Malignant neoplasms may be composed of several cell groups, including cancer stem cells (CSC). These cells have been related with the capacity of metastasis, relapse and resistance to multiple drugs during chemotherapy. This study aims to identify CSC biomarkers and their expression pattern in human head and neck carcinomas. This study was conducted following the PRISMA checklist. The search for articles was carried out in five databases (PubMed, Scopus, Web of Science, Lilacs and Scielo). The articles found were selected in two phases: 1) reading the titles and / or abstract and 2) reading the full text. At the end, the selected articles were evaluated by QUADAS-2. Most studies evaluated oral neoplastic tissues and, as a control, samples of normal local mucosa. All studies performed immunohistochemistry as a method of immunolocalization and some also applied immunofluorescence. The most commonly used biomarker was CD44. However, other such as Sox2, Oct4, Nestin, Nanog, BMI1, ALDH1, CD133 and CD166 were also found. Several biomarkers were (ALDH1, Sox2, Oct4, ABCB5, AGR2 and TAZ) correlated with clinical characteristics of the tumor, such as staging, tumor size and lymph node metastasis. These data reinforce the CSC theory and favor the use of these biomarkers as possible determinants of prognosis.

In in vitro culture systems, dexamethasone (DEX) has been applied with ascorbic acid (ASC) and β-glycerophosphate (βGLY) as culture media supplementation to induce osteogenic differentiation of mesenchymal stem cells. However, there are some inconsistencies regarding the role of DEX as osteogenic media supplementation. Therefore, this study verified the influence of DEX culture media supplementation on the osteogenic differentiation, especially the capacity to mineralize the extracellular matrix of stem cells from human exfoliated deciduous teeth (SHED). Five groups were established: G1—SHED + Dulbecco’s Modified Eagles’ Medium (DMEM) + fetal bovine serum (FBS); G2—SHED + DMEM + FBS + DEX; G3—SHED + DMEM + FBS + ASC + βGLY; G4—SHED + DMEM + FBS + ASC + βGLY + DEX; G5—MC3T3-E1 + α Minimal Essential Medium (MEM) + FBS + ASC + βGLY. DNA content, alkaline phosphatase (ALP) activity, free calcium quantification in the extracellular medium, and extracellular matrix mineralization quantification through staining with von Kossa, alizarin red, and tetracycline were performed on days 7 and 21. Osteogenic media supplemented with ASC and β-GLY demonstrated similar effects on SHED in the presence or absence of DEX for DNA content (day 21) and capacity to mineralize the extracellular matrix according to alizarin red and tetracycline quantifications (day 21). In addition, the presence of DEX in the osteogenic medium promoted less ALP activity (day 7) and extracellular matrix mineralization according to the von Kossa assay (day 21), and more free calcium quantification at extracellular medium (day 21). In summary, the presence of DEX in the osteogenic media supplementation did not interfere with SHED commitment into mineral matrix depositor cells. We suggest that DEX may be omitted from culture media supplementation for SHED osteogenic differentiation in vitro studies.

Objective To propose a biofunctionalized prosthetic abutment by analyzing physico‐chemical and morphological properties, simvastatin (SIM) release, and biocompatibility of titanium (Ti) disks coated with poly(lactic‐co‐glycolic) acid (PLGA) incorporating SIM. Methods Titanium disks (8 × 3 mm) were distributed into four groups: Ti: pure Ti; Ti + PLGA: Ti coated with PLGA; Ti + PLGA + SIM6%: Ti + PLGA with 6% SIM; and Ti + PLGA + SIM0.6%: Ti + PLGA incorporating 0.6% SIM. PLGA was prepared through chloroform evaporation technique. After complete dissolution of PLGA, SIM was diluted in the solution. Ti + PLGA, Ti + PLGA + SIM6%, and Ti + PLGA + SIM0.6% were dip coated with PLGA and PLGA + SIM, respectively. Samples were sterilized by ethylene oxide. For SIM release assay, disks were submerged in PBS, pH 7.4, 37°C, 30 rpm up to 600 hours. At different time intervals, SIM was quantified by spectrophotometry (238 nm). For characterization of the biomaterial components, it was performed Fourier‐transform infrared spectroscopy, differential scanning calorimetry, scanning electron microscopy (SEM), optical profilometry, and atomic force microscopy. Biocompatibility analyses were performed by MTS colorimetric assay on murine fibroblasts L929, human gingival fibroblasts (HGFs), and stem cells from human exfoliated deciduous teeth (SHEDs). Absorbance was measured at 490 nm, and percentages of viable cells were calculated in relation to positive control (Ti). SEM images were obtained to verify cell adhesion and morphology. One‐way ANOVA followed by Tukey's post hoc test was applied (P < 0.05) for statistical analyses. Results SIM release was slow and continuous, reaching about 21% of the incorporated SIM after 600 hours. Topographical analyses revealed success in coating Ti disks with PLGA incorporating SIM. Regarding biocompatibility test, Ti + PLGA + SIM0.6% showed the highest percentage of L929 viability at days 3 and 7. There was no significant difference for Ti, Ti + PLGA, and Ti + PLGA + SIM0.6% groups on cell viability of both SHEDs and HGFs at days 3 and 7. SEM corroborates that SHEDs and HGFs were able to adhere and proliferate on Ti, Ti + PLGA, and Ti + PLGA + SIM0.6% surfaces. Conclusion A slow and controlled release of SIM was achieved, attributed to a diffusional mass transfer mechanism. Moreover, a homogenous coating topography was obtained. Additionally, 0.6% SIM incorporated into PLGA coating improved fibroblasts L929 viability compared to titanium or PLGA. Also, 0.6% SIM incorporated into PLGA promoted cell viability of about 100% for HGFs and approximately 150% for human mesenchymal stem cells. Therefore, this study allows to consider the use of PLGA‐coated titanium incorporating SIM as a biofunctionalized abutment for dental implants.

Simvastatin embedded into poly(lactic-co-glycolic acid) (PLGA)-based scaffolds can stimulate bone regeneration in preclinical models. However, the ideal pharmacological dose has not been evaluated. This systematic review reports on the simvastatin doses used in preclinical studies and evaluates the regeneration of critical-sized bone defects. References were selected in a two-phase process. Electronic databases (Embase, LILACS, LIVIVO, PubMed, SCOPUS, and Web of Science) and grey literature databases (Google Scholar, Open Grey, and ProQuest) were searched until September 2022. The risk of bias was considered to be low based on the SYRCLE tool. We identified four studies in rat, two in parietal and two in calvaria bone, one in mouse parietal bone, and one in rabbit femur bone. Simvastatin, ranging from 8 to 100 µg, significantly increased bone formation in five studies, as compared to the scaffold alone based on µ-computed tomography, histomorphometric, and radiography analysis. The median increase in bone formation caused by simvastatin was 2.1-fold compared to the PLGA-based scaffold alone. There was, however, no significant correlation between the relative bone gain and the doses of simvastatin (p = 0.37). The data suggest that relatively lower doses of simvastatin can consistently promote preclinical bone regeneration. However, the interpretation of these data must consider the heterogenicity of the PLGA-scaffolds, the defect anatomy, the observation period, and the evaluation method.

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