Arthrofibrosis - Result of a T cell mediated immune response?

Aim: Detection of a T cell mediated immune response as a cause of arthrofib rosis. Methods: Tissue samples were taken from 7 patients (mean age: 31.8 years; r ange 18-50) undergoing open arthrolysis of the knee joint because of sympto matic arthrofibrosis following ligament injuries. The average time interval between trauma and arthrolysis was 16.4 months (range 4-48 m). Before arth rolysis, the mean range of motion was 77.8 degrees C (70 -110 degrees). Any other inflammatory disease was excluded by history. Tissue samples were fi xed in formalin and embedded in paraffin. Sections were stained with HE. Mo noclonal antibodies were used for immunohistological localization of MHC cl ass II expressing cells as well as CD68, CD83, CD3, CD4, CD25 and CD20 posi tive cells. The ABC reaction and DAB or AEC were used for immunostaining an d hemalum for counterstaining. Synovial tissue samples from 5 knees without any pathology served as controls. Results: Arthrofibrotic tissue revealed synovial hyperplasia, fibrotic enla rgement and infiltration of inflammatory cells. Expression of MHC class II indicating antigen-presenting cells is increased in synovial macrophages (C D68+) and dendritic cells (CD83+). Positive immunostaining for CD4 (helper T cells) was also increased and mainly present around MHC class II expressi ng cells. There were also CD3+, CD25+ and CD20+ cells. Conclusion: A T cell mediated immune response may play a crucial role in th e mechanism of arthrofibrosis. MHC class II expressing cells can present an tigens that are recognized by helper T cells. This promotes an immune respo nse followed by stimulation of other cells and formation of extracellular m atrix.