Inflammatory arthritis spans a number of diseases. The most prevalent is rheumatoid arthritis (RA). Others include psoriatic arthritis (PsA), reactive arthritis, ankylosing spondylitis (AS) and arthritis in patients with inflammatory bowel disease (IBD).

A number of disorders in which inflammatory arthritis is sometimes seen, are not usually considered to be a part of the inflammatory arthropathies. These disorders include:

The known causal factors for inflammatory arthritis include genetic risks (particularly in RA and AS), exposure to infection (particularly in reactive arthritis), environmental factors (particularly smoking in RA) and demographic factors (such as age and sex). Most of the diseases are thought to involve autoimmune triggers and immunological mechanisms. There has been extensive speculation about the roles of infective or viral triggers, but no firm conclusions have been reached.

Treatment of these disorders is broadly similar. All respond to symptomatic treatment with analgesics and anti-inflammatory drugs. DMARDs and biologics are often used to both improve symptoms and reduce arthritis disease activity. Non-pharmacological therapies such as exercise and physiotherapy are also recommended. The similar management of these diseases is the main reason for considering them together under the umbrella term of “inflammatory arthropathies”.

The spondyloarthropathies are best considered to form a spectrum of diseases characterised by several key features comprising enthesitis, iritis, spinal involvement, the presence of HLA-B27 and absence of rheumatoid factor (RF). Overlap between these disorders is common with many AS patients having microscopic colitis on colonic biopsy. To an extent it is the presence of associated features outside the joints (termed extra-articular features) that differentiates them. However, in many patients it may be difficult to tell them apart, and often they are considered to be undifferentiated.

Most types of inflammatory arthritis were identified in the nineteenth century, though their exact classification was only finalised in the last 50 years. Prior to 1850 there was considerable uncertainty about how to differentiate different forms of arthritis, and a number of complex, somewhat confusing names were used, such as chronic rheumatic gout. Rheumatic fever, which was commonplace at that time, also caused considerable uncertainly.

The concept of “rheumatoid arthritis” dates from Victorian times and the term was introduced by Sir Archibald Garrod, an academic clinician in London, to distinguish the disease from gout and rheumatic fever. It took many years before the term RA achieved universal recognition. It was not officially taken up by the Empire Rheumatism Council until the 1920s and by the American Rheumatism Association in the 1940s.

The roots of seronegative arthritis can be traced back further to antiquity. AS was present in ancient Egypt and has been identified in mummified remains. There is evidence that several pharaohs including Rameses II (“The Great”, 1290–1221BC) had AS. PsA may also have been an ancient disease; skeletons from early Christian society, in a fifth century AD Byzantine monastery in the Judean Desert contained features of PsA. Reactive arthritis has a more recent provenance. Although there have been suggestions that Christopher Columbus may have had reactive arthritis, this is speculative. It was first noted associated with venereal disease at the end of the eighteenth century. These disorders were often “rediscovered”. There are several good examples from the 1914–1918 European war. In 1916, two French physicians, Fiessinger and Leroy described four cases of conjunctivitis and arthritis after diarrhoeal illness. The same year Reiter reported a young officer in the Balkan front who after acute diarrhoea developed arthritis, urethritis and conjunctivitis.