Arthrofibrosis is a disabling complication after trauma and surgery due to
massive connective tissue proliferation. The etiology and pathogenesis have
never been fully understood. A strong immune response may lead to activati
on and proliferation of fibroblasts with excessive and disordered depositio
n of matrix proteins. In similar pathological conditions, like lung fibrosi
s or superficial fibromatoses with fibrotic transformation an increased exp
ression of collagen type VI has been reported. We investigated fibrotic tis
sue samples taken from 18 patients (average age: 32,7 years), who underwent
arthrolysis of the knee joint because of symptomatic arthrofibrosis follow
ing ligament injury. The mean interval between trauma and arthrolysis was 1
3,8 months (range 4-50 months). Tissue samples were taken from the infrapat
ellar fat pad and intercondylar connective tissue. All samples were stained
with HE. The expression of type III and VI collagen was studied immunohist
ochemically using an immunoperoxidase method for light microscopic visualiz
ation. Histologic analysis from patients with arthrofibrosis showed a synov
ial hyperplasia with cell infiltration and vascular proliferation compared
to synovial tissue samples from knee joints without any detectable patholog
y. Subsynovial an increased deposition of matrix proteins was visible. Type
VI collagen was widely distributed as a network subsynovial and around cap
illary walls. Type III collagen showed a diffuse distribution. Arthrofibrot
ic tissue is, similar to pathological conditions with fibrotic transformati
on characterized by an increased expression of collagen type VI. Collagen t
ype VI may play an important role in matrix homeostasis. It serves as an an
choring element between collagen fibers and as a cell binding structure.