Osteoarthritis in patients with anterior cruciate ligament rupture: A review of risk factors

Louboutin H, Debarge R, Richou J, Ait Si Selmi T, Donnell AT, Neyret P and Dubrana F. (2009) The Knee. 16:239-244.

This is the editor's interpretation of a paper published in the orthopaedic literature in 2009 - our attempt to make relevant medical articles accessible to lay readers. If you wish to read the original it is easy to ask your librarian to obtain a reprint for you from any medical library.


This paper is a review where the authors look at the risk factors for developing osteoarthritis (OA) in patients who have had a rupture of their anterior cruciate ligament (ACL).

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 -

Primary damage - ie occurring at the time of the initial injury

At the time of injury, other structures besides the ACL may also be damaged - the joint surface, menisci, capsule, other ligaments - and the more bits that are damaged the greater the risk of developing OA in the untreated knee.

 

Secondary damage - ie occurring because of giving way and instability

This may affect the joint cartilage, the meniscus and other ligaments, which may become stretched.

 

Tertiary damage - ie due to alteration of the mechanics due to abnormal shearing forces

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.

 

The paper in full makes very good reading, and the authors discuss many factors affecting the development of OA after ACL rupture. Finally, the authors present a very informative flowchart which they have put together from several studies, a summary of which is -

  • At the time of the initial ACL rupture, 20% of patients also have a meniscal tear and 16% show damage to the joint cartilage.
  • Without ACL reconstruction, after 20 years 60-100% of patients have OA. After 30 years 86-100% have OA, and 42% go on to a total knee replacement.
  • With reconstuction the figures are better, but are also influence by whether or not any meniscal tear was repaired rather than removed (meniscectomy). If the meniscus was normal or was repaired, after 20 years the incidence of OA was 14-26%, but this went up to 37% if there was a meniscectomy.

They conclude that the principle reason for developing OA after ACL rupture is the shear force leading to the tibia slipping forward (anterior translation). The more normal the knee at the time of reconstruction, particularly the posterior horn of the medial meniscus, the lower the risk of OA. Delay in reconstruction increases the risk because of all the secondary damage that can occur.

 

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