Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Introduction: B27-associated diseases.

D A Brewerton1

  • 1Department of Therapeutics, Charing Cross and Westminster Medical School, London, U.K.

Scandinavian Journal of Rheumatology. Supplement
|January 1, 1990
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Echocardiographic diastolic abnormalities of the left ventricle in inflammatory joint disease.

Annals of the rheumatic diseases·1991
Same author

Regional distribution of mast cells and peptide containing nerves in normal and adjuvant arthritic rat synovium.

The Journal of rheumatology·1991
Same author

Increased calcitonin gene-related peptide (CGRP), substance P, and enkephalin immunoreactivities in dorsal spinal cord and loss of CGRP-immunoreactive motoneurons in arthritic rats depend on intact peripheral nerve supply.

Journal of molecular neuroscience : MN·1991
Same author

Nerves in inflammatory synovium: immunohistochemical observations on the adjuvant arthritis rat model.

The Journal of rheumatology·1990
Same author

Polymorphonuclear leucocyte motility in men with ankylosing spondylitis.

Annals of the rheumatic diseases·1989
Same author

Ankylosing spondylitis without B27: no evidence for gene conversion.

Annals of the rheumatic diseases·1988
Same journal

How should impaired morning function in rheumatoid arthritis be treated?

Scandinavian journal of rheumatology. Supplement·2011
Same journal

Morning stiffness and other patient-reported outcomes of rheumatoid arthritis in clinical practice.

Scandinavian journal of rheumatology. Supplement·2011
Same journal

How should morning function in rheumatoid arthritis be assessed? Bibliographic study of current assessment.

Scandinavian journal of rheumatology. Supplement·2011
Same journal

How much is a reduction in morning stiffness worth to patients with rheumatoid arthritis?

Scandinavian journal of rheumatology. Supplement·2011
Same journal

Impact of impaired morning function on the lives and well-being of patients with rheumatoid arthritis.

Scandinavian journal of rheumatology. Supplement·2011
Same journal

Morning symptoms in rheumatoid arthritis: a defining characteristic and marker of active disease.

Scandinavian journal of rheumatology. Supplement·2011
See all related articles

This study proposes a ten-mechanism hypothesis for the cause of inflammatory arthritis, including ankylosing spondylitis and rheumatoid arthritis. It then discusses ten clinical issues and poses four questions for clinicians.

Area of Science:

  • Rheumatology
  • Immunology
  • Pathophysiology

Background:

  • Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and rheumatoid arthritis are distinct inflammatory arthropathies.
  • Understanding the precise causation of these conditions remains a significant clinical challenge.

Purpose of the Study:

  • To present a novel hypothesis for the unified causation of four major inflammatory arthritis types.
  • To stimulate discussion on ten key clinical issues arising from this hypothesis.
  • To articulate four critical questions from a clinical perspective.

Main Methods:

  • A hypothesis outlining ten fundamental causative mechanisms was developed.
  • Ten distinct clinical issues were identified and presented for discussion.
  • Four questions were formulated based on clinical observations and the proposed hypothesis.

Related Experiment Videos

Main Results:

  • A comprehensive hypothesis for the pathogenesis of ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and rheumatoid arthritis is detailed.
  • Ten clinically relevant issues are presented, supported by existing evidence.
  • Four pertinent questions are posed to advance clinical understanding and management.

Conclusions:

  • The proposed hypothesis offers a framework for understanding the shared and distinct mechanisms in inflammatory arthritis.
  • Further clinical discussion and research are warranted to validate the proposed mechanisms and address the posed questions.
  • Bridging basic science and clinical practice is essential for improving patient outcomes in inflammatory arthritis.