Blocking Posttraumatic Arthritis: A Way to Prevent OA?
Furman BD, Mangiapani DS, Zeitler E, et al
Arthritis Res Ther. 2014;16:R134
Furman and colleagues report their findings from a series of experiments in which they first performed an articular fracture of the knee in mice, then gave the mice an interleukin-1 receptor antagonist (IL-1ra) or soluble tumor necrosis factor receptor II either intra-articularly or systemically for 4 weeks.
They found that after the fracture, intra-articular injection of IL-1ra reduced cartilage degeneration and synovial inflammation, and did not adversely affect bone morphology. In contrast, systemic IL-1ra and local and systemic soluble tumor necrosis factor receptor II provided no benefit or were associated with increased joint damage.
They concluded that local IL-1 inhibition may be an option to prevent post-traumatic arthritis.
These are exciting findings demonstrating that intra-articular IL-1 inhibition can diminish the progression of post-traumatic arthritis. This provides information about the role that IL-1 may play in this process, as well as a potential avenue for treatment to prevent post-traumatic arthritis. These experiments will need to be expanded and ultimately done in humans.
Furthermore, the potential benefit in osteoarthritis (which may ultimately be a form of post-traumatic arthritis on a smaller and more persistent scale) will need to be explored. For example, Sharma and colleagues recently reported that baseline MRI abnormalities of the knee predicted future joint symptoms and MRI progression of disease. Could patients with early joint damage be identified with MRI and then be targeted with IL-1 inhibition, perhaps along with other approaches (eg, gait improvement), to prevent worsening of the disease? We will need more data to answer that question, but it is exciting to envision that ultimately, such approaches may be useful to prevent progression of post-traumatic arthritis as well as osteoarthritis.
Targeting Pro-inflammatory Cytokines Following Knee Injury: Acute Intra-articular Inhibition of Interleukin-1 Following Knee Injury Prevents Post-traumatic Arthritis
Furman BD, Mangiapani DS, Zeitler E, et al
Arthritis Res Ther. 2014;16:R134
Study Summary
Furman and colleagues report their findings from a series of experiments in which they first performed an articular fracture of the knee in mice, then gave the mice an interleukin-1 receptor antagonist (IL-1ra) or soluble tumor necrosis factor receptor II either intra-articularly or systemically for 4 weeks.
They found that after the fracture, intra-articular injection of IL-1ra reduced cartilage degeneration and synovial inflammation, and did not adversely affect bone morphology. In contrast, systemic IL-1ra and local and systemic soluble tumor necrosis factor receptor II provided no benefit or were associated with increased joint damage.
They concluded that local IL-1 inhibition may be an option to prevent post-traumatic arthritis.
Viewpoint
These are exciting findings demonstrating that intra-articular IL-1 inhibition can diminish the progression of post-traumatic arthritis. This provides information about the role that IL-1 may play in this process, as well as a potential avenue for treatment to prevent post-traumatic arthritis. These experiments will need to be expanded and ultimately done in humans.
Furthermore, the potential benefit in osteoarthritis (which may ultimately be a form of post-traumatic arthritis on a smaller and more persistent scale) will need to be explored. For example, Sharma and colleagues recently reported that baseline MRI abnormalities of the knee predicted future joint symptoms and MRI progression of disease. Could patients with early joint damage be identified with MRI and then be targeted with IL-1 inhibition, perhaps along with other approaches (eg, gait improvement), to prevent worsening of the disease? We will need more data to answer that question, but it is exciting to envision that ultimately, such approaches may be useful to prevent progression of post-traumatic arthritis as well as osteoarthritis.
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