An evaluation of prophylactic treatments to prevent post-traumatic joint stiffness.
Efird W, Kellam P, et al. J Orthop Res. 2014;32(11):1520-4. doi: 10.1002/jor.22700.
Take Home Message: Three agents that target different aspects of the inflammatory pathways decreased joint stiffness after joint trauma in rats.
Arthrofibrosis and joint stiffness are problems for many patients who experience serious joint trauma, and so far no prophylactic treatments for joint stiffness have been identified. Without a preventative option, many patients must undergo surgical intervention to treat the stiffness after it occurs. Identifying a safe and effective prophylaxis to alter the inflammatory pathways and prevent joint stiffness in susceptible patients is an ideal conservative therapy option. The purpose of this animal study was to examine three therapeutic agents to assess prophylactic treatment (i.e. prevention) of arthrofibrosis by inhibiting components in the inflammatory process. The researchers used montelukast, a leukotriene inhibitor, forskolin, a transforming growth factor-beta1 blocker, and triamcinolone acetonide, a corticosteroid. Surgery was performed on 48 male rats; the right patella was laterally dislocated and repaired with a pro-inflammatory suture and immobilized in full flexion. The rats were placed into four treatment groups after surgery including the control group that received no prophylaxis. The montelukast group received 3.75 mg/kg/day in their food. The forskolin and corticosteroid group received two injections. The forskolin and corticosteroid groups received injections one day and four days after the operation. Two weeks after the surgery, the rats were euthanized and the researchers used radiographs to measure the femorotibial angle. During the femorotibial angle measurement, the joint capsule was intact but both cruciate ligaments and the posterior joint capsule had been cut. All animals who received an intervention showed less contracture than the control group. The corticosteroid group had less contracture than the montelukast and forskolin groups, developing only a 7° loss of extension. The corticosteroid group formed less contracture than all other groups. In conclusion, all three interventions caused reductions in joint stiffness, but the corticosteroid was the most effective agent.
This study highlights the possibility that targeting inflammatory pathways may reduce the risk of post-traumatic joint stiffness. Animals in the corticosteroid group formed the least amount of contracture but experienced unwanted weight loss as a side effect. A human dose of triamcinolone acetonide would be small enough to avoid these potential adverse effects. Now that we see evidence that we can reduce post-traumatic joint stiffness with these interventions, it would be useful to see more studies that help us understand dose-response interactions to achieve a greater decrease in joint contracture. It may be pertinent for athletes seeking treatment for joint stiffness to have either forskolin or montelukast perfected as a treatment option in humans, to avoid unnecessary use of corticosteroids. It may also be informative if future studies examine how these interventions influence healing after various types of injury. Implementing these drug therapies effectively may lead to fewer patients underging surgical intervention to decrease joint contracture and stiffness following joint trauma.
Questions for Discussion: Do you know any other treatments that would be effective to decrease joint contractures and joint stiffness? Have any of your patients used these similar drug therapies to prevention joint stiffness?
Written by: Kristin Gibson and Daniel Clark
Reviewed by: Kim Pritchard