J. Bruns et al., PRESSURE DISTRIBUTION IN THE KNEE-JOINT - INFLUENCE OF FLEXION WITH AND WITHOUT LIGAMENT DISSECTION, Archives of orthopaedic and trauma surgery, 113(4), 1994, pp. 204-209
Biomechanical factors influencing the patterns of pressure distributio
n at the articular surface and the subchondral bone are suggested to b
e most important in the pathogenesis of osteoarthritis and ostechondri
tis dissecans at the knee joint. Besides this, chronic joint instabili
ty is another important factor under discussion in the etiology of ost
eoarthritis of the knee. The patterns of pressure distribution on the
femoral condyles of weight-bearing knee joints were investigated in a
biostatic cadaver model. The pressure on the femoral condyles was eval
uated using pressure-sensitive films with the knee in different physio
logical joint positions (extension, 15-degrees and 30-degrees flexion)
with and without division of either the medial collateral ligament (M
CL), the lateral collateral ligament (LCL), the MCL and the anterior c
ruciate ligament (ACL), or the LCL and the ACL. Results showed that th
e location of the contact area and peak pressure depended on the joint
position and stage of ligament division. Without ligainent division t
he maximum peak pressure was always observed on the medial condyle. On
ly after MCL and combined MCL + ACL division did the lateral condyle s
how in extension a higher peak pressure than the medial condyle. Divis
ion of the LCL and LCL + ACL resulted in an increase in peak pressure
on the medial condyle, particularly in flexion. The highest peak press
ure of all was measured in the 30-degrees flexion position on the medi
al condyle after division of the LCL. The lowest at all was found on t
he lateral condyle in 15-degrees flexion after LCL division. Additiona
l ACL division resulted in only minor further changes. These results a
re important for the interpretation of clinically observed factors dis
cussed in the etiology of secondary osteoarthritis of the knee and con
tribute to the theory of mechanical induction of osteoarthritis and os
teochondritis dissecans.