Download PDFPDF
Animal models for arthritis: innovative tools for prevention and treatment
Compose Response

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g.
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests


  • Responses are moderated before posting and publication is at the absolute discretion of BMJ, however they are not peer-reviewed
  • Once published, you will not have the right to remove or edit your response. Removal or editing of responses is at BMJ's absolute discretion
  • If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patient's written consent to publication and send them to the editorial office before submitting your response [Patient consent forms]
  • By submitting this response you are agreeing to our full [Response terms and requirements]

Vertical Tabs

Other responses

  • Published on:
    Bone appearance in human tumor necrosis factor transgenic mice model: A model of rheumatoid arthritis or of hyperparathyroidism?

    Dear Editor,

    Kollias et al. [1] presented an eloquent discussion of animal models of arthritis, remarking on their imperfect modeling of rheumatoid arthritis.
    Among the models discussed was the human tumor necrosis factor (TNF) transgenic mice model. Examination of images of bone damage2 in this model3 suggested a previously unrecognized, intriguing effect/role of TNF. We use the phrase bone damage, as the most imp...

    Show More
    Conflict of Interest:
    None declared.