POSTTRAUMATIC JOINT CONTRACTURES IN A RABBIT MODEL: TESTING THE MAST CELL - MYOFIBROBLAST AXIS

Michael Monument, M.D.
Calgary, AB

K. Hildebrand

Background: The elbow is quite vulnerable to chronic posttraumatic contracture formation and in the setting of a congruent articular surface, the joint capsule is the critical causal agent of contracture. Capsular tissue becomes fibrotic, characterized by elevated numbers of myofibroblasts and altered collagen production.  This parallels other fibrotic conditions such as Dupytrens' contracture, pulmonary fibrosis and idiopathic frozen shoulder. There is an abundance experimental evidence suggesting that mast cell activity is linked to myofibroblast differentiation and increased mast cells counts have been reported within fibrotic tissue.

Hypothesis: Systemic mast cell inhibition will impede the genesis of posttraumatic knee joint contractures in a rabbit model.

Methods: Injury and immobilization of the knee joint was surgically created in skeletally mature New Zealand white rabbits. Three groups were studied: a nonoperative control group, an operative control group and an operative group treated with a mast cell stabilizer, Ketotifen fumurate. After 8 weeks immobilization, flexion contractures were measured.

Results: Relative to the nonoperative group (n=8), flexion contractures in the operative control group (n=14) and Ketotifen group (n=9) were 31° and 15°, respectively (p = 0.01).

Conclusions: Using this rabbit model, posttraumatic flexion contractures were reduced by 52% in rabbits treated with a mast cell stabilizer.