Changes in circulating monocytes may contribute to pain and disease progression.
Monocyte activation plays a pivotal role in the degree of pain and disease progression associated with osteoarthritis (OA), according to researchers at McMaster University in Hamilton, Ontario, Canada.1
The study, published in Osteoarthritis and Cartilage, found that monocytes were more activated and pro-inflammatory in women with OA, and that elevated inflammation and body mass index (BMI) were associated with this increased activation.
The study included 22 women with OA, and 22 healthy age- and sex-matched controls. The researchers measured markers of soluble and cellular inflammation in the peripheral blood.
Serum C-reactive protein (CRP) levels were elevated in participants with OA, who also had a lower proportion of circulating monocytes. Increased expression of the activation markers CD16, CCR2, and HLA-DR was found in monocytes from women with OA; these monocytes induced greater production of tumor necrosis factor (TNF) and interleukin-1Î² than in healthy controls. BMI and higher serum TNF levels were correlated with increased monocyte expression of CCR2.
Implications for physicians
“It is the first study, to our knowledge, to specifically characterize changes in circulating monocytes in individuals with OA compared to healthy women,” said senior author Dawn Bowdish, a professor of pathology and molecular medicine at McMaster, and member of the McMaster Institute for Research on Aging.
“We know that changes in monocytes contribute to the development of chronic inflammatory conditions. If we can target these monocytes in OA, we may be able to slow down disease progression or decrease the risk of other chronic inflammatory diseases,” she said.
This study was supported by a grant from McMaster University’s Labarge Optimal Aging Initiative.
1. Loukov D, Karampatos S, Maly MR, Bowdish DME. Monocyte activation is elevated in women with knee-osteoarthritis and associated with inflammation, BMI and pain. Osteoarthritis Cartilage. 2017 Nov 8. pii: S1063-4584(17)31300-6. doi:10.1016/j.joca.2017.10.018. [Epub ahead of print]