Arthrofibrosis is the result of a T cell mediated immune response.

It is thought that an excessive fibrotic healing response with diffuse intra-articular scarring leads to arthrofibrosis after trauma and surgery around joints. To clarify the specific cellular mechanism of arthrofibrosis during arthrolysis we took fibrotic tissue samples from 18 patients at varying periods after knee trauma or surgery. Sections were stained with hematoxylin and eosin to study the overall histopathological changes. Major histocompatibility complex (MHC) class II expressing cells as well as CD3, CD4, CD25, CD28, CD68, CD80, and CD83 positive cells were localized immunohistologically. The results demonstrated synovial hyperplasia with fibrotic enlargement of the subintima and infiltration of inflammatory cells. The number of MHC 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 cells (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 differentiation. 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 immunohistological study we conclude that a T cell mediated immune response plays a crucial role in the mechanism of arthrofibrosis.