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The pharmacology of pain associated with the monoiodoacetate model of osteoarthritis

Research output: Contribution to journalArticle

Original languageEnglish
Article number974
JournalFrontiers in Pharmacology
Volume10
DOIs
Published2019

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  • Author's Proof (4)

    Author_s_Proof_4_.pdf, 1.32 MB, application/pdf

    Uploaded date:10 Sep 2019

    Version:Accepted author manuscript

King's Authors

Abstract

The high incidence of osteoarthritis (OA) in an increasingly elderly population anticipates a
dramatic rise in the number of people suffering from this disease in the near future. Because
pain is the main reason patients seek medical help, effective pain management—which is
currently lacking—is paramount to improve the quality of life that OA sufferers desperately
seek. Good animal models are, in this day and age, fundamental tools for basic research
of new therapeutic pathways. Several animal models of OA have been characterized,
but none of them reproduces entirely all symptoms of the disease. Choosing between
different animal models depends largely on which aspect of OA one aims to study. Here,
we review the current understanding of the monoiodoacetate (MIA) model of OA. MIA
injection in the knee joint leads to the progressive disruption of cartilage, which, in turn, is
associated with the development of pain-like behavior. There are several reasons why the
MIA model of OA seems to be the most adequate to study the pharmacological effect of
new drugs in pain associated with OA. First, the pathological changes induced by MIA
share many common traits with those observed in human OA (Van Der Kraan et al., 1989;
Guingamp et al., 1997; Guzman et al., 2003), including loss of cartilage and alterations in
the subchondral bone. The model has been extensively utilized in basic research, which
means that the time course of pain-related behaviors and histopathological changes, as
well as pharmacological profile, namely of commonly used pain-reducing drugs, is now
moderately understood. Also, the severity of the progression of pathological changes
can be controlled by grading the concentration of MIA administered. Further, in contrast
with other OA models, MIA offers a rapid induction of pain-related phenotypes, with the
cost-saving consequence in new drug screening. This model, therefore, may be more
predictive of clinical efficacy of novel pharmacological tools than other chronic or acute
OA models

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