scholarly journals Malnutrition and Fracture Healing: Are Specific Deficiencies in Amino Acids Important in Nonunion Development?

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1597 ◽  
Author(s):  
Dennis Meesters ◽  
Karolina Wijnands ◽  
Peter Brink ◽  
Martijn Poeze
Keyword(s):  
Nitric Oxide ◽  
Fracture Healing ◽  
Inflammatory Responses ◽  
Repair Process ◽  
Absolute Number ◽  
Fracture Repair ◽  
Influential Factor ◽  
Protein Amino Acid ◽  
Collagen Formation ◽  
Nitric Oxide Metabolism

With the increasing incidence of fractures now, and in the future, the absolute number of bone-healing complications such as nonunion development will also increase. Next to fracture-dependent factors such as large bone loss volumes and inadequate stabilization, the nutritional state of these patients is a major influential factor for the fracture repair process. In this review, we will focus on the influence of protein/amino acid malnutrition and its influence on fracture healing. Mainly, the arginine-citrulline-nitric oxide metabolism is of importance since it can affect fracture healing via several precursors of collagen formation, and through nitric oxide synthases it has influences on the bio-molecular inflammatory responses and the local capillary growth and circulation.

Systemic Mesenchymal Stem Cell Delivery and Axial Mechanical Stimulation Accelerate Fracture Healing

2008 ◽  
Author(s):  
Aaron S. Weaver ◽  
Yu-Ping Su ◽  
Dana L. Begun ◽  
Ralph T. Zade ◽  
Andrea I. Alford ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Bone Repair ◽  
Local Environment ◽  
Cell Types ◽  
Repair Process ◽  
Fracture Site ◽  
Fracture Repair ◽  
Stem Cell Delivery ◽  
Numerous Cell ◽  
Local Cell

Fracture healing is a complex process involving numerous cell types, whose actions are regulated by many factors in their local environment. Mechanical factors are known to exert a strong influence on the actions of these cells and the progression of the repair process. While prior studies have investigated the effect of physical forces on cell differentiation, biofactor expression, and mechanical competence of repair, the mechanosensory and response mechanisms are poorly understood. This study was designed to explore the influence of a controlled mechanical environment on temporal aspects of the bone repair process. Specifically, this study examines how the timing of an applied strain influences local cell behavior during fracture repair, and how this load affects the migration of systemically introduced mesenchymal stem cells (MSCs) to the fracture site.

scholarly journals Interactions between MSCs and Immune Cells: Implications for Bone Healing

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Tracy K. Kovach ◽  
Abhijit S. Dighe ◽  
Peter I. Lobo ◽  
Quanjun Cui
Keyword(s):  
Fracture Healing ◽  
Bone Healing ◽  
Immune Cells ◽  
Bone Repair ◽  
Repair Process ◽  
The United States ◽  
Fracture Repair ◽  
Cell Based Therapy

It is estimated that, of the 7.9 million fractures sustained in the United States each year, 5% to 20% result in delayed or impaired healing requiring therapeutic intervention. Following fracture injury, there is an initial inflammatory response that plays a crucial role in bone healing; however, prolonged inflammation is inhibitory for fracture repair. The precise spatial and temporal impact of immune cells and their cytokines on fracture healing remains obscure. Some cytokines are reported to be proosteogenic while others inhibit bone healing. Cell-based therapy utilizing mesenchymal stromal cells (MSCs) is an attractive option for augmenting the fracture repair process. Osteoprogenitor MSCs not only differentiate into bone, but they also exert modulatory effects on immune cells via a variety of mechanisms. In this paper, we review the current literature on bothin vitroandin vivostudies on the role of the immune system in fracture repair, the use of MSCs in the enhancement of fracture healing, and interactions between MSCs and immune cells. Insight into this paradigm can provide valuable clues in identifying cellular and noncellular targets that can potentially be modulated to enhance both natural bone healing and bone repair augmented by the exogenous addition of MSCs.

scholarly journals Systemic Administration of Recombinant Irisin Accelerates Fracture Healing in Mice

2021 ◽  
Vol 22 (19) ◽  
pp. 10863
Author(s):  
Silvia Concetta Colucci ◽  
Cinzia Buccoliero ◽  
Lorenzo Sanesi ◽  
Mariella Errede ◽  
Graziana Colaianni ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Mineral Content ◽  
Histological Analysis ◽  
Early Stage ◽  
Fold Increase ◽  
Repair Process ◽  
Fracture Repair ◽  
Bone Fracture Healing ◽  
Bony Callus ◽  
Callus Volume

To date, pharmacological strategies designed to accelerate bone fracture healing are lacking. We subjected 8-week-old C57BL/6 male mice to closed, transverse, mid-diaphyseal tibial fractures and treated them with intraperitoneal injection of a vehicle or r-irisin (100 µg/kg/weekly) immediately following fracture for 10 days or 28 days. Histological analysis of the cartilaginous callus at 10 days showed a threefold increase in Collagen Type X (p = 0.0012) and a reduced content of proteoglycans (40%; p = 0.0018). Osteoclast count within the callus showed a 2.4-fold increase compared with untreated mice (p = 0.026), indicating a more advanced stage of endochondral ossification of the callus during the early stage of fracture repair. Further evidence that irisin induced the transition of cartilage callus into bony callus was provided by a twofold reduction in the expression of SOX9 (p = 0.0058) and a 2.2-fold increase in RUNX2 (p = 0.0137). Twenty-eight days post-fracture, microCT analyses showed that total callus volume and bone volume were increased by 68% (p = 0.0003) and 67% (p = 0.0093), respectively, and bone mineral content was 74% higher (p = 0.0012) in irisin-treated mice than in controls. Our findings suggest that irisin promotes bone formation in the bony callus and accelerates the fracture repair process, suggesting a possible use as a novel pharmacologic modulator of fracture healing.

Endothelin-1 May Be a Potential Biomarker for Monitoring Changes in Nitric Oxide Metabolism in Pulmonary Hypertension

2020 ◽  
Vol 26 (10) ◽  
pp. S17-S18
Author(s):  
Adil Yunis ◽  
Mehdi Nouraie ◽  
Noel Britton ◽  
Yingze Zhang ◽  
Nicole Helbling ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Endothelin 1 ◽  
Nitric Oxide Metabolism ◽  
Potential Biomarker

Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: Implications for nitric oxide production

2006 ◽  
Vol 41 (7) ◽  
pp. 820-825 ◽  
Author(s):  
Eric A. G. Demoncheaux ◽  
David A. Elphick ◽  
Marc B. Dürner ◽  
Gail E. Higgins ◽  
David Crowther ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Whole Body ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Nitric Oxide Metabolism ◽  
Human Alcoholic

Nitric oxide increases IL-8 gene transcription and mRNA stability to enhance IL-8 gene expression in lung epithelial cells

2004 ◽  
Vol 287 (4) ◽  
pp. L764-L773 ◽  
Author(s):  
Loretta Sparkman ◽  
Vijayakumar Boggaram
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Inflammatory Responses ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Lung Epithelial

Interleukin (IL)-8, a C-X-C chemokine, is a potent chemoattractant and an activator for neutrophils, T cells, and other immune cells. The airway and respiratory epithelia play important roles in the initiation and modulation of inflammatory responses via production of cytokines and surfactant. The association between elevated levels of nitric oxide (NO) and IL-8 in acute lung injury associated with sepsis, acute respiratory distress syndrome, respiratory syncytial virus infection in infants, and other inflammatory diseases suggested that NO may play important roles in the control of IL-8 gene expression in the lung. We investigated the role of NO in the control of IL-8 gene expression in H441 lung epithelial cells. We found that a variety of NO donors significantly induced IL-8 mRNA levels, and the increase in IL-8 mRNA was associated with an increase in IL-8 protein. NO induction of IL-8 mRNA was due to increases in IL-8 gene transcription and mRNA stability. NO induction of IL-8 mRNA levels was not inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823, inhibitors of soluble guanylate cyclase and protein kinase G, respectively, and 8-bromo-cGMP did not increase IL-8 mRNA levels. This indicated that NO induces IL-8 mRNA levels independently of changes in the intracellular cGMP levels. NO induction of IL-8 mRNA was significantly reduced by inhibitors of extracellular regulated kinase and protein kinase C. IL-8 induction by NO was also reduced by hydroxyl radical scavengers such as dimethyl sulfoxide and dimethylthiourea, indicating the involvement of hydroxyl radicals in the induction process. NO induction of IL-8 gene expression could be a significant contributing factor in the initiation and induction of inflammatory response in the respiratory epithelium.

scholarly journals A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Peng Yu ◽  
Xiang-Lin Chi ◽  
Li-Jun Liu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
The Brain

Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH). Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

Angiotensin II increases neurogenic nitric oxide metabolism in mesenteric arteries from hypertensive rats

Life Sciences ◽  
2001 ◽  
Vol 68 (10) ◽  
pp. 1169-1179 ◽  
Author(s):  
Mercedes Ferrer ◽  
M Jesús Alonso ◽  
Mercedes Salaices ◽  
Jesús Marı́n ◽  
Gloria Balfagón
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
Nitric Oxide Metabolism
Sign in / Sign up

Export Citation Format

Share Document