To the Editors:

We are delighted to have the opportunity to respond to Dr. Falsetti and colleagues. They provide interesting additional insight into the pathophysiology of shoulder pain in the spondylarthropathies. Their experience with ultrasound has revealed observations in the soft tissues similar to our own, particularly at the deltoid insertion on the scapular spine and acromion process. We agree that the sensitivity of MRI to inflammatory changes in bone marrow is the likely explanation for the higher prevalence of enthesopathy observed in our population. We also agree that the relatively long disease duration could be a contributing factor to the higher prevalence of both the entheseal changes and the rotator cuff abnormalities that were identified in our patients, although it was not possible to determine the actual duration of shoulder symptoms.

The distribution of fibrocartilage (most pronounced in the origin of the posterior limb and least pronounced at the clavicular origin) is an observation that lends further credence to the current hypothesis that the inflammatory basis of the spondylarthropathies might reflect immunity to fibrocartilage. Although not expressly specified within our publication, we also did not observe any soft tissue or bone marrow abnormality at the distal diaphyseal insertion of the deltoid or the shaft of the humerus.

We concur with the proposition that deltoid acromial enthesopathy is likely a hallmark of all spondylarthropathies and not only of AS, and that patients with this underlying condition and shoulder symptoms may very well benefit from cross-sectional imaging (ultrasound or MRI) to fully assess the many structures that can be a source of symptoms in this population.

Robert G. Lambert FRCP(C)*, Walter P. Maksymowych FRCP(C)*, * University of Alberta, Edmonton, Alberta, Canada.