Extraction treatment using Invisalign Technique

The Invisalign method is gaining an increasing interest as an alternative treatment option in adult patients and in difficult orthodontic cases. The aim of this work is to show a class II malocclusion with severe crowding in the upper and lower arches treated with the extraction of the upper first premolars performed by means of Invisalign. The alignment phase was successfully completed but the space closure achieved with crown tipping and without correct root inclination making a further fixed appliance phase necessary.     

Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis

The sequence of events associated with the development of gastric cancer has been described as “the gastric precancerous cascade”. This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia. According to this model, Helicobacter pylori (H. pylori) infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis. The presence of virulence factors in the infecting H. pylori drives the carcinogenesis process. Independent epidemiological and animal studies have confirmed the sequential progression of these precancerous lesions. Particularly long-term follow-up studies estimated a risk of 0.1% for atrophic gastritis/intestinal metaplasia and 6% in case of dysplasia for the long-term development of gastric cancer. With this in mind, a better understanding of the genetic and epigenetic changes associated with progression of the cascade is critical in determining the risk of gastric cancer associated with H. pylori infection. In this review, we will summarize some of the most relevant mechanisms and focus predominantly but not exclusively on the discussion of gene promoter methylation and miRNAs in this context.     

DLA-identical bone marrow grafts after low-dose total body irradiation: the effect of canine recombinant hematopoietic growth factors

Previous studies found that bone marrow (BM) allografts from DLA- identical littermates resulted in survival of two thirds of recipient dogs after otherwise lethal doses of 450 to 600 cGy of total body irradiation (TBI) because of successful allografts or autologous recovery after rejection of the allografts. The current study asked whether survival could be further improved by treating allograft recipients with recombinant canine granulocyte colony-stimulating factor (G-CSF), stem cell factor (SCF), or G-CSF/SCF. Of 21 dogs, 14 (67%) receiving allografts but no growth factors survived, 10 with successful allografts (including 5 mixed chimeras) and 4 with autologous recovery; whereas 7 animals died, 5 from infections during BM aplasia and 2 from acute graft-versus-host disease. By comparison, 30 of 34 dogs (88%) receiving hematopoietic growth factors in addition to the BM graft survived, 17 with successful allografts (including 10 mixed chimeras) and 13 with autologous recovery; whereas 4 died, all with infection related to BM aplasia after rejection of the allograft. Survival was similar for recipients of G-CSF, SCF, or the combination of G-CSF and SCF. Logistic regression analyses, which accounted for possible effects of TBI dose, showed a trend for improved survival in dogs receiving growth factors (P = .09), no change in allogeneic engraftment (P = .74), and a slight increase in autologous recovery (P = .22). In agreement with previous data, we found that grafts of BM from DLA-identical littermates improved survival of recipient dogs exposed to low but otherwise lethal doses of TBI. A further improvement in survival could be achieved by additional treatment with G-CSF, SCF, or G-CSF/SCF. Results suggest that treatment by hematopoietic growth factors along with BM grafts should be considered for victims of radiation accidents.     

Lymphoid proliferations and lymphomas associated with gastric metaplasia, dysplasia, and carcinoma.

Gastric carcinomas are invariably accompanied by lymphoid proliferations. We studied their features in 22 resected gastric carcinomas in which the lymphoid proliferations ranged from reactive lymphoid follicles to mucosa-associated lymphoid tissue (MALT) lymphomas. In most cases, the collections of lymphocytes were abundant, which is remarkable considering the lack of lymphoid tissue in the normal stomach. They were not haphazardly located but in direct contact with the metaplastic, dysplastic, and neoplastic epithelial cells, in positions suggestive of defense barriers. They consisted of newly formed lymphoid follicles with reactive germinal centers sometimes high up in the superficial mucosa, collections of plasma cells beneath the surface epithelium, and large aggregates of B cells above and below the muscularis mucosae as well as abundant T cells. The latter, both CD4+ and CD8+, were seen within metaplastic epithelial cells as well as within carcinomatous glands that were partially destroyed, resembling apparent neoplastic lympho-epithelial lesions (LEL). In three cases, the B cells infiltrating the gastric muscular layers represented MALT-lymphomas adjacent to gastric carcinomas, as confirmed by polymerase chain reaction (PCR) analysis in two cases. In a case of lymphoepithelioma-like carcinoma, the excessive lymphoid cells were predominantly of T-CD8+ type. In this case, EBV identified by EBV-encoded RNA and latent membrane protein was present in large amounts. Helicobacter pylori was seen in only six cases in areas of chronic gastritis that were distant from carcinoma. H. pylori was not present in the areas of metaplasia, dysplasia, or carcinoma. It appears that the lymphoid proliferations accompanying these gastric changes do not arise in response to the pathogenic agent H. pylori, which caused the persistent infection leading to them yet is no longer present, but rather in response to the existence of the abnormal epithelial cells. Thus the lymphoid proliferations consistently associated with gastric metaplasia, dysplasia, and neoplasia may be regarded as immune reactions to the long-term cellular changes triggered by the initial chronic gastritis. On rare occasions, the exaggerated lymphoid proliferations may reach the end of the spectrum, resulting in MALT lymphomas coexistent with gastric carcinomas.