Introduction

The development of degenerative changes within the knee following anterior cruciate ligament (ACL) injury is well recognized. However, defining the exact incidence of arthrosis following an ACL injury or after reconstruction of the ACL is a challenge for several reasons. Long-term clinical follow-up studies are difficult to perform because most patients presenting with an ACL injury are young and many will change geographical location in the years following surgery. Outcome studies with long-term follow-up periods tend to have a large number of patients lost to follow-up for this reason.

Furthermore, the group of patients with these injuries is heterogenous, with widely varying ages, preinjury levels of activity, and different expectations following treatment. ACL tears may occur in isolation, but a significant proportion is associated with collateral ligament injuries and concomitant or subsequent meniscal tears, which may also influence the development of degenerative change. In addition to these considerations, some patients may have a previous history of knee injury or surgery and may already have significant degenerative changes within the knee at the time the ACL injury is sustained.

Although most ACL reconstructions are carried out using either hamstring or patellar tendon autografts, there is wide variation in the surgical techniques used to prepare and anchor grafts, which may also influence development of osteoarthritis (OA). The timing of surgical reconstruction after injury may also be of considerable importance. Access to expert orthopaedic opinion and treatment varies considerably with geographical location, and in some areas the duration from injury to surgery may be prolonged. In this chapter we consider the existing evidence linking ACL injury and treatment to subsequent development of OA.

Pathophysiology of Osteoarthritis Following Anterior Cruciate Ligament Injury

Previous studies have shown that restoring knee stability through ACL reconstruction does not necessarily decrease the incidence of posttraumatic OA.^1,2 It therefore follows that other mechanisms, rather than the initial mechanical disturbance of stability at the time of injury, may be responsible for the development of OA, both in the chronic ACL deficient knee and in the reconstructed knee.

Several biochemical mechanisms have been proposed. It has been shown that an early increase in the proteoglycan content of articular cartilage adjacent to the torn ligament occurs following ACL rupture.³ Other studies^4,5 have shown an increase in collagenase activity leading to increased denaturation and loss of type II collagen in the articular cartilage of the knee following injury. These changes are also seen in the knee with idiopathic OA.

Intraarticular pro-inflammatory cytokines are also increased immediately after ACL rupture.^6,7 These include interleukins (IL) -1, -6, and -8, tumor necrosis factor alpha (TNF-α), and keratan sulfate. Of note, IL-1 (in both its alpha and beta forms) and TNF-α have direct chondrodestructive effects independent of their inflammatory properties. These cytokines are present in higher concentrations with more severe chondral damage, and levels fall gradually beginning approximately 3 months postinjury. Granulocyte-macrophage colony-stimulating factor (GM-CSF) concentrations are initially normal but become grossly elevated beginning approximately 3 months postinjury. Conversely, the chondroprotective cytokine IL-1Ra concentration decreases with increasing severity of chondral damage and with chronic ACL deficiency.

These findings suggest the existence of important contributory biochemical factors in the development of OA in the ACL deficient knee. Elevated intraarticular concentrations of several cytokines are present during the acute inflammation following ACL rupture, and this inflammation subsides but does not completely resolve in the subacute and chronic phases postinjury. Instead, a potentially chondrodestructive cytokine imbalance persists that can eventually lead to OA.

It has been shown that ligamentous knee injury is strongly associated with bone bruising.⁸ Magnetic resonance imaging (MRI) scans performed acutely following ACL rupture have shown occult subchondral lesions in 85% of patients, mainly involving the lateral femoral condyle and lateral tibial plateau.⁹ Although the majority of these lesions resolved with time, permanent chondral damage is known to have occurred in some lesions. Histological analysis of these bone bruises has shown associated areas of chondrocyte degeneration and necrotic osteocytes, which suggests that significant damage to the articular cartilage is sustained at the time of injury.¹⁰

Following ACL reconstruction, further factors may play an additional role in the development of arthrosis. It has been shown that pretensioning the graft can cause changes in joint biomechanics that may lead to arthrosis in the long term.^11,12 Shortening of the patellar tendon may occur after patellar tendon autograft, which has been shown to lead to patellofemoral arthrosis and a worse functional outcome, both of which are directly associated with the degree of shortening of the patellar tendon.¹³

Any intraarticular damage that requires treatment with meniscectomy will diminish the joint contact surface area and increase the stress on the tibia.¹⁴ The resultant increased stress on the knee joint has been shown to accelerate the development of OA.¹⁵

Natural History of the Untreated Anterior Cruciate Ligament Deficient Knee

The development of arthrosis following ACL rupture is widely recognized,^16,17 and in a review by Gillquist and Messner¹⁸ it was concluded that in the long term (i.e., 10 to 20 years), as many as 70% of all ACL deficient knees had radiological signs of arthrosis, although clinical symptoms of knee arthritis were infrequent. Segawa et al¹⁹ found radiographic changes of OA in 63% of patients who were followed for 12 years after a conservatively treated ACL rupture. The main risk factor for arthrosis was shown to be meniscectomy, in combination with the risk factors for primary OA, such as increased age at time of injury, increased level of sports activity, obesity, and OA of the contralateral knee.

In a study of patients with symptomatic knee OA, 22.8% had complete ACL rupture identified at MRI, compared with 2.7% of controls.²⁰ Patients with OA in the presence of an ACL rupture had more severe radiological OA.

A cohort of female soccer players in Sweden was assessed 12 years after a known ACL injury, and although radiographic evidence of OA was seen in 82%, there was no difference in the incidence of OA between those ACL injuries treated nonoperatively (38%) and those treated with reconstruction, and the same proportion (75%) of those without radiographic OA had knee symptoms.² Comparable results were seen in a similar study of male soccer players in Sweden 14 years following a known ACL injury.²¹

In children and adolescents with ACL rupture, nonoperative treatment is often favored to avoid drilling surgical tunnels across physeal growth plates. However, it has been shown that ACL injuries treated nonoperatively in this age group are likely to develop instability and poor function, with development of radiological signs of degeneration in almost half of children.²² Subsequent studies have shown that ACL reconstruction can be safely undertaken in adolescents nearing skeletal maturity.²³ It has not yet been proven that this can be safely performed in very young children with opened physes.

Despite this evidence, some studies challenge the concept that ACL tears are inextricably linked to development of arthritis. It has been shown that in older patients (40 to 60 years old) with an ACL rupture treated nonoperatively, 87% had little or no radiographic changes at a mean of 7 years postinjury.²⁴ In 46 young recreational athletes followed up at an average of 5 years following conservative treatment of an ACL tear diagnosed at arthroscopy, only 17.4% had mild radiographic osteoarthritic changes, and only one patient (2.2%) was symptomatic.²⁵

Arthrosis Following Anterior Cruciate Ligament Reconstruction

With the knowledge that ACL tears are associated with an increased risk of OA, it would seem reasonable to assume that ACL reconstruction would play a useful role in prevention of arthrosis in the long term. The difficulties in implementing large long-term follow-up studies following ACL reconstruction have already been mentioned. Table 8-1 summarizes the recent literature that has evaluated the incidence of arthrosis following ACL reconstruction. Analysis of these studies clearly suggests that surgical reconstruction of the ligament does not prevent the development of radiological OA. A meta-analysis by Lohmander and Roos²⁶ found no evidence that ACL reconstruction slowed the progression of arthrosis following ACL rupture, and it does not seem that ACL reconstruction reduces the clinical symptoms of OA in the long term.² However, it is noteworthy that most authors have found the majority of patients to be essentially asymptomatic at follow-up, regardless of the radiological changes, which are often mild. Clearly a spectrum of joint changes exists, with many patients demonstrating minimal radiographic change and few clinical symptoms, although unfortunately a minority will go on to have symptomatic arthrosis (Fig. 8-1).

Fig. 8-1 Anteroposterior (AP) (A) and lateral (B) radiographs of the knee of a man who underwent an anterior cruciate ligament (ACL) reconstruction associated with a medial meniscectomy 11 years previously. The initial femoral tunnel was too anterior. The graft was revised, but the patient presented with symptomatic arthritis at age 34 years.

As with conservatively managed ACL tears, the major risk factor associated with the development of OA is meniscal damage²⁷ and the need for meniscal resection at the time of surgery.^28–35 Some authors maintain that chondral damage is of more importance than medial meniscal tears, which in turn are more significant than lateral meniscal tears in the development of OA.³⁴ However, even in the absence of chondral damage or meniscal injury, early mild degenerative changes may occur after successful ACL reconstruction.³⁶ Other risk factors appear to be female gender and age older than 30 years,^36,37 presence of persistent pivot shift following reconstruction,³² bone–patellar tendon–bone autograft compared with hamstring autograft,^38,39 time to surgery,^27,33,40 synthetic graft material,^37,41 and maintenance of high levels of sporting activity after surgery.⁴² Surgery within 12 months of injury^40,42 appears to reduce the incidence of arthrosis. There does not appear to be any benefit to surgery earlier than 3 months postinjury.⁴³ Anteroposterior (AP) instability post reconstruction does not appear to be a risk.^36,32

Looking at the most up-to-date studies that have followed patients undergoing ACL reconstruction using modern graft materials, it appears that the rate of radiographic degenerative changes is between 4% and 47% between 5 and 10 years of follow-up. This figure has been shown to rise as high as 100% following ACL reconstruction with a total meniscectomy.³⁵ It has even been reported that the rate of degenerative change is higher in the reconstructed knee compared with the chronic ACL deficient knee.¹ This is probably due to the fact that those patients who have symptomatic instability and require ACL reconstruction are more likely to have concomitant meniscal and/or chondral damage predisposing to the development of OA. By comparison, those patients with normal articular cartilage and menisci can often be satisfactorily managed conservatively.

In our own study⁴⁰ we investigated the relationship of time from injury to surgery on the incidence of meniscal tears and degenerative change. We evaluated 183 patients who underwent ACL reconstruction for isolated ACL tears using a quadruple hamstring graft. An arthroscopically assisted single-incision technique was used. Patients were divided into an early group (surgery within 12 months of injury) and a late group (surgery more than 12 months from injury). The late group was also subdivided into four groups of 12-month periods ranging from 1 year to more than 4 years after injury. There was a significantly higher incidence of meniscal tears in patients undergoing reconstruction after 12 months compared with those in the early group (71.2% versus 41.7%, P < 0.001) (Fig. 8-2). This was due to a large increase in medial meniscal tears in the late group. The incidence of lateral meniscal tears remained relatively unchanged with time. This may indicate that lateral meniscal tears occur at the time of ACL injury or very early after injury, whereas the majority of medial meniscal tears are acquired after the initial ACL tear. The increase in medial meniscal tears after 12 months probably correlates with an attempted return to preinjury levels of sporting activity. The data are consistent with development of knee instability associated with a return to sport, with increased torsional and shear forces resulting in acquired medial meniscal injuries and acceleration of degenerative change in the knee.

Fig. 8-2 Percentage of patients with meniscal pathology undergoing surgery 0–12 months after injury or more than 12 months after injury.

We also found an increased incidence of degenerative change in the late group (31.3% versus 10.7%, P < 0.001) (Fig. 8-3), even though the majority of patients in both groups had no degenerative change at all. The findings in the study indicate that reconstruction carried out within 1 year of injury is associated with a very low incidence of degenerative change. It remains to be seen whether an ACL reconstruction carried out at this stage confers a longer-term benefit in prevention of late degenerative change. In a recent study⁴⁴ using modern reconstruction techniques with a hamstring autograft, the reported incidence of significant radiographic degenerative change at 2- to 8-years follow-up was only 4%, and these occurred in patients who had undergone meniscectomy. It is possible, therefore, that early reconstruction carried out in the presence of intact menisci may carry a more favorable prognosis with a lower incidence of arthrosis in the longer term.

Fig. 8-3 Incidence of degenerative change found at surgery 0–12 months and more than 12 months after injury.

Conclusion

The development of arthrosis is a well-recognized complication following ACL rupture. The ACL injury itself is unlikely to be the sole causative mechanism, and initial chondral damage at the time of injury combined with various biochemical mediators may also be implicated. Meniscal damage, either directly at the time of injury or subsequent to chronic ACL deficiency, also plays a key role in the development of arthrosis.

It is well recognized that the untreated ACL deficient knee has an increased risk of developing degenerative change. However, there is evidence to show that a significant number of patients also develop radiographic signs of arthrosis following ACL reconstruction. Despite this, the majority of ACL reconstructed patients have a very satisfactory functional outcome. The radiographic appearances are usually minimal, and patients are essentially asymptomatic despite these early degenerative changes.

Several problems lie in meaningfully interpreting the literature on outcomes following ACL reconstruction. Study cohorts vary widely in terms of age, level of sports activity, outcome measures, and duration of follow-up. All recent studies have suboptimal follow-up rates, none of which was longer than 10 years. Most studies in the literature have looked at patients who have undergone ACL reconstruction using bone–patellar tendon–bone autograft, although hamstring autografts are now a popular choice. However, there is no sound evidence linking graft choice to the rate of post ACL reconstruction arthrosis.

Although there is no definite evidence that ACL reconstruction prevents arthrosis in the long term, the literature indicates that chronic ACL deficiency and meniscal tears are the most important factors associated with the development of degenerative change. Delays to reconstruction for periods of longer than 12 months are associated with a greater risk of meniscal tears and degeneration. The evidence also suggests that early reconstruction of the ACL within 12 months of injury minimizes the rate of meniscal tears and consequently should lead to lower rates of arthrosis. We would advocate undertaking surgery within this timeframe. Furthermore, we would also recommend that every effort be made to repair meniscal injuries, as the loss of meniscal tissue is a major risk factor in post-reconstruction arthrosis. The most recent studies seem to indicate that early ACL reconstruction in knees with a normal articular surface and intact menisci will delay and may even prevent the development of arthrosis. More evidence from clinical studies with longer-term follow-up is required to support this view.