Plica Syndrome

Etiology

Healthcare professionals do not universally agree upon the embryological development of the knee joint. One common theory is the menisci, cruciate ligaments, and a joint cavity all develop when the fetus is 8 weeks old. Over the next 2 weeks, the septa of the synovium are resorbed, and larger cavitation develops which ultimately becomes the knee joint. If this larger cavitation fails to join together fully, mesenchymal tissue may develop synovial folds. These synovial folds are plicae.[1]

Epidemiology

The literature varies widely regarding the estimated prevalence of plica syndrome. Most report a 10% prevalence of plica syndrome based on arthroscopic studies.[1] It is estimated that plica syndrome is underdiagnosed because the symptoms are similar to other etiologies of knee pain. A study in Japan looked at 3889 knee joints during arthroscopy and found the incidence of medial plica to be 79.9%.[2] This did not specify that the plica was the etiology of symptoms in all these patients and thus this was the incidence of plica, not plica syndrome. Other literature reviews show autopsy results that found plica are present in approximately 50% of individuals.[3] Thus, the prevalence of plica on arthroscopy does not correlate with the prevalence of clinical plica syndrome.

Pathophysiology

Plicae are normal structures in the knee joint that come together in utero. Plicae typically involute when the fetus is around 12 weeks old, but autopsy results indicate plicae are present in 50% of individuals.[3]

For the approximately 50% of people who have a plica, there are four different normal plicae. These are suprapatellar, infrapatellar, medial, and lateral. It is not uncommon for a patient to have more than one plica.

The suprapatellar plica is found between the knee joint and the suprapatellar bursa. The infrapatellar plica is found between the intercondylar notch and the synovium around the infrapatellar fat pad. The medial plica is found between the infrapatellar fat pad and the medial aspect of the knee joint. Medial plicae are the most common type of plicae and are the most common to be symptomatic.[4] The lateral plica is the rarest of the plica. It is found between the infrapatellar region and the lateral patellar facet.

It is important to note that not all plicae cause pain. Normal plicae can become painful as a result of undergoing inflammation. This inflammation can then lead to a tight, fibrotic plica that can manifest in symptoms during flexion of the knee when it leads to impingement between the patella and femur.

History and Physical

Patients with plica syndrome will experience pain on the anterior aspect of the knee associated with clicking or popping. The anterior knee pain is a hallmark of plica syndrome. Pain can be brought on by rising from a chair, squatting, stairs, or other activities that load the patellofemoral joint. The history may include a twisting injury or blunt trauma, or there could be no history of injury or trauma. There are secondary causes of plica that should be considered when obtaining a history. These include hemarthrosis secondary to hemophilia, intra-articular lesions, loose foreign bodies, and rheumatoid arthritis.

On physical exam, a taut band may be palpable under the skin which may be tender to palpation. If this is the case, the contralateral knee should be examined to see if there is a plica causing tenderness to palpation on that knee as well. Other findings on physical exam may include an effusion, tight hamstrings, and tight quadriceps.

Two physical exam techniques can suggest plica syndrome. These tests are the Stutter test and the Hughston test. When both tests are positive, the diagnosis of plica syndrome should be suspected. If only 1 of the 2 is positive, plica syndrome is less suspicious, but should still be considered. The Stutter test is performed by having the patient sit upright with the legs dangling off the edge of the exam table at a 90-degree angle. The examiner places his or her index and middle fingers on the center of the patella of the affected leg. The patient then extends the affected leg while the examiner feels for a stutter of the patella. Feeling a stutter is a positive test. In the Hughston test, the patient lies supine with the knee extended. The examiner stands on the side of the affected knee with one hand around the plantar aspect of the patient's heel and the other palm covering the patient's patella. The examiner then pushes the patella medially and internally rotates the tibia while taking the patient's knee through flexion and extension. A positive Hughston's test is when the patient experiences pain or the practitioner appreciates popping during the range of motion.

Evaluation

Anteroposterior (AP), lateral, and skyline radiographs should be obtained when plica syndrome is suspected, although they will often be normal even if plica syndrome is the diagnosis.

The utility of magnetic resonance imaging (MRI) is controversial in the workup of plica syndrome. Plicae are only occasionally apparent on MRI. It is easier to see plica on MRI when an effusion is present. If plicae are apparent, they will appear with low-signal intensity. Symptomatic plicae can sometimes be differentiated from normal plicae on MRI because symptomatic plicae could appear thick and may have synovitis. This is opposed to normal plicae which may appear thin.[5] As a result, MRI can be useful as part of pre-operative planning and is important in evaluating other potential causes of knee pain.

A literature review revealed multiple studies which looked at 492 knees and compared the sensitivity and specificity of physical exam compared to ultrasound and MRI. The results were that physical exam had a 90% sensitivity and 89% specificity, ultrasound had 90% sensitivity and 83% specificity, and MRI had 77% sensitivity and 58% specificity. The gold standard for diagnosis is arthroscopy.[6]

Treatment / Management

Treatment options for plica syndrome include stretching and strengthening, intraplical corticosteroid injections, and arthroscopy.

The Sakakibara classification system is important when considering treatment because type A and B have a low likelihood to cause pain. Type C and D, on the other hand, can impinge on the medial condyle due to their larger size. Type A and B respond much better to conservative therapies than C and D do. As a result, patients with type A and B should be encouraged to attempt conservative therapy first.

Conservative treatment for plica syndrome can either be performed at home by the patient or via formal physical therapy. Either way, this would involve lower extremity stretching and knee extension exercises with the goal of strengthening the joint capsule musculature, hamstrings, and quadriceps. Nonsteroidal anti-inflammatory drugs (NSAIDs) and ice are reasonable treatments at this stage to calm down inflammation. Conservative management also includes avoiding activities that incite pain. At least 3 months of conservative treatment is recommended before advancing to more aggressive therapies. One study demonstrated that 49 of 55 patients treated conservatively returned to their prior baseline without a return of symptoms. The remaining 6 patients were also able to return to their prior baseline, but they reported an occasional return of symptoms, which were tolerable.[7]

Often the next step if stretching and strengthening do not release symptoms is intraplical corticosteroid injection. This is a reasonable treatment option, especially early in the disease process when conservative management has not provided relief. Research of 31 patients with medial plica syndrome treated with intraplical steroid injection found that 73% had a full return to activity with complete pain relief.[8]

Resection via arthroscopy is a favorable option for medial plicae that do not respond to conservative treatment. Resection is also reasonable when cartilage damage is suspected, such as in type C and D lesions, even if conservative measures have not been completed for 3 months. Another study showed that compared to conservative treatment, arthroscopy yields a greater therapeutic effect for plica syndrome and the effect is longer lasting.[9]

Differential Diagnosis

Symptoms of plica syndrome are often similar to many other etiologies of knee pain. As a result, the differential diagnosis can be lengthy and may include osteochondritis dissecans, patellofemoral syndrome, patellofemoral subluxation, meniscal disease, osteoarthritis, patellar tendonitis, cruciate ligament pathology, and pigmented villonodular synovitis. These differential diagnoses can be differentiated from plica syndrome as follows:

• Osteochondritis dissecans: Differentiated with radiographs and MRI.
• Patellofemoral syndrome: Patellofemoral knee pain can be difficult to distinguish from plica syndrome as the symptoms overlap significantly. Other causes of patellofemoral pain, such as chondromalacia, may be apparent in history and imaging.
• Patellofemoral subluxation: Patients with patellofemoral subluxation will often provide a history consistent with subluxation and may have apprehension with a displacement of the lateral patella.
• Meniscus pathology: Meniscus pathology will have tenderness at the joint line, whereas plica pain tends to localize above the joint line. Also, physical exam tests such as Apley, Thessaly, bounce home, and/or McMurray can help distinguish the 2 entities.
• Osteoarthritis: Differentiated with radiographs showing decreased joint space, osteophytes, subchondral sclerosis, subchondral cysts, among others, although this does not rule out also having symptomatic plicae.
• Patellar tendonitis: Differentiated by palpating the patellar tendon on either the proximal or distal attachment.
• Cruciate ligament dysfunction: Differentiated by physical exam techniques suggesting laxity including Lachman, anterior drawer, or posterior drawer that would likely be positive in cruciate ligament injury.
• Pigmented villonodular synovitis (PVNS): Differentiated via MRI.

Staging

Medial plicae are most commonly symptomatic and can be classified by the Sakakibara arthroscopic classification:

• Type A: Elevation in the synovial wall
• Type B: Appear shelf-like, but not covering the anterior surface of the medial femoral condyle
• Type C: Large, shelf-like appearance and covering the anterior surface of the medial femoral condyle
• Type D: Fenestrated plica with a central defect

Prognosis

Once appropriately treated, there is a favorable prognosis for plica syndrome. One study of 969 patients found that at a median follow-up of 27.5 months, 10% had not responded to treatment, whereas 26% improved, and 64% were symptom-free.[10]

Complications

One study suggests that the friction between a medial plica and the medial femoral condyle may lead to cartilage damage.[11] Another study that looked at 48 patients who had severe medial compartment osteoarthritis requiring total knee replacement supported this. All 48 of these patients had a medial plica and a cartilaginous lesion on the medial femoral condyle abutting the plica.[12]

If left untreated, medial plica syndrome can cause grade IV Outerbridge chondral lesions, which is when the subchondral bonehead is exposed.[13] These are difficult to treat and preventing grade IV Outerbridge lesions from occurring highlights the importance of prompt diagnosis and treatment of plica syndrome.