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Accelerated return to sport after anterior cruciate ligament injury: a risk factor for early knee osteoarthritis?
  1. Adam G Culvenor1,2,
  2. Kay M Crossley2
  1. 1Paracelsus Medical University, Institute of Anatomy Salzburg & Nuremburg, Salzburg, Austria
  2. 2La Trobe University, School of Allied Health, Bundoora, Victoria, Australia
  1. Correspondence to Professor Kay M Crossley, School of Allied Health, La Trobe University, Melbourne, VIC 3086, Australia; k.crossley{at}latrobe.edu.au

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Returning to preinjury level of sports participation is a primary goal of anterior cruciate ligament reconstruction (ACLR). Indeed, surgical success is often judged on return-to-sport rates. While timeframes of 6–12 months postsurgery are typically expected, in reality, fewer than two-thirds of individuals return-to-sport within the first year post-ACLR.1 Conservatively managed individuals have similar clinical outcomes—future knee function relies on optimal rehabilitation, irrespective of surgery.2 Although consensus for the most effective rehabilitation approach is lacking, contemporary treatment programmes worship at the altar of accelerated return-to-sport.

Although the finish line for ACL rehabilitation is often defined as resuming sporting pursuits, consequences of ACL injury, including the high reinjury and contralateral injury risk, extend for many years, possibly a lifetime. Radiographic knee osteoarthritis (OA) is inevitable for 50–60% of individuals ≥10 years post-ACL injury and reconstruction.3 Given that typical ACL injured patients are young, this early-onset OA often engenders considerable morbidity and impact on healthcare resources. Could our short-sighted fixation on a fast-tracked return-to-sport be linked to these alarming premature OA rates?

Post-traumatic OA, like its non-traumatic sibling, is a complex multifactorial entity that cannot be explained by one factor alone. However, evidence is emerging that an early return-to-sport may contribute to post-traumatic OA.

Early return-to-sport and its consequences for articular cartilage

Recent insights indicate that knee cartilage has low in vivo resilience 6 months post-ACLR, and repetitive high-impact on this qualitatively diminished cartilage may contribute to OA.4 Altered cartilage homeostasis post-ACLR (eg, prolonged presence of inflammatory biomarkers damaging type-II collagen network) may not cope with the rapid load increase, as evidenced by a return to high-impact activity before 5 months engendering even poorer cartilage quality.4 Higher physical activity levels within 12 months of injury have also been associated with cartilage thinning, particularly in the patellofemoral joint (PFJ).5 The influence of concomitant meniscal or cartilage injury/surgery on the risk of cartilage loss with an early return-to-sport is unknown. Additionally, a return-to-sport with persistent impairments in muscle strength and lower-extremity function may remove an important level of joint protection. Poor physical performance post-ACL rehabilitation predicted worse patient-reported outcomes 2 and 5 years postinjury.2 Individuals returning to high-impact activities without optimal strength and neuromuscular control may also place themselves at an elevated risk of early OA.

Knee OA is typically considered a long-term outcome post-ACL injury and reconstruction, primarily affecting the tibiofemoral joint. This view is largely held because investigations of post-traumatic OA almost exclusively involve ≥5 year follow-up, to enable degeneration to be detected from anteroposterior radiographs alone. However, more advanced imaging modalities challenge this dogma. Within a year of ACL injury, femoral trochlear cartilage quality deteriorated rapidly,5 and in young adults 1 year post-ACLR, we reported a high prevalence (31%) of MRI-diagnosed OA, most frequently affecting the PFJ.6

The impact of returning to sport, at any time-point post-ACLR, on the development of OA has not been evaluated. However, given the possible danger to articular cartilage with a premature return-to-sport, we call for the research and clinical focus to include more specific elements of maintaining long-term joint health, particularly in trials addressing early return-to-sport. This is pertinent, not only for the tibiofemoral joint, but also for the PFJ, which until recently, has been an under-recognised source of pathology and symptoms post-ACLR.3

What is the role of loading in articular cartilage post-ACL injury?

Although the ability to slow structural disease progression remains elusive, optimising load has potential to interrupt the rapid cartilage deterioration observed post-ACLR. Neuromuscular exercises can improve knee cartilage quality (glycosaminoglycan content) in middle-aged adults postmeniscectomy, potentially by optimising joint loads.7 ACL injury provides a model to evaluate the influence of specific interventions on disease modification because the acute injury event defines disease onset, so management strategies can be implemented at an early stage when they are likely most effective. Individuals in their third decade (>26 years) may benefit most from early intervention as they are particularly at risk of cartilage loss within the first year post-ACLR.6

Given the high rates of PFJ OA and symptoms independent of graft type,3 ,6 ,8 clinicians should recognise the contribution of the PFJ and include interventions that reduce patellofemoral pain during postoperative rehabilitation.9 ,10 Although randomised controlled trials are required to evaluate the effect of specific exercise modifications for the PFJ, adjustments such as closed kinetic chain exercises at <60° of knee flexion, combined with optimal quadriceps and hamstring activation minimise patellofemoral loads and may aid in limiting patellofemoral dysfunction.9

It is paramount that we continue to strive for improved medium and long-term postinjury outcomes for patients who have suffered an ACL injury. We must not simply be content with a satisfactory short-term outcome. Despite the best efforts of primary injury prevention, ACL injuries continue to be a source of great individual and societal burden. We can, and need to, do better.

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Footnotes

  • Contributors Both authors designed the study. AGC drafted the manuscript. KMC revised the manuscript for important intellectual content. Both authors approved the final version for publication.

  • Funding AGC is supported by a European Union Seventh Framework Programme (FP7-PEOPLE-2013-ITN; KNEEMO) under grant agreement number 607510. The funding source had no involvement in any aspect of this editorial.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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