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Knee Arthrofibrosis

Prevention and Management of a Potentially Devastating Condition

Colin L. Eakin, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO. 3 - MARCH 2001


In Brief: Knee arthrofibrosis, which usually occurs after trauma or surgery, can inhibit joint biomechanics. An elaborate interaction of growth factors and other inflammatory mediators initiates and coordinates this deleterious tissue proliferation. Knowledge of risk factors can aid clinicians in helping patients avoid knee arthrofibrosis. Once the condition is present, a history and examination are imperative to institute the most appropriate treatment regimen. Nonoperative measures can be used as therapy, though surgery is often necessary for optimal results.

Arthrofibrosis is an abnormal proliferation of fibrous tissue in and around a joint that can lead to loss of motion. This condition is especially common at the knee and represents a challenge for the clinician. Widespread fibrous tissue growth can fundamentally alter knee biomechanics. The adhesions that form often lead to stiffness and abnormal joint contact pressures and predispose the joint to cartilage degeneration. Attempts to regain normal function of an arthrofibrotic joint can lead to further tissue injury, resulting in swelling and additional discomfort. Injudicious surgical release or removal of this tissue can stimulate more fibrous tissue formation and worsen the condition.

Since arthrofibrosis of the knee can involve a wide variety of types, causes, and severities, statistics on its incidence depend on the parameter assessed. Studies of knee motion loss following surgery document incidences between 4% and 35% (1-4). Harner et al (5) reported an 11% incidence in patients who had had anterior cruciate ligament (ACL) reconstruction. Arthrofibrosis in their report was defined as loss of extension of more than 10° or flexion of less than 125°. Other authors (6,7) have reported similar incidences. The incidence of fibrous tissue proliferation in the intercondylar notch following ACL reconstruction, the so-called cyclops lesion, is between 2% and 4% (8,9). Some authors have noted that men have a higher incidence of arthrofibrosis than women (5).

Pathogenesis

Arthrofibrosis is thought to result from abnormal fibrous tissue hyperplasia (10,11) and usually follows injury or surgery to the knee. Trauma initiates the clotting cascade and is followed by migration of inflammatory cells, then fibroblasts, to the injured tissue. The ensuing surge in collagen synthesis is regulated by an incompletely understood interaction of growth factors, including platelet-derived growth factor, fibroblast growth factor, insulin-like growth factor-1, and transforming growth factor-beta. An abnormal expression of these proteins may accentuate the degree of fibrous tissue formation (12,13). Recently, researchers have isolated a high concentration of type 6 collagen in tissue samples from the infrapatellar fat pad and intercondylar synovium in arthrofibrotic knees, suggesting that disordered regulation of collagen 6 synthesis may contribute to arthrofibrosis (14).

Concomittant ACL injury. An overwhelming number of the studies evaluating arthrofibrosis pathogenesis have examined its incidence following ACL injury and reconstruction (2,5,8,11,15-24). In one series (25), 40 of 44 patients presenting with arthrofibrosis had undergone ACL reconstruction. In studying synovial tissue after ACL injury, Murakami et al (12) demonstrated the presence of fibrogenic cytokines and growth factors at sites of fibrosis up to 3 months after injury. The researchers proposed that such cytokines may be involved in new collagen synthesis and the accumulation of collagen in the synovium following ACL injury and reconstruction (12,13), but they did not demonstrate a direct correlation between synovial collagen content and loss of knee flexion or extension (13).

Joint motion. The sites of fibrous tissue formation can have implications for subsequent motion limitations (26). Presence of such tissue near the cruciate ligaments and tibiofemoral joint is thought to be primarily responsible for extension loss, with flexion loss resulting from fibrous tissue formation around the patellofemoral articulation and subsequent adherence of the patella to the trochlear groove (27). Similarly, fibrous tissue formation at the tibial attachment of the ACL following reconstruction—the cyclops lesion—has been postulated to block terminal extension (2,8,28). Some authors (28) have observed a transformation of this fibroconnective tissue into fibrocartilage over time and postulate that this process occurs in response to compression loading of the nodule.

Biomechanics. The predominant effect of knee fibrosis that has been studied is the alteration in patellofemoral articulation. Fibrosis lowers the patella, a condition termed infrapatellar contraction syndrome (11), patella infera, or patella baja (29,30). Both extrinsic mechanisms, such as quadriceps muscle weakness, and intrinsic mechanisms, such as abnormal collagen response to injury, can contribute to this process (29). Wojtys et al (29) have proposed that active contraction of myofibroblasts within the matrix may lead to collagen bundle folding and contribute to intrinsic shortening of the tendon. Immobilization and the lack of active quadriceps contraction may exacerbate tendon shortening (29,31-34).

Van Eijden et al (35) used a mathematical model to show that patellar tendon shortening causes the anterior tibial translational forces to increase near terminal extension. They theorized that as the patellar tendon shortened, the quadriceps force necessary to generate the same extension moment would have to increase, yielding greater contact pressures between the patella and femur.

This model has since been confirmed experimentally. Using a cadaveric model, Ahmad et al (36) fastened a metal plate across the patellar tendon to simulate adhesions between the tendon and proximal tibia. Patellar tendon adhesion was observed to translate the patella more medially and distally, creating an apparent patella infera. This effect was more pronounced at knee angles near full extension. Although adhesion did not change the total area of patellofemoral contact, the contact position of both the patella and femur shifted distally. Finally, effective patellar tendon length and knee extension force both were significantly reduced by patellar tendon adhesion, with the effect greatest at full extension and diminishing with flexion (figure 1). Ahmad et al concluded that patellar tendons adhesions could lead to increased patellofemoral joint reaction force. They also suggested that the altered location of contact could cause anterior knee pain after knee trauma or surgery.

[Figure 1]

Ultimately, these biomechanical changes lead to patellofemoral arthrosis, and many have commented on the risk of progressive joint deterioration and patellofemoral arthrosis to the affected knee (1,11,25,29,30). Cosgarea et al (30) observed degenerative changes in 89% of patients who underwent surgery for arthrofibrosis. Sachs et al (37) noted an association between persistent flexion contracture, resultant quadriceps weakness, and the presence of patellar pain.

Etiology

The development of knee arthrofibrosis is likely multifactorial, with a number of risk factors identified. Immobilization or immobility after trauma or surgery can facilitate the proliferation of fibrous tissue and is a known risk factor (11,27,30,38). Even without external immobilization, quadriceps inhibition or inactivity following injury can limit knee motion and predispose the patient to fibrous tissue proliferation (11,29).

Knee injury severity can affect the return of motion and development of arthrofibrosis. Several authors have reported an increased incidence of arthrofibrosis following multiple-ligament injuries and when multiple procedures are performed (3,5,21,39). In particular, simultaneous medial collateral ligament (MCL) repair appears to increase the incidence of arthrofibrosis following ACL reconstruction (5,21). More proximal MCL injuries may have a higher association with knee motion limitation (39). The effect of simultaneous ACL reconstruction and meniscal repair is less clear: One study (40) showed a slight increase in arthrofibrosis (6% to 10%), while another (6) found no significant increase.

Timing. The timing of ACL reconstruction is thought to play a role also. Many authors (2,5-7,12,17,24,30,41) have suggested that surgery performed in the acute postinjury period (within 3 or 4 weeks) has a higher risk of arthrofibrosis. Shelbourne and Johnson (22) reported that eight of nine consecutive patients referred because of arthrofibrosis had undergone ACL reconstruction within 2 weeks of injury. However, other authors (42) have reported no difference in the rate of loss of extension between acute and delayed ACL reconstructions. Bach et al (43) proposed that ACL injuries sustained during loading activities such as football, basketball, volleyball, and rugby may involve a heightened inflammatory response compared with those that occur during unloading activities such as skiing, and may therefore warrant greater delay before surgery.

Graft substrates. Choice of graft material may be a factor in the development of fibrotic changes following ACL reconstruction. Burks et al (44) demonstrated patellar tendon shortening after harvest of the central third in dogs, even when the defect was not reapproximated and there was no postoperative immobilization. Other authors (45) have shown extensive tendon and fat pad proliferation and fibrosis following autogenous patellar tendon graft harvest and ACL reconstruction. However, a study by Murakami et al (13) showed no significant difference in synovial fibrosis between semitendinosus-gracilis graft harvest and patellar tendon graft harvest used for ACL reconstruction, suggesting that other factors are equally or more important than graft type in predicting postoperative fibrosis. To date, no studies have directly compared the risk of arthrofibrosis with autograft and allograft materials.

Technique errors. Intraoperative technical errors can also predispose the joint to arthrofibrosis (43). The most common error leading to loss of flexion occurs when the graft is misplaced anteriorly on the femur. As the femoral condyles roll back during knee flexion, excessive strain develops within the substance of the graft, leading to the limitation of knee flexion, failure of the graft, or both. Another common mistake is graft placement in the anterior tibial tunnel, which may result in impingement in extension (46,47). Excessive graft tension that overstrains the joint has also been implicated in loss of knee motion (15,43). Open arthrotomy has also been identified as a factor in the development of arthrofibrosis, presumably because of increased trauma to the tissues about the knee (17).

Exercise timing. Finally, the timing of knee range of motion has been shown to affect the incidence of postoperative arthrofibrosis (17,18,48,49). In their retrospective study of 373 patients who underwent intra-articular ligament reconstruction, Graf et al (17) found that delaying motion until the second day following surgery significantly increased the incidence of arthrofibrosis. Cosgarea et al (6) reported a nearly eightfold decrease in the incidence of arthrofibrosis following ACL reconstruction if surgery was delayed until 3 weeks after injury, the leg was braced in full extension postoperatively, and a range-of-motion program was started within 24 hours after surgery. Other authors have reported similar experiences (2,5,17,24).

Clinical Evaluation

History. A thorough history is imperative in evaluating the patient who has knee arthrofibrosis. Complete accounts should be obtained of any knee injuries and treatments received, including reports from any previous surgeries. Often, patients have pain as the chief complaint rather than limited motion. Any pain should be localized, if possible, and its nature sought. Constant aching that is difficult to localize is typical of diffuse synovitis or fibrosis, whereas complaints of sharp, pinching pain can indicate the presence of impinging fibrous tissue. The patient can often provide insight about presence and location of fibrous tissue by describing various positions or activities that reproduce discomfort.

While the link between knee fibrosis and pain is well documented (11,13), the exact relationship requires clarification. Possible explanations include coexisting intra-articular pathology (such as meniscal lesions or degenerative arthrosis) or the stiffer fibrotic tissue causing adjacent parts of the synovial membrane to stretch with knee motion (13). Impingement of the fibrotic fat pad on the femur has also been described (50,51) and may hasten the development of cartilage degeneration at the trochlear groove or patella.

Ongoing treatments, such as anti-inflammatory or other medications and any past or current courses of physical therapy should be noted. Understanding the patient's activities and goals can help the clinician recommend an appropriate treatment regimen. Having the patient rate how well the knee functions at the initial evaluation can be useful when reviewing the result of subsequent treatment.

If patients are aware of limited knee motion, they can help identify how activities are affected. They can, for example, relate problems with gait or difficulty with flexion or extension. Associated symptoms to recognize include popping or cracking, swelling, buckling, catching, or locking.

Physical exam. The physician begins with observation of the patient's knee, making note of the location and quality of scars from previous surgeries. Any asymmetries between the involved and uninvolved knees should be noted, including differences in muscle development or color. Similarly, skin texture and temperature abnormalities can signal the presence of reflex sympathetic dystrophy. Gait and the ability to squat should be assessed, with the degree and location of any crepitus noted. The knee should then be palpated for areas of tenderness. In particular, the physician should assess the suppleness of the patellar tendon and fat pad. Joint-line tenderness may indicate concomitant meniscal pathology. Effusion or warmth in comparison to the other knee may indicate ongoing synovitis.

Active and passive range of motion should be observed and measured with a goniometer. The clinician should attempt to identify whether a loss of extension represents a flexion contracture (indicative of posterior capsular scarring) or an extension block (indicative of excessive fibrous tissue anteriorly in the intercondylar notch and fat pad). Such differentiation has important implications for subsequent treatment. Patients may sometimes be able to give their impressions of the reason for any flexion or extension limitation. Physicians should also document any pain elicited throughout the range of motion.

Audible indications of fibrous tissue should be noted; these include clunking, popping, and grating. Anterior scar tissue formation (eg, cyclops lesions) will cause clunking and popping during the terminal 25° to 30° of extension and can thus be differentiated from patellofemoral crepitus. The knee should also be assessed for locking. Finsterbush et al (52) reported on 12 of 51 patients with partial or complete ACL tears who had locked knees on examination, and they found at arthroscopy that fibrosis and adhesions of the fat pad and the synovium adjacent to the ACL stump had caused the locking.

Special assessment should be made of the patella, including its tracking, tilt, and overall mobility. Fibrosis of the fat pad or medial or lateral gutters will often severely limit patellar mobility. Noting the patellar location with respect to the tibial tuberosity can help in assessing possible patellar infera.

Typically, instability is not a concern with arthrofibrosis. However, patients will occasionally have concomitant chronic ligamentous insufficiency or failed ligament reconstruction. For this reason, knee laxity in all directions should be graded using standard tests, comparing the involved with the uninvolved knees. An arthrometric evaluation to assess for residual laxity is performed on all knees that have undergone ACL reconstruction.

Imaging. When arthrofibrosis is suspected, imaging can provide valuable additional information. A complete set of radiographs of both knees should also be obtained. Evaluation of the anteroposterior and Rosenberg posteroanterior (53) views (taken with the patient's knees flexed 30° to 45° and the beam angled down) can indicate the degree of arthrosis, if any. Merchant views (taken tangential to the patellofemoral joint with the knee in approximately 30° of flexion) can show changes consistent with patellofemoral arthrosis. Lateral views at 30° and 60° are also helpful in determining the presence of patellofemoral arthrosis and changes in patellar height that may signal patella infera or infrapatellar contraction syndrome (11,29). In patients who have undergone ACL or other ligament reconstruction, radiographs can be used to assess tunnel placement (54).

Although the clinical examination should provide the basis for establishing the diagnosis, magnetic resonance imaging (MRI) has been increasingly used in the evaluation of patients with arthrofibrosis (48,55,56). Recht et al (56) showed the efficacy of MRI for identifying anterior arthrofibrosis (cyclops lesions) in patients with complaints of anterior knee pain following ACL reconstruction, and Howell et al (47) demonstrated abnormal signal changes in impinged grafts when compared with normal knees. MRI in these patients has the added value of being able to help exclude the presence of any concomitant pathology, including chondral defects, loose bodies, and meniscus tears.

Nonoperative Treatments

Prevention. By far, the most effective approach to knee arthrofibrosis is prevention. As previously noted, this includes early restoration of knee motion following injury or surgery and delaying surgical reconstruction until joint inflammation has subsided and normal or near-normal range of motion has been restored. In the past, it was not uncommon for patients undergoing ligament reconstruction to have the knee immobilized in a cast or brace so grafts could heal without undue tension and stretching. As confidence in graft fixation has increased, immobilization has been eliminated because of the risk of arthrofibrosis and the recognition of the benefits of early motion on graft healing (25,57).

Most clinicians now advocate an accelerated rehabilitation program after cruciate ligament reconstruction such as the one described by Shelbourne et al (24). These early range-of-motion exercises help prevent the development of contractures (2,23,37), and immediate knee range of motion can be initiated without risk of ACL graft injury if graft placement is anatomic (43). Roberts and Terry (58) have outlined factors that can impair return of motion and thus increase risk for postoperative arthrofibrosis (table 1).


TABLE 1. Conditions That Increase the Risk of Loss of Motion After Knee Surgery and Their Treatment

Condition Treatment

Hemarthrosis Aspirate early
Large effusion Aspirate early
Immobilization Early recognition and debridement
Multiple procedures Consider CPM postoperatively
Combined knee and femoral fracture Early stabilization and CPM
Nonisometric cruciate reconstruction Early recognition or notchplasty; manipulation
Cyclops lesion Resection
Reflex sympathetic dystrophy Early recognition, aggressive treatment; consider CPM
Traction Avoid prolonged skeletal traction

CPM = continuous passive motion

Reproduced with permission from DeLee JC, Drez D (eds): Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 1994, pp 1528-1539.


Drugs and other modalities. Anti-inflammatory modalities have a role in minimizing the formation of adhesions following injury or surgery to the knee. Some authors (1) have used intravenous corticosteroids in the immediate postoperative period. In addition, oral nonsteroidal anti-inflammatory drugs are commonly prescribed for several days to weeks to reduce postoperative inflammation. Cryotherapy is often encouraged as well to limit swelling and inflammation. Certain nutritional supplements have been recommended by some clinicians for the prevention of postoperative arthrofibrosis, though currently little basic science or clinical research has demonstrated their efficacy.

Physical therapy and casts. Once arthrofibrosis is diagnosed, a course of physical therapy is often recommended to regain range of motion through gentle manipulation. Little data exist, however, as to the efficacy of nonoperative treatment of knee arthrofibrosis. Some authors have proposed the use of supplemental dropout or extension casts (19,22) or Dynasplints (25) (Dynasplint Systems, Inc, Severna Park, Maryland) in conjunction with physical therapy to facilitate the return of range of motion.

Operative Therapies

The decision window. Determining when to cease nonoperative measures and resort to surgery is sometimes a difficult decision (figure 2: not shown). Several authors (11,29,30) have stressed the importance of early identification and expeditious management of arthrofibrosis before the process can lead to irreversible changes. Some studies (11,29) note a finite period of about 3 months in which the effects of arthrofibrosis such as patella infera can be corrected. After that, irreversible ultrastructural changes occur within the patellar tendon, and cartilage degeneration from abnormal joint loading can occur at the patellofemoral articular interface. However, some authors recommend that surgical intervention be withheld until active quadriceps muscle function has been restored. Otherwise, quadriceps muscle function can be further inhibited and the patient can be predisposed to recurrent infrapatellar contracture (29).

Surgical techniques. Once the decision to proceed with surgical intervention has been made, an appropriate technique must be chosen. Manipulation under anesthesia is commonly proposed as a first-line treatment for knee arthrofibrosis. While this can be a simple means of correcting contractures, it involves indiscriminate tearing of connective tissues that can take place in tissue planes different from the original planes (38). Avulsion of softened articular cartilage and fractures are additional hazards. Most clinicians recommend that manipulation, if performed, be done with great care, and it is usually more effective for patients with flexion, rather than extension loss.

Arthroscopic lysis of adhesions has been well described as effective (2,8,19,22,30,59-64) and can usually be performed on an outpatient basis (figures 3 and 4). Some authors have suggested that this technique is more effective for localized as opposed to diffuse forms of arthrofibrosis, which might regain a satisfactory arc of motion but often remain symptomatic from other factors (59). Cosgarea et al (30) suggest that patients with localized fibrous tissue in the anterior interval of the knee may respond better to this treatment. Arthroscopic resection of a cyclops lesion at the anterior region of the intercondylar notch has been shown to improve extension and relieve pain (8). If graft impingement occurs in extension, this technique is combined with notchplasty (46).

[Figure 3]

[Figure 4]

Shelbourne et al (19) have recently proposed a classification scheme for the arthroscopic treatment of patients with arthrofibrosis (table 2). In a study on the treatment of 72 patients according to this scheme, patients with type 1 arthrofibrosis noted 7° improved extension, type 2, 14° extension, type 3, 13° extension and 28° flexion, and type 4, 18° extension and 27° flexion. All groups had less stiffness postoperatively and improved self-evaluation and functional knee scores.


TABLE 2. A Classification System for Arthroscopic Treatment of Patients With Arthrofibrosis

Type Extension Loss Flexion Loss Proposed Treatment

1 <10° None Arthroplastic debridement, notchplasty

2 >10° None Arthroplastic debridement, notchplasty, anterior scar resection

3 >10° >25°, tight patella Arthroplastic debridement, notchplasty, anterior scar resection, medial or lateral gutter release

4 >10° >30°, patella infera Arthroplastic debridement, notchplasty, anterior scar resection, more extensive medial or lateral gutter release to completely free patella

Adapted from Shelbourne et al (19).


When nonoperative and arthroscopic techniques are unsuccessful at restoring knee motion, open debridement is usually recommended. Various techniques have been employed, usually involving extensive release of the involved capsule and resection of all fibrous tissue (1,11,25,65). Lobenhoffer et al (65) reported successful treatment of knee flexion contractures with posterior capsulotomy via a posteromedial incision.

Postoperative management. Care after surgery is critical to ensuring a successful result and preventing recurrence. As noted, a key element of such management is immediate initiation of a range-of-motion program to maintain the gains obtained in surgery. Adequate pain control is crucial to allow intensive physical therapy in the immediate postoperative period. Epidural anesthesia has been used effectively for several days in patients to provide effective pain relief (1,7). Continuous passive motion has been described in the treatment of arthrofibrosis, though some literature suggests limited benefit after 3 days following ligament reconstruction (66).

Parting Advice

The treatment of the patient with knee arthrofibrosis remains a challenge. Despite advances in treatment, some patients who develop knee arthrofibrosis continue to have limited range of motion or pain, and many note at least some limitation in their activities. With this in mind, the clinician must be cognizant of the risk factors that can lead to this potentially devastating condition and manage it expeditiously.

References

  1. Millett PJ, Williams RJ III, Wickiewicz TL: Open debridement and soft tissue release as a salvage procedure for the severely arthrofibrotic knee. Am J Sports Med. 1999;27(5):552-561
  2. Fisher SE, Shelbourne KD: Arthroscopic treatment of symptomatic extension block complicating anterior cruciate ligament reconstruction. Am J Sports Med 1993;21(4):558-564
  3. Noyes FR, Barber-Westin SD: Reconstruction of the anterior and posterior cruciate ligaments after knee dislocation: use of early protected postoperative motion to decrease arthrofibrosis. Am J Sports Med 1997;25(6):769-778
  4. Strum GM, Friedman MJ, Fox JM, et al: Acute anterior cruciate ligament reconstruction: analysis of complications. Clin Orthop 1990;253(Apr):184-189
  5. Harner CD, Irrgang JJ, Paul J, et al: Loss of motion after anterior cruciate ligament reconstruction. Am J Sports Med 1992;20(5):499-506
  6. Cosgarea AJ, Sebastianelli WJ, DeHaven KE: Prevention of arthrofibrosis after anterior cruciate ligament reconstruction using the central third patellar tendon autograft. Am J Sports Med 1995;23(1):87-92
  7. Wasilewski SA, Covall DJ, Cohen S: Effect of surgical timing on recovery and associated injuries after anterior cruciate ligament reconstruction. Am J Sports Med 1993;21(3):338-342
  8. Jackson DW, Schaefer RK: Cyclops syndrome: loss of extension following intra-articular anterior cruciate ligament reconstruction. Arthroscopy 1990;6(3):171-178
  9. 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 1996;4(4):194-199
  10. Lindenfeld TN, Wojtys EM, Husain A: Operative treatment of arthrofibrosis of the knee. J Bone Joint Surg (Am) 1999;81(12):1772-1784
  11. Paulos LE, Rosenberg TD, Drawbert J, et al: Infrapatellar contracture syndrome: an unrecognized cause of knee stiffness with patella entrapment and patella infera. Am J Sports Med 1987;15(4):331-341
  12. Murakami S, Muneta T, Furuya K, et al: Immunohistologic analysis of synovium in infrapatellar fat pad after anterior cruciate ligament injury. Am J Sports Med 1995;23(6):763-768
  13. Murakami S, Muneta T, Ezura Y, et al: Quantitative analysis of synovial fibrosis in the infrapatellar fat pad before and after anterior cruciate ligament reconstruction. Am J Sports Med 1997;25(1):29-34
  14. Zeichen J, van Griensven M, Albers I, et al: Immunohistochemical localization of collagen VI in arthrofibrosis. Arch Orthop Trauma Surg 1999;119(5-6):315-318
  15. Bach BR Jr, Jones GT, Sweet FA, et al: Arthroscopy-assisted anterior cruciate ligament reconstruction using patellar tendon substitution: two- to four-year follow-up results. Am J Sports Med 1994;22(6):758-767
  16. Graf B, Uhr F: Complications of intra-articular anterior cruciate reconstruction. Clin Sports Med 1988;7(4):835-848
  17. Graf BK, Ott JW, Lange RH, et al: Risk factors for restricted motion after anterior cruciate reconstruction. Orthopedics 1994;17(10):909-912
  18. Noyes FR, Mangine RE, Barber S: Early knee motion after open and arthroscopic anterior cruciate ligament reconstruction. Am J Sports Med 1987;15(2):149-160
  19. 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
  20. Shelbourne KD, Patel DV: Management of combined injuries of the anterior cruciate and medial collateral ligaments. Instr Course Lect 1996;45:275-280
  21. Shelbourne KD, Baele JR:Treatment of combined anterior cruciate ligament and MCL injuries. Am J Knee Surg 1988;1:56-58
  22. Shelbourne KD, Johnson GE: Outpatient surgical management of arthrofibrosis after anterior cruciate ligament surgery. Am J Sports Med 1994;22(2):192-197
  23. Shelbourne KD, Trumper RV: Preventing anterior knee pain after anterior cruciate ligament reconstruction. Am J Sports Med 1997;25(1):41-47
  24. 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 1991;19(4):332-336
  25. Steadman JR, Burns TP, Peloza J et al: Surgical treament of arthrofibrosis of the knee. J Orthop Tech 1993;1:119-127
  26. Mariani PP, Santori N, Rovere P, et al: Histological and structural study of the adhesive tissue in knee fibroarthrosis: a clinical-pathological correlation. Arthroscopy 1997;13(3):313-318
  27. Enneking WF, Horowitz M: The intra-articular effects of immobilization on the human knee. J Bone Joint Surg (Am) 1972;54(5):973-985
  28. Marzo JM, Bowen MK, Warren RF, et al: Intraarticular fibrous nodule as a cause of loss of extension following anterior cruciate ligament reconstruction. Arthroscopy 1992;8(1):10-18
  29. Wojtys EM, Oakes B, Lindenfeld TN, et al: Patella infera syndrome: an analysis of the patellar tendon pathology. Instr Course Lect 1997;46:241-250
  30. Cosgarea AJ, DeHaven KE, Lovelock JE: The surgical treatment of arthrofibrosis of the knee. Am J Sports Med 1994;22(2):184-191
  31. Tardieu C, Blanchard O, Tabary JC, et al: Tendon adaptation to bone shortening. Connect Tissue Res 1983;11(1):35-44
  32. Tipton CM, Matthes RD, Maynard JA, et al: The influence of physical activity on ligaments and tendons. Med Sci Sports 1975;7(3):165-175
  33. Piper TL, Whiteside LA: Early mobilization after knee ligament repair in dogs: an experimental study. Clin Orthop 1980;150(Jul-Aug):277-282
  34. Vailas AC, Tipton CM, Matthes RD, et al: Physical activity and its influence on the repair process of medial collateral ligaments. Connect Tissue Res 1981;9(1):25-31
  35. van Eijden TM, Kouwenhoven E, Weijs WA: Mechanics of the patellar articulation: effects of patellar ligament length studied with a mathematical model. Acta Orthop Scand 1987;58(5):560-566
  36. Ahmad CS, Kwak SD, Ateshian GA, et al: Effects of patellar tendon adhesion to the anterior tibia on knee mechanics. Am J Sports Med 1998;26(5):715-724
  37. Sachs RA, Daniel DM, Stone ML, et al: Patellofemoral problems after anterior cruciate ligament reconstruction. Am J Sports Med 1989;17(6):760-765
  38. Evans EB, Eggers GW, Butler JK, et al: Experimental immobilization and remobilization of rat knee joints. J Bone Joint Surg (Am) 1960;42:737-758
  39. Robins AJ, Newman AP, Burks RT: Postoperative return of motion in anterior cruciate ligament and medial collateral ligament injuries: the effect of medial collateral ligament rupture location. Am J Sports Med 1993;21(1):20-25
  40. Austin KS, Sherman OH: Complications of arthroscopic meniscal repair. Am J Sports Med 1993;21(6):864-868
  41. Mohtadi NG, Webster-Bogaert S, Fowler PJ: Limitation of motion following anterior cruciate ligament reconstruction: a case-control study. Am J Sports Med 1991;19(6):620-624
  42. Marcacci M, Zaffagnini S, Iacono F, et al: Early versus late reconstruction for anterior cruciate ligament rupture: results after five years of follow-up. Am J Sports Med 1995;23(6):690-693
  43. Bach BR Jr, Wojtys EM, Lindenfeld TN: Reflex sympathetic dystrophy, patella infera contracture syndrome, and loss of motion following anterior cruciate ligament surgery. Instr Course Lect 1997;46:251-260
  44. Burks RT, Haut RC, Lancaster RL: Biomechanical and histological observations of the dog patellar tendon after removal of its central one-third. Am J Sports Med 1990;18(2):146-153
  45. Atkinson TS, Atkinson PJ, Mendenhal HV, et al: patellar tendon and infrapatellar fat pad healing after harvest of an ACL graft. J Surg Res 1998;79(1):25-30
  46. Howell SM: Arthroscopic roofplasty: a method for correcting an extension deficit caused by roof impingement of an anterior cruciate ligament graft. Arthroscopy 1992;8(3):375-379
  47. Howell SM, Clark JA, Farley TE: Serial magnetic resonance study assessing the effects of impingement on the MR image of the patellar tendon graft. Arthroscopy 1992;8(3):350-358
  48. Noyes FR, Butler DL, Paulos LE, et al: Intra-articular cruciate reconstruction: I. perspectives on graft strength, vascularization, and immediate motion after replacement. Clin Orthop 1983;172(Jan-Feb):71-77
  49. Shelbourne KD, Nitz P: Accelerated rehabilitation after anterior cruciate ligament reconstruction. Am J Sports Med 1990;18(3):292-299
  50. Krebs VE, Parker RD: Arthroscopic resection of an extrasynovial ossifying chondroma of the infrapatellar fat pad: end-stage Hoffa's disease? Arthroscopy 1994;10(3):301-304
  51. Ogilvie-Harris DJ, Giddens J: Hoffa's disease: arthroscopic resection of the infrapatellar fat pad. Arthroscopy 1994;10(2):184-187
  52. Finsterbush A, Frankl U, Mann G: Fat pad adhesion to partially torn anterior cruciate ligament: a cause of knee locking. Am J Sports Med 1989;17(1):92-95
  53. Rosenberg TD, Paulos LE, Parker RD, et al: The forty-five degree posteroanterior flexion weight-bearing radiograph of the knee. J Bone Joint Surg Am 1988;70(10)1479-1483
  54. Manaster BJ, Remley K, Newman AP, et al: Knee ligament reconstruction: plain film analysis. AJR Am J Roentgenol 1988 Feb;150(2):337-342
  55. Jacobson JA, Lenchik L, Ruhoy MK, et al: MR imaging of the infrapatellar fat pad of Hoffa. Radiographics 1997;17(3):675-691
  56. Recht MP, Piraino DW, Cohen MA, et al: Localized anterior arthrofibrosis (cyclops lesion) after reconstruction of the anterior cruciate ligament: MR imaging findings. AJR Am J Roentgenol 1995;165(2):383-385
  57. Gomez MA, Woo SL, Amiel D, et al: The effects of increased tension on healing medial collateral ligaments. Am J Sports Med 1991;19(4):347-354
  58. Roberts TS, Terry R: Complications of knee surgery, in DeLee JC, Drez D (eds): Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 1994, pp 1528-1539
  59. Aglietti P, Buzzi R, De Felice R, et al: Results of surgical treatment of arthrofibrosis after ACL reconstruction. Knee Surg Sports Traumatol Arthrosc 1995;3(2):83-88
  60. Sprague NF: Motion-limiting arthrofibrosis of the knee: the role of arthroscopic management. Clin Sports Med 1987;6(3):537-549
  61. Vaquero J, Vidal C, Medina E, et al: Arthroscopic lysis in knee arthrofibrosis. Arthroscopy 1993;9(6):691-694
  62. Klein W, Shah N, Gassen A: Arthroscopic management of postoperative arthrofibrosis of the knee joint: indication, technique, and results. Arthroscopy 1994;10(6):591-597
  63. Parisien JS: The role of arthroscopy in the treatment of postoperative fibroarthrosis of the knee joint. Clin Orthop 1988;229(Apr):185-192
  64. Richmond JC, al Assal M: Arthroscopic management of arthrofibrosis of the knee, including infrapatellar contraction syndrome. Arthroscopy 1991;7(2):144-147
  65. Lobenhoffer HP, Bosch U, Gerich TG: Role of posterior capsulotomy for the treatment of extension deficits of the knee. Knee Surg Sports Traumatol Arthrosc 1996;4(4):237-241
  66. Richmond JC, Gladstone J, MacGillivray J: Continuous passive motion after arthroscopically assisted anterior cruciate ligament reconstruction: comparison of short- versus long-term use. Arthroscopy 1991;7(1):39-44

Dr Eakin is an orthopedic surgeon and chairman in the department of sports medicine at the Palo Alto Medical Clinic in Palo Alto, California. Address correspondence to Colin L. Eakin, MD, 795 El Camino Real, Palo Alto, CA 94301; e-mail to [email protected].


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