Histology and Cytology

  • Cell Death Pathways on Cancer Therapy

    Introduction: Cancer is a disease characterized by uncontrolled cell proliferation. The development of new drugs effective in the cancer treatment seeks the selectivity in inducing cell death. Different cell death pathways are known to date, the main ones are apoptosis, necrosis and autophagy. Objective: To describe the main cell death regulatory pathways and the possible targets of new anticancer drugs. Methodology: A bibliographic review of the scientific literature published in international journals was carried out. Results and Discussion: Apoptosis is a programmed cell death that controls the balance between death and tissue proliferation, and cancer cells are able to evade this mechanism. It can be induced by the extrinsic pathway, where receptors of the TNF- or CD95 family are activated on the cell surface, which subsequently activate cytosolic proteases, the caspases; or by the intrinsic pathway, where apoptosis is induced by the release of apoptogenic factors by mitochondria. Bcl-2 family proteins are highly involved in this pathway. Autophagy is a type of death in which the cell eliminates unhealthy cytoplasmic components by lysosomal degradation. The autophagic process is highly controlled, among others, by components of the PI3K-Akt-mTOR pathway, becoming key targets in anticancer therapy via autophagy induction. Finally, necrosis is a passive cell death that generally does not depend on a specific signaling pathway. It usually occurs as a final step of apoptosis or necrosis or by other factors which affect cellular homeostasis, such as physical damage and mechanical stresses, leadind to cell volume augmentation and membrane disruption, resulting in loss of cell integrity. Conclusion: Thus, the search or development of new molecules that act against one or more of the cell death activation pathways may reveal new and promising therapeutic agents against cancer.

  • Differential Diagnosis for Incisive Channel Cysts

    Introduction: Nasopalatine duct cysts are common entities of the jaw, but may resemble clinical and radiographic findings to other cystic and solid lesions of the medial anterior maxilla. It can develop at any age, but it is more frequent between the fourth and sixth decades of life affecting men more frequently. Its etiology seems to be associated with the proliferation of epithelial remnants of the nasopalatine duct or from oronasal ducts within the incisor canal. Objective: To discuss the relevant microscopic and differential diagnosis features in clinical dental practice through recent publications. Methodology: An integrative review was performed on the MEDLINE and LILACS databases, using the descriptors: Cyst, Incisor channel, lesions. Inclusion criteria were: full-text articles available in Portuguese or English and with a temporal cut between 2013 and 2017. Results: Five articles were selected that fit the inclusion criteria. Discussion: Nasopalatine duct cyst is the most common non-odontogenic cyst of maxillary intraosseous cyst. Due to its specific anatomical location and its proximity to the upper central incisors, this lesion is often confused with periapical cysts, which leads to difficulties in establishing the best therapy by the clinician. Its radiographic appearance shows a radiolucent area, unilocular, oval or rounded, well delimited and located along the midline of the maxilla, between the apexes of the central incisors or higher on the hard palate. The main differential diagnoses usually provided include, in addition to the nasopalatine duct cyst itself, the pe- triapical cyst located apical or laterally to the roots and odontogenic keratocyst (or keratocystic odontogenic tumor). Conclusion: Nasopalatine duct cysts usually affect adult men, resembling the periapical cysts associated with the upper central incisors, which should be treated through surgical procedures with a subsequent microscopic evaluation of the specimen removed.

  • Genetic Factors and Clinical Characteristics of Early Alzheimer

    Introduction: Alzheimer’s disease (AD) is an irreversible and progressive neurodegenerative disorder of insidious onset that causes loss of memory and various cognitive disorders. Early AD represents 5% of all cases of this pathology, demonstrating a family recurrence that initially presents a relative preservation of cognition. Its development is directly related to mutated genes that cause changes in the proteins encoded by them. Objectives: To describe the genetic factors and clinical characteristics of early Alzheimer’s disease. Methodology: Articles published between 2000 and 2010 were pre-selected through the PubMed and SciELO databases, using the descriptor: alzheimer. A total of 73 texts were analyzed, of which 54 were selected after the study of titles and abstracts. Considering inclusion and exclusion criteria, only 13 were included in the review because they refer to Early AD theme in the descriptors and abstracts. Results and Discussion: The genetic factor is considered crucial in the disease. The cases behave according to an autosomal dominant monogenic hereditary pattern in heterozygous individuals for the mutated gene (Aa), since the dominant gene is rare in the population. Studies suggest that the reduction in the level or activity of APP fragments plays a critical role in cognitive dysfunction, including the genes of PSEN1 and PSEN2 as well as responsible for this involvement. Early signs tend to be ignored because of their early character, presenting characteristics of behavioral changes, personality or depressive symptoms, with relative cognitive preservation. Conclusion: Early AD has low incidence and a great genetic relation, which makes it necessary to know the genetic factors for the specificity of the diagnosis since its clinical manifestation can confuse the family of the affected one due to its prematurity and the symptoms, being of great importance the diagnosis differential through complementary exams, along with the clinic, to the exclusion of other types…