Dental terminology "discoloration" or "pigment dystrophy" - a review and practical recommendations.

A range of issues related to using English attributive phrases formed by the prefix + noun model in dental literature by modern scientists is considered. Such words' syntactic structure does not correspond to the disease's pathogenesis, which creates certain difficulties in terms of the perception of these syntactic constructions by General Practitioners and Pathologists Our work is devoted to finding an adequate equivalent replacement for the ingrained semantics of phrases that are implicit in nature. Using the term "discoloration", in our opinion, is due to the simplicity of explaining to the patient the change in tooth color under the influence of various exogenous and endogenous factors. Using the term 'pigment dystrophy' for dental patients is a complicated psychological factor. Therefore, there is a substitution of 'pigment dystrophy' to "discoloration" in modern dental literature. The term 'pigment dystrophy' is more pathologically and pathogenetically determined and is more suitable for explaining pathological processes in the teeth' hard tissues. There is no concept of "pigment dystrophy" and "discoloration" of teeth in the current classification of diseases World Health Organization (WHO) ICD-10. As a result of the analysis of the rules and semantics of the terms used by scientists, they are incorrect in many cases.

Pathogenesis of Warthin's tumors.

INTRODUCTION: Warthin's tumor, also known as papillary cystadenoma lymphomatosum, monomorphic adenoma, or adenolymphoma, is a benign cystic tumor of the salivary glands containing abundant lymphocytes and lymph node-like stroma. It is named after the pathologist Aldred Scott Warthin, who described two cases in 1929. OBJECTIVE: The aim of this study is to analyze the pathogenesis of Warthin's tumor. METHODS: A total of 15 patients with Warthin's tumor were studied. Hematoxylin and eosin stains, which have been used for at least a century and are still essential for recognizing various tissue types and the morphologic changes for cancer diagnosis, were used. Warthin's tumor was evaluated for the expression of MGMT, CD3, HSP90AA1, MMP-1, Bcl-2, CD79A, IgG, Ki-67, p53, IgM, OPN, S100, myeloperoxidase, and VEGF by immunohistochemistry. RESULTS: Immunohistochemical staining confirmed that the immune cells within the follicles of Warthin's tumor were positive for MGMT (10.0 ± 0.34%), Ki-67 (13.3 ± 0.45%), Bcl-2 (42.6 ± 8.33), and p53 (11.6 ± 2.3). The immune cells associated with CD3 were present at the stroma of residual cells (47.3 ± 3.89); however, they were not present in the epithelium cell layers. B cells (CD79A) consistent with germinal centers were present within the immune cells and formed follicles (43.2 ± 13.5%). CONCLUSIONS: 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.

S100, bcl2 and myeloperoxid protein expirations during periodontal inflammation.

BACKGROUND: Periodontal 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. METHODS: 27 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. RESULTS: Giant-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. CONCLUSION: The 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.

Mechanisms of morphogenetic disorders in the lower jaw under the influence of heavy metal salts on the body.

In the experiment on the 36 mature rats, the peculiarities of morphological disorders in the lower jaw of rats under the influence of salts of chromium, lead, zinc, iron, copper, and manganese are showed. Profound morphological changes in bone and cartilaginous tissues of lower jaw are followed by disorders of bone mineral content. The importance of the S100 protein in morphological changes in bone and cartilaginous tissues under the influence of heavy metal salts is shown.

Pathogenetic mechanisms of heavy metals effect on proapoptotic and proliferative potential of breast cancer.

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 effects of cells. This can cause the tumor progression and the destabilization of the genome, which is reflected in the increased DNA fragmentation.