Histopathological analysis of the stroma and parenchyma revealed balanced distribution of epithelial and stromal component. Epithelial component of the Warthin's tumor is the trigger for the tumor process. This study indicates that the Warthin tumor is a consequence of inflammatory etiology.

BackgroundPeriodontal inflammation is characterized by injuries in collagen, epithelial, bone tissues. The hypotheses to be tested were relationship between the s100, bcl2 and myeloperoxidase in gingival tissues (MPO does affect the level of s100, bcl2). The object of this study was to investigate of s100 expression, bcl2 expression and myeloperoxidase expression in periodontal inflammation.Methods27 patients (giant-cell epulis) and 30 patients (acute and chronic inflammations) were included in the study for s100 expression, bcl2 expression and myeloperoxidase expression by immunohistochemistry and hematoxylin - eosin.ResultsGiant-cells in epulis positivity for myeloperoxidase has been observed in 100 % However, only 75.31 % of giant-cells were positive for bcl2 expression. Acute 98.2 %, and chronic 89.28 % inflammation was a significant positive for myeloperoxidase. The immunohistochemical findings of s100, bcl 2 and myeloperoxidase in epithelial layers have showed the result of 100 %, 82,2 %, 100 % positive cells in acute and 100 %, 78.25 %, 100 % in chronic process of inflammation respectively.ConclusionThe results indicate that the pathogenesis of periodontal inflammation might involve inhibition of cell death, through the overexpression of bcl-2, due to identifying factors myeloperoxidase (result in the DNA damage by the product of catalysis). The highest levels of s100 activity have been found at sites with chronic inflammation.

a b s t r a c tBackground: Nowadays multiple primary tumor is characterized by growth and development of two or more tumors in one patient. The total world sickness rate ranges from 1% to 37%. The presence of four or more tumors in one patient is rare case and presented as casuistry. Case presentation: We showed a case of multiple primary tumor with metahronic lesion of the thyroid, uterus and breast, followed by synchronous benign tumors of the subcutaneous fat, urinary bladder and gallbladder were considered. The development of all malignant tumors in all cases was accompanied by the presence of benign precancerous processes. Analysis of neoplasia histology shows the predominance of poorly differentiated forms of cancers in women with increased aggressiveness of cancerous tissue in each subsequent case and the growth of metastatic ability. The influence of heredity on the tumors progress is confirmed by immunohistochemical characteristics of cancer cells. Steroid-sensitive tissue of the uterus and breast in both cases didn't express ER and PR, in all cases the tissue had overexpression of Ki-67, p53, bax and bcl-2 receptors. The results of DNA testing for determination the Lynch syndrome revealed the presence of microsatellite instability in genetic material. The results of studies revealed the absence of mutations in these genes (MLH1, MSH2 and MSH6). Despite the negative results of the study, it doesn't exclude the possibility of Lynch syndrome for 100%, and its presence may be caused by the mutations of other genes (PMS1, PMS2 and MLH3), responsible for DNA repair. Unfortunately there wasn't any opportunity to study their mutations. Conclusions: While studying the anamnesis of life and disease of women it was revealed that she had multiple primary tumor with lesions of the breast, urinary bladder, thyroid, uterus and other organs. This study shows that neoplastic tissue in all cases had high rates of cell proliferation, their antiapoptotic stability, expression of prognostically unfavorable-receptors, and absence of favorable prognostic markers. Histological study revealed high rates of malignant neoplastic tissue. It indicates to the existence of common mechanisms of malignant tumors and their genetic predisposition that can be clearly observed in many generations of patient.

Materials and Methods:Chemical composition was studied with the help of the scanning electron microscope with energy-dispersion spectrometer. Immunohistochemical reaction showed the p53 and Ki-67 receptors expression. The study of DNA fragmentation was performed in agarose gel. Results: There was an interrelation between the accumulations of the trace elements with the degree of cancer malignancy. There were 85% of cases with positive reaction to Ki-67 and 40% cases with positive reaction to p53. We found a moderate correlation between the accumulation of microelements in the breast cancer tissue and the level of proliferative activity. We noted the combination of the increase of DNA fragmentation with the expression of p53 and Ki-67 receptors. Conclusions: The trace elements can cause the initiation and the progression of the tumorous growth, which is expressed in the increased proliferation of tumor cells. This leads to the destabilization of the genetic material which can be expressed in the synthesis of mutant p53 protein. Finally, it leads to the block of apoptosis and regulatory eff ects of cells. This can cause the tumor progression and the destabilization of the genome, which is refl ected in the increased DNA fragmentation.

Background. The association between periodontitis and collagen damage with immune cells is an actual problem. Periodontitis is a bacterially induced exacerbation of chronic process and chronic inflammatory disease that destroys teeth supporting connective tissue. Bacteria initiate periodontitis and destruction of the alveolar periodontal connective tissue. Objectives. Immune cells location between damaged collagen fibers remains obscure and this is the purpose of the current study. Results. We have determined five variants of immune cells microenvironment: nodular, trabecular, diffuse, mixed. We have observed five types of collagen structures destruction in exacerbation of chronic process and chronic periodontal inflammation. They are characterized by swelling, pulping and insignificant necrosis. Conclusion. Connective tissue has signs of swelling and destruction during inflammation; edema is observed between collagen fibers. Collagen fiber damage during periodontitis is caused by neutrophils. Widespread edema of collagen fibers increasing of depth cells infiltration during chronic inflammation. Nodular type of immune cells microenvironment is observed during outcome of chronic inflammation. Trabecular type of immune cells microenvironment is observed during exacerbation of chronic process. Diffuse type of immune cells microenvironment is observed during chronic inflammation process.