Experimental evaluation of three osteosynthesis devices used for stabilizing condylar fractures of the mandible.

INTRODUCTION: The purpose of the study is to evaluate experimentally the quality of the primary stability achieved in treating low subcondylar fractures by means of three different osteosynthesis devices. MATERIAL AND METHODS: The devices, a standard four-hole plate, an axial lag screw and a three-dimensional rectangular plate were tested on fresh isolated human mandibles. Testing was done on a test bench by reproducing static biting exercises between the first molars on the side of the fracture. The quality of the osteosynthesis was assessed by measuring the macroscopic amount of fragment displacement and on the device's ability to diffuse the mechanical strain within the fractured area by photoelastic stress analysis. RESULTS: The straight plates provided the worst restoration. This was explained by the unfavourable position of the plate along compression lines. The axial lag screws allowed average stability. This was due to the difficulty of intra-medullary positioning of the screw, and by the compression of the fracture line. Rectangular plates allowed good stability associated with rather good restitution of the strains. These good results were assigned to the shape of the plate, one of its arms approximating the tensile strain lines. CONCLUSION: Positioning and shape of the osteosynthesis device are of prime importance for condylar fracture stabilization. None of the three tested devices was optimal but the three-dimensional plate was the best. There is a need to develop the geometry of new plates.     

Reported use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors was not associated with reduced recurrence of colorectal adenomas.

We did a secondary analysis of data from three large colorectal adenoma chemoprevention trials to assess the association between 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor use and reduced risk of recurrent colorectal adenomas. Reported use of HMG-CoA reductase inhibitors was not associated with a reduced recurrence of colorectal adenomas, multiple adenomas, or advanced adenomas. Lack of statistical power from limited exposure to HMG-CoA reductase inhibitors might be responsible for the lack of association.     

Vitamin-D Deficiency and Supplementation Altered the Network of the Coronary Arteries in a Rodent Model—In Situ Video Microscopic Technique

The aim of our study was to identify whether vitamin-D deficiency (VDD) can alter the geometry of the coronary-resistance-artery system. Male Wistar rats were divided into vitamin-D-deficient (VD−, n = 10) and vitamin-D-supplemented (VD+, n = 8) groups. After eight weeks, branches and segments of the left-anterior-descending-coronary-artery (LAD) network were analyzed by a video-microscopy technique. Segments were divided into 50 μm-long cylindrical ring units. VDD did not increase the number of morphological abnormalities. The number of segments did not differ between the groups (VD−: 210 and VD+: 224; pooled data of 8 networks). A larger lumen area of branches was found in VD+ group, while 1–4-order branches were lengthier in the VD− group. VD− rats had less rich coronary-resistance-artery networks in terms of 50 µm-long units. (VD−: 6365 vs. VD+: 6602; pooled data of 8 networks). VD+ animals were richer in the 100–350 µm outer diameter range, and VD− animals were richer in the 400–550 µm-diameter units. In VD− rats, 150–200 and 300 µm units were almost missing at higher flow distances from the orifice. Serum vitamin-D alterations caused by dietary changes can affect the geometry of the coronary-artery network, which may contribute to vitamin-D-dependent changes in cardiovascular mortality.     

Assessment of Angiogenesis and Cell Survivability of an Inkjet Bioprinted Biological Implant in an Animal Model

The rapidly growing field of tissue engineering hopes to soon address the shortage of transplantable tissues, allowing for precise control and fabrication that could be made for each specific patient. The protocols currently in place to print large-scale tissues have yet to address the main challenge of nutritional deficiencies in the central areas of the engineered tissue, causing necrosis deep within and rendering it ineffective. Bioprinted microvasculature has been proposed to encourage angiogenesis and facilitate the mobility of oxygen and nutrients throughout the engineered tissue. An implant made via an inkjet printing process containing human microvascular endothelial cells was placed in both B17-SCID and NSG-SGM3 animal models to determine the rate of angiogenesis and degree of cell survival. The implantable tissues were made using a combination of alginate and gelatin type B; all implants were printed via previously published procedures using a modified HP inkjet printer. Histopathological results show a dramatic increase in the average microvasculature formation for mice that received the printed constructs within the implant area when compared to the manual and control implants, indicating inkjet bioprinting technology can be effectively used for vascularization of engineered tissues.