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      Differences in structural and pain phenotypes in the sodium monoiodoacetate and meniscal transection models of osteoarthritis

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          Summary

          Objectives

          To characterize differences in joint pathology and pain behavior between two rat models of osteoarthritis (OA) in order to inform selection of animal models for interventional studies.

          Method

          Knee OA was induced in Sprague Dawley rats by either meniscal transection (MNX) or intra-articular injection of monosodium iodoacetate (MIA). Controls were subjected to sham surgery or saline-injection. In a separate experiment, a single intra-articular injection of triamcinolone acetonide was administered 14 days after MNX or MIA arthritis induction. Pain behavior and joint pathology were quantified.

          Results

          Both models displayed synovial inflammation, chondropathy and osteophytosis. Chondropathy scores increased with time similarly in the two models. Inflammation and osteophyte scores were greater in MNX model compared to the MIA model. At day 49, the MNX model exhibited a greater number of channels crossing the osteochondral junction compared to all other groups. The MNX model exhibited greater weight bearing asymmetry compared to the MIA model, whereas the MIA model displayed more consistent hindpaw allodynia. Triamcinolone attenuated weight bearing asymmetry and distal allodynia to control levels in the MNX model, but distal allodynia was unaltered in the MIA model.

          Conclusions

          The comparison of the two models of OA in rats, using identical assessment tools has demonstrated that although both models display features of OA, there are differences between the models which may represent different aspects of human OA. Thus, model selection should be based on the pathological aspects of OA under investigation.

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          Most cited references29

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          Pathogenesis and management of pain in osteoarthritis.

          The term osteoarthritis describes a common, age-related, heterogeneous group of disorders characterised pathologically by focal areas of loss of articular cartilage in synovial joints, associated with varying degrees of osteophyte formation, subchondral bone change, and synovitis. Joint damage is caused by a mixture of systemic factors that predispose to the disease, and local mechanical factors that dictate its distribution and severity. Various genetic abnormalities have been described, but most sporadic osteoarthritis probably depends on minor contributions from several genetic loci. Osteoarthritic joint damage may be associated with clinical problems, but the severity of joint disease is only weakly related to that of the clinical problem. For this reason the associations and pathogenesis of pain are in as much need of investigation as joint damage. Subchondral bone and synovium may be responsible for nociceptive stimuli, and peripheral neuronal sensitisation is an important feature, and can result in normal activities (such as walking) causing pain. Central pain sensitisation can also occur, and psychosocial factors are important determinants of pain severity. We present a stepwise approach to the management of osteoarthritis.
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            The OARSI histopathology initiative - recommendations for histological assessments of osteoarthritis in the rat.

            During the development of disease-modifying osteoarthritis (OA) drugs, rat models of OA are frequently used for a first assessment of in vivo efficacy. The most efficacious compound in the rat model may then be tested in a larger animal model before entering human trials. The aim of this study was to describe a histologic scoring system for use in different models of OA in rats that allows standardization and comparison of results obtained by different investigators. The experience of the authors with current scoring systems and the range of lesions observed in rat and human OA studies were considered in recommending this common paradigm for rat histologic scoring. Considerations were made for reproducibility and ease of use for new scorers. Additional scoring paradigms may be employed to further identify specific effects of some disease-modifying drugs. Although the described scoring system is more complex than the modified Mankin scores, which are recommended for some other species, the reliability study showed that it is easily understood and can be reproducibly used, even by inexperienced scorers. The scoring paradigm described here has been found to be sufficiently sensitive to discriminate between treatments and to have high reproducibility. Therefore we recommend its use for evaluation of different rat OA models as well as assessment of disease-modifying effects of treatments in these models. Copyright © 2010 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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              The formalin test in mice: dissociation between inflammatory and non-inflammatory pain.

              The formalin test in mice is a valid and reliable model of nociception and is sensitive for various classes of analgesic drugs. The noxious stimulus is an injection of dilute formalin (1% in saline) under the skin of the dorsal surface of the right hindpaw. The response is the amount of time the animals spend licking the injected paw. Two distinct periods of high licking activity can be identified, an early phase lasting the first 5 min and a late phase lasting from 20 to 30 min after the injection of formalin. In order to elucidate the involvement of inflammatory processes in the two phases, we tested different classes of drugs in the two phases independently. Morphine, codeine, nefopam, and orphenadrine, as examples of centrally acting analgesics, were antinociceptive in both phases. In contrast, the non-steroid anti-inflammatory drugs indomethacin and naproxen and the steroids dexamethasone and hydrocortisone inhibited only the late phase, while acetylsalicylic acid (ASA) and paracetamol were antinociceptive in both phases. The results demonstrate that the two phases in the formalin test may have different nociceptive mechanisms. It is suggested that the early phase is due to a direct effect on nociceptors and that prostaglandins do not play an important role during this phase. The late phase seems to be an inflammatory response with inflammatory pain that can be inhibited by anti-inflammatory drugs. ASA and paracetamol seem to have actions independent of their inhibition of prostaglandin synthesis and they also have effects on non-inflammatory pain.
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                Author and article information

                Journal
                Osteoarthritis Cartilage
                Osteoarthr. Cartil
                Osteoarthritis and Cartilage
                W.B. Saunders For The Osteoarthritis Research Society
                1063-4584
                1522-9653
                1 September 2013
                September 2013
                : 21
                : 9
                : 1336-1345
                Affiliations
                []Arthritis Research UK Pain Centre, University of Nottingham, UK
                []School of Clinical Sciences, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham NG5 1PB, UK
                [§ ]School of Biomedical Sciences, Queens Medical Centre, University of Nottingham, Nottingham NG7 2UH, UK
                Author notes
                []Address correspondence and reprint requests to: P.I. Mapp, Arthritis Research UK Pain Centre, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham NG5 1PB, UK. Tel: 44-(0)115-823-1758; Fax: 44-(0)115-823-1757. Paul.Mapp@ 123456nottingham.ac.uk
                Article
                S1063-4584(13)00891-1
                10.1016/j.joca.2013.06.031
                3790974
                23973148
                6b0db85d-874a-46a1-8e15-442ce76dc49f
                © 2013 Elsevier Ltd.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 16 January 2013
                : 19 June 2013
                Categories
                Article

                Rheumatology
                osteoarthritis,animal models,pain,inflammation,glucocorticosteroids
                Rheumatology
                osteoarthritis, animal models, pain, inflammation, glucocorticosteroids

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