Twenty years ago, Verna Wright commented, “clinicians may all too easily spend years writing ‘doing well’ in the notes of patients who become progressively more crippled before their eyes.” Thankfully much of this has changed. Clinicians increasingly understand the advantages of early intervention, particularly in inflammatory joint diseases,1 ,2 and we now have better, more targeted treatments. During this time, however, our methods of objectively assessing and quantifying joint damage have remained largely unchanged. As a result, it is likely that early joint damage in patients goes undetected and untreated.

Although magnetic resonance imaging initially promised much, it has delivered little outside highly specialised centres, where software, coils, and scan sequences change with every passing season. The “gold standard” for assessing joint damage is still the plain radiograph. This mainly images only the bone and is insensitive to change, with reliable differences requiring at least 12 months to evolve. The scoring of radiographs is also time consuming and it does not lend itself to routine monitoring. Importantly, all imaging techniques also only provide a historical view of damage that has already occurred. Even after repeated measures, they are of limited use in informing the clinician of continuing or future damage. Existing serological measures, such as erythrocyte sedimentation rate or C reactive protein, also fall short of requirements.3 They are neither specific to joint disease nor of much use in non-inflammatory conditions. Known genetic and environmental factors that have been associated with various arthritic diseases might also be considered to be markers, but they are often not modifiable nor do they provide any direct information on the extent of joint disease. There is an urgent need for reliable, quantitative, and dynamic tests that will detect damage early and allow the response of treatments targeted at joint destruction to …