Response to ‘Interspinous bursitis is common in polymyalgia rheumatica, but is not associated with spinal pain’

In a recent contribution to this journal,Camellino and colleagues 1] reported that asymptomatic inflammation of the interspinous bursas is a common occurrence
in patients with polymyalgia rheumatica. Thus, they confirm the findings of three
other studies which found florid inflammation (which was felt to be symptomatic) at
these sites between the spinous processes of adjacent vertebrae. Why would this be
so when bursitis at more accessible locations is not recognized as a part of this
syndrome? One possible explanation might be found in the proximity of each interspinous
bursa to its adjacent ligamentum flavum 2]. If the fundamental process is an auto-immune response to elastic tissue, then this
most elastic of all anatomical structures would be an appropriate target and a ‘sympathetic
effusion’ might be expected in adjacent tissues such as the interspinous bursas.

A similar situation could explain the characteristic synovitis of large joints in
polymyalgia. There, scanning techniques demonstrate an unequivocal inflammatory cause
for the joint pain and stiffness, but the effusions are small, synovial fluid findings
are unimpressive, and the synovitis is not destructive. This, too, could represent
an immune response to aging elastic tissue of the joint capsule with the synovitis
being secondary.

Possible elastic antigenicity is not a new idea in giant cell arteritis 3]. Localization of inflammatory cells around the internal elastic laminas of temporal
artery biopsies was prominent from the first recognition of this entity and remains
so today 4]. Apparent elastic fragments within giant cells, immunoglobulin deposits adjacent
to the internal elastic lamina, proliferative responses of lymphocytes to arterial
tissue in vitro, and a striking response of mononuclear cells to elastin peptides all lend support
to this idea, although none of these findings have been replicated convincingly 5].

Polymyalgia rheumatica can be excruciating, giant cell arteritis can be lethal, and
both conditions respond dramatically to appropriate therapy. Yet their diagnosis can
be difficult, and their common link has not been found. Confirmation of elastic antigenicity
would provide much-needed understanding of the basic pathophysiology and could thereby
facilitate both diagnosis and management. Does not someone want to take another look
at the possibility that these findings and concepts may be held together with an elastic
band?