Sub-chondral RA bone erosion explored | Arthritis Information

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Annals Rheum Dis 2008; Advance online publication

 Bone erosion in patients with rheumatoid arthritis (RA) is not limited to synovial tissue and is probably a consequence of increased osteoclast production and RANKL expression in sub-chondral bone regions, researchers in New Zealand believe.

The advent of magnetic resonance imaging (MRI) revealed that RA is a disease that affects not just synovial tissues but also sub-chondral bone.

Sub-chondral changes can be seen on MRI scans as bone edema, which Nicola Dalbeth (University of Auckland) and co-workers say is "clinically important as it frequently presents in patients with early disease and is a key predictor of plain radiographic erosive joint damage."

For the current study, Dalbeth and team aimed to gain a better understanding of the form bone edema takes in RA and to more exactly define the link between bone edema and erosion.

To do this, the researchers used immunohistochemistry and MRI techniques to study 28 bones in 11 individuals with RA.

As published in the Annals of the Rheumatic Diseases, the bones of individuals showing edema had a significantly higher osteoclast density than the bones of those without edema, suggesting higher bone resorption in those with edema (0.1 vs 3.35 osteoclasts per field of vision).

RANKL expression was also significantly higher in bone samples taken from patients with than those without edema (RANKL score 1.0 vs 2.0). Of note, this increased RANKL expression was linked to the increase in osteoclast number associated with edema.

"This study is the first to histologically characterize the cellular composition of MRI bone edema in RA," the investigators summarize.

The authors acknowledge that their findings are limited by the small size of the study, but conclude that, "despite these limitations, this work has provided insights into the mechanisms of bone damage in RA, implicating chronic inflammation and RANKL-induced osteoclastogenesis within bone marrow.

"These findings support the hypothesis that bone erosion in RA occurs through activation of local bone resorption mechanisms within sub-chondral bone as well as through synovial invasion into bone," they add.

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