Ankylosing
enthesopathy is a spontaneously occurring progressive stiffening of the ankle and/or tarsal joints in mice of C57Black background. In C57BL/10 mice and mice of the same genetic background that had been made transgenic for
HLA-B27, the start of the disease was detected by weekly testing for decreased mobility in the ankle/tarsus region. Ankylosing
enthesopathy was found to begin with a short phase of proliferative
inflammation of the joints and adjacent tissues, with some fibrinous exsudation, some leucocytic infiltration and slight bone erosion. This
inflammation is soon accompanied and followed by proliferation of cartilaginous cells at the bone insertions of joint capsule ligaments (entheses). Ossification of the cartilage proliferations and some
desmal ossification lead to large
osteophytes that inhibit mobility. Fusion of
osteophytes occasionally leads to marginal
ankylosis. The histopathology of the successive stages of murine ankylosing
enthesopathy and the preponderance in males and
HLA-B27 transgenic mice are reminiscent of
ankylosing spondylitis in man. The spine, however, was not affected.