Entheseal inflammation is a hallmark feature of spondyloarthritis (SpA). New bone formation is thought to be part of the pathogenesis of joint damage and ankylosis in SpA. A progression from enthesitis to new bone formation and joint damage has been postulated but is difficult to assess as a process in vivo. Conventional radiography cannot visualize tendons, and MRI may be less sensitive in detecting small calcifications than ultrasound (US). The aim of this study was to assess development of enthesitis in vivo using serial high resolution US.
144 images and video clips of 8 clinically symptomatic and sonographically abnormal entheses in 7 patients with SpA (psoriatic arthritis, n=4; reactive arthritis, n=2; ankylosing spondylitis (AS), n=1) were obtained over 2 years (long and short axis views in gray scale and power Doppler, and video clips to document pulsatile flow). The 8 entheses included: origin of patellar ligament: n=3; insertion of Achilles tendon, n=4; insertion of medial collateral ligament of first metatarsophalangeal joint, n=1. US criteria for enthesitis were: 1) cortical irregularity at interface of ligament or tendon and bone; 2) pulse synchronous Doppler signal at interface and within body of tendon or ligament; 3) loss of densely packed fibrillar pattern with decrease of hyperechogenicity and increased thickness of tendon or ligament at insertion or origin (edema). Criterion for entheseal new bone formation was: hyperechoic material within body of tendon or ligament that was not seen on prior studies. All studies were performed by a rheumatologist certified in musculoskeletal ultrasound, with 20 years' experience. Transducer frequencies of 10-18 MHz were used. All patients underwent treatment: NSAIDs alone, n=1; methotrexate and NSAIDs, n=1, methotrexate and TNF-inhibitor, n=5.
Inflammatory changes by US criteria decreased in all 8 entheses followed after 15-24 months: No more Doppler signal was seen at the entheses, hypoechogenicity and thickness had decreased in all at the time of the last study. CRP and ESR levels had remained within normal limits in all patients throughout the observation period, and were not suitable as markers of entheseal inflammation in our patients. Clinical entheseal pain was present in all at study entry and none at the time of the last US study. Newly formed hyperechoic material was eventually seen in all entheses (mean time to development 17 months). This calcific appearing material was present at the site of previously seen Doppler signal in all cases (Figure). In the case of AS, enthesitis led to calcification of a collateral ligament.
Conclusion: Within entheses, sites of deposition of calcified material correlate with sites of prior hyperemia. In AS, enthesitis preceded collateral ligament calcification in our study. Serial US can document disease development from enthesitis to new bone formation.
Disclosure: R. G. Thiele, None; B. A. Marston, None; D. Tabechian, None; A. P. Anandarajah, None; C. T. Ritchlin, None.