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No Clear Connection Between Inflammation & Disease Progression in AS

  |  Issue: October 2010  |  

Mean change in mSASSS from baseline to two years was 0.8 for the patients treated with adalimumab and 0.9 for those who had not received the TNF blocker, a non-statistically significant difference.4 The same was found in other trials that compared radiographic progression between patients treated with a TNF blocker and patients in the OASIS cohort, Dr. van der Heijde said.

Even though there was no effect on structural damage, there were “striking effects of MRI activity of the spine,” leading to questions about whether this contributes to formation of syndesmophytes, she said.

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Three independent studies have looked at this correlation, with all patients given an MRI at baseline and over time. The MRI looked at the vertebral edge, with analysis of each vertebra as an independent unit.

Results showed that formation of new syndesmophytes is rare at sites with inflammation. “If there is a syndesmophyte, the majority are not associated with inflammation,” Dr. van der Heijde said.

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“What we know now about TNF blockers is that they don’t seem to inhibit structural damage,” she continued. “However, it is still good to use them because they are effective on symptoms and signs of the disease,” and on functioning, spinal mobility, quality of life, inflammation as assessed on MRI, and bone mineral density.

Using Mouse Models

Rik Lories, MD, PhD, of the division of rheumatology at the Laboratory for Skeletal Development and Joint Disorders in KU Leuven, Belgium, said that progression of AS is characterized by spine or joint ankylosis due to new cartilage and bone formation that originates from extra- or intraarticular entheses.

His research has used mouse models of AS to understand the mechanisms of new bone formation in spondyloarthritides (SpAs). Dr. Lories and colleagues have proposed that bone morphogenetic protein is a critical player in the early phases of ankylosis in SpA and that WNT signaling through beta-catenin plays a crucial supportive role in this process, in particular in the progression of endochondral bone formation.

Their research, reported in Arthritis Research and Therapy, has culminated in an hypothesis about how the disease develops. “Activation of entheseal cells could lead to a double phenomenon: triggering of new tissue formation and production of proinflammatory molecules. The former can lead to restoration of tissue integrity or tissue remodeling. The latter phenomenon can develop into a chronic inflammatory process in which cytokines such as TNF play a pivotal role,” Dr. Lories and colleagues noted.

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