Musculotendinous Inflammation: The Defining Pathology of Polymyalgia Rheumatica?

Abstract

Despite being the most common inflammatory rheumatic disease of the elderly, and despite significant scientific breakthroughs in the related condition giant cell arteritis (GCA), the paradigm of polymyalgia rheumatica (PMR) has failed to progress beyond its earliest descriptions as a glucocorticoid-responsive syndrome of shoulder and pelvic girdle pain and stiffness. In the absence of a gold standard test, diagnosis is based on laboratory evidence of systemic inflammation and the exclusion of other relevant differentials. Ultrasound findings including subacromial bursitis, biceps tenosynovitis, and glenohumeral synovitis at the shoulders, and synovitis and trochanteric bursitis at the hips, improve the specificity of clinical classification criteria1. However, the precise pathology underpinning PMR remains unclear2. A mild synovitis with CD4+ T cell and macrophage infiltration characterizes arthroscopic biopsies taken from the glenohumeral joints of patients with PMR, while histopathologic studies of muscle have consistently revealed only minor immunologic abnormalities3,4. Such uncertainty surrounding disease pathophysiology has undoubtedly hindered therapeutic advances in PMR, with the majority of patients still condemned to longterm prednisolone treatment and its attendant glucocorticoid-related complications.\n\nModern advances in our understanding of PMR as a distinct disease entity have come largely courtesy of imaging. McGonagle, et al first reported an anatomical difference in the distribution of inflammation in their magnetic resonance imaging (MRI) study contrasting the shoulders of PMR and rheumatoid arthritis (RA) patients5. Extracapsular soft tissue edema differentiated the PMR group from its RA counterpart, whereas bursitis, tenosynovitis, and joint effusion did not. A subsequent study by the same authors investigating MRI findings at the metacarpophalangeal joints in PMR and RA similarly documented comparable rates of synovitis, tenosynovitis, and even bone erosions, with a much greater degree of gadolinium-enhancement noted in the extracapsular soft tissues of patients with PMR6. More recently, … \n\nAddress correspondence to Dr. C.E. Owen, Rheumatology Department, Austin Health, Repatriation Campus, Level 1, North Wing, 300 Waterdale Road, Heidelberg West, Victoria, Australia 3081. E-mail: claire.owen{at}austin.org.au