Reactive oxygen species and oxidative stress in osteoclastogenesis, skeletal aging and bone diseases

Osteoclasts are cells derived from bone marrow macrophages and are important in regulating bone resorption during bone homeostasis. Understanding what drives osteoclast differentiation and activity is important when studying diseases characterized by heightened bone resorption relative to formation,...

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Bibliographic Details
Published in:Journal of bone and mineral metabolism 2015-07, Vol.33 (4), p.359-370
Main Authors: Callaway, Danielle A., Jiang, Jean X.
Format: Article
Language:English
Subjects:
Aging
Animals
Bone and Bones - metabolism
Bone and Bones - pathology
Bone Diseases - metabolism
Bone Diseases - pathology
Bone Resorption
Calcium - metabolism
Cell Differentiation
Cytosol - metabolism
Homeostasis
Humans
Hydrogen Peroxide - chemistry
Invited Review
MAP Kinase Signaling System
Medicine
Medicine & Public Health
Metabolic Diseases
Mitochondria - metabolism
NADPH Oxidases - chemistry
NF-kappa B - metabolism
Orthopedics
Osteoclasts - cytology
Oxidative Stress
Protein Isoforms
RANK Ligand - metabolism
Reactive Nitrogen Species
Reactive Oxygen Species - metabolism
Signal Transduction
Superoxides - metabolism
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Summary:Osteoclasts are cells derived from bone marrow macrophages and are important in regulating bone resorption during bone homeostasis. Understanding what drives osteoclast differentiation and activity is important when studying diseases characterized by heightened bone resorption relative to formation, such as osteoporosis. In the last decade, studies have indicated that reactive oxygen species (ROS), including superoxide and hydrogen peroxide, are crucial components that regulate the differentiation process of osteoclasts. However, there are still many unanswered questions that remain. This review will examine the mechanisms by which ROS can be produced in osteoclasts as well as how it may affect osteoclast differentiation and activity through its actions on osteoclastogenesis signaling pathways. In addition, the contribution of ROS to the aging-associated disease of osteoporosis will be addressed and how targeting ROS may lead to the development of novel therapeutic treatment options.
ISSN:0914-8779
1435-5604
DOI:10.1007/s00774-015-0656-4