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Studies on Arthritis and Joint Disorders pp 275–295Cite as

Antioxidants in the Treatment of Osteoarthritis and Bone Mineral Loss

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Abstract

The concept that inflammatory diseases of bones and joints can be postponed or even prevented naturally by consuming certain foods or food-derived substances is currently eliciting considerable interest from researchers, clinicians and patients. Oxidative stress results in the production of reactive oxygen species (ROS), which play important roles in the development of many diseases including those relating to bones and joints. Metabolic reactions in osteoblasts, osteoclasts, chondrocytes and synoviocytes produce free radicals, ROS and their derivatives. These dangerous chemicals can accumulate in bones and synovial joints, and in combination with inflammatory mediators they can cause extensive structural damage, inflammation and cell death. Antioxidants are naturally occurring reducing agents capable of inhibiting ROS formation, scavenging free radicals and removing ROS derivatives. Antioxidant vitamins have major roles in modulating oxidative stress, regulating immune responses and contributing to cell differentiation. Vitamin C (ascorbic acid), vitamin E, thiols (glutathione) and plant polyphenols have the capacity to neutralize ROS in joints and decrease the oxidative stress associated with the progression of arthritis. This chapter focuses on antioxidants and their potential for the treatment of diseases of bones and joints, particularly focusing on osteoarthritis (OA) and bone mineral loss.

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Notes

  1. 1.

    http://www.un.org/

  2. 2.

    http://www.who.int/en/

  3. 3.

    http://www.arthritis.org/

  4. 4.

    http://www.niams.nih.gov/

  5. 5.

    http://www.cdc.gov/

  6. 6.

    http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/overview.asp

  7. 7.

    PYCARD promotes caspase-mediated apoptosis. Its proapoptotic activity is mediated predominantly through the activation of caspase 9. It may be a component of the inflammasome and part of a protein complex whose function would be the activation of pro-inflammatory caspases.

    GeneCards entry: http://www.genecards.org/cgi-bin/carddisp.pl?gene=PYCARD

  8. 8.

    NALP (NLR family, pyrin domain containing 1) is a protein involved in activation of caspase 1 and caspase 5 as part of the NALP1 inflammasome complex which leads to processing and release of IL-1β and IL-18.

    GeneCards entry: http://www.genecards.org/cgi-bin/carddisp.pl?gene=NLRP1

  9. 9.

    http://www.fda.gov/

Abbreviations

AP-1:

Activator protein 1

AR:

Androgen receptor

BMD:

Bone mineral density

CBP:

CREB-binding protein or CREBBP

CDC:

Centers for Disease Control and Prevention

cGMP:

current Good Manufacturing Practices

COX:

Cyclooxygenase

EFSA:

European Food Safety Authority

EGR-1:

Early growth response protein 1

eNOS:

Endothelial NOS

EpRE:

Electrophile-responsive element

FA:

Fatty acids

FDA:

Food and Drug Administration

GSH:

Glutathione or gamma-l-glutamyl-l-cysteinylglycine

H2O2 :

Hydrogen peroxide

IFN-γ:

Interferon gamma

IGF-I:

Insulin-like growth factor I

IGF-IR:

Insulin-like growth factor I receptor

IL-1β:

Interleukin 1 beta

iNOS:

Inducible NOS

JSW:

Joint space width

LOX:

Lipoxygenase

LPS:

Lipopolysaccharides

NAC:

N-acetylcysteine

NADPH:

Nicotinamide adenine dinucleotide phosphate

NALP:

Pyrin-like protein containing a pyrin domain

NF-κB:

Nuclear factor kappa B

NIAMS:

National Institute of Arthritis and Musculoskeletal and Skin Diseases

NO:

Nitric oxide

NOS:

Nitric oxide synthase

NRF-2:

Nuclear respiratory factor 2

NSAID:

Nonsteroidal anti-inflammatory drug

OA:

Osteoarthritis

p300:

E1A binding protein p300

p53:

Protein 53 or tumour protein 53

PGE2 :

Prostaglandin E2

PPAR-γ:

Peroxisome proliferator-activated receptor gamma

PYCARD:

Apoptosis-associated speck-like protein containing a caspase-recruitment domain (CARD)

RA:

Rheumatoid arthritis

RANK:

Receptor activator of nuclear factor kappa B

RANKL:

Receptor activator of nuclear factor kappa B ligand

ROS:

Reactive oxygen species

Sirt-1:

Sirtuin (silent mating type information regulation 2 homolog) 1

SLE:

Systemic lupus erythematosus

SOD:

Superoxide dismutase

STAT:

Signal transducer and activator of transcription

TGF-β:

Transforming growth factor beta

UN:

United Nations

WHO:

World Health Organization

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Acknowledgments

A. Mobasheri wishes to acknowledge the financial support of the Wellcome Trust, the National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC3Rs) (grant number: Mobasheri.A.28102007), the Biotechnology and Biological Sciences Research Council (BBSRC) (grants BBSRC/S/M/2006/13141 and BB/G018030/1) and the Engineering and Physical Sciences Research Council (EPSRC). A. Mobasheri and Y. Henrotin are members of the D-BOARD Consortium funded by European Commission Framework 7 program (EU FP7; HEALTH.2012.2.4.5–2, project number 305815, NovelDiagnostics and Biomarkers for Early Identification of Chronic Inflammatory Joint Diseases).

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Authors and Affiliations

  1. Musculoskeletal Research Group, Division of Veterinary Medicine, School of Veterinary Medicine and Science, Faculty of Medicine and Health Sciences, The University of Nottingham, Sutton Bonington Campus, College Road, Sutton Bonington, Leicestershire, LE12 5RD, UK

    Ali Mobasheri D.Phil. (Oxon)

  2. Musculoskeletal Research Group, Institute of Anatomy, Ludwig-Maximilian-University Munich, Munich, Germany

    Mehdi Shakibaei D.V.M., Ph.D.

  3. Department of Biological Chemistry and Nutrition, Institute of Biological Chemistry and Nutrition, University of Hohenheim, Stuttgart, Germany

    Hans Konrad Biesalski M.D., Ph.D.

  4. Bone and Cartilage Research Unit, Institute of Pathology, University of Liege, Sart-Tilman, Liege, Belgium

    Yves Henrotin Ph.D.

  5. Physical Therapy and Rehabilitation Department, Princess Paola Hospital, Vivalia, Marche-en-Famenne, Belgium

    Yves Henrotin Ph.D.

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  1. Ali Mobasheri D.Phil. (Oxon)
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  2. Mehdi Shakibaei D.V.M., Ph.D.
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  3. Hans Konrad Biesalski M.D., Ph.D.
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  4. Yves Henrotin Ph.D.
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Corresponding author

Correspondence to Ali Mobasheri D.Phil. (Oxon) .

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Editors and Affiliations

  1. Fac Farmacia, Department of Pharmacology, University of Valencia, Av Vicent Andres Estelles S/n Burjasot, Valencia, 46100, Spain

    Maria Jose Alcaraz

  2. , NEIRID Lab, Santiago University Clinical Hospital, Trav. Choupana sn, Santiago de Compostela, 15706, Spain

    Oreste Gualillo

  3. Fundación Jiménez Díaz Hospital, Rheumatology Division, Autonoma University, Avda Reyes Católicos 2, Madrid, 28040, Spain

    Olga Sánchez-Pernaute

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Conflict of Interest

This chapter was written by the authors within the scope of their academic and research positions at their host institutions. None of the authors has a financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of this chapter.

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Mobasheri, A., Shakibaei, M., Biesalski, H.K., Henrotin, Y. (2013). Antioxidants in the Treatment of Osteoarthritis and Bone Mineral Loss. In: Alcaraz, M., Gualillo, O., Sánchez-Pernaute, O. (eds) Studies on Arthritis and Joint Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4614-6166-1_15

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