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CC BY-NC-ND 4.0 · Revista Chilena de Ortopedia y Traumatología 2025; 66(01): e37-e41
DOI: 10.1055/s-0045-1809064
Artículo de Revisión | Review Article

Triggering Factors of Arthrofibrosis Following Anterior Cruciate Ligament Reconstruction

Article in several languages: español | English
Alejandro Antonio Monzón Rodas 
1   Universidad de San Carlos de Guatemala, Ciudad de Guatemala, Guatemala
,
Cristel Carolina Ramírez Rodas 
1   Universidad de San Carlos de Guatemala, Ciudad de Guatemala, Guatemala
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Abstract

Arthrofibrosis corresponds to an intra- and periarticular invasion of fibrous tissue responsible for joint ankylosis. It is a complication that arises due to multiple factors that promote excessive proliferation of myofibroblasts, regulated by reduced apoptosis, adhesions, and aggressive synthesis of extracellular matrix. An incidence of 5–35% has been reported, which is higher in women. The most common triggering factors include the presence of concomitant injuries in the knee joint, limited preoperative range of motion, chronic inflammation in the knee prior to surgery, surgical trauma, errors in surgical technique, postoperative infection, inadequate rehabilitation, and prolonged immobilization after surgery. Understanding the etiology of this condition is essential to identify individuals at higher risk of developing this complication and to develop prevention strategies and appropriate treatment to minimize the risk of arthrofibrosis.


 

Keywords

arthrofibrosis - anterior cruciate ligament - triggering factors - arthroscopy

Introduction

The anterior cruciate ligament is an essential structure for knee stability, providing resistance to excessive forward displacement of the tibia relative to the femur. The femur is composed of collagen fibers surrounded by loose connective tissue and synovial fluid. Injury to the ligament can result in joint instability and functional limitations. ACL reconstruction surgery is a commonly performed procedure to restore knee stability, but it can lead to complications such as arthrofibrosis.

Arthrofibrosis is defined as the diffuse proliferation of scar tissue within a joint, forming adhesions between joint structures. This process produces inflammatory agents, growth factors, and cytokines, which initiate a series of events that generate extracellular matrix production. This process, when overexpressed, causes the tissue to become proinflammatory and fibrosis to develop. After surgery, arthrofibrosis manifests as severe pain with limited joint mobility in extension, flexion, or both, with an immobile patella causing knee stiffness. The identification and timely management of these factors can prevent, as far as possible, the appearance of arthrofibrosis after anterior cruciate ligament reconstruction.


 

Materials and Methods

Inductive method. Conducting a retrospective longitudinal descriptive study.

Biological Factors

The biological factors that make an individual more likely to develop arthrofibrosis are genetic predisposition, age, gender, and weight, the latter being the only modifiable factor when considering prevention. Regarding genetic predisposition, presenting the alleles HLA-Cw*07, HLA-Cw*08 and HLA-DQB1*06 predisposes to the development of arthrofibrosis, although it is not yet clear whether this is due to weakened defense mechanisms or increased susceptibility. The allele that has been detected in the highest proportion is HLA Cw*08.[1] [2]

The incidence increases in children under 18 years of age, due to the increasing prevalence of ACL injuries in the active adolescent population and in older adults, especially those over 40 years of age, due to degenerative changes in the joint. The age-related risk of developing arthrofibrosis is attributed to the mechanism of injury, activity level, and preoperative factors.[3] [4]

Females are 2.5 to 2.8 times more likely to develop arthrofibrosis, which is attributed to a combination of social, psychological, musculoskeletal, and hormonal factors. These include social pressure, fear and anxiety, joint laxity and muscle strength, smaller femoral notch, estrogen levels, and the menstrual cycle.[4] [5] [6]

A high body mass index increases the risk of ACL rupture and of developing arthrofibrosis following its reconstruction. This is associated with participation in high-impact sports.[7] An HbA1c greater than 6.5% is associated with a higher risk of arthrofibrosis, with a rate of 44%, the probability of its development is 16 times higher compared to those who do not suffer from diabetes, this is due to both systemic and localized inflammation observed due to diabetes and surgical intervention.[8]


 

Trauma-Related Factors

According to the literature, meniscal and concomitant ligament injuries contribute to 5.2% of the development of arthrofibrosis following ACL reconstruction. The development of arthrofibrosis associated with meniscal injury is primarily due to meniscal suturing and a restrictive rehabilitation regimen following surgery.[9] Injuries to three or more ligaments requiring surgical intervention are associated with increased stiffness. Damage to articular cartilage due to the injury increases the risk of arthrofibrosis due to the formation of bone hematomas. More severe ACL injuries are more likely to develop arthrofibrosis because extensive soft tissue damage provokes a more intense inflammatory response and requires a longer surgical time.[10]


 

Surgical Factors

Surgical factors such as early surgical intervention, reduced preoperative range of motion (ROM), graft type, poor graft placement, extra-articular procedures, and meniscus repair favor increased myofibroblast proliferation and reduced apoptosis, leading to increased concentration of myofibroblasts in the synovial membrane, causing arthrofibrosis.[10] [11]

The most important factor in the development of arthrofibrosis is the time elapsed between the injury and surgery. Performing surgery before muscle tone and full mobility has been restored increases the risk of arthrofibrosis. It should be delayed until the inflammatory response subsides and the knee has significantly improved, as evidenced by a reduction in edema, swelling, and joint effusion, along with improved mobility.[7] [12]

According to current guidelines, surgery is performed between the 3rd week and the 5th month after the injury, ideally in the first 3 months, to allow for the reduction of irritation, initiate preoperative rehabilitation, and minimize the risk of damage to other tissues. After the 5th month, the risk of meniscal and chondral injuries increases.[5] [13] [14] [15]

Studies have shown that a reduced preoperative knee ROM is a risk factor for arthrofibrosis because the preoperative range of motion predicts the arc of motion after ligament reconstruction.[16] Preoperative rehabilitation should be initiated, consisting of short-term progressive exercise therapy focused on maximizing ROM and improving knee function.[17]

The choice of graft for ACL reconstruction may influence the development of arthrofibrosis. Previous studies have identified that patellar tendon and quadriceps tendon autografts pose a higher risk due to their greater stiffness and higher collagen content.[4] However, patellar tendon autograft remains the gold standard for ACL reconstruction due to its rapid integration into bone tunnels compared to other grafts. Studies suggest that allografts are associated with a lower risk of arthrofibrosis than autografts.[13]

Technical errors during ACL reconstruction are the main cause of failure of primary surgery. Improper graft positioning and excessive tension are most often associated with the development of arthrofibrosis. Tension depends on the position of the femoral and tibial tunnels, as they determine the graft insertion points. Ideally, the graft should be positioned at the anatomical site of the ACL; its correct placement achieves tension similar to that of the native ACL.[18] [19] [20]

During reconstruction, the reaction to debridement, perforation during tibial tunnel formation, and microtrauma of the graft are traumas to the soft tissues and the joint itself, which lead to an inflammatory response, promote the activation and proliferation of fibroblasts, resulting in the formation of a large amount of extracellular matrix and, ultimately, in the formation of fibrosis.[21] [22]

ACL reconstruction with concomitant procedures increases surgical trauma to the joint, triggering a more intense inflammatory response and predisposing to the development of arthrofibrosis.[23] [24] Repair of other ligaments is associated with longer postoperative immobilization. Meniscal repair increases the risk of arthrofibrosis by 10% due to a more restrictive rehabilitation protocol.[5]


 

Post-surgical Factors

Postoperative factors that influence the development of arthrofibrosis after ACL reconstruction include prolonged immobilization, inadequate rehabilitation, complex regional pain syndrome, infection, hematoma, and synovitis.[7] These factors promote a chronically inflamed joint, which undergoes cycles of oxidative stress in which cytokines and growth factors are released that intensify the inflammatory response, increasing the recruitment of inflammatory cells that promote fibroblast proliferation and reduce vascularization, leading to arthrofibrosis.[25]

Prolonged postoperative immobilization results in some degree of permanent loss of mobility, primarily 2-week immobilization.[1] An immobilized joint following trauma favors elevated levels of transforming growth factor beta 1 mRNA and proteins, which is chemoattractant and mitogenic for fibroblasts that can upregulate collagen synthesis due to the release of growth factors and proteases mediated by myofibroblasts and mast cells, this produces excess collagen in the joint which leads to stiffness and fibrosis.[26]

Inadequate postoperative rehabilitation promotes knee pain and inflammation, resulting in the formation of scar tissue that causes arthrofibrosis.[7] [12] Therapy begins without resistance for the first 2 weeks to reduce joint irritation, and resistance is added after 6 weeks. Continuous passive motion reduces the risk of postoperative stiffness by reducing pain and initiating joint movement early.[27]

Fear of pain or damage to the ligament reconstruction leads to avoidance of movements perceived as risky, and postoperative pain and inflammation lead to avoidance of full range of motion, limiting joint ROM. Inadequate pain management limits the ability to perform movements necessary to regain active knee range of motion. Analgesia and functional rehabilitation are crucial to prevent the progression of arthrofibrosis. Providing an educational plan and incorporating neuromuscular education techniques can benefit the patient.[28]

Infection following ACL reconstruction is a complication that can occur in approximately 0.14–5.7% of cases and reduces the likelihood of a good functional outcome due to knee stiffness and cartilage damage. It manifests as a very swollen and painful knee, limited ROM, a sudden increase in throbbing pain, persistent and rapidly increasing joint effusion, local erythema, warmth, intermittent fever, and hyperemia with discharge. Infection is primarily of bacterial origin and is due to contamination of the graft with bacterial flora from the skin during harvesting or graft preparation.[29] [30]

A hematoma after ACL reconstruction increases the risk of developing arthrofibrosis because blood products generate an accumulation of inflammatory mediators in the joint that promote the formation of excessive scar tissue. It is characterized by persistent pain, and swelling, reduces the patient's willingness to begin rehabilitation, and is mainly associated with the use of pharmacological thromboprophylaxis. Agents such as low molecular weight heparin, factor Xa inhibitors, fondaparinux, and warfarin increase the risk of requiring another intervention for arthrofibrosis 2.6 times more, while the use of aspirin does not.[5] [31]


 

 

Conclusion

Arthrofibrosis following ACL reconstruction has a multifactorial etiology, with key factors including sex, age, genetic predisposition, timing of the surgical intervention, reduced preoperative range of motion, graft type, technical errors, prolonged immobilization, inadequate rehabilitation, infection, and hematoma. These factors dysregulate the inflammatory response, leading to excessive extracellular matrix production and the development of fibrosis. Early identification of these factors can reduce the risk of arthrofibrosis development.

ACL reconstruction requires careful preoperative planning and meticulous surgical technique. Graft selection should be individualized and meet the biomechanical properties of the native ACL. It is important to consider that certain graft types and surgical techniques may increase the risk of arthrofibrosis. Currently, patellar tendon autografts are more commonly associated with this complication, whereas the use of allografts is linked to a reduced risk.


 

 

Conflicto de Interés

Ninguno.

Evidence Level

EBM: Recommendation: Grade A Level of Scientific Evidence: Level IV



Address for correspondence

Alejandro Antonio Monzón Rodas
Universidad de San Carlos de Guatemala
Ciudad de Guatemala
Guatemala   

Publication History

Received: 19 March 2025

Accepted: 02 April 2025

Article published online:
20 May 2025

© 2025. Sociedad Chilena de Ortopedia y Traumatologia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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