Updated: Jun 30, 2009
Understanding of the importance of the menisci in the biomechanics of the knee has progressed steadily since 1968, when Jackson wrote, "The exact function of that structure (meniscus) is still a matter of some conjecture."1 At that time, it was common to remove the entire substance if any doubt existed regarding the integrity of the meniscus. Today, it is known that the menisci are not optional or expendable structures; they have an integral role in normal knee joint mechanics. The physician treating an athlete with a known or suspected meniscal tear needs to understand the structure and function of the meniscus and the factors involved in treating an athlete with nonoperative versus operative treatment. This article presents a program for rehabilitation after meniscal injuries, meniscectomy, and meniscal repair based on current knowledge of knee biomechanics. (See images below and Images 1, 2.)
Anatomy
The menisci are C-shaped wedges of fibrocartilage located between the tibial plateau and femoral condyles. The menisci contain 70% type I collagen. The larger semilunar medial meniscus is attached more firmly than the loosely fixed, more circular lateral meniscus. The anterior and posterior horns of both menisci are secured to the tibial plateaus. Anteriorly, the transverse ligament connects the 2 menisci; posteriorly, the meniscofemoral ligament helps stabilize the posterior horn of the lateral meniscus to the femoral condyle. The coronary ligaments connect the peripheral meniscal rim loosely to the tibia. Although the lateral collateral ligament (LCL) passes in close proximity, the lateral meniscus has no attachment to this structure.
The joint capsule attaches to the entire periphery of each meniscus but adheres more firmly to the medial meniscus. An interruption in the attachment of the joint capsule to the lateral meniscus, forming the popliteal hiatus, allows the popliteus tendon to pass through to its femoral attachment site. Contraction by the popliteus during knee flexion pulls the lateral meniscus posteriorly, avoiding entrapment within the joint space. The medial meniscus does not have a direct muscular connection. The medial meniscus may shift a few millimeters, while the less stable lateral meniscus may move at least 1 cm.
In 1978, Shrive et al reported that the collagen fibers of the menisci are oriented in a circumferential pattern.2 When a compressive force is applied in the knee joint, a tensile force is transmitted to the menisci. The femur attempts to spread the menisci anteroposteriorly in extension and mediolaterally in flexion. Shrive et al further studied the effects of a radial cut in the peripheral rim of the menisci during loading. In joints with intact menisci, the force was applied through the menisci and articular cartilage; however, a lesion in the peripheral rim disrupted the normal mechanics of the menisci and allowed it to spread when a load was applied. The load now was distributed directly to the articular cartilage. In light of these findings, it is essential to preserve the peripheral rim during partial meniscectomy to avoid irreversible disruption of the structure's hoop tension capability.
Blood supply
The blood supply to the menisci is limited to their peripheries. The medial and lateral geniculate arteries anastomose into a parameniscal capillary plexus supplying the synovial and capsular tissues of the knee joint. The vascular penetration through this capsular attachment is limited to 10-25% of the peripheral widths of the medial and lateral meniscal rims. In 1990, Renstrom and Johnson reported a 20% decrease in the vascular supply by age 40 years, which may be attributed to weight bearing over time.3
The presence of a vascular supply to the menisci is an essential component in the potential for repair. The blood supply must be able to support the inflammatory response normally seen in wound healing. Arnoczky, in 1982, proposed a classification system that categorizes lesions in relation to the meniscal vascular supply.4
Repair of lesions in the red zone has yielded good results, according to Stone. Reports describe techniques for manufacturing a vascular access channel from the peripheral vasculature to improve the chance that tissue in the central region will repair itself.
Biomechanics
The menisci follow the motion of the femoral condyle during knee flexion and extension. Shrive et al presented a model of normal meniscal function.2 During extension, the femoral condyles exert a compressive force displacing the menisci anteroposteriorly. As the knee moves into flexion, the condyles roll backward onto the tibial plateau. The menisci deform mediolaterally, maintaining joint congruity and maximal contact area. As the knee flexes, the femur externally rotates on the tibia, and the medial meniscus is pulled forward. Studies by Shrive, Fukubayashi, Walker, and Kurosawa state that the menisci directly influence the transmission of forces, distribution of load, amount of contact force, and pressure distribution patterns.
Mechanism of injury
Meniscal injuries, particularly sports-related injuries, usually involve damage due to rotational force. A common mechanism of injury is a varus or valgus force directed to a flexed knee. When the foot is planted and the femur is internally rotated, a valgus force applied to a flexed knee may cause a tear of the medial meniscus. A varus force on a flexed knee with the femur externally rotated may lead to a lateral meniscus lesion. According to Ricklin, the medial meniscus is attached more firmly than the relatively mobile lateral meniscus, and this may result in a greater incidence of medial meniscus injury.
Although the exact incidence and prevalence of meniscal injury are unknown, it is a fairly common sports-related injury among adults. Although less common than in adults, knee meniscal injuries do occur in individuals who are skeletally immature. Meniscal injuries are rare in children younger than 10 years with morphologically normal menisci.5
Meniscal injuries usually are associated with pain that results in gait deviation and loss of time from work and/or sport.
A correlation of race and meniscal injuries is not known to exist.
Meniscal injuries are more common in males, which may be a reflection of males being more involved in aggressive sporting and manual activities that predispose to rotational injuries of the knee.
Meniscal injuries are common in young males who are involved in sporting or manual activities. A second peak of incidence is observed in elderly persons older than 55 years; this incidence is secondary to a degenerate meniscus being susceptible to injuries with minor trauma.6 Meniscal injuries are rare in children younger than 10 years with morphologically normal menisci.5
A thorough subjective history can help the examiner choose the appropriate clinical tests to include in the physical examination. A complete understanding of the exact mechanism of injury helps determine what type of meniscal involvement to look for. Initial symptoms may include the following:
During clinical examination, use the uninvolved leg as the reference for comparison with qualitative and quantitative findings of the involved leg. Examination should include inspection, palpation, range of motion (ROM), gait, girth measurements, and tests for integrity of menisci and other structures of the knee joint.9
Most commonly, meniscal injuries are due to a traumatic event (especially in athletes) or degenerative changes in older individuals. Meniscal tears are caused by twisting motions with the knee in a flexed position (eg, pivoting in basketball). Chronic or repetitive stress also may cause degenerative tears of the menisci.
A Danish study investigated whether an association exists between meniscal injuries and occupations that require kneeling.10 Magnetic resonance imaging (MRI) of the knees was conducted in 92 male floor layers and compared with MRI scans from referents, in this case 49 male graphic designers. (The mean age for all persons in the study was 55.6 years.) The incidence of degenerative tears of the medial meniscus was significantly higher in floor layers than in graphic designers, the odds ratio (OR) being 2.28. Medial tears in both knees also occurred more frequently in floor layers (OR 3.46). Tears in the lateral meniscus, however, were no more prevalent in floor layers than in graphic designers.
Anterior Cruciate Ligament Injury
Posterior Cruciate Ligament Injury
Collateral ligament injuries
Loose bodies in the knee
Osteochondritis dissecans
Initial phase
When the patient first reports to outpatient physical therapy 4-7 days after surgery, he or she usually is able to bear full weight or as much weight as tolerated on the involved leg. Modalities are used as needed to decrease pain or swelling, including heat/ice contrasts, ice alone, transcutaneous electrical nerve stimulation (TENS), electric galvanic stimulation, and phonophoresis. As needed, the patient should perform flexibility exercises for the lower extremity musculature, including the hamstrings, quadriceps femoris, hip flexors, hip adductors, and calf muscles.
During the initial stage, the emphasis should be placed on overcoming any limitations to ROM. To increase passive flexion ROM, the patient should complete exercises such as wall slides. The patient uses the uninvolved leg to control the speed of descent and to push the involved leg back up into extension. The patient does not have to use the quadriceps muscle of the involved leg for this exercise, but he or she can use it if there is no pain.
After the patient attains 110-115° of flexion, he or she may substitute heel slides for supine wall slides to increase flexion ROM. Isometric exercises for the quadriceps muscle assist in strengthening the quadriceps muscle, especially the VMO segment. Electrical muscle stimulation may be used to help retrain poorly contracting VMO or quadriceps femoris muscles. Short-arc quadriceps femoris muscle exercises strengthen the quadriceps femoris muscle.
Additional exercises to strengthen the lower extremity musculature (eg, hamstrings, hip adductors, hip abductors, calf muscles) are included in the program. The patient can begin isotonic strengthening exercises for the hamstring muscles when he or she can flex the knee to at least 80-90°. Hip abduction strengthening may begin when VMO muscle contraction and strength is adequate. If the patient begins hip abduction exercises before the quadriceps femoris muscle is strong enough, the exercises may contribute to increased lateral tracking of the patella. The tensor fasciae latae muscle inserts into the iliotibial band distally, and contraction of this muscle increases the tightness of the fascial sheath, contributing to lateral patellar tracking.
Depending on weight-bearing ability and other symptoms, the patient can begin toe raise exercises to strengthen the lower leg. Proper foot placement is important, as it influences the stresses at the knee. Supination of the foot causes tibial external rotation and a varus force at the knee joint, resulting in increased pressure in the medial compartment. Pronation causes tibial internal rotation, a valgus force at the knee joint, and increased lateral compartment pressure.
Stationary bicycling may be implemented into the rehabilitation program when the patient attains 115-120° of knee flexion. This exercise increases joint lubrication, which helps to improve ROM. Tension and resistance should be adjusted according to the presence of effusion or the patient's complaints of pain. If the patient's ROM is not adequate, bicycling may cause forced motion and increased pressure, irritating the knee.
Intermediate phase
The patient should have full ROM to begin this phase. Modalities are continued as indicated by symptoms. Flexibility and strengthening exercises are continued, increasing resistance as tolerated. The patient may progress to isokinetic strength and endurance training.
The patient also may begin closed kinetic chain exercises during this phase. If the quadriceps femoris muscle is strong enough (ie, if the patient can lift 10 lb during short-arc quadriceps femoris muscle exercise), the running program may be initiated. The first stage of the running program is jogging in place on a trampoline. Unless pain or swelling occurs, the patient gradually progresses to jogging for 10-15 minutes.
Advanced phase
During the advanced phase, the patient continues to progress in strength-training exercises while beginning to return to sports activities. Track running may begin when the patient is able to run on the treadmill for 10-15 minutes at a pace of 7-8 minutes per mile (depending upon the patient's previous activity level). Once mileage on the track has reached 2-3 miles, agility drills and sport-specific activities may be performed.
The program for rehabilitation following meniscus repair is similar in principle to the program that follows meniscectomy; however, more limitations are put on the patient's weight-bearing status, and the duration of each phase of rehabilitation is longer to allow for healing. Full weight bearing is postponed until 4-6 weeks after surgery to reduce the tensile and compressive forces on the repair site. During the initial phase of rehabilitation, more attention should be paid to applying modalities to decrease pain and effusion. ROM exercises are performed with caution so that the healing process is not delayed. Mobilization of the patella may be required to ensure proper mechanics of the patellofemoral joint. Stretching exercises include calf stretches to reduce the possibility of Achilles tendinitis when the patient resumes weight bearing on the involved leg. Ankle ROM exercises also may be required to maintain adequate ankle ROM before weight bearing begins.
Open kinetic chain strengthening exercises may begin during the initial phase, but caution must be used and the exercises must be reduced or suspended if the patient reports pain. Isokinetic training should not begin until the patient is able to lift 10 lb on the short-arc quadriceps muscle exercise. The running program may begin when the quadriceps femoris and hamstring muscles of the involved leg have reached approximately 70% of the strength of the same muscles of the uninvolved leg, as demonstrated by an isokinetic strength test.
Nonoperative rehabilitation
The program for nonoperative rehabilitation is similar in principle to the program that follows meniscectomy. Cryotherapy and nonsteroidal anti-inflammatory drugs (NSAIDs) play a very important role in the management of nonoperative meniscal injury. These medications help control the amount of swelling and provide some pain relief. Sometimes, aspiration is useful to decrease the effusion, and, rarely, an athlete may need a judicious 1-time corticosteroid injection. Although not routinely advocated, an injection may provide an athlete with a way to control the irritation within the knee so that performance may not falter. Maintenance of ROM of the knee is important, as are muscular strength and endurance.
A reasonable goal before return to athletic activity is strength of the injured lower extremity within 20-30% of the contralateral side. Initially, activity modification is useful, particularly in athletes who are "weekend warriors." The time frame for return to activity depends on a number of factors. Returning to competition depends on the demands and motivation of the athlete, as well as on the severity of the meniscal tear.
Operative versus nonoperative treatment
Multiple factors are involved in making decisions regarding the management of an athlete with a known or suspected meniscal tear. Factors such as the severity of the symptoms, the ability to perform one's activity, and the timing of possible surgery must be taken into account. The need for surgical management is quite evident in an individual with significant symptoms, such as a locked knee or debilitating pain with clinical or MRI evidence of a meniscal tear. A treatment decision may be much more difficult to make on an individual who has relatively mild symptoms of a meniscal tear and who is participating in a sporting event that is in the middle-to-late part of the season.
The severity of the symptoms can vary for different types of meniscal tears. A bucket-handle tear may cause the knee to lock and be quite painful, whereas a small vertical or radial tear that displaces may cause occasional symptoms of giving way and only mild pain. If the symptoms are infrequent and locking does not occur, then an initial period of conservative management may be indicated, depending on the activity level and demands of the athlete. If the athlete's ability to compete is impaired because of the symptoms, then nonoperative management is unlikely to be satisfactory and arthroscopic surgery should be helpful, although it may mean a delay of 1-4 weeks in returning to competition.
An athlete with recurrent mild symptoms but without impairment in the ability to compete may be a suitable candidate for delayed operative management. Thorough consultation between the athlete, the physician, and the athletic trainer must be undertaken before any decision is made. The athlete must be given a clear explanation of what a meniscus tear is and of what the potential ramifications of delaying surgery are. The potential ramifications of delaying surgery include the possibility of propagation of the tear or significant symptoms during a competition, which may preclude further participation at a particular event. Few published studies have examined the results of nonoperative treatment of meniscal tears, and, to the authors' knowledge, none have been performed in a prospective randomized fashion.
Operative management
Once a decision has been made to proceed with operative management, further decisions regarding the surgical treatment of the meniscus tear need to be made (see images below and Images 3, 4). Intraoperatively, a decision has to be made whether to repair, excise, or leave the tear in the meniscus alone.
When a patient is implementing nonoperative rehabilitation, an aspiration of the knee joint sometimes is useful to decrease effusion. Rarely, an athlete may need a judicious 1-time injection of a corticosteroid. Although not routinely advocated, an injection may provide an athlete with a way to control the irritation within the knee so that performance may not falter.
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained injuries.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible following various dose levels in those with chronic alcoholism; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products, and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Designated chemically as 2-[(2,6-dichlorophenyl)amino] benzeneacetic acid, monosodium salt, with an empirical formula of C14 H10 Cl2 NO2 NA. One of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. Believed to inhibit COX, which is essential in biosynthesis of prostaglandins. Can cause hepatotoxicity; hence, monitor liver enzyme levels in first 8 wk of treatment.
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Delayed-release, enteric-coated form is diclofenac sodium, and immediate release form is diclofenac potassium. Has relatively low risk for bleeding GI ulcers.
25 mg PO bid/tid
If well tolerated, increase by 25 or 50 mg qwk until satisfactory response is obtained or total daily dose of 150-200 mg PO is reached
Higher doses generally do not increase effectiveness
<12 years: Not established
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; do not administer into CNS or give to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, and those at high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely, and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs
Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and by inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; severe heart failure and hyponatremia may occur because celecoxib may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction
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meniscal injury, meniscus, knee surgery, knee injury, knee injuries, meniscus tear, torn meniscus, medial meniscus, lateral meniscus, meniscus surgery, knee meniscus, medial meniscus tear, meniscus injury, meniscus repair, meniscus treatment, meniscal tear, menisci, lateral meniscus tear
Sarjoo M Bhagia, MD, Honorary Teaching Faculty, Charlotte Institute of Rehabilitation, Consulting Staff, Physical Medicine and Rehabilitation, OrthoCarolina
Sarjoo M Bhagia, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Michael Weinik, DO, Associate Chairman, Associate Professor, Physical Medicine and Rehabilitation, Temple University Hospital
Michael Weinik, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Selina Yingqi Xing, MD, MS, Staff Physician, Department of Physical Medicine and Rehabilitation, Temple University
Selina Yingqi Xing, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Texas Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
The authors and editors wish to thank Kavita Gupta, DO, MEng, Department of Orthopedics, Center of Physical Medicine and Rehabilitation, University of Dentistry and Medicine of New Jersey, for his previous contributions to this article.
Further ReadingRelated eMedicine topics:
Anterior Cruciate Ligament Injury [Physical Medicine and Rehabilitation]
Anterior Cruciate Ligament Injury [Sports Medicine]
Anterior Cruciate Ligament Pathology
Knee, Anterior Cruciate Ligament Injuries (MRI)
Knee Injury, Soft Tissue
Knee, Meniscal Tears (MRI)
Meniscus Injuries
Clinical guidelines:
ACR Appropriateness Criteria® nontraumatic knee pain. American College of Radiology - Medical Specialty Society. 1995 (revised 2005). 9 pages. [NGC Update Pending] NGC:004631
Knee & leg (acute & chronic). Work Loss Data Institute - Public For Profit Organization. 2003 (revised 2008 May 7). 289 pages. NGC:006561
Clinical trials:
Chondrocyte Maturation and Cartilage Loss Following Meniscal Injury
Comparing Knee Cartilage Surgery Versus Standard Physical Therapy in Treating People With a Meniscal Tear and Osteoarthritis
Meniscal Repair: A Randomized Prospective Trial of FAST-FIX vs. Meniscal Suturing
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