Degenerative changes have been considered to be a cause for spontaneous qua
driceps tendon rupture. Aim of this study is to investigate the microvascul
ature of the quadriceps tendon by injection techniques and immunohistochemi
cal methods (antibodies against laminin) with regard to the pathogenesis of
tendon degeneration. The blood supply of the quadriceps tendon arises from
descending branches of the lateral circumflex femoral artery, by branches
of the descending geniculate artery and by branches of the medial and later
al superior geniculate arteries. Blood vessels penetrate the tendon from th
e surrounding connective tissue and anastomose with a longitudinally orient
ated intraligamentous network. Compared to the surrounding synovial layer,
the amount of vessels in the tendon substance is greatly reduced. The distr
ibution of blood vessels within the quadriceps tendon is not homogenous. Th
e anterior or superficial part of the tendon has a complete vascular networ
k that extends from the musculo-tendinous junction to the patella. Within t
he deep portion of the quadriceps tendon there is an oval shaped avascular
area which measures app. 30 mm in length and app. 15 mm in width. Within th
is area the immunohistochemical proof of laminin is negative. An explanatio
n for the absence of blood vessels may be compressive stress caused by the
patellar groove which serves as hypomochlion for the quadriceps tendon when
the knee is flexed. The occurrence of an avascular zone within the deep la
yer of the tendon that is directed to the joint cavity may explain the freq
uency of degenerative changes in this region.