Plica Syndrome

Plica syndrome of the knee is a constellation of signs and symptoms that occur secondary to injury or overuse. Plica is a Latin word meaning "fold." This term is simply a descriptive one; there is no empiric evidence that true folding of the synovial lining ever occurs.

Synovial plicae are normal structures found in many knees. Under normal circumstances, these plicae are not associated with any painful conditions. However, with the right combination of events they can become quite painful.[1] These events almost certainly include a somewhat exuberant plical shelf at baseline combined with an inciting event (either discrete macrotrauma or repeated microtrauma). Once an inflammatory process is established, the normal plical tissue may hypertrophy into a truly pathologic structure (see the image below).[2]  

Plica syndrome. Typical appearance of a large beefy medial parapatellar plica.

Both the normal and the pathologic aspects of various synovial plicae readily became apparent to orthopedic surgeons with the advent of arthroscopy. Arthroscopy is a Japanese innovation that changed the face of orthopedics forever. Kenji Takagi (1888-1963) and Masaki Watanabe and others in Japan drove its early development, and early adopters in North America, such as Robert Jackson and Lanny Johnson, helped popularize this technology.[3, 4]

Future treatment of plica syndrome may be supplemented further by improved brace designs and pharmacologic treatments. Earlier recognition of patients with the syndrome might facilitate syndrome resolution by such means, in contrast to patients who experience years of symptoms.

This article provides an overview of the pertinent anatomy and of diagnosis and treatment of plica syndrome of the knee.[5, 6]

During embryonic development, the knee is divided initially by synovial membranes into three separate compartments. By the third or fourth month of fetal life, the membranes are resorbed, and the knee becomes a single chamber. If the membranes resorb incompletely, various degrees of septation may persist. These embryonic remnants are known as synovial plicae. Four types of synovial plicae of the knee have been described in the literature.[7, 8]

The suprapatellar plica (plica synovialis suprapatellaris) divides the suprapatellar pouch from the remainder of the knee. Rarely, it may initiate a suprapatellar bursitis or perhaps chondromalacia, and symptoms secondary to these conditions may be present.[9] Anatomically, this plica can be complete or in the form of a porta, which only partially separates the compartments. It courses from the anterior femoral metaphysis or the posterior quadriceps tendon to the medial wall of the joint. It usually begins proximal to the superior pole of the patella but may begin anywhere.

The mediopatellar plica (referred to by some as the Aoki ledge or Iino band) is the most frequently cited cause of plica syndrome. It lies on the medial wall of the joint, coursing from a suprapatellar origin obliquely down to insert on the infrapatellar (ie, Hoffa) fat pad. This plica, sometimes known as a shelf, lies in the coronal plane.[10, 11, 12]

The rare and poorly documented lateral synovial plica is a wider and thicker band than the medial plica. It is located along the lateral parapatellar synovium, inserting on the lateral patellar facet and extending distally toward the infrapatellar region. It has been argued that the lateral plica, rather than being a vestigial septum, is derived from the parapatellar adipose synovial fringe.

The plica that is the least symptomatic of all, the infrapatellar plica (ligamentum mucosum) is, ironically, the one most commonly encountered. Some authors even claim that the infrapatellar plica is never responsible for plica syndrome. This bell-shaped remnant originates in the intercondylar notch, widens as it sweeps through the anterior joint space, and attaches to the infrapatellar fat pad. This plica's ability to obscure portal entry sites or interfere with visualization during arthroscopy is touted as its only significance.

Kim et al classified ligamentum mucosum (ie, infrapatellar plica) into the following five groups[13] :

• Separate type - 60.5%
• Split type - 13.5%
• Vertical septum type - 10.5%
• Fenestra type - 1.0%
• None present - 14.5%

In a clinical study of 400 knees in more than 350 patients, Kim and Choe found suprapatellar plicae in 87%, mediopatellar plicae in 72%, infrapatellar plicae in 86%, and lateral plicae in 1.3%.[14]

Not all synovial plicae are symptomatic. For those that are, the cause may not always be apparent.

Inflammation leads to edema, thickening, and decreased elasticity of the plica. The plica may develop irregular edges and may snap over the femoral condyle, leading to a secondary synovitis and chondromalacia. Loose areolar fatty tissue appears to become gristlelike, and when plicae are soft, wavy, and vascular with synovium-covered edges, they are not pathologic. Numerous studies describe pathologic plicae as thick, fibrotic, white, and inelastic. Histologically, fibrosis, hyalinization, and calcification are present.[6]

The etiology of symptomatic plica is unclear. Potential causes of inflammation include repetitive stress, a single blunt trauma, loose bodies, osteochondritis dissecans, meniscal tears, or other aggravating knee pathology. The most common symptomatic plica is medial plica; occasionally, suprapatellar plica may also be symptomatic.[15, 16, 17, 18, 19]

A popular theory for the initiation of inflammation is that the plica is converted to a bowstring, which causes it to contact the medial femoral condyle. During flexion of the knee, the plica causes an abrasion to the condyle, resulting in symptoms. Others contend that a plica need not contact the femoral condyle to cause symptoms.

One study found that the onset of symptoms was usually delayed until adolescence. Possible explanations include a decrease in tissue elasticity with age, and a biomechanical change resulting from a growth spurt.

The precise incidence of plica syndrome is a source of ongoing controversy. The incidence of symptomatic or pathologic plica versus asymptomatic plica is even more debatable. Some authors contend that distribution is regional. Distribution differences based on race or ethnicity may exist.

The incidence of suprapatellar plica has been reported to be as low as 11%; however, one study reported a rate of 89% on autopsy.

Medial plica has a reported incidence of 18-60%. The incidence of medial plica in anatomic studies is similar to that in arthroscopic studies. The most commonly cited incidence range in the literature is approximately 20-25%. Nakayama investigated the incidence of medial plicae in 3889 knee joints in the Japanese population and classified the plicae into four types according to Sakakibara’s classification, as follows[20] :

• Type A - Those with a cordlike elevation in the synovial wall
• Type B - Those with a shelflike appearance but not covering the anterior surface of the medial femoral condyle
• Type C - Those with a large shelflike appearance covering the anterior surface of the medial femoral condyle
• Type D - Those with double insertions into the medial wall or having a central defect

The incidence of medial plicae was 79.9%; the incidence of Sakakibara types A, B, C, and D medial plicae was 35.2%, 22.4%, 12.3%, and 10%, respectively.[20]

Little literature exists on lateral plica. Most of this literature is Japanese, and few cases have been reported in English.[21]  The incidence of this kind of plica is lower than 1%.

Dupont et al found some type of inferior plica in 65% of their 200 dissected cadaveric knees. They stated that it was the most frequently found plica. In their review of the literature, infrapatellar plica was most common in some studies but not in others.[7]

The outcome of surgical treatment for well-selected patients with plica syndrome is very good.[22, 23, 24] A clinical trial conducted by Johnson et al in England demonstrated a success rate higher than 80%.[25] In this same study, nearly 50% of patients in the control group experienced continued symptoms severe enough that they later returned for definitive arthroscopic resection of their plicae.

In a predominantly adult population (average age, 25 years; range, 11-56 years), Kasim and Fulkerson reported 88% moderate-to-substantial improvement at an average of more than 4 years after resection of localized segments of painful retinacula (ie, plicae) about the knee.[26]

The spectrum and diversity of symptoms can make plica syndrome difficult to pinpoint. Often, symptoms resemble or overlap with those of other pathologic conditions.[27, 28]

Reported symptoms include the following:

• Anterior or anteromedial knee pain
• Intermittent or episodic pain
• Clicking
• High-pitched snapping
• Occasional giving way
• Locking (really pseudolocking) and catching
• Aggravation of symptoms by activity, by stair climbing, or by prolonged standing, squatting, or sitting

Meniscal tears, patellar tendinitis, Osgood-Schlatter disease, Sinding-Larsen-Johansson disease, and patellar instability are the most commonly found concomitant conditions.

On physical examination, the patient typically has tender points along the medial and inferior aspect of the patella (see the first image below); in some instances, a painful, hypertrophied membrane is palpable. The inferomedial quadrant (see the second image below) is the most consistently painful region. Occasionally, a medial apprehension test of the patella elicits a positive response, but careful evaluation reveals that it is due to direct tenderness to palpation in the region of the plica and is not true patellar instability.

Plica syndrome. Patient pointing to the painful area of her knee.

Plica syndrome. The inferomedial quadrant is usually the most painful region by physical examination. This area is highlighted by several X's in this figure. A painful taut band of tissue that emanates from the central portion of the medial patella may often be palpated (3 o'clock position on the figure).

Rovere et al stated that a palpably tender plica in the absence of an intra-articular effusion conclusively establishes a diagnosis of plica syndrome, provided that other causes of knee pain are ruled out.[29] A taut articular band that reproduces the patient's pain upon palpation of the medial peripatellar region is virtually pathognomonic for plica syndrome. This may be referred to as a positive TARP sign, in which TARP stands for the following:

• T - Taut
• A - Articular band
• R - Reproduces
• P - Pain

In addition to the history and physical examination, a radiograph is recommended to exclude other causes of knee pain. As stated previously, plica syndrome is difficult to differentiate from other pathology and remains a diagnosis of exclusion. Other adjunctive diagnostic studies include contrast pneumoarthrography and double-contrast arthrography, yet arthroscopy remains the diagnostic standard.[30, 31]

Plain radiographs of the knee are appropriate in the evaluation of a patient with plica syndrome. However, they are useful only in that they help eliminate other diagnoses.[32]

Magnetic resonance imaging (MRI) is of limited value in detecting normal or pathologic plicae about the knee.[33] It rarely demonstrates these structures conclusively (see the image below). Jee et al published one of the only papers that touts the usefulness of MRI in diagnosing medial parapatellar plicae.[34] They reported 95% sensitivity and 72% specificity with their MRI approach. It should also be noted that plica syndrome has been a major research interest at their center. To the best of the authors' knowledge, no other center has matched these numbers.

Plica syndrome. Axial MRI demonstrating abundant medial plical tissue.

Arthroscopy is the standard for definitive diagnosis of plica syndrome.[30, 31]  Most plicae are found incidentally during knee arthroscopy.

Munzinger classified the mediopatellar plica into four types on the basis of appearance, as follows[35] :

• A - Cordlike
• B - Shelflike, does not cover medial femoral condyle
• C - Does cover medial femoral condyle
• D - Double insertion

Other authors believe that to differentiate between symptomatic and asymptomatic plicae, the following criteria must be met upon arthroscopic examination:

• Plica must appear
• Impingement must be visualized
• Chondromalacia must be present in the areas of impingement

The histology of a symptomatic plica is typically that of synovial tissue (type A macrophagelike cells and type B fibroblastlike cells) immersed in an inflammatory reaction.[36] In other instances, the histology may show dense fibrotic tissue that only secondarily impinges upon articular surfaces to produce pain. Kasim and Fulkerson found fibrosis, vascular proliferation, and small nerves with deceased myelin (neuromata) on histologic analysis of specimens from their plica patients.[26]

Jee et al staged medial parapatellar plicae according to how far the plica extends into the region of the patellofemoral joint, as follows[34] :

• 1+ (does not extend to the medial edge of the patella)
• 2+ (extends to the medial third of medial facet of the patella)
• 3+ (extends over one third to two thirds of the medial facet)
• 4+ (extends over more than two thirds of the medial facet)

The most common symptomatic plica is medial parapatellar plica. Surgical intervention for plica syndrome should be considered when symptoms have persisted and efforts at nonoperative management have failed for a period typically approaching 6 months. Permanent modification of athletic activity is usually another option, but patients rarely find it acceptable. Moreover, surgical treatment offers such predictable results that withholding treatment could arguably be considered ethically questionable. Longer periods between symptom onset and surgical treatment appear to be associated with cartilage damage.[37]

Patients with absolute contraindications for surgical treatment include those who are considered unfit for surgery from a medical standpoint. Active soft-tissue infection around the knee that precludes the use of standard arthroscopic portals is another contraindication. Relative contraindications include hypercoagulability syndromes that predispose the patient to thrombotic complications, as well as excessive risk for reflex sympathetic dystrophy (RSD).

Medical treatment of plica syndrome has been driven largely by empiric evidence. A structured program of stretching and strengthening exercises often leads to some improvement. This may include short-arc quadriceps extension exercises (terminal ~20° of extension). These exercises are aimed at optimizing patellofemoral biodynamic relationships in an effort to control symptoms.

A patellar knee sleeve worn during sporting activities (usually a neoprene-type brace) may also be a useful adjunct for many athletes. In addition, nonsteroidal anti-inflammatory drugs (NSAIDs) are a time-tested and confirmed aid for many athletes with plica syndrome.

Surgical therapy for plica syndrome is virtually always arthroscopic. The arthroscopic surgeon must exclude other potential intra-articular causes of knee pain and then address any pathologic plicae. Plica resection may be performed with arthroscopic hand instruments, a motorized soft-tissue resector, or certain commercially available electrothermal devices.

Preparation for surgery

The preoperative phase of treatment involves optimizing the patient's knee strength and flexibility in an effort to streamline postoperative rehabilitation. Preoperative preparation of the patient also involves education and appropriate goal setting. For instance, the patient should understand that therapeutic exercises typically begin shortly after surgery (hours to days) and that a full return to sports can be realized soon thereafter (days to weeks). Patients who know this in advance tend to achieve these goals quite readily.

Operative details

After arthroscopic evaluation establishes that no other intra-articular abnormalities must be addressed, the plica can be resected. With whatever tools work best, the plica should be resected back to a point where it no longer impinges on articular structures. With beefy synovitic plicae extending into the patellofemoral joint space (typically ≥ 50%; see the first image below), this may require extensive debridement (see the second image below). With tough, fibrotic plicae draping over the medial femoral condyle, this may involve little more than disruption of the tight band.

Plica syndrome. Preoperative appearance of medial parapatellar plica (a 4+ plica by the Jee classification, extending across more than two thirds of the medial facet of the patella).

Plica syndrome. Postoperative appearance of the same patient as in Image 5 after plical resection.

At times, even a suprapatellar plica may lead to symptoms. Strover et al reported on an arthroscopic technique demonstrating the pathomechanics of such suprapatellar plicae.[38] They recommended that the arthroscope should be inserted through a lateral suprapatellar portal. Proximal visualization is then optimized.

In those patients whose suprapatellar plica is symptomatic, progressive flexion of the knee results in the plical tissue becoming taut. It also makes contact with the medial femoral condyle and even becomes entrapped between the quadriceps tendon and the medial femoral condyle.[38]

Postoperatively, the patient is started on a structured course of therapeutic exercise that initially emphasizes reestablishment of active quadriceps control and firing. This progresses to regaining full range of motion and then full strength. The patient concludes therapeutic recovery by gradually performing more and more sport-specific exercises until a controlled reentry to the sport is achieved.

Complications of surgical treatment of plica syndrome are really complications associated with arthroscopic surgery of the knee. These include septic arthritis, neurapraxias or neuromas, and synovial fistulae. RSD may also occur after such surgery. The incidence of each of these complications is extremely low (< 1% in most cases). Only patients with particular risk factors (eg, diabetes, steroid dependence, or history of RSD) may be at significantly higher risk.

Follow-up care focuses on confirmation that symptoms have abated. True recurrence of the original plical pathology is quite rare and is more likely to represent either an incomplete resection or entirely new knee pathology. Continued use of a patellar stabilizing-type brace is preferred by many patients.