Post-Traumatic Osteoarthritis Following ACL Injury

Li-Juan Wang; Ni Zeng; Zhi-Peng Yan; Jie-Ting Li; Guo-Xin Ni


Arthritis Res Ther. 2020;22(57) 

In This Article

ACL Injury and PTOA

The ACL plays an important role in the stabilization of the knee by restricting anterior translation of tibial and rotational forces at the tibiofemoral joint.[6] As a common orthopedic injury, the annual incidence of isolated ACL injury in the general population is 68.6 per 100,000 people.[7] ACL injury may cause pain, range of motion limitation, muscle weakness, knee instability, altered biomechanics, and reduction in physical activity levels, which place a great economic burden on the health care system.[6] It commonly occurs during sudden deceleration and direction change in non-contact situations.[3] Adolescents and young adults who participate in sports requiring pivoting and frequent direction changes have a high incidence of ACL injury. The risk in young women performing pivoting sports is 3–5 times higher than in men.[5]

As reported, 50–90% of ACL injuries progress to PTOA.[6] After ACL injury, grade III or IV radiologic changes in the Kellgren–Lawrence classification system are nearly 5 times more likely than in contralateral knees without a history of ACL injury.[8] A number of factors may mediate the risk of PTOA after ACL injury, such as gender (female), age, high body mass index (BMI), obesity, physical activity level, smoking, low education level, subsequent surgery, time interval between injury and surgery, and varus alignment of the uninjured knee.[2,5,9,10]

Older age leads to a disturbance of the balance between anabolic and catabolic processes.[5] Evidence suggests that it is related to medial compartment joint space narrowing.[9] Similarly, BMI is associated with joint space narrowing after ACL injury.[5] Obesity is also believed to have a great influence on OA progress in many ways. One is increased joint loading. Another could be the catabolic effect of inflammatory substances released by adipose tissue, including free fatty acids, reactive oxygen species cytokines, and adipokines on joint tissues. Additionally, obesity is related to increased levels of IL-6 and TNF-α, which are pro-inflammatory indicators of PTOA development.[11] Although the level of physical activity is also considered a risk factor, no consensus has been reached to date. On one hand, physical activity is often recommended to improve function and promote overall health. A lack of mechanical loading contributes to thinning of articular cartilage. A low level of physical activity is associated with a higher BMI, which may lead to the progression of OA. On the other hand, the repetitive use of joints and joint overload may result in matrix loss and chondrocyte apoptosis.[2]