SEATTLE – C-reactive protein is associated with the presence and progression of bone marrow lesions in patients with osteoarthritis of the knee, according to data from a cohort study of 192 patients that were reported at the World Congress on Osteoarthritis.
“Osteoarthritis has predominantly been viewed as a degenerative joint disease driven by continued and irreversible deterioration of joints,” said lead investigator Zhaohua (Alex) Zhu, a PhD candidate at the Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia. “However, current studies suggest a different way of understanding this disease, showing that the development of osteoarthritis may be in great part driven by a low-grade inflammatory process.”
Zhaohua (Alex) Zhu
He and his colleagues analyzed data from the randomized phase III VIDEO trial (Vitamin D Effect on Osteoarthritis), which enrolled patients aged 50-79 years who had symptomatic knee osteoarthritis and vitamin D deficiency. Analyses were based on 192 patients who had measurement of high-sensitivity C-reactive protein (CRP) and resistin (a proinflammatory cytokine secreted by adipose tissue) at baseline and again 2 years later.
Bone marrow lesions also were assessed at both time points with a modified version of the whole-organ magnetic resonance imaging score (WORMS). “Bone marrow lesions may represent areas of edema, inflammation, and remodeling,” Mr. Zhu explained. “Plenty of studies have shown that bone marrow lesions are linked to knee pain, cartilage volumes, and cartilage defect changes, so it’s a very important subchondral feature in knee osteoarthritis. But so far, the cause of bone marrow lesions remains unclear.”
Multivariate analyses showed that, as patients’ baseline CRP quartile increased, so did their odds of having total knee bone marrow lesions at that time (odds ratio, 1.45) and worsening of these lesions during follow-up (odds ratio, 1.56), according to data reported at the meeting, which was sponsored by the Osteoarthritis Research Society International. Additionally, the absolute change in CRP level during follow-up was positively associated with a worsening of lesions.
Associations for resistin were generally weaker or absent, with the only significant one seen between baseline quartile of that marker and bone marrow lesions at that time, reported Dr. Zhu.
In an interview, Dr. Timothy McAlindon, one of the session’s comoderators and professor of medicine at Tufts University in Boston, said that the study helps elucidate a possible role for adipose tissue, overweight, and adipocytokines in one subphenotype of osteoarthritis. “They found some associations, and I think those associations are probably the basis for further study and hopefully more understanding of what they mean,” he commented.
Dr. Rik Lories, the other session comoderator and professor at the University of Leuven (Belgium), noted that research on this topic is complicated. “You can ask questions about the chicken and the egg in this case because, if you are obese, you have a higher fat mass, so you are more likely to produce proinflammatory mediators, which can then induce your CRP. The fact that you have more inflammatory mediators could also contribute to the fact that you get these bone marrow lesions,” he elaborated. “But on the other hand, if you put more weight on your knees, the impact may also play a role. So it remains a very, very difficult thing to study and to come up with clear answers.”
Dr. Zhu disclosed no relevant conflicts of interest.