Summary. In contrast to the current literature, myofibroblasts are not present in chronic posttraumatic elbow contractures. However, myofibroblasts are present in the acute phase after an elbow fracture and/or dislocation. This suggests a physiological role in normal capsule healing and a potential role in the early phase of posttraumatic contracture formation. Introduction. Elbow stiffness is a common complication after elbow trauma. The elbow capsule is often thickened, fibrotic and contracted upon surgical release. The limited studies available suggest that the capsule is contracted because of fibroblast to myofibroblast differentiation. However, the timeline is controversial and data on human capsules are scarce. We hypothesise that myofibroblasts are absent in normal capsules and early after acute trauma and elevated in patients with posttraumatic elbow contracture. Patients & Methods. We obtained twenty-one human elbow joint capsules within fourteen days after an elbow fracture and/or dislocation and thirty-four capsules from thirty-four patients who had operative release of posttraumatic contractures greater than five months after injury. Myofibroblasts in the joint capsules were quantified using immunohistochemistry. Alpha-smooth muscle actin (α-SMA) was used as a marker for myofibroblasts. Samples were characterised and scored by an independent pathologist blinded for clinical data. Results. Eleven capsules were associated with the acute phase after trauma (hours to 7 days), and staining for α-SMA was negative in all eleven specimens. Ten specimens were associated with a later phase post trauma with myofibroblasts staining positive for α-SMA in all but two. All, but two, thirty-four long standing contractures showed a histological pattern consistent with chronic stages of fibrosis, characterised by increased fibroblast-like cell proliferation and higher cellular density of fibroblast-like cells with highly unstructured collagen. There was no staining of α-SMA in fibroblast-like cells in, all but two of these longstanding contractures suggesting absence of myofibroblasts. Conclusions. This study present ‘negative results’ on the hypothesis that myofibroblast numbers are elevated in longstanding (> 5 months) human posttraumatic elbow capsules. This is in contrast to all studies on human tissue in the literature to date. One recent animal study is in agreement withy our data. We did find some myofibroblasts in elbow capsules in the late-phase posttrauma (between 7 and 14 days) suggesting a potential role in early phase of posttraumatic contracture formation

Aims

Animal models have been developed that allow simulation of post-traumatic joint contracture. One such model involves contracture-forming surgery followed by surgical capsular release. This model allows testing of antifibrotic agents, such as rosiglitazone.