title: Homocysteine as a Pathological Biomarker for Bone Disease.
abstract: In the last few decades, perturbation in methyl-group and homocysteine (Hcy) balance have emerged as independent risk factors in a number of pathological conditions including neurodegenerative disease, cardiovascular dysfunction, cancer development, autoimmune disease, and kidney disease. Recent studies report Hcy to be a newly recognized risk factor for osteoporosis. Elevated Hcy levels are known to modulate osteoclastgenesis by causing detrimental effects on bone via oxidative stress induced metalloproteinase-mediated extracellular matrix degradation and decrease in bone blood flow. Evidence from previous studies also suggests that the decreased chondrocytes mediated bone mineralization in chick limb-bud mesenchymal cells and during the gestational period of ossification in rat model. However, Hcy imbalance and its role in bone loss, regression in vascular invasion, and osteoporosis, are not clearly understood. More investigations are required to explore the complex interplay between Hcy imbalance and onset of bone disease progression. This article reviews the current body of knowledge on regulation of Hcy mediated oxidative stress and its role in bone remodeling, vascular blood flow and progression of bone disease. J. Cell. Physiol. 232: 2704-2709, 2017. © 2016 Wiley Periodicals, Inc.
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Jyotirmaya
authors.initials: J
authors.lastname: Behera
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Jyoti
authors.initials: J
authors.lastname: Bala
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Mohammed
authors.initials: M
authors.lastname: Nuru
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Suresh C
authors.initials: SC
authors.lastname: Tyagi
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Neetu
authors.initials: N
authors.lastname: Tyagi
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D016723:Bone Remodeling; D001842:Bone and Bones / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019902:Chondrocytes / Q000378:metabolism / Q000473:pathology; D003094:Collagen / Q000378:metabolism; D018450:Disease Progression; D006710:Homocysteine / Q000378:metabolism*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020782:Matrix Metalloproteinases / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D010010:Osteoclasts / Q000378:metabolism / Q000473:pathology; D010012:Osteogenesis; D010024:Osteoporosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D018384:Oxidative Stress; D012039:Regional Blood Flow
chemical_list: D015415:Biomarkers; D006710:Homocysteine; D003094:Collagen; D020782:Matrix Metalloproteinases