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Knee Arthrofibrosis

The term Knee arthrofibrosis has been used to describe a spectrum of knee conditions in which loss of motion is the major finding. It is perhaps best defined as a condition of restricted knee motion characterized by dense proliferative scar formation, in which intra-articular and extra-articular adhesions can progressively spread to limit joint motion. This dense scar tissue can obliterate the parapatellar recesses, suprapatellar pouch, intercondylar notch, and eventually the articular surfaces. Patella infera and chronic patellar entrapment also may develop as a consequence of this process.

Knee Arthrofibrosis was described as the fibroplastic response of the joint to trauma in 1951.

Knee Arthrofibrosis Causes

Knee Arthrofibrosis may occur as the result of the inflammatory cascade after injury or operative treatment. Although inflammation is undoubtedly present in a large number of individuals, it is not clear why an aggressive form of this condition may develop in some patients.

To diagnose Knee arthrofibrosis accurately, other causes of restricted active and passive motion of the knee must first be eliminated. Mechanical causes include loss of articular congruency (e.g., as a result of fracture, meniscal tear, or loose body), interruption of the extensor or flexor mechanism, substantial effusion, or nonisometric placement of a graft during reconstruction of the ACL.

Some investigators believe that an ACL reconstruction performed within 3 weeks after an injury may increase the likelihood of Knee arthrofibrosis although others disagree. Poor or unsupervised rehabilitation preoperatively or postoperatively, with delayed motion protocols, may further increase the risk.

Adhesions in the suprapatellar pouch
Adhesions in the suprapatellar pouch between the anterior femur and quadriceps muscle causing loss of flexion

Clinical Evaluation

Symptoms vary and often do not correlate with the severity of the condition. Since knee arthrofibrosis usually occurs after trauma or an operative procedure, pain and stiffness may be the initial symptoms:

  1. The presence of pain may complicate preexisting knee stiffness. Although pain can be present early, it often becomes more prominent when joint degeneration and arthritis occur because of long-standing Knee arthrofibrosis. Pain may also be constant, especially when it is associated with complex regional pain syndrome (CRPS).
  2. Decreased ROM
  3. Decreased patellar glide from cranially to caudally (best test)
  4. Decreased patellar tilt
  5. Warmth and swelling with surrounding atrophy
  6. Flexed-knee gait
  7. Shelf sign (late finding).
See Also: Complex Regional Pain Syndrome (CRPS)
Positive shelf sign
Positive shelf sign characterized by an increased slope between the inferior pole of the patella and the proximal tibia with the knee in extension. This occurs secondary to obliteration of the retropatella tendon bursa with adhesions to the anterior tibia

Patients with Knee arthrofibrosis present with persistent stiffness, pain, and typically a painful flexed-knee gait. Warmth and swelling will be present in the active phase, and there will commonly be surrounding atrophy. Notable physical findings include decreased ROM and decreased patellar glide. However, one must be aware that during the normal healing response, the patella will exhibit decreased mobility between weeks 4 and 12, with a gradual return of mobility as week 16 approaches.

Quadriceps function can be decreased or absent because of pain. As function of the quadriceps muscle decreases, the ability of the muscle to act as a shock absorber is lessened, which may lead to additional articular degeneration. Often, the knee is held in a flexed position, which encourages tightening of the posterior part of the capsule and the hamstrings.

Crepitus and weakness are frequently present with swelling following prolonged standing or walking. Even when the patient does not have pain, loss of motion and quadriceps weakness can be substantial impediments to the performance of activities of daily living. An antalgic, flexed-knee gait is often seen. Although effusion may be present, swelling is more often a result of inflamed, thickened capsular and pericapsular tissues.

Active and passive knee flexion and extension often are restricted in a capsular pattern, and the mediolateral and superoinferior patellar glides are reduced. This restriction of passive motion often has a spring-like end-feel, reflecting the density and stiffness of the thickened, inflamed, or scarred peripatellar tissue.


Standard x-rays: Anteroposterior, bent knee posteroanterior, and Merchant view x-rays should be obtained, in addition to an excellent lateral image of the knee in 30 degrees of flexion. The lateral image is crucial to evaluate for patella infera, which can be measured using the modified Insall-Salvati method.

The length of the patella tendon is measured from its origin from the inferior pole of the patella to its insertion at the proximal pole of the tibial tubercle. The length of the patella is then measured at its greatest diagonal length from its superior to inferior pole. The normal ratio of length of the patellar tendon:length of the patella should be approximately 1:1, with some minor gender variation. A ratio of less than 0.8 indicates patella infera.

patella infera
Lateral x-ray with the knee flexed 30 degrees demonstrating marked patella infera

Magnetic resonance imaging (MRI): MRI can be helpful to evaluate for causes of anterior impingement, including improper graft placement and exuberant scar formation anteriorly as well as the presence of a “pseudopatella tendon”.

infrapatellar contraction syndrome
Sagittal MRI of a patient with advanced infrapatellar contraction syndrome. A prominent pseudotendon can be seen posterior to the patellar tendon. This represents fibrosis and remodeling of the fat pad

Arthrofibrosis Classification

Knee motion loss can be graded based on deviation from normal flexion and extension or by the pathoanatomy causing the motion loss. Del Pizzo et al classified motion loss into the following 3 groups:

  1. Group 1 consisted of knees with extension less than 5 degrees and flexion greater than 110 degrees,
  2. Group 2 had extension of 5 to 10 degrees with flexion between 90 and 110 degrees,
  3. Group 3 was limited to extension greater than 10 degrees or flexion less than 90 degrees.

These were characterized as mild, moderate, and severe, respectively.

Knee Arthrofibrosis has also been classified by its pathoanatomy:

In the suprapatellar classification by Sprague et al:

  1. Group 1 consisted of discreet bands or a single sheet of adhesions traversing the suprapatellar pouch.
  2. Group 2 involved complete obliteration of the suprapatellar pouch and peripatellar gutters with masses of adhesions,
  3. Group 3 included the above with extracapsular involvement with bands of tissue from the proximal patella to anterior femur. Suprapatellar adhesions result in flexion loss only.

Infrapatellar entrapment may be associated with atypical pain, loss of extension and flexion, and sometimes patella infera. It can be classified as primary or secondary, such as entrapment caused by nonisometric graft placement. It can also be divided into 3 distinct stages:

  1. Stage I, the prodromal stage, there is periarticular inflammation and swelling combined with immobility and quadriceps weakness as demonstrated by an extension lag. Tenderness is noted about the patellar tendon and active ROM is painful. There is decreased excursion of patellar glide tests and patellar tilt, although not rigidly fixed in the early stage.
  2. Stage II, the active stage, there is essentially no patellar tilt, decreased medial to lateral glide, and loss of anterior tilt. There may be a positive shelf sign. A positive shelf sign is characterized by an increased slope between the inferior pole of the patella and the proximal tibia with the knee in extension. A positive shelf sign is typically a late finding that indicates significant chronicity and possible patella infera. Its appearance is due to the adhesion of the patella tendon to the anterior tibia.
  3. Stage III, the residual stage, is characterized by slightly more supple peripatellar and retinacular tissues but with more significant patellofemoral arthrosis as demonstrated by patellofemoral crepitation on examination and decreased joint space seen on x-rays. Patella infera is usually present.

Knee Arthrofibrosis Treatment

Knee Arthrofibrosis Treatment includes:

  1. Anti-inflammatory drugs
  2. ROM exercises and the stretching of specific structures.
  3. When a plateau has been reached during rehabilitative efforts to restore motion or when there is progressive loss of motion, additional intervention of a gentle manipulation of the knee under anesthesia may result in improvement. Closed manipulation or vigorous attempts to gain passive motion may cause indiscriminate tearing of intraarticular tissue, excessive tibiofemoral and patellofemoral compression with the risk of chondral damage or fracture, rupture of the patellar ligament, and even femoral fracture. Manipulation has also been noted to initiate complex regional pain syndrome (CRPS).

Operative treatment of Knee Arthrofibrosis indications include:

  1. Decreased ROM: Pain and decreased ROM after ligament reconstruction surgery, especially when performed during the acute phase and in combination with extra-articular procedures.
  2. Failure of nonoperative treatment or manipulation alone: Patients who have failed to regain full ROM within 4 to 6 weeks after surgery should be counseled regarding possible intervention for Knee arthrofibrosis.
  3. If manipulation followed by judicious physical therapy, anti-inflammatory drugs, and hamstring stretching exercises between weeks 6 and 12 fails to bring about progress, then arthroscopic management is indicated typically between weeks 10 and 12.

Active inflammation: Surgical intervention should not be considered if the knee is still actively inflamed.

Extensor lag: Surgery should be delayed when there is an extensor lag. There should be full quad activation and strength prior to consideration of arthroscopic lysis of adhesions in the joint so as to maintain extension gains.


  1. Usher KM, Zhu S, Mavropalias G, Carrino JA, Zhao J, Xu J. Pathological mechanisms and therapeutic outlooks for arthrofibrosis. Bone Res. 2019 Mar 26;7:9. doi: 10.1038/s41413-019-0047-x. PMID: 30937213; PMCID: PMC6433953.
  2. Shelbourne KD, Patel DV, Martini DJ. Classification and management of arthrofibrosis of the knee after anterior cruciate ligament reconstruction. Am J Sports Med. 1996 Nov-Dec;24(6):857-62. doi: 10.1177/036354659602400625. PMID: 8947412.
  3. Sprague NF, III.: Motion-limiting arthrofibrosis of the knee: the role of arthroscopic management. Clin Sports Med 6:537–549, 1987.
  4. Steadman JR, Burns TP, Peloza J, et al: Surgical treatment of arthrofibrosis of the knee. J Orthop Tech 1:119–127, 1993
  5. Cosgarea AJ, DeHaven KE, Lovelock JE: The surgical treatment of arthrofibrosis of the knee. Am J Sports Med 22:184–191, 1994
  6. Klein W, Shah N, Gassen A: Arthroscopic management of postoperative arthrofibrosis of the knee joint: Indication, technique, and results. Arthroscopy 10:591–597, 1994.
  7. Sebastianelli WJ, Gillespie MJ, Hicks DG, et al: The histopathology of arthrofibrosis. Arthroscopy 9:359–360, 1993.
  8. Shelbourne KD, Johnson GE: Outpatient surgical management of arthrofibrosis after anterior cruciate ligament surgery. Am J Sports Med 22:192–197, 1994.
  9. Lindenfeld TN, Wojtys EM, Husain A: Operative Treatment of Arthrofibrosis of the Knee. J Bone Joint Surg Am 81-A:1772–1784, 1999.
  10. Delcogliano A, Franzese S, Branca A, et al: Light and scan electron microscopic analysis of cyclops syndrome: Etiopathogenic hypothesis and technical solutions. Knee Surg Sports Traumatol Arthrosc 4:194–199, 1996.
  11. Jackson DW, Schaefer RK: Cyclops syndrome: Loss of extension following intra-articular anterior cruciate ligament reconstruction. Arthroscopy 6:171–178, 1990.
  12. Shelbourne KD, Wilckens JH, Mollabashy A, et al: Arthrofibrosis in acute anterior cruciate ligament reconstruction. The effect of timing of reconstruction and rehabilitation. Am J Sports Med 19:332–336, 1991.
Last Reviewed
November 27, 2022
Contributed by

Orthofixar does not endorse any treatments, procedures, products, or physicians referenced herein. This information is provided as an educational service and is not intended to serve as medical advice.

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