In their introduction the authors highlight that untreated ruptures of the anterior cruciate ligament lead to degenerative changes in the tibiofemoral joint (joint surfaces of tibia or femur bone), but they point out that there is a discrepancy between the presence of OA reported from X-rays and the presence of symptoms reported by the patients. They also offer the concept of 'copers' and 'non-copers' and suggest that most reports are those of the non-copers.
Phases of damage
The authors consider the three phases when damage can occur to other structures in the knee after ACL injury and they list the risk factors for developing OA in each of these phases -
Tertiary damage may include -
- increased anterior tibial displacement - the torn ligament allows abnormal slippage of the tibia forwards underneath the femur as there is no ACL to restrain this. This leads to shearing forces on the medial (inner) aspect of the joint, and the posterior horn of the meniscus gets wedged between the tibia and the back of the rounded condyle of the femur, resulting in longitudinal splits in the posterior horn. Initially these splits are only partial, but eventually the split goes right through the meniscus, forming a bucket-handle tear of the meniscus. Within 10 years all patients who have had an ACL tear and who do not undergo reconstruction are likely to have a medial meniscus tear.
- loss of the posterior horn results in aggravated tendency of the tibia to slip forwards, as the intact meniscus acts as a bearing and is one of the normal anatomic restraints - then this further shearing damages the joint cartilage.
- as this process progresses, the fibrous capsule starts to stretch at the back on the knee on the inner (medial) side, and the cartilage damage goes right down to the bone. Where the posteromedial capsule is stretched a mushroom-like bony outgrowth can form (an osteophyte or spur), and X-rays may show the rounded end (condyle) of the femur riding onto this prominence.