Arthrofibrosis is a severe complication after anterior cruciate ligament (ACL) reconstruction, characterized by excessive scar tissue formation in the knee joint. It causes painful restriction of knee motion, frequently involving both extension and flexion loss. Primary arthrofibrosis occurs without clear secondary causes such as prolonged immobilization, infection, or surgical errors. The pathophysiology involves fibroblast proliferation and increased production of extracellular matrix proteins, mediated by growth factors and cytokines. Genetic factors likely contribute to risk.
The pathophysiology of primary arthrofibrosis implicates inflammatory cells, fibroblasts, cytokines, and growth factors. inflammatory cells such as macrophages likely initiate the process through release of fibrogenic cytokines like TGF-β1 and PDGF-B.1,2 These stimulate fibroblast proliferation and collagen synthesis, leading to disorganized scar tissue deposition in the knee joint. The fibrotic process shows similarities to other conditions like pulmonary fibrosis and scleroderma.
The factors predisposing to primary arthrofibrosis after ACL reconstruction are not fully defined. Younger age, closed kinetic chain exercises early after surgery, and concomitant injuries/procedures have been associated with increased risk.4 There is growing evidence for genetic susceptibility related to variations in HLA antigens.5 The study by Skutek et al in the original post found associations between arthrofibrosis and HLA-Cw*08 as well as HLA-Cw*07 and DQB1*06 negativity. Larger studies are needed to confirm these preliminary HLA findings.
Prevention through early mobilization and gradual rehabilitation is important. Once arthrofibrosis develops, nonsurgical modalities include physical therapy for range of motion and strength and intra-articular corticosteroid injections. Operative treatment is often necessary, involving arthroscopic or open surgical lysis of adhesions and scar tissue combined with manipulation under anesthesia to regain knee extension and flexion. Results are generally good, but some residual stiffness may persist.
In summary, primary arthrofibrosis is a challenging complication after ACL surgery. The pathophysiology suggests complex interactions between inflammatory cells, fibroblasts, and mediators that stimulate excessive scar formation. Certain genetic factors may confer increased risk. Early rehabilitation and motion are critical to prevention. Further research is warranted to better define the mechanisms and risk factors for arthrofibrosis after ACL reconstruction.
1. Bosch U, Zeichen J, Skutek M, et al. Arthrofibrosis is the result of a T cell mediated immune response. Knee Surg Sports Traumatol Arthrosc. 2001;9(5):282-289.
2. Murakami S, Muneta T, Furuya K, Saito I, Miyasaka N, Ezura Y. Immunohistologic analysis of synovium in infrapatellar fat pad after anterior cruciate ligament injury. Am J Sports Med. 1995;23(6):763-768.
3. Marshall RP, McAnulty RJ, Laurent GJ. The pathogenesis of pulmonary fibrosis: is there a fibrosis gene? Int J Biochem Cell Biol. 1997;29(1):107-120.
4. Millett PJ, Wickiewicz TL, Warren RF. Motion loss after ligament injuries to the knee. Part I: Causes. Am J Sports Med. 2001;29(5):664-675.
5. Skutek M, Elsner HA, Slateva K, et al. Screening for arthrofibrosis after anterior cruciate ligament reconstruction: analysis of association with human leukocyte antigen. Arthroscopy. 2004;20(5):469-473.
6. Shelbourne KD, Patel DV, Martini DJ. Classification and management of arthrofibrosis of the knee after anterior cruciate ligament reconstruction. Am J Sports Med. 1996;24(6):857-862.