Pullout strength of monocortical and bicortical screws in metaphyseal and diaphyseal regions of the canine humerus.

OBJECTIVE: Monocortical screws are commonly employed in locking plate fixation, but specific recommendations for their placement are lacking and use of short monocortical screws in metaphyseal bone may be contraindicated. Objectives of this study were to evaluate axial pullout strength of two different lengths of monocortical screws placed in various regions of the canine humerus compared to bicortical screws, and to derive cortical thickness and bone density values for those regions using quantitative computed tomography analysis (QCT). METHODS: The QCT analysis was performed on 36 cadaveric canine humeri for six regions of interest (ROI). A bicortical, short monocortical, or 50% transcortical 3.5 mm screw was implanted in each ROI and axial pullout testing was performed. RESULTS: Bicortical screws were stronger than monocortical screws in all ROI except the lateral epicondylar crest. Short monocortical metaphyseal screws were weaker than those placed in other regions. The 50% transcortical screws were stronger than the short monocortical screws in the condyle. A linear relationship between screw length and pullout strength was observed. CLINICAL SIGNIFICANCE: Cortical thickness and bone density measurements were obtained from multiple regions of the canine humerus using QCT. Use of short monocortical screws may contribute to failure of locking plate fixation of humeral fractures, especially when placed in the condyle. When bicortical screw placement is not possible, maximizing monocortical screw length may optimize fixation stability for distal humeral fractures.

High fat diet induces dysregulation of hepatic oxygen gradients and mitochondrial function in vivo.

NAFLD (non-alcoholic fatty liver disease), associated with obesity and the cardiometabolic syndrome, is an important medical problem affecting up to 20% of western populations. Evidence indicates that mitochondrial dysfunction plays a critical role in NAFLD initiation and progression to the more serious condition of NASH (non-alcoholic steatohepatitis). Herein we hypothesize that mitochondrial defects induced by exposure to a HFD (high fat diet) contribute to a hypoxic state in liver and this is associated with increased protein modification by RNS (reactive nitrogen species). To test this concept, C57BL/6 mice were pair-fed a control diet and HFD containing 35% and 71% total calories (1 cal approximately 4.184 J) from fat respectively, for 8 or 16 weeks and liver hypoxia, mitochondrial bioenergetics, NO (nitric oxide)-dependent control of respiration, and 3-NT (3-nitrotyrosine), a marker of protein modification by RNS, were examined. Feeding a HFD for 16 weeks induced NASH-like pathology accompanied by elevated triacylglycerols, increased CYP2E1 (cytochrome P450 2E1) and iNOS (inducible nitric oxide synthase) protein, and significantly enhanced hypoxia in the pericentral region of the liver. Mitochondria from the HFD group showed increased sensitivity to NO-dependent inhibition of respiration compared with controls. In addition, accumulation of 3-NT paralleled the hypoxia gradient in vivo and 3-NT levels were increased in mitochondrial proteins. Liver mitochondria from mice fed the HFD for 16 weeks exhibited depressed state 3 respiration, uncoupled respiration, cytochrome c oxidase activity, and mitochondrial membrane potential. These findings indicate that chronic exposure to a HFD negatively affects the bioenergetics of liver mitochondria and this probably contributes to hypoxic stress and deleterious NO-dependent modification of mitochondrial proteins.