Arthrofibrosis is the result of a T cell mediated immune response

It is thought that an excessive fibrotic healing response with diffuse intr a-articular scarring leads to arthrofibrosis after trauma and surgery aroun d joints. To clarify the specific cellular mechanism of arthrofibrosis duri ng arthrolysis we took fibrotic tissue samples from 18 patients at varying periods after knee trauma or surgery. Sections were stained with hematoxyli n and eosin to study the overall histopathological changes. Major histocomp atibility complex (MHC) class II expressing cells as well as CD3, CD4, CD25 , CD28, CD68, CD80, and CD83 positive cells were localized immunohistologic ally. The results demonstrated synovial hyperplasia with fibrotic enlargeme nt of the subintima and infiltration of inflammatory cells. The number of M HC class II expressing cells was increased. Mainly, intimal macrophages and dendritic cells showed positive immunostaining for MHC class II antigens. In the subintima moderate infiltration of T cells including activated T cel ls (CD25), CD4(+) T helper (Th) cells and Th1 and Th2 subsets was detected. There was a slight polarization of the Th1/Th2 balance towards Th1 differe ntiation. Positive immunostaining for CD80/CD28 indicated the costimulatory signal for T cell activation and clonal expansion. These findings strongly support an immune response as the cause of capsulitis leading to formation of diffuse scar tissue within the knee joint. Based on our immunohistologi cal study we conclude that a T cell mediated immune response plays a crucia l role in the mechanism of arthrofibrosis.