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Article summary:

1. Osteoarthritis (OA) is a structural and symptomatic disease that has been difficult to study due to the lack of reliable tools.

2. Pain in OA is variable, with some individuals presenting with pain and little change on X-ray, while others present after considerable damage has occurred.

3. Rodent models of OA have been used to study pain behaviour, including monosodium iodoacetate (MIA) and surgical destabilisation of the joint models.

Article analysis:

The article provides an overview of peripheral pain mechanisms in osteoarthritis, discussing the difficulty in studying structural and symptomatic disease due to the lack of reliable tools, as well as the course of pain in human OA and rodent models used to study pain behaviour. The article is generally well-written and provides a comprehensive overview of the topic, however there are some potential biases that should be noted.

First, the article does not provide any evidence for its claims about the difficulty in studying structural and symptomatic disease due to lack of reliable tools or about the course of pain in human OA. This could lead readers to believe that these claims are true without any supporting evidence or research backing them up. Additionally, there is no discussion about possible counterarguments or alternative perspectives on this topic which could lead readers to form one-sided opinions on this issue.

Second, there is no mention of potential risks associated with using rodent models for studying pain behaviour in OA which could lead readers to believe that these methods are safe without considering any potential risks involved. Furthermore, there is no discussion about how these methods may be limited or biased which could lead readers to form an overly positive opinion on their use without considering any potential drawbacks or limitations associated with them.

Finally, there is no mention of other methods for assessing central sensitisation such as qualitative pain questionnaires which could lead readers to believe that quantitative sensory testing is the only method available when this may not be true. Additionally, there is no discussion about how these methods may be limited or biased which could lead readers to form an overly positive opinion on their use without considering any potential drawbacks or limitations associated with them.

In conclusion, while this article provides a comprehensive overview of peripheral pain mechanisms in osteoarthritis, it does not provide sufficient evidence for its claims nor does it explore alternative perspectives or discuss potential risks associated with using rodent models for studying pain behaviour in OA which could lead readers to form one-sided opinions on this issue without considering all sides equally.