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Low dose native type II collagen prevents pain in a rat osteoarthritis model
BACKGROUND: Osteoarthritis is the most widespread joint-affecting disease. Patients with osteoarthritis experience pain and impaired mobility resulting in marked reduction of quality of life. A progressive cartilage loss is responsible of an evolving disease difficult to treat. The characteristic of...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751133/ https://www.ncbi.nlm.nih.gov/pubmed/23915264 http://dx.doi.org/10.1186/1471-2474-14-228 |
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author | Di Cesare Mannelli, Lorenzo Micheli, Laura Zanardelli, Matteo Ghelardini, Carla |
author_facet | Di Cesare Mannelli, Lorenzo Micheli, Laura Zanardelli, Matteo Ghelardini, Carla |
author_sort | Di Cesare Mannelli, Lorenzo |
collection | PubMed |
description | BACKGROUND: Osteoarthritis is the most widespread joint-affecting disease. Patients with osteoarthritis experience pain and impaired mobility resulting in marked reduction of quality of life. A progressive cartilage loss is responsible of an evolving disease difficult to treat. The characteristic of chronicity determines the need of new active disease modifying drugs. Aim of the present research is to evaluate the role of low doses of native type II collagen in the rat model of osteoarthritis induced by sodium monoiodoacetate (MIA). METHODS: 1, 3 and 10 mg kg(-1) porcine native type II collagen were daily per os administered for 13 days starting from the day of MIA intra-articular injection. RESULTS: On day 14, collagen-treated rats showed a significant prevention of pain threshold alterations induced by MIA. Evaluation were performed on paws using mechanical noxious (Paw pressure test) or non-noxious (Electronic Von Frey test) stimuli, and a decrease of articular pain was directly measured on the damaged joint (PAM test). The efficacy of collagen in reducing pain was as higher as the dose was lowered. Moreover, a reduced postural unbalance, measured as hind limb weight bearing alterations (Incapacitance test), and a general improvement of motor activity (Animex test) were observed. Finally, the decrease of plasma and urine levels of CTX-II (Cross Linked C-Telopeptide of Type II Collagen), a biomarker of cartilage degradation, suggests a collagen-dependent decrease of structural joint damage. CONCLUSIONS: These results describe the preclinical efficacy of low dosages of native type II collagen as pain reliever by a mechanism that involves a protective effect on cartilage. |
format | Online Article Text |
id | pubmed-3751133 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-37511332013-08-24 Low dose native type II collagen prevents pain in a rat osteoarthritis model Di Cesare Mannelli, Lorenzo Micheli, Laura Zanardelli, Matteo Ghelardini, Carla BMC Musculoskelet Disord Research Article BACKGROUND: Osteoarthritis is the most widespread joint-affecting disease. Patients with osteoarthritis experience pain and impaired mobility resulting in marked reduction of quality of life. A progressive cartilage loss is responsible of an evolving disease difficult to treat. The characteristic of chronicity determines the need of new active disease modifying drugs. Aim of the present research is to evaluate the role of low doses of native type II collagen in the rat model of osteoarthritis induced by sodium monoiodoacetate (MIA). METHODS: 1, 3 and 10 mg kg(-1) porcine native type II collagen were daily per os administered for 13 days starting from the day of MIA intra-articular injection. RESULTS: On day 14, collagen-treated rats showed a significant prevention of pain threshold alterations induced by MIA. Evaluation were performed on paws using mechanical noxious (Paw pressure test) or non-noxious (Electronic Von Frey test) stimuli, and a decrease of articular pain was directly measured on the damaged joint (PAM test). The efficacy of collagen in reducing pain was as higher as the dose was lowered. Moreover, a reduced postural unbalance, measured as hind limb weight bearing alterations (Incapacitance test), and a general improvement of motor activity (Animex test) were observed. Finally, the decrease of plasma and urine levels of CTX-II (Cross Linked C-Telopeptide of Type II Collagen), a biomarker of cartilage degradation, suggests a collagen-dependent decrease of structural joint damage. CONCLUSIONS: These results describe the preclinical efficacy of low dosages of native type II collagen as pain reliever by a mechanism that involves a protective effect on cartilage. BioMed Central 2013-08-01 /pmc/articles/PMC3751133/ /pubmed/23915264 http://dx.doi.org/10.1186/1471-2474-14-228 Text en Copyright © 2013 Di Cesare Mannelli et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Di Cesare Mannelli, Lorenzo Micheli, Laura Zanardelli, Matteo Ghelardini, Carla Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title | Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title_full | Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title_fullStr | Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title_full_unstemmed | Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title_short | Low dose native type II collagen prevents pain in a rat osteoarthritis model |
title_sort | low dose native type ii collagen prevents pain in a rat osteoarthritis model |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751133/ https://www.ncbi.nlm.nih.gov/pubmed/23915264 http://dx.doi.org/10.1186/1471-2474-14-228 |
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