Grading of monosodium iodoacetate-induced osteoarthritis reveals a concentration-dependent sensitization of nociceptors in the knee joint of the rat

Schuelert, Niklas; McDougall, Jason J.

doi:10.1016/j.neulet.2009.08.063

Cited by 115 publications

(94 citation statements)

References 27 publications

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“…These models include single injections in the knee of inflammatory agents, immunotoxins, collagenase, papain, or monoiodoacetate, which can be toxic if they escape the joint space. Of all chemical models of OA, MIA is the one most often used, particularly to test the efficacy of pharmacologic agents to treat pain, as this model generates a reproducible, robust, and rapid pain-like phenotype that can be graded by altering MIA dosage [11][12][13][14][15] . Intra-articular injection of MIA in rodents reproduces OA-like lesions and functional impairment that can be analyzed and quantified.…”

Section: Introductionmentioning

confidence: 99%

The Monoiodoacetate Model of Osteoarthritis Pain in the Mouse

Pitcher

Valente

Malcangio

2016

JoVE

108

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A major symptom of patients with osteoarthritis (OA) is pain that is triggered by peripheral as well as central changes within the pain pathways. The current treatments for OA pain such as NSAIDS or opiates are neither sufficiently effective nor devoid of detrimental side effects. Animal models of OA are being developed to improve our understanding of OA-related pain mechanisms and define novel pharmacological targets for therapy. Currently available models of OA in rodents include surgical and chemical interventions into one knee joint. The monoiodoacetate (MIA) model has become a standard for modelling joint disruption in OA in both rats and mice. The model, which is easier to perform in the rat, involves injection of MIA into a knee joint that induces rapid pain-like responses in the ipsilateral limb, the level of which can be controlled by injection of different doses. Intra-articular injection of MIA disrupts chondrocyte glycolysis by inhibiting glyceraldehyde-3-phosphatase dehydrogenase and results in chondrocyte death, neovascularization, subchondral bone necrosis and collapse, as well as inflammation. The morphological changes of the articular cartilage and bone disruption are reflective of some aspects of patient pathology. Along with joint damage, MIA injection induces referred mechanical sensitivity in the ipsilateral hind paw and weight bearing deficits that are measurable and quantifiable. These behavioral changes resemble some of the symptoms reported by the patient population, thereby validating the MIA injection in the knee as a useful and relevant pre-clinical model of OA pain.The aim of this article is to describe the methodology of intra-articular injections of MIA and the behavioral recordings of the associated development of hypersensitivity with a mind to highlight the necessary steps to give consistent and reliable recordings.

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Section: Introductionmentioning

confidence: 99%

The Monoiodoacetate Model of Osteoarthritis Pain in the Mouse

Pitcher

Valente

Malcangio

2016

JoVE

108

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“…Intra-articular injection leads to the destruction of chondrocytes in rodents and non-rodents. When it is used in rodent, cartilage lesions with loss of proteoglycan matrix and functional changes with stiffness similar to those observed in human osteoarthritis, are produced 10,11 . Given the importance of the synovial membrane and subchondral bone in the pathogenesis of joint pain in osteoarthritis, many experimental studies have been published with monosodium iodoacetate, but most of them only evaluated histopathological and radiological aspects, and not functional ones.…”

Section: Introductionmentioning

confidence: 99%

Osteoarthritis model induced by intra-articular monosodium iodoacetate in rats knee

et al. 2016

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PURPOSE:To evaluate the usefulness of a knee osteoarthritis model through functional, radiological and microscopic changes of the synovial membrane. METHODS:Forty eight rats were divided randomly into two groups. The first received 0.9% saline in the joint and corresponded to the control group. The second was submitted to experimental osteoarthritis of the right knee induced by monosodium iodoacetate and corresponded to the osteoarthritis group. All animals were subjected to comparative tests of forced ambulation and joint movements, inability to articulate and tactile allodynia on day 1 post-experiment by forced ambulation (Roto-rod test), joint assessment of disability (weight bearing test) and assessment of tactile allodynia (Von Frey test). After inflammatory induction they were divided into four subgroups corresponding to the scheduled death in 7, 14, 21 and 28 days when they were submitted to radiographic examination of the knee, arthrotomy and collection of the synovial membrane. RESULTS:The osteoarthritis group showed significant differences compared to control group on days 7 and 14 in Roto-rod, in weight bearing and Von Frey tests in all days, and in radiological evaluation. Microscopic examination of the synovial membrane showed abnormalities of inflammatory character at all stages. CONCLUSION:The osteoarthritis induced by intra-articular monosodium iodoacetate in rats knee is a good model to be used in related research, because it provides mensurable changes on joint movements, tactile allodynia, progressive radiological degeneration and microscopic inflammation of the synovial membrane, that represent markers for osteoarthritis evaluation

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“…Hence, the use of electrophysiological recordings of nerve fibers has helped provide direct insight into the underlying nociceptive processes. Electrophysiological recordings of the firing frequency of primary afferent nerve fibers from the rat knee joint in response to normal and noxious rotation was shown to be higher in animals that had received MIA, and there was a direct relationship between the dose of MIA and the sensitivity of the nerve fibers [139]. This in turn appeared to correlate with the dosedependent increases in joint destruction and pain scores that were observed in this model.…”

Section: Enzymatic and Chemical Models Of Oamentioning

confidence: 73%

A Review of Current Animal Models of Osteoarthritis Pain

D’Souza

Ng²,

Youngblood³

et al. 2011

CPB

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Osteoarthritis (OA) is a complex disease plagued by a significant unmet need for treatment. To date, no disease- modifying OA drugs (DMOADs) exist and the available symptom-modifying OA drugs (SMOADs) have limitations. Although a complete understanding of the mechanisms of OA pain in humans is lacking, animal models have helped provide insight into the multifaceted origin and manifestation of OA pain. Success in discovering new therapeutics will likely require reliance on good animal models. This review summarizes the animal models available for studying pain associated with OA.

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Grading of monosodium iodoacetate-induced osteoarthritis reveals a concentration-dependent sensitization of nociceptors in the knee joint of the rat

Cited by 115 publications

References 27 publications

The Monoiodoacetate Model of Osteoarthritis Pain in the Mouse

The Monoiodoacetate Model of Osteoarthritis Pain in the Mouse

Osteoarthritis model induced by intra-articular monosodium iodoacetate in rats knee

A Review of Current Animal Models of Osteoarthritis Pain

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