Posterior Cruciate Ligament Pathology

Updated: Oct 19, 2021

Author: Matthew Lawless, MD; Chief Editor: Thomas M DeBerardino, MD

Overview

Practice Essentials

The posterior cruciate ligament (PCL) of the knee has been the subject of many debates. The role of the PCL has become a topic of interest across the subspecialties of trauma, sports medicine,[1] and knee arthroplasty. What, if any, treatment is required for a PCL-deficient knee is still a widely debated topic.

Isolated PCL injuries are defined by the degree of posterior translation of the tibia with respect to the distal femoral condyles with the knee in 90° of flexion. These injuries can be tears in continuity or complete ruptures of the PCL.

The consequences of an isolated PCL injury are poorly understood. PCL reconstruction has been advocated to restore knee kinematics to normal, which decreases the perceived risk of early degenerative joint disease.

Many procedures have been described that are no longer in general use and are mentioned here only for the sake of completeness and historical interest. These were nonanatomic reconstructions using transfers of various structures, including the medial head of the gastrocnemius, the popliteus, and the semimembranosus.[2] Current reconstruction is anatomic and attempts to recreate the PCL in the same manner as is done in anterior cruciate ligament (ACL) reconstruction.

Although the development of early degenerative disease is controversial and has not been proved with clinical studies, the ability to restore normal knee kinematics with PCL reconstruction has also not been demonstrated in vivo. Thus, the PCL continues to be a topic of research and debate.

Anatomy

The PCL originates from the junction of the femoral notch roof and the medial femoral condyle roughly 1 cm proximal to the articular surface.[3] The insertion of the PCL is on the posterior aspect of the proximal tibia at the fovea, a depression between the tibial plateaus 1 cm distal to the articular surface.[4] (See the images below.)

A view of the broad origin of the posterior cruciate ligament (PCL) on the medial femoral condyle of a left knee. The anterior cruciate has been removed for surgical reconstruction. Image courtesy of Janos P. Ertl, MD.

An additional view of the posterior cruciate ligament (PCL) broad origin and insertion in a knee pending anterior cruciate ligament (ACL) reconstruction. Image courtesy of Janos P. Ertl, MD.

The PCL is an intra-articular ligament but remains extrasynovial.[5, 6] The PCL is just medial to the center of the knee and averages 38 mm in length and 13 mm in thickness.[7] At its origin, the PCL averages 32 mm thickness, is narrowest at its mid substance, and then fans out to an average of 13 mm at its insertion.[7]

The PCL consists of two bundles, the anterolateral and posteromedial bundles. The anterolateral bundle originates anteriorly and inserts laterally. It is largest at the mid substance and is taut in flexion. The posteromedial bundle originates posteriorly and inserts medially. It is tight in extension and contains a small component that is isometric.[7, 8]

The vascular supply of the PCL depends in large part on the middle geniculate artery. A small component of the nutrient supply of the PCL is contributed by the synovium. Capsular branches of the inferior geniculate and popliteal arteries supply the PCL insertion.[9]

Fibers of the posterior articular nerve, a branch of the tibial nerve, are in the posterior capsule and the synovium lining the cruciate ligaments.[10] At the insertion of the cruciate ligaments, Golgi tendon–like organs are found and may play a role in proprioception.[11, 12]

The meniscofemoral ligaments contribute to the function of the PCL. The ligament of Humphrey is less than a third of the size of the PCL. It traverses anterior to the PCL origin and attaches to the posterior horn of the lateral meniscus. The ligament of Wrisberg is nearly half the size of the PCL. It traverses posterior to the PCL origin and inserts onto the posterior horn of the lateral meniscus.[13]

Pathophysiology

The PCL is stronger than its counterpart, the ACL, and it is less frequently injured.[14, 15] The PCL is the primary restraint to posterior tibial translation between 30° and 90°. At 90°, the PCL accepts 95% of posterior translational forces.[16] The in-situ forces of the PCL are 36 N in knee extension and 112 N in knee flexion.[17] Quadriceps and popliteus loading and weightbearing decreases the in-situ PCL forces, whereas hamstring loading increases the forces.[18, 19, 20]

Gollehon et al applied a 100 N posterior load to cadaver knees at 90° of flexion and reported that the normal posterior translation was 5 mm.[21] After isolated PCL sectioning, the posterior translation increased to 16 mm, whereas isolated lateral collateral ligament (LCL) and deep ligament complex sectioning increased the posterior translation by less than 3 mm. Sectioning of the PCL combined with sectioning of the LCL and deep ligament complex resulted in 25-30 mm translation; this amount was consistent throughout all positions of knee flexion.

The authors concluded that the PCL is the only primary restraint to posterior translation throughout the entire knee range of motion (ROM). Secondary restraints have a decreased role between 60° and 90° of knee flexion. With isolated PCL sectioning, external rotation and varus stability of the knee remained unchanged.[21]

The tensile strength of the PCL is greater than that of the ACL.[14] The ultimate load of the PCL, averaging 1627 N, is also greater than that of the ACL.[15, 22] The contributions to the PCL ultimate load of the anterolateral and posteromedial bundles remains controversial.[22, 23] The stiffness of the PCL averages 204 N/mm.[15]

The importance of the posteromedial bundle in bearing forces throughout knee ROM has been established.[18, 24, 25] Posteromedial-bundle forces have been found to exceed anterolateral-bundle forces in all angles of knee flexion.[18] Codominance of the anterolateral and posteromedial bundles has gained acceptance, instead of anterolateral bundle dominance.[24]

Etiology

Several mechanisms are responsible for PCL injuries. A direct posterior force on the proximal tibia with the knee flexed is commonly described. This mechanism occurs in dashboard injuries and in falls in which the foot is plantarflexed such that the tibial tubercle strikes the ground first. Hyperextension injuries of the knee are the most common cause of PCL tears from sports participation. Another mechanism related to sports injuries involves the combination of valgus and external rotation forces on a planted but unloaded lower extremity. The axial load of weightbearing is protective.[26, 27]

Epidemiology

The incidence of PCL injury is thought to be one tenth to one twentieth of that of ACL injury.[28] PCL injuries are present in 3.3-6.5% of all acute knee injuries.[29, 30]

Also, 40% of PCL injuries, including grade 1 and grade 2, are isolated injuries.[31] Some have estimated that 51% of PCL injuries are combined with other ligament injuries of the knee, most commonly the medial collateral ligament (MCL).[32, 33, 34] Grade 3 injuries are more likely to be combined injuries. However, many isolated PCL injuries are believed to be undiagnosed. About 2-5% of the participants at a National Football League Combine event were found to have isolated PCL laxity, and most could not recall having a significant injury.[35]

Prognosis

No series of acute isolated PCL reconstruction exists. The results in the literature are difficult to interpret because of variations in case selection and methods of evaluation. Techniques of reconstruction and the lengths of follow-up also vary. Consequently, the reported results vary.

Lipscomb et al reported the results for 25 patients with isolated acute or chronic PCL injuries treated with single-tunnel technique. At an average of 7 years after surgery, 60% had degenerative changes identified on radiographs.

Degenerative joint disease of the medial compartment is the most common late sequelae of PCL injury. Degeneration of the patellofemoral compartment also occurs, but less often.

Stannard et al reported the results of 30 multiligament knee injuries with PCL ruptures. This was the first reported series of PCL reconstructions using the combination of the tibial inlay technique and the double-tunnel technique. At a mean follow-up of 25 months, no statistical difference was found between injured knees and normal knees.

The outcome following PCL reconstruction for chronic PCL insufficiency has been worse than that of reconstruction for acute injuries. Postoperative posterior tibial laxity is greater after reconstruction for chronic PCL insufficiency than it is after acute PCL insufficiency, and patients with this injury cannot safely return to athletics. The diminished results of PCL reconstruction in patients with chronic knee insufficiency are thought to be the result of attenuation of the secondary restraints over time. PCL reconstruction inevitably fails if the posterolateral corner is insufficient or if the patient has developed a lateral thrust and the other pathology is not addressed.

Grade 1 and 2 PCL injuries have been reported to heal without any progression of posterior tibial laxity. Grade 3 tears do not heal and progressive laxity may develop as secondary and tertiary posterior tibial stabilizers are stressed over time.

Presentation

History

Patients with acute posterior cruciate ligament (PCL) injuries have a presentation similar to that of patients with most other knee injuries. Patients with acute isolated PCL injuries often have minimal symptoms consisting of pain, swelling, and instability. In many cases, a near-normal gait pattern is seen.[36]

Physical Examination

PCL injury should be suspected at the time of physical examination of any acute knee injury. (See the image below.) Complete examinations of the contralateral and injured knees should be performed for comparison. If a PCL insufficiency is noted, care must be taken to evaluate the competency of the posterolateral corner.

Clinical examination photograph of a ruptured posterior cruciate ligament (PCL) confirmed on a posterior sagittal radiograph. Image courtesy of Mervyn J. Cross, MBBS, FRACS.

With acute isolated PCL injuries, patients typically do not have joint-line tenderness. An effusion may or may not be present. Varus, valgus, and rotational stressing reveal no instability.

The posterior drawer test is the most reliable indicator during physical examination for a PCL injury.[37, 38] Positive posterior drawer test results are graded as follows:

Grade 1 - Laxity is noted compared with the contralateral knee, but the tibia remains anterior to the anterior aspect of the femoral condyles
Grade 2 - The anterior tibia can be subluxated equal to the anterior aspect of the femoral condyles
Grade 3 - The tibia subluxates posterior to the anterior aspect of the femoral condyles

With internal rotation, the posterior drawer test may elicit normal results for a PCL-insufficient knee because of the secondary restraint effect of the meniscofemoral ligaments.[39] If more than 10 mm of posterior tibial translation is noted at 90° of knee flexion, a combined PCL and posterolateral corner injury is present. The posterior drawer test result demonstrates more than 10 mm posterior translation at 30° of knee flexion when the posterolateral corner is disrupted, either in isolation or in combination with a PCL injury.

The dial test helps identify an associated or isolated posterolateral corner injury. Greater than 10° of increased external rotation of the leg compared with the contralateral leg at 30° and 90° of knee flexion is a positive finding signifying a posterolateral corner injury with a PCL injury.[2] A posterolateral corner injury has increased external rotation at 30º of flexion that (with PCL injury) stays the same or increases at 90º of flexion, whereas, at 90º of flexion without a PCL injury, less external rotation occurs.

Care must be taken in evaluating a knee with a positive dial test result to note that the lateral tibial plateau is subluxating posteriorly so that anterior subluxation of the medial tibial plateau secondary to an anterior cruciate ligament(ACL) and/or medial collateral ligament (MCL) disruption is not misinterpreted.[40]

The posterior sag, quadriceps active, external rotation recurvatum, and reverse pivot shift tests also aid in evaluating an acutely injured knee for PCL pathology.[41] (See the images below.)

The photo on the left demonstrates the clinical finding of the posterior tibia sag sign. A line drawn parallel to the patella accentuates the posterior tibia sag. The photo on the right demonstrates the quadriceps active drawer test described by Daniels; with the knee in 70-90° of flexion, the extensor mechanism is contracted, pulling the tibia anteriorly into a reduced position. Image courtesy of Janos P. Ertl, MD.

Close-up view of a posterior tibia sag with an incompetent posterior cruciate ligament (PCL). Image courtesy of Janos P. Ertl, MD.

Posterior sag of the left posterior cruciate ligament–deficient knee in comparison to the right knee. Note the posterior subluxation of the tibia relative to the femur of the left knee. Image courtesy of Robert Bronstein, MD.

Workup

Imaging Studies

Radiography

Initial radiographs should include weightbearing 45° posteroanterior (PA), lateral, and Merchant views. (See the images below.)

Lateral radiograph of a normal knee. In a normal knee, a line drawn along the posterior femoral condyle does not intersect the posterior tibial condyle. Image courtesy of Janos P. Ertl, MD.

Lateral radiograph of a knee with a posterior cruciate ligament injury. Note that the same line as in the image above bisects the posterior tibial condyle due to a posterior sag and an incompetent PCL. Image courtesy of Janos P. Ertl, MD.

An avulsion fracture from the origin of the posterior cruciate ligament (PCL) may be seen with hyperextension injuries. Avulsion fractures from the insertion of the PCL are associated with flexion injuries.[2] (See the images below.)

Radiograph depicting a chronic avulsed posterior cruciate ligament (PCL). Image courtesy of Mervyn J. Cross, MBBS, FRACS.

Sagittal view radiograph showing a posterior cruciate ligament (PCL) rupture. Note the posterior positioning of the tibia in relation to the femur. Image courtesy of Mervyn J. Cross, MBBS, FRACS.

Stress views are more sensitive than physical examination for diagnosing PCL tears. Posterior tibia translation of more than 8 mm on stress radiographs is consistent with a complete PCL tear, and translation of less than 8 mm suggests a partial tear.[42]

Magnetic resonance imaging

Magnetic resonance imaging (MRI) is 97-100% sensitive for PCL injuries.[43, 44, 45, 46, 47, 48, 49, 50, 51] (See the image below.) However, MRI is only 67% sensitive in distinguishing between partial and complete PCL tears.[52, 53]

An MRI showing a torn posterior cruciate ligament (PCL). Image courtesy of Mervyn J. Cross, MBBS, FRACS.

Bone scanning

A bone scan can be used to evaluate patients with chronic PCL insufficiency for early chondrosis. Increased signal at the medial femoral condyle and the patellofemoral compartment suggests degenerative changes secondary to PCL insufficiency.[2, 54]

Treatment

Approach Considerations

The long-term outcome of posterior cruciate ligament (PCL) insufficiency is difficult to predict, as is the outcome of PCL reconstruction.[55] Current reconstruction techniques (ie, the tibial inlay and double-tunnel methods) are promising with regard to their ability to create more normal knee responses to a posterior tibial force. However, the value of restoring knee posterior-tibial stability has not yet been correlated with patient function and outcome.

Many also believe that PCL reconstruction cannot prevent or delay the onset of degenerative changes in patients who have had a PCL injury.[29] One certainty is that isolated PCL tears are not benign injuries. Reconstruction is advocated for patients with grade 3 PCL injuries. The natural history of isolated grade 1 and grade 2 PCL injuries has been established, and the outcome following PCL reconstruction must prove to be better to warrant the procedure and lengthy rehabilitation.

Medical Therapy

The natural history of PCL insufficiency has been a subject of controversy. Several reports with small cohorts have reported good outcomes with conservative treatment. These reports include patients with acute and chronic PCL insufficiency, as well as isolated and combined PCL injuries.[56, 57, 58] Several authors have reported late chondrosis of the medial femoral condyle and the patellofemoral compartment in patients with PCL insufficiency.[39, 59, 60, 61, 62] The development of meniscus tears and abnormal contact pressures have been reported.[61, 63, 64]

Geissler et al evaluated patients with PCL injuries treated conservatively with arthroscopy at a mean of 2.2 years. They reported that 49% had grade 2 or higher articular cartilage lesions, and 36% had meniscal tears.[61]

Keller et al monitored 40 patients with isolated PCL injuries treated conservatively an average of 6 years. Among the patients, 90% complained of knee pain, 65% had activity limitations secondary to the knee, and 43% had difficulty walking. The patient complaints were correlated with objective measures of posterior laxity. In addition, the incidence of radiographic abnormalities increased in relation to the duration of follow-up.[60]

Boynton et al reported findings in 38 patients at a mean of 13.4 years after an isolated PCL injury treated conservatively. Among the patients, 81% complained of occasional knee pain, and 56% reported occasional knee swelling. Radiographic analysis also correlated the degree of degenerative changes to the duration of follow-up.[62]

Shelbourne et al reported that of 133 athletic patients treated conservatively for isolated acute PCL tears, 68 patients returned for clinical follow-up at a mean of 5.4 years. The other 65 patients complete a modified Noyes Knee Questionnaire. The mean questionnaire score was 84.2. A score of 94 has been found to be normal for athletes of the same age.[65]

Findings in this cohort led to the following conclusions:

Healing of PCL injuries occurs, and residual laxity does not increase over time
Subjective scores are poorly correlated with the degree of posterior knee laxity
Objective and subjective knee function is independent of the grade of posterior knee laxity
A trend toward medial compartment arthrosis exists but does not correlate with the degree of posterior knee laxity
Meniscus tears are rare
Independent of laxity, one half of patients can return to the same sport at the same level, one third can return to the same sport at a lower level, and one sixth cannot return to the same sport

Although these results are comparable to those reported after PCL reconstruction, this cohort had laxity of grade 2 or less, and no distinction between partial and complete PCL tears was made in this study.[26, 65]

Surgical Therapy

PCL reconstruction begins with an examination with the patient under anesthesia to rule out concomitant ligament injuries.[66] Diagnostic arthroscopy should be performed, and any meniscus or cartilage procedures should be performed. Findings such as abnormal lateral joint opening at 25° of knee flexion during knee arthroscopy are also suggestive of posterolateral corner insufficiency.[40, 67] Arthroscopic findings consistent with an isolated PCL injury are as follows[30, 68] :

Anterior cruciate ligament (ACL) pseudolaxity
Medial femoral condyle and patellofemoral compartment chondrosis
Abnormal relation of the medial femoral condyle to the medial meniscus

Arthroscopic debridement of the PCL should be performed, leaving any fibers in continuity to lie over the graft and leaving enough remnants to identify the PCL footprints. A limited notchplasty (see the image below) can be performed for visualization; notch impingement is not a factor for PCL reconstruction, unlike ACL reconstruction.[69]

A right knee pending posterior cruciate ligament (PCL) reconstruction. A minimal notchplasty is completed. Two guide pins are advanced into the medial femoral condyle for tunnel placement to reconstruct the two bundles of the PCL. Image courtesy of Janos P. Ertl, MD.

Tibial graft fixation can utilize a tunnel or an inlay technique. The tunnel technique is simpler, avoiding posterior knee dissection. However, the angle the graft must make at the back of the tibial articular surface has been termed the killer turn.[40, 54, 69] A cadaveric study demonstrated that the PCL graft has increased laxity and evidence of degradation after 72 cyclic loads, after tibial tunnel PCL reconstruction.[70]

The tibial inlay technique can be performed with the patient in a lateral position or else requires the patient to be turned from supine to prone and back to supine.[71] Decreased posterior tibial translation has been demonstrated after the tibial inlay technique.[70, 72]

Femoral graft placement has been performed with single-tunnel and, subsequently, double-tunnel techniques. Single-tunnel techniques were designed to recreate the stabilizing effect of the anterolateral bundle of the PCL. This was based on the belief that the anterolateral bundle of the PCL is dominant.[73] The inability of single-tunnel techniques to restore posterior tibial translation throughout knee range of motion (ROM) led to further studies.[39, 74, 75, 76]

Isometric PCL reconstruction has been advocated to recreate normal PCL function. Studies have shown that the isometric region of the PCL is a small portion of the ligament.[40, 69] Isometric reconstructions restored normal posterior translation only at low angles of knee flexion, not at knee flexion greater than 60°.[77] Nonisometric reconstruction with the femoral tunnel placed distal to the isometric region, in the anterior aspect of the PCL footprint, 7-10 mm proximal to the articular surface better restores posterior translational stability throughout knee range of motion (ROM) than isometric reconstruction.[40, 69, 77]

Codominance of the anterolateral bundle (larger aspect of the PCL) is taut in flexion (also becomes tighter in internal rotation), and the smaller posteromedial bundle is taut in extension. The two bundles are inseparable. Subsequently, double-tunnel or double-bundle techniques have been developed with the goal of restoring normal knee kinematics.[25, 39, 74, 75, 76, 77, 78] Split- or Y-graft may be used, or else two separate grafts are needed. (See the images below.)

The two femoral tunnels are created by reaming from outside in; 8- to 9-mm tunnels are made depending on the patient size and graft used. Image courtesy of Janos P. Ertl, MD.

Two red Robinson catheters are advanced through the femoral tunnels. Image courtesy of Janos P. Ertl, MD.

The catheters have premade holes that are used for suture retrieval. Image courtesy of Janos P. Ertl, MD.

The catheters are advanced and threaded out the posterior knee. In this case, a posterior tibial inlay graft from an Achilles tendon allograft is used. The two bundles are secured to the catheters and advanced into the joint through the tunnels. Image courtesy of Janos P. Ertl, MD.

The two Achilles tendon bundles are secured with a baseball whipstitch, threaded through the catheter holes, and advanced into the femoral condyle tunnels. Image courtesy of Janos P. Ertl, MD.

Additional view of the placement and advancement of the Achilles allograft. Image courtesy of Janos P. Ertl, MD.

Completion and seating of the femoral allograft reconstruction. The two bundles are secured or stabilized by suturing over a post and washer. Note the re-establishment of the broad surface area for the reconstructed posterior cruciate ligament (PCL) origin. Image courtesy of Janos P. Ertl, MD.

Completion of the tibial inlay two-bundle Achilles tendon allograft/posterior cruciate ligament (PCL) reconstruction. The bony calcaneus remnant is secured to the posterior tibia with one or two interfragmentary compression screws into a trough into the posterior tibia at the level of the PCL insertion. Care is taken not to penetrate the anterior tibial cortex with these screws. Note the intact original anterior cruciate ligament (ACL). Image courtesy of Janos P. Ertl, MD.

With the double-tunnel technique, the anterolateral bundle graft should be tensioned in 90° of knee flexion with anterior tibial translation.[69, 71] Tension of the posteromedial bundle graft has been advocated with the knee in extension and with the knee in 30° of flexion with the tibia anteriorly translated.[69, 71] Debate also persists as to whether a bone bridge is needed at the articular surface between the two femoral tunnels.

In-vitro studies support the double-bundle technique over the single-bundle technique.[74, 77, 78] The double-bundle technique has been shown to restore results of the posterior drawer test to normal.[78, 79, 80]

All other ligament laxities, especially the lateral side, should be addressed. Contraindications for PCL reconstruction include active infection and lack of full motion.

Postoperative Care

Postoperative management should include a wound drain and neurovascular examination in the recovery room. Neurapraxia is the most common complication of PCL reconstruction.[69] Passive ROM from 0º to 90° and quadriceps-strengthening exercises should be initiated immediately after surgery.

Patients should be restricted to toe-touch weightbearing with an extension brace for the first 2 weeks after surgery. The brace is kept locked in extension for a total of 4 weeks, then 0-90° motion is allowed for the next 4 weeks. Full extension must be achieved by postoperative weeks 3-6, or else intervention is required.

Patients are restricted from squatting, downhill walking, or sudden deceleration for 6 months. At 6 months, patients may begin straight run-walking if quadriceps and hamstring deficits are less than 20%. Once patients can run straight ahead at full speed, they may progress to lateral running, crossovers, cutting drills, and figure-eight exercises.[40]

Author

Matthew Lawless, MD Assistant Professor of Orthopedic Surgery, Wright State University School of Medicine; Consulting Surgeon, Department of Orthopedic Surgery, Miami Valley Hospital and Dayton Veterans Affairs Medical Center

Matthew Lawless, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Damian M Andrisani, MD Staff Physician, Department of Orthopedic Surgery, Wright State University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Thomas M DeBerardino, MD Orthopedic Surgeon, The San Antonio Orthopaedic Group; Professor of Orthopedic Surgery, Baylor College of Medicine as Co-Director, Combined Baylor College of Medicine-The San Antonio Orthopaedic Group, Texas Sports Medicine Fellowship; Medical Director, Burkhart Research Institute for Orthopaedics (BRIO) of the San Antonio Orthopaedic Group; Consulting Surgeon, Sports Medicine, Arthroscopy and Reconstruction of the Knee, Hip and Shoulder

Thomas M DeBerardino, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of North America, Herodicus Society, International Society of Arthroscopy, Knee Surgery and Orthopaedic Sports Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Arthrex, Inc.; MTF; Aesculap; ABMT; Conmed; JRF<br/>Received research grant from: Arthrex, Inc.; MTF.

Additional Contributors

Phillip J Marone, MD, MSPH Clinical Professor, Department of Orthopedic Surgery and Department of Rehabilitation Medicine, Jefferson Medical College of Thomas Jefferson University

Phillip J Marone, MD, MSPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Medical Association, American Orthopaedic Society for Sports Medicine, Philadelphia County Medical Society

Disclosure: Nothing to disclose.

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