Risk of osteoarthritis after an ACL tear and ACL reconstruction

 Risk of osteoarthritis after an ACL tear and ACL reconstruction
                    

                                    Dr. KS Dhillon

Introduction

Osteoarthritis (OA) is the most common type of arthritis. OA is the leading cause of mobility-related disability. Post-traumatic osteoarthritis (PTOA), a subtype of  OA develops after an injury to the joint. The injuries include intra-articular fractures,  ligament injuries, and cartilage (articular or meniscus) injuries. PTOA  accounts for nearly 12% of all arthritis [1].

Unlike idiopathic OA which occurs in older people, PTOA represents a cause of functional disability in a younger population because joint injuries are more often sustained by younger individuals [2]. 

Risk factors for knee PTOA are anterior cruciate ligament (ACL) injury, meniscus tears, patellar dislocation, posterior cruciate ligament tears, and intra-articular fractures.

The incidence of ACL injury is high in adolescents playing sports that involve pivoting. The reported incidence of PTOA following ACL injury is particularly high.

ACL injury and PTOA

ACL rupture is a common and debilitating injury that occurs in athletes who are involved in pivoting sports such as basketball, American football, and soccer. The incidence of ACL tears has been estimated at 0.8 per 1,000 people in the general population. This number is likely to be much higher in younger, more athletic populations [11]. 

Gender is an important risk factor for ACL injuries. Younger women are roughly twice as likely to suffer ACL rupture than young men [4].

About 80,000 to 250,000 ACL ruptures occur annually, and the majority of them in individuals below the age of 30 [5,6,7].

ACL deficiency leads to suboptimal kinematics of the knee since effective transfer of loads relies on mechanical stability. ACL laxity causes deterioration of the physiologic roll-glide mechanism. This results in increased anterior tibial translation as well as increased tibial internal rotation [8]. ACL deficiency results in increased mean contact stress in the posterior parts of the medial and lateral compartments under anterior and rotational loads, respectively [9].

When there is muscle fatigue or poor neuromuscular control, patients with ACL deficiency experience combined anterior and rotatory instability as subluxation of the tibiofemoral joint occurs. In ACL deficient knees the failure of a primary restraint necessitates recruitment of secondary structures such as the menisci to resist external forces and to stabilize the joint. The higher loads borne by secondary structures can make them more susceptible to injury and degeneration [10]. 

ACL injury is usually associated with cartilage injury. Potter et al. [11] prospectively evaluated 40 knees with an acute isolated ACL injury and they found that all patients sustained a chondral injury at the time of ACL tear. They also found that there was an association between the initial size of bone marrow oedema pattern and subsequent degeneration of cartilage [11]. All of these changes may correlate with the eventual development of posttraumatic OA in the knee after an ACL injury. 

About 50% of ACL tears are accompanied by meniscal injury at the time of the acute injury. In the chronic ACL-deficient knee, meniscal tears have been seen in about 80% of the patient population [12,13]. 

Meniscectomy is an important risk factor for developing knee osteoarthritis after an ACL injury. The amount of meniscus resected is the most important surgical predictive factor for the development of OA. 

Lie et al [14] carried out an updated systematic review to assess the prevalence of knee OA at 10 years after an anterior cruciate ligament injury. They found that the prevalence of radiographic knee OA varied from 0% to 100%. They also found that the prevalence of symptomatic knee OA in the tibiofemoral joint was 35% and in the patellofemoral joint 15%.

Øiestad et al [15] carried out a systematic review to study the prevalence of osteoarthritis in the tibiofemoral joint more than 10 years after an anterior cruciate injury. Seven of the studies were prospective and 24 retrospective studies. They found that the prevalence of knee osteoarthritis for subjects with isolated anterior cruciate ligament injury was between 0% and 13% and for subjects with anterior cruciate ligament and additional meniscal injury, the prevalence varied between 21% and 48%. The study also found that the most frequently reported risk factor for the development of knee osteoarthritis was meniscal injury.

After ACL injury, grade III or IV radiologic changes in the knee are nearly 5 times more likely than in contralateral knees without a history of ACL injury. 

There are several risk factors for the development of OA after knee injuries. Meniscectomy is a consistent risk factor for radiographic OA. Meniscus injury often treated by meniscectomy occurs in approximately 75% of patients with ACL injury [14].

The menisci play an important role in providing stability to the tibiofemoral joint. It helps to distribute the load, absorb shock, lubricate the knee joint as well as protect the articular cartilage from excessive axial loading [16]. When the meniscus is damaged the axial loading on the articular cartilage increases and this predisposes and increases the risk of development of OA development [17]. There is a strong correlation between meniscal lesions, cartilage loss, and subchondral bone marrow lesions and these are important factors in the development of OA [18]. Meniscal injuries are common in patients with an acute ACL injury and meniscal injuries can also occur subsequent to ACL injuries. The incidence of OA is higher in patients with combined ACL and meniscus injuries as compared to patients with isolated ACL injuries [14].

Besides meniscectomy, the other risk factors for radiographic OA include gender (female) age, higher body mass index (BMI), obesity, physical activity level, smoking, low education level, subsequent surgery, the time interval between injury and surgery, and varus alignment of the uninjured knee, range of motion loss and articular cartilage damage. 

With older age, there is a disturbance of the balance between anabolic and catabolic processes. There is evidence that suggest that it is related to medial compartment joint space narrowing [19]. It is well known that BMI is associated with the onset and progression of knee OA in patients without ACL rupture. Multiple studies have found that patient BMI is correlated with joint space narrowing and OA following injury to the ACL [20]. Obesity also has a great influence on OA progress in several ways. One is increased joint loading and others include the catabolic effect of inflammatory substances released by adipose tissue, such as free fatty acids, reactive oxygen species cytokines, and adipokines, on joint tissues. 

Physical activity is also considered a risk factor for OA but there appears to be no consensus so far. Physical activity is usually recommended to improve function and promote health. A lack of mechanical loading is also known to contribute to thinning of articular cartilage. A low level of physical activity can lead to an increase in BMI, which is known to lead to the progression of OA.  Repetitive use of joints and joint overload can lead to matrix loss and chondrocyte apoptosis [21].

Some studies have report quadriceps weakness as a risk factor while there are others which state that quadriceps weakness is not a risk factor for radiographic OA [14].

Age has been identified as a risk factor for the development of PTOA. Chondrocyte senescence and preexisting joint degeneration seen in older people increases the possibility of developing OA. 

There have been several studies that have showed that chondral damage is a risk factor for OA [20]. Recurrent episodes of giving way of the knee after an ACL injury can also lead to chondral damage thereby increasing the risks of OA.

Chondral injuries are also known to produce a biochemical cascade, which increases the concentrations of chondrodestructive cytokines and decreases the concentration of chondroprotective cytokines as compared to the contralateral knee [20].

There is some evidence that a time delay between injury and surgery may be a risk factor for tibiofemoral OA. Studies have shown that early reconstruction of the ACL reduces the development of OA when compared with late reconstruction [20].

ACL reconstruction, however, cannot prevent the development of OA and OA can develop regardless of whether a patient undergoes ACL reconstruction or conservative treatment. There is a 57% incidence of knee OA 14 years following ACL reconstruction, as compared to an 18% incidence of knee OA in the contralateral knee [22]. 

A 2014 meta-analysis by Cinque et al [23] showed that the relative risk (RR) of developing radiographic moderate to severe osteoarthritis (grade III or IV) was 3.84. The incidence of moderate to severe OA was 20.3% in ACL-injured knees as compared to 4.9% in the uninjured contralateral knees at an average of 10 years following ACL reconstruction. 

The RR of developing OA in the ACL-injured knees not treated with surgery was significantly higher 4.98 as compared to an RR of 3.62 in knees that were treated with surgery [24]. A more recent meta-analysis showed that the prevalence of radiographic knee OA following ACL reconstruction at 5, 10, and 20 years was  11.3%, 20.6%, and 51.6% respectively [23].

ACL reconstruction does not prevent OA, but ACL reconstruction can delay its onset [25]. 

This is in sharp contrast to other studies that have found no statistical difference in knee osteoarthritis between operative versus nonoperative treatment groups [26,27]. 

A study by Daniel et al [28] concluded that patients who had undergone ACL reconstruction had a higher level of arthrosis by radiograph and bone scan evaluation. Overall, a comparison of bone scan scores for patients who ACL reconstruction as compared to those who did not have surgery revealed a greater incidence of arthrosis in patients who had reconstructed knees.

Risk of arthroplasty after ACL injury

Studies evaluating the risk of knee replacement after ACL injuries is lacking probably because the incidence is very low. Leroux et al (22) did a population-based matched cohort study to evaluate the risk of arthroplasty following ACL reconstruction. They obtained administrative databases of patients who had ACL reconstruction in Ontario, Canada, from 1993 to 2008. They identified 30,301 patients who had ACL reconstruction and 151,362 individuals from the general population with similar demographic variables. They found that 209 patients with ACL reconstruction and 125 patients from the general population had knee arthroplasty. The cumulative incidence of knee arthroplasty following ACL reconstruction after 15 years was low at 1.4% and in the general population, it was 0.2%. Age of 50 years or more, female sex, comorbidity, surgeon annual volume of ACL reconstruction of 12 or less per year, and reconstruction of the ACL done at a university-affiliated hospital, increased the odds of knee arthroplasty. Male sex and an age of 20 years or less were protective indicators. Meniscal tears, however, were not associated with an increased risk of knee arthroplasty.

The limitations of this level 3 study was that it is not known how many of these patients had OA at the time of ACL reconstruction and neither was information about concomitant PCL injury and revision reconstructions available.

Conclusion

Post-traumatic osteoarthritis (PTOA) develops after injury to the joint. The injuries include intra-articular fractures, ligament injuries, and cartilage (articular or meniscus) injuries. PTOA  accounts for nearly 12% of all arthritis.

Unlike idiopathic OA which occurs in older people, PTOA represents a cause of functional disability in a younger population because joint injuries are more often

sustained by younger individuals. 

Risk factors for knee PTOA are anterior cruciate ligament (ACL) injury, meniscus tears, patellar dislocation, posterior cruciate ligament tears, and intra-articular fractures.

ACL injuries are a common cause of PTOA of the knee. The incidence of ACL tears has been estimated at 0.8 per 1,000 people in the general population. About 50% of ACL tears are accompanied by meniscal injury at the time of the acute injury. In the chronic ACL-deficient knee, meniscal tears have been seen in about 80% of the patient population. The incidence of knee OA is higher when there is an ACL tear with a meniscal tear.

The prevalence of radiographic knee OA at 10 years after an anterior cruciate ligament injury varies from 0% to 100%. The prevalence of symptomatic knee OA in the tibiofemoral joint is 35% and in the patellofemoral joint 15%, following an ACL injury.

ACL reconstruction does not prevent OA. Some studies suggest that the incidence of OA is lower after ACL reconstruction as compared to no surgery, others say that the incidence is the same and there is also evidence to show that the incidence is higher after ACL reconstruction.

The cumulative incidence of knee arthroplasty following ACL reconstruction after 15 years is low at 1.4% and in the general population, it is 0.2%. Meniscal tears, however, are not associated with an increased risk of knee arthroplasty.

 

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