Three-dimensional (3D) printing technology has revolutionized tissue engineering field because of its excellent potential of accurately positioning cell-laden constructs. One of the main challenges in the formation of functional engineered tissues is the lack of an efficient and extensive network of microvessels to support cell viability. By printing vascular cells and appropriate biomaterials, the 3D printing could closely mimic in vivo conditions to generate blood vessels. In vascular tissue engineering, many various approaches of 3D printing have been developed, including selective laser sintering and extrusion methods, etc. The 3D printing is going to be the integral part of tissue engineering approaches; in comparison with other scaffolding techniques, 3D printing has two major merits: automation and high cell density. Undoubtedly, the application of 3D printing in vascular tissue engineering will be extended if its resolution, printing speed, and available materials can be improved.

The investigation and determination of the significance of neoVASCULARIZATION in the progression of soft tissue sarcoma is currently of increasing clinical importance. Microvessel density is the morphologic evidence of neoangiogenesis in the process of malignant progression of sarcomata. This brief review of the markers commonly used in clinical practice was undertaken to determine the validity of the application of these markers in the quantitation of neoangiogenesis in sarcomata. The material selection was based only on primary material from untreated cases that were part of the inhospital and consultation practices. From this investigation, one can conclude that not all markers have equal value in either the qualitative or quantitative assessment of VASCULARIZATION in tumors. Laminin was found to have low sensitivity. Factor VIII was found to have extreme sensitivity but lack specificity. A combination of collagen IV, smooth muscle actin, CD34 and CD31 markers were found to represent the most reliable identificators of blood vessels in sarcomata. Morphological identification of vessels may be further supplemented by proliferation markers (e.g. PCNA, Ki67) as indicators for, not only the presence of blood vessels, but also to determine the activity of endothelial cells in blood vessel growth.

Background & objective: Changes in submucosal VASCULARIZATION and inflammation, determined by immunohistochemistry staining, were shown to be correlated with the development of dysplasia and invasiveness of epithelial cells in premalignant and malignant lesions. This study evaluated changes in sections routinely stained with Hematoxylin and Eosin (H& E) in order to investigate vascular density and intensity of inflammatory cells infiltration during the progression of oral leukoplakia with mild dysplasia to Squamous Cell Carcinoma (SCC).The aim of the research was to determine whether changes in sub-mucosal vascularity and inflammatory infiltration of leukoplakia in routine H& E-stained sections could contribute to the assessment of severity of the lesion.Methods: In this cross-sectional, comparative and descriptive study, vascular density and inflammation intensity of 125 available samples of H& E-stained sections, consisting of 35 cases of mild and moderate dysplasia, 38 severe dysplasia and carcinoma in situ, and 52 SCC, were investigated. To analyze the data, chi-square test, Mann-Whitney test, Kruskal-Wallis test, Tukey’s post hoc test, and cumulative ordinal logistic regression were conducted.Results: There was a significantly higher vascular density in cases with severe dysplasia, in situ carcinoma, and SCC compared to those with mild to moderate dysplasia (P<0.0001). However, the difference in vascularity was not statically significant between severe dysplasia, carcinoma in situ, and SCC (P=0.78). Intensity of inflammatory cells infiltration in the underlying connective tissue was significantly different among the three groups (P<0.0001), and the highest intensity of inflammatory cells infiltration was seen in the SCC group.Conclusions: Increased submucosal VASCULARIZATION and inflammatory cells infiltration can contribute further to predicting more aggressive epithelial dysplasia.