Cell proliferation markers in the odontogenic keratocyst: effect of inflammation.

The immunohistochemical expression of PCNA and Ki-67 proteins and the histochemical expression of AgNORs were studied in 20 odontogenic keratocysts in order to assess the relationship between epithelial cell proliferation and inflammation within the capsule. Immunostained cells were quantified by conventional methods, and both quantitative and morphometric analyses of AgNORs were performed by TV image analysis. Non-inflamed odontogenic keratocysts showed a typical epithelial lining and inflamed odontogenic keratocysts were lined also by hyperplastic non-keratinized stratified squamous epithelium. A statistically significant increase of PCNA+ and Ki-67+ cells and of AgNOR numbers was detected in the linings of inflamed odontogenic keratocysts compared to non-inflamed lesions. The results suggest the existence of greater proliferative activity in the epithelial cells of inflamed odontogenic keratocysts, which may be associated with the disruption of the typical structure of odontogenic keratocyst linings.

Immunohistochemical expression of p53, MDM2, Ki-67 and PCNA in central giant cell granuloma and giant cell tumor.

Central giant cell granuloma (CGCG) is a reactive bone lesion that occurs mainly in the jaws. The giant cell tumour (GCT) is a benign locally aggressive neoplasm located near the articular end of tubular bones. Both lesions are characterised histologically by multinucleated giant cells in a background of ovoid to spindle-shaped mesenchymal cells. There is a basic question whether both lesions are separate entities or variants of the same disease. The study of cell cycle-associated proteins may give insights into clarifying such question. The expression of these proteins is also important to determine the cell cycle regulation in both tumours. The purpose of this study was to evaluate the immunohistochemical expression of p53, MDM2, Ki-67 and PCNA in CGCG and GCT. The results demonstrated that, despite the lack of p53 immunoreactivity, all the samples showed wide expression of MDM2. The percentage of Ki-67- and PCNA-positive cells in CGCG was statistically higher than that of GCT Our findings show that CGCG has a higher proliferative activity compared with that of the GCT. Our results also suggest that p53 inactivation by MDM2 expression may be involved in the pathogenesis of giant cell lesions of the jaws and long bones.

Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease.

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P > 0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (16.4 (6.9-54.4) vs 59.3 (29.6-113.8), P < 0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.