| Description |
- Traumatic etiology is implicated in up to 12% of the cases of osteoarthritis in the United States. This type of arthritis, termed post traumatic osteoarthritis (PTOA), has been proposed to be mediated in part through an imbalance in inflammatory processes. Important mediators of this process are T-cells and, depending on the subtype, they can either promote or inhibit inflammation. In murine models, athymic mice deficient in T-cells have been shown to develop more severe PTOA after intraarticular fracture than control animals. Conversely, MRL/MpJ mice, a “super healer” strain, have demonstrated accelerated and improved healing in a variety of injury models including PTOA after intra-articular fracture. Lesser severe osteoarthritis (OA) develops in MRL mice after intra-articular fracture irrespective of fracture displacement. A subtype of these T-cells, called regulatory T-cells (T-regs), can suppress the activity of innate and adaptive immune cells including other T-cell subsets thereby reducing inflammation. T-regs have been shown to be a protective factor in several inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease and acute respiratory distress syndrome to name a few. FOXP3 protein (transcription factor) and CD25 (IL-2 receptor) are expressed by T-regs and can be used as cell markers8. To assess the potential importance of T-regs in development of PTOA, we sought to quantify differences in T-reg population within the synovium in B6 (native) mice versus MRL-MpJ mice following intra-articular fracture. We hypothesize that there would be a greater number T-regs as indicated by measuring the number of Foxp3 and CD25 receptor positive cells and lower histologic synovial inflammation scores in the MRL mice when compared to the B6 mice.
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