopalatine canal contains the nasopalatine nerve, the terminal branch of the nasopalatine artery, fibrous connective tissue, adipose tissue, and minor salivary glands. The purpose of this article was to report a case of a trifid nasopalatine canal detected by cone beam computed tomography prior to dental implant placement. A 47-year-old female patient was submitted to cone beam computed tomography. Axial and sagittal sections revealed a trifurcation of the nasopalatine canal. Each canal was separated from the other by bony septa and extended independently from the floor of the nasal cavity to the incisive foramen in the remnant of the alveolar process in the anterior region of the maxilla. Cone beam computed tomography has permitted better visualization of the details and anatomical variations of the nasopalatine canal. Detailed knowledge of variations in the shape, number and size of the nasopalatine canal is fundamental for surgical procedures, such as local anesthesia in the anterior maxillary region and placement of dental implants, in order to prevent damage to important arteries and nerves(AU)

El canal nasopalatino es una larga estructura delgada presente en la línea media del maxilar anterior que conecta el palato al suelo de la cavidad nasal. El canal nasopalatino contiene el nervio nasopalatino, la rama terminal de la arteria nasopalatina, el tejido conectivo fibroso, el tejido adiposo y las glándulas salivales menores. El propósito de este artículo es presentar el caso de un canal nasopalatino trifid detectado a través de tomografía computarizada de haz cónico anterior a la colocación de implantes dentales, en una paciente de femenino 47 años de edad. Secciones axiales y sagitales revelaron la trifurcación del canal nasopalatino. Cada canal se apartó del otro por tabiques ósea y extendida independientemente del suelo de la cavidad nasal para el agujero incisivo en el remanente del proceso alveolar en la región anterior del maxilar. La tomografía computarizada de haz cónico ha permitido una mejor visualización de los detalles y variaciones anatómicas del canal nasopalatino. El conocimiento detallado de las variaciones en su forma, el número y el tamaño del canal nasopalatino es fundamental para los procedimientos cirúrgicos, así como la anestesia local en la región anterior del maxilar superior y la colocación de los implantes dentales, con el fin de prevenir el daño a las arterias y a los nervios importantes(AU)