A 10-year study of specimens submitted to oral pathology laboratory analysis: lesion occurrence and demographic features

The purpose of the present paper was to describe the range of lesions histologically diagnosed in an oral pathology laboratory in southern Brazil. A retrospective study of 8,168 specimen analyses recorded between 1995 and 2004 was conducted. The records were retrieved from the Oral Pathology Laboratory, School of Dentistry, Federal University of Rio Grande do Sul, RS, Brazil. A total of 6,831 valid cases (83.63%) were examined. Of these, inflammatory lesions were the most common occurrences (n = 4,320; 63.24%). Benign and malignant tumors accounted for 7.66% (n = 523) and 1.9% (n = 130) of the occurrences, respectively. Significant associations were observed between nonneoplastic proliferative disorders and benign mesenchymal tumors in females, and between squamous cell carcinoma and leukoplakia in males. Most diagnoses were benign in nature and had an inflammatory etiology. The association of some demographic characteristics with the occurrence of lesions suggests that these characteristics should be considered in performing differential diagnoses

Esôfago de Barrett: aspectos fisiopatológicos e moleculares da seqüência metaplasia-displasia-adenocarcinoma - artigo de revisão

The Barrett's esophagus (BE) is defined as endoscopically visible columnar mucosa at the distal esophagus, of any extension, proved to harbor intestinal metaplasia on biopsy, highlighted by the presence of goblet cells. BE denotes long-standing gastroesophageal reflux disease (GERD) and is an important risk factor for the development of esophageal adenocarcinoma (EAC). Therefore, these patients must be on follow-up, in order to diagnose cancer early. BE patients have frequent alterations in esophageal physiologyc studies. Alkaline duodenogastroesophageal reflux seems to have important role. The development BE occurs in steps, initially with formation of cardiac type mucosa subsequent intestinalization. Futher progression can follow a sequence, from low grade dysplasia, to high grade dysplasia and esophageal adenocarcinoma. Current follow-up is based on the presence of dysplasia. It has limitations, grouping patients heterogeneously. Different steps of carcinogenesis have been studied looking for an ideal prognostic marker. Uncontrolled proliferative activity, apoptosis inhibition, angiogenesis, tissue invasion and metastases formation are all implicated in cancer origin. Some cycle cell molecules have been studied in BE, such as retinoblastoma protein, ciclins, kinase dependent ciclins and cell cycle inhibitors. The P53 protein is one of the most investigated in the metaplasia-adenocarcinoma progression. Growth Factors, apoptotic proteins, telomers and DNA ploidy have also been searched. Increased proliferative activity has been implicated in Barrett's carcinogenesis and the Ki-67 antigen, through imunohistochemical analysis, has become the the method of choice. Present in the nucleus, it is found in proliferative cells only. Some studies suport association between Ki-67 activity and the metaplasia-dysplasia-adenocarcinoma sequence.The results, however, are inconclusive and research should follow this way