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Muscle paralysis induces bone marrow inflammation and predisposition to formation of giant osteoclasts.
- Source :
-
American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2017 Nov 01; Vol. 313 (5), pp. C533-C540. Date of Electronic Publication: 2017 Aug 30. - Publication Year :
- 2017
-
Abstract
- Transient muscle paralysis engendered by a single injection of botulinum toxin A (BTxA) rapidly induces profound focal bone resorption within the medullary cavity of adjacent bones. While initially conceived as a model of mechanical disuse, osteoclastic resorption in this model is disproportionately severe compared with the modest gait defect that is created. Preliminary studies of bone marrow following muscle paralysis suggested acute upregulation of inflammatory cytokines, including TNF-α and IL-1. We therefore hypothesized that BTxA-induced muscle paralysis would rapidly alter the inflammatory microenvironment and the osteoclastic potential of bone marrow. We tested this hypothesis by defining the time course of inflammatory cell infiltration, osteoinflammatory cytokine expression, and alteration in osteoclastogenic potential in the tibia bone marrow following transient muscle paralysis of the calf muscles. Our findings identified inflammatory cell infiltration within 24 h of muscle paralysis. By 72 h, osteoclast fusion and pro-osteoclastic inflammatory gene expression were upregulated in tibia bone marrow. These alterations coincided with bone marrow becoming permissive to the formation of osteoclasts of greater size and greater nuclei numbers. Taken together, our data are consistent with the thesis that transient calf muscle paralysis induces acute inflammation within the marrow of the adjacent tibia and that these alterations are temporally consistent with a role in mediating muscle paralysis-induced bone resorption.<br /> (Copyright © 2017 the American Physiological Society.)
- Subjects :
- Animals
Bone Marrow pathology
Bone Resorption etiology
Botulinum Toxins, Type A toxicity
Female
Inflammation physiopathology
Mice
Mice, Inbred C57BL
Neuromuscular Agents toxicity
Paralysis chemically induced
Paralysis immunology
T-Lymphocytes immunology
Bone Resorption physiopathology
Inflammation etiology
Muscle, Skeletal drug effects
Osteoclasts pathology
Paralysis physiopathology
Subjects
Details
- Language :
- English
- ISSN :
- 1522-1563
- Volume :
- 313
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- American journal of physiology. Cell physiology
- Publication Type :
- Academic Journal
- Accession number :
- 28855162
- Full Text :
- https://doi.org/10.1152/ajpcell.00363.2016