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The purpose of this study is to outline relevant elements regarding the biochemical interactions between prosthetic materials used for obtaining implant-supported restorations and the oral environment. Implant-supported prostheses have seen unprecedented development in recent years, benefiting from the emergence of both new prosthetic materials (with increased biocompatibility and very good mechanical behavior), and computerized manufacturing technologies, which offer predictability, accuracy, and reproducibility. On the other hand, the quality of conventional materials for obtaining implant-supported prostheses is acknowledged, as they have already proven their clinical performance. The properties of PMMA (poly (methyl methacrylate))-which is a representative interim material frequently used in prosthodontics-and of PEEK (polyether ether ketone)-a biomaterial which is placed on the border between interim and final prosthetic use-are highlighted in order to illustrate the complex way these materials interact with the oral environment. In regard to definitive prosthetic materials used for obtaining implant-supported prostheses, emphasis is placed on zirconia-based ceramics. Zirconia exhibits several distinctive advantages (excellent aesthetics, good mechanical behavior, biocompatibility), through which its clinical applicability has become increasingly wide. Zirconia's interaction with the oral environment (fibroblasts, osteoblasts, dental pulp cells, macrophages) is presented in a relevant synthesis, thus revealing its good biocompatibility.

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Colorectal cancer (CRC) is a predominant malignancy worldwide, being the fourth most common cause of mortality and morbidity. The CRC incidence in adolescents, young adults, and adult populations is increasing every year. In the pathogenesis of CRC, various factors are involved including diet, sedentary life, smoking, excessive alcohol consumption, obesity, gut microbiota, diabetes, and genetic mutations. The CRC tumor microenvironment (TME) involves the complex cooperation between tumoral cells with stroma, immune, and endothelial cells. Cytokines and several growth factors (GFs) will sustain CRC cell proliferation, survival, motility, and invasion. Epidermal growth factor receptor (EGFR), Insulin-like growth factor -1 receptor (IGF-1R), and Vascular Endothelial Growth Factor -A (VEGF-A) are overexpressed in various human cancers including CRC. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) and all the three major subfamilies of the mitogen-activated protein kinase (MAPK) signaling pathways may be activated by GFs and will further play key roles in CRC development. The main aim of this review is to present the CRC incidence, risk factors, pathogenesis, and the impact of GFs during its development. Moreover, the article describes the relationship between EGF, IGF, VEGF, GFs inhibitors, PI3K/AKT/mTOR-MAPK signaling pathways, and CRC.

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It has become widely accepted that insulin resistance and glucose hypermetabolism can be linked to acute pathologies, such as burn injury, severe trauma, or sepsis. Severe burns can determine a significant increase in catabolism, having an important effect on glucose metabolism and on muscle protein metabolism. It is imperative to acknowledge that these alterations can lead to increased mortality through organ failure, even when the patients survive the initial trauma caused by the burn. By limiting the peripheral use of glucose with consequent hyperglycemia, insulin resistance determines compensatory increased levels of insulin in plasma. However, the significant alterations in cellular metabolism lead to a lack of response to insulin's anabolic functions, as well as to a decrease in its cytoprotective role. In the end, via pathological insulin signaling associated with increased liver gluconeogenesis, elevated levels of glucose are detected in the blood. Several cellular mechanisms have been incriminated in the development of insulin resistance in burns. In this context, the main aim of this review article is to summarize some of the drugs that might interfere with insulin resistance in burns, taking into consideration that such an approach can significantly improve the prognosis of the burned patient.

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Burns can be caused by various factors and have an increased risk of infection that can seriously delay the wound healing process. Chronic wounds caused by burns represent a major health problem. Wound healing is a complex process, orchestrated by cytokines, growth factors, prostaglandins, free radicals, clotting factors, and nitric oxide. Growth factors released during this process are involved in cell growth, proliferation, migration, and differentiation. Reactive oxygen species are released in acute and chronic burn injuries and play key roles in healing and regeneration. The main aim of this review is to present the roles of growth factors, reactive oxygen species, and metformin in the healing process of burn injuries.

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Oral cancer represents one of the most common types of cancer worldwide, with oral squamous cell carcinoma (OSCC) being the most frequently diagnosed. Cytokines play a crucial role in inflammation, apoptosis and metastasis. Interleukin (IL)-8 promotes the direct migration of inflammatory cells. IL-6 induces tumor cell proliferation, increases expression of invasiveness and angiogenetic factors or matrix metalloproteinases (MMPs), promoting metastasis. Tissue inhibitor of metalloproteinases (TIMPs) blocks the action of MMPs controlling extracellular matrix degradation and inhibiting metastasis. The aim of our study was to analyze the existence of correlations between inflammation markers (IL-6 and IL-8) and extracellular degradation protection markers such as TIMP-1 in OSCC tumors. Our study included 20 patients (12 females and 8 males) diagnosed with OSCC, recruited from January to April, 2020. IL-8, IL-6 and TIMP-1 levels were measured in the tumor cell lysates by ELISA technique, using relevant assay kits. Our results showed a positive and significant correlation between IL-6 and IL-8 (P=0.005, R=0.517) indicating that high IL-8 levels can be associated with high IL-6 levels. We also found a significant and high negative correlation (P<0.001, R=-0.673) between IL-6 and TIMP-1 and a significant and high negative correlation (P<0.001, R=-0.684) between IL-8 and TIMP-1 indicating that high levels of IL-8 and IL-6 are significantly associated with lower levels of TIMP-1. In conclusion, our study confirms the available literature data on IL-6 and IL-8 as potential markers for oral cancers such as OSCC and affect the tumor microenvironment by decreasing TIMPs. All three biomarkers included in this study have the potential to be used as detection or prognostic factors for oral cancer.

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The purpose of this study was to analyze the oxidative stress level and inflammatory status of saliva in the presence of certain materials used for obtaining interim prosthetic restorations. Four types of interim resin materials were investigated: a pressure/heat-cured acrylic resin (Superpont C+B, SpofaDental a.s Czech Republic, /KaVo Kerr Group), a milled resin (Telio CAD polymethyl methacrylate, Ivoclar Vivadent AG, Liechtenstein), a 3D printed resin (NextDent C&B MFH, NextDent by 3D Systems, the Netherlands), and a pressure/heat-cured micro-filled indirect composite resin (SR Chromasit, Ivoclar Vivadent AG, Liechtenstein). The disk-shaped resin samples (30 mm diameter, 2 mm high) were obtained in line with the producers' recommendations. The resulting resin specimens were incubated with saliva samples collected from twenty healthy volunteers. In order to analyze the antioxidant activity of the tested materials, certain salivary parameters were evaluated before and after incubation: uric acid, gamma glutamyl transferase (GGT), oxidative stress responsive kinase-1 (OXSR-1), and total antioxidant capacity (TAC); the salivary levels of tumor necrosis factor (TNFα) and interleukin-6 (IL-6) (inflammatory markers) were measured as well. The obtained results are overall favorable, showing that the tested materials did not cause significant changes in the salivary oxidative stress level and did not influence the inflammatory salivary status.

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We have studied Na/K-ATPase and Mg-ATPase activities in red blood cells of diabetic rats treated in vivo with sodium vanadate. To our knowledge the effect of in vivo vanadate treatment on these two enzymes has not been studied. Red blood cell Na/K-ATPase plays a central role in the regulation of intra- and extra cellular cation homeostasis. Alteration of this transport enzymes is thought to be linked to several complications of diabetes mellitus: hypertension, nephropathy, peripherical neuropathy and microangiopathy. An Mg2+-dependent ATPase activity located in the erythrocyte membrane appears to be responsible for controlling the smoothing of echinocytic erythrocytes to discocytes and stomatocytes. Our results show that in alloxan diabetes activities of both ATPases are reduced (especially the activity of Na/K-ATPase). Vanadate treatment of normal animals reduced the activities of both enzymes: with 33.08% for Na/K-ATPase and 22.76% for Mg-ATPase. Vanadate treatment of diabetic animals did not affect significantly the inhibition process for Na/K-ATPase. For Mg-ATPase we have obtained a significant cumulative inhibition. These results stand out the different functions and physiologic control mechanism of these two ionic pump in red blood cells.

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