eMedicine Specialties > Sports Medicine > Knee

Patellofemoral Joint Syndromes

Jane T Servi, MD, Consulting Staff, Northern Colorado Orthopedic Associates

Updated: Jul 15, 2009

Introduction

Background

Patellofemoral joint complaints are one of the most common musculoskeletal complaints in all age groups. Complaints vary from anterior knee pain to peripatellar knee pain to retropatellar knee pain.^{1,2,3,4,5,6,7} Nonspecific complaints may include global or generalized knee pain, joint line pain, or posterior knee pain. Often, there is a paucity of objective findings despite subjective complaints. The problem may vary from one of short duration to one of a recurrent or chronic nature.

The etiology of patellofemoral joint syndrome is multifactorial and results from a combination of intrinsic and extrinsic factors.^{1,2,3,4,5,6,7}  Treatment is often conservative in nature. Because of the variable nature of the complaints and an often lack of objective identifiable pathologic cause of patellofemoral joint complaints, this condition can be difficult to evaluate, diagnose, and treat, which may cause great frustration for the physician and patient alike.⁵

For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center; Breaks, Fractures, and Dislocations Center; Arthritis Center; and Osteoporosis and Bone Health Center. Also, see eMedicine's patient education articles Knee Pain Overview and Knee Injury.

Frequency

United States

Patellofemoral joint syndrome may affect as many as 25% of all athletes.

Functional Anatomy

The patellofemoral joint is composed of the articulation of the patella with the femoral condyles of the femur. The patella has a configuration of a triangle with its apex directed inferiorly. Superiorly, it articulates with the trochlea, the distal articulating surface of the femur.

The patella is the largest sesamoid bone in the body and protects the knee from direct trauma. Localized within the quadriceps tendon, the patella also acts as a fulcrum for extension of the quadriceps.

Medial movement of the patella is controlled by the vastus medialis oblique (VMO) muscle. Lateral tracking is guided by both the vastus lateralis and the iliotibial band. Patellar motion is further constrained by the patellofemoral ligament, the patellotibial ligament, and the retinaculum.

The patella is engaged with the trochlea at 20-30 º of knee flexion. At 90 º, the patella contacts the lateral and medial femoral facets within the condylar fossa. At 130-135 º of knee flexion, the medial facets of the patella contact the articulating surface of the femoral condyles. In knee extension, the patella abuts the suprapatellar fat pad.

Sport-Specific Biomechanics

The patella lies within the quadriceps tendon and thereby increases the mechanical advantage of the quadriceps mechanism. Not only does the patella increase the force of knee extension by 50%, but it also provides stability to the patellar tendon and minimizes the forces placed on the femoral condyles.

Tracking of the patella begins with the lower patellar border lying in contact with the suprapatellar fat pad when the knee is fully extended. With knee flexion, the patella moves proximally with a lateral shift, which is limited in excursion by the lateral retinaculum. As the knee continues to flex, the tibia internally rotates and the patella moves upward. The amount of force placed on the patellofemoral joint increases with increasing knee flexion. On the other hand, knee hyperflexion increases patellofemoral stress, as does extreme extension.

The vector force placed on the patella may be affected by the Q-angle. The Q-angle is a line created from the anterior superior iliac spine (ASIS) to the mid patella, which intersects with a line from the mid patella to the tibial tubercle when the knee is in full extension. An average Q-angle for a male is 14 º, whereas that for a female is 17 º. Q-angles larger than average can indicate abnormal patellar tracking.

Other factors that may affect the vector force on the patella include the following:

• Femoral anteversion
• Tibial torsion
• Hyperpronation of the foot
• Atrophy of the VMO muscle
• A tight lateral retinaculum
• Patella position (patella alta/baja or subluxation)
• Inflexibility of the quadriceps, hamstring, iliotibial, and calf muscle-tendon units
• General ligamentous laxity

Clinical

History

The presenting symptom in patients with patellofemoral joint syndrome is knee pain.

• The quality of the knee pain varies from dull and achy to sharp and shooting; occasionally, there is a burning sensation.
• The location of the pain may also vary. The pain may be described as anterior knee pain, retropatellar knee pain, peripatellar knee pain, global knee pain, posterior knee pain, joint line pain, or a combination of these.
• Patients may complain of painful or painless retropatellar crepitation. Symptoms may also include a painful catching sensation and a painful giving way of the knee.
• The pain may have an obvious etiology. Pain is often related to overuse or a change in exercise intensity.
  • Some activities that frequently trigger symptomatology are stair climbing, uphill running, hiking, deep knee bends, and squatting. The pain is often not noted until completion of the activity. The patient may also complain of pain with prolonged sitting in which the knees are in flexion.
  • Pain may be related to trauma, most frequently from falls onto the anterior knee or from the impact of the knees on the dashboard in motor vehicle accidents. Most commonly though, an inciting event cannot be determined.
  • A family history of anterior knee pain may be positive.
  • Children going through growth spurts may experience painful knees, which occurs as the bone grows and stimulates musculotendinous growth through traction. This results in a relative period of inflexibility, which translates to abnormal vector forces placed at the patella and patellar maltracking.

Related eMedicine topics:
Knee Injury, Soft Tissue
Knee Osteochondritis Dissecans
Osgood-Schlatter Disease
Overuse Injury

Physical

• The clinician should make a general observation for the presence of any predisposing factors, which may include the following:
  • Gait (walking and running) – Inversion/eversion of the hindfoot
  • Femoral anteversion or tibial torsion
  • Genu varus, genu valgus, or genu recurvatum
  • Foot with pes planus or pronation
• Examination of the tibiofemoral joint (the anterior knee, not the joint lines) should include the following:
  • Assess range of motion (ROM). Most often the ROM is within normal limits; genu recurvatum may be present.
  • Look for the presence of any effusion, which is often absent.
  • Assess for ligamentous laxity. No laxity should be noted.
  • Assess for joint line tenderness, which is more prone to be present anteriorly if it is elicited.
  • Perform the McMurray maneuver, in which the examiner concurrently extends and rotates the patient's affected lower limb. When the patient complains of pain with this maneuver, the pain is usually localized to the anterior knee.
• Examination of the patellofemoral joint
  • Observe the position of the patella with the knee in 90° of flexion. Patella alta, patella baja, or patellar lateralization may be present.
  • Observe patellar tracking in terminal extension (30-0°). A J-curve may be present.
  • Assess the patellar glide. A tight lateral retinaculum can decrease the medial glide. A medial glide of less than 5 mm (1 quadrant) can indicate a tight retinaculum. If a positive apprehension sign (fear of the patella popping out of position) is elicited with assessment of the patellar glide, suspect a patella subluxation or dislocation.
  • Palpate for pain. Tenderness is often found on the patellar facets, the trochlea, and the peripatellar soft tissue. Tenderness to palpation at the superior or inferior poles of the patella usually indicates another pathology.
  • Assess the patella compression test. Compress and push the affected patella distally. Pain is a positive test associated with anterior knee pain. An active test, in which the patient contracts the quadriceps tendon against a compressed patella, has a high false-positive rate.
  • Assess the Q-angle. The Q-angle is the angle formed by a line created from the ASIS to the mid patella intersecting with a line created from the mid patella to the tibial tubercle with the knee in full extension. The average Q-angle for males is 14°, and the average for females is 17°. An increase in this angle can indicate abnormal patellar tracking.
• Muscle force vectors may be unequal and cause patellar maltracking.
  • Assess hamstring flexibility. Tight hamstrings antagonize the quadriceps function and increase patellofemoral joint loading. Iliotibial band and rectus femoris flexibility should likewise be assessed. In a study of 12 patients with patellofemoral pain syndrome, Hudson and Darthuy noted that these patients had a tighter iliotibial band.⁸ However, it was unclear whether patellofemoral pain syndrome is caused by or results in a tighter iliotibial band.
  • Assess the muscle bulk of the VMO. The VMO controls medial movement of the patella.

Related eMedicine topics:
Osgood-Schlatter Disease
Osteochondritis Dissecans
Patellar Injury and Dislocation
Pes Planus

Causes

• Genetics may predispose a person to develop patellofemoral joint syndrome. Genetic factors that are commonly associated with this condition include the following:
  • Hyperlaxity of the knee (genu recurvatum) or patellofemoral joint
  • Genu varus or genu valgus
  • Femoral anteversion or tibial torsion
  • Wide pelvic girdle
  • Pes planus or pronation of the foot
  • Muscle tightness, which itself may have a genetic component
  • Abnormal concentration of forces over a smaller articular surface of the patellofemoral joint.
• This condition may either be caused or aggravated by overuse or a change in activity level. Repetitive knee flexion, especially on a weighted joint (eg, stair climbing, hiking, uphill running, kneeling, squatting, prolonged sitting with knee flexion) can cause symptomatology.
• Trauma can be the underlying cause.
• A forceful compression of the patellofemoral joint (eg, a fall onto the anterior knees, impact of the knees on a dashboard during a motor vehicle accident) may precipitate this condition.
  • Patellofemoral syndrome may occur after a patella subluxation or dislocation.
  • Patients may develop this condition after having ACL reconstruction with a bone-patellar tendon-bone technique. One year postoperatively, one third of these patients may have patellofemoral symptoms secondary to a weak quadriceps from patellar irritability or flexion contracture.
• Osgood-Schlatter disease may be a predisposing factor to the development of patellofemoral pain later in life.
  • These patients continue to have the predisposing factors, such as muscle imbalance, that caused the Osgood-Schlatter disease.
  • Assess muscle strength, particularly VMO strength. Weakness is often associated with a decrease in muscle bulk. VMO weakness causes poor patellar tracking. The VMO displaces the patella medially during knee extension, thus guiding it through the trochlear groove during quadriceps contraction.

Related eMedicine topics:
Knee Injury, Soft Tissue
Osgood-Schlatter Disease
Overuse Injury
Patellar Injury and Dislocation
Pes Planus

Differential Diagnoses

Osgood-Schlatter Disease
Slipped Capital Femoral Epiphysis

Other Problems to Be Considered

Chondromalacia patella
Complex regional pain syndrome type I (Reflex sympathetic dystrophy)
Crystal arthropathy
Excessive lateral pressure syndrome
Infection
Legg-Calve-Perthes Disease
Loose body
Meniscal tear
Neoplasm
Osteochondritis dissecans
Rheumatoid arthritis /Psoriatic arthritis
Patellar/quadriceps tendinitis
Patellar subluxation
Plica
Postoperative considerations (after ACL reconstruction)
Sinding-Larsen-Johansson disease
Stress fracture of the hip or femur
Suprapatellar/prepatellar/infrapatellar tendinitis
Trauma from a direct blow to the knee

Workup

Laboratory Studies

• Laboratory studies are not indicated for patellofemoral joint syndromes, unless there is a need to rule out other potential causes, such as systemic, inflammatory, or metabolic disease.
  • Erythrocyte sedimentation rate (ESR) is elevated in an inflammatory process.
  • Liver and renal function may be abnormal in metabolic disease.
  • Antibody tests are elevated for rheumatoid arthritis or ankylosing spondylitis.
  • Knee aspirates show an elevated white blood cell (WBC) count in an inflammatory process, an abnormal Gram stain and culture in infection, and crystals when crystal arthropathy is present.

Imaging Studies

• Radiographic imaging is not necessary to make the diagnosis of patellofemoral joint syndrome, but these studies can be helpful to the physician when excluding other potential causes (see Differentials and Other Problems to Be Considered). Particular findings can support the diagnosis, including the following:
  • Lateral plain films show the presence of patella alta or patella baja.
  • A sunrise or Merchant's view reveals lateral tilt and the relative height of the femoral condyles.
  • Magnetic resonance imaging (MRI), computed tomography (CT) scanning, and bone scanning are not needed in the evaluation of patellofemoral joint syndromes, but these imaging modalities may be used to evaluate other pathologic conditions of the knee if the diagnosis is in doubt. Dynamic CT scanning, 0-120 º, is useful in assessing patellar tracking in recalcitrant cases in which surgery is being considered. This study can be used in the rare patient who is suspected of having a patellar tilt or subluxation but whose radiographs are normal.

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Conservative treatment is successful in 80% of cases of patellofemoral joint syndromes. The goal of treatment is to control the symptoms. Underlying strength and flexibility deficits need to be addressed. 

• Start by having the patient modify his/her activity level. Decrease activities that increase patellofemoral pressure (eg, jumping, squatting, kneeling). Gentle eccentric loading activities may be initiated.
• Apply ice for 10-15 minutes, 4-6 times per day, especially after activity.
• Increase muscle strength, especially of the VMO, with short-arc quadriceps sets, knee presses, isometric quadriceps sets, and straight-leg raises with the leg externally rotated. Biofeedback may aid in teaching recruitment of the VMO.
• Improve flexibility of the hamstrings, vastus lateralis, and iliotibial band. Stretch tight retinacular structures.
• Initiate proprioceptive exercises.
• Ultrasound or phonophoresis may decrease pain symptoms.
• A patellofemoral brace with a patella cutout and lateral stabilizer or McConnell taping/Kinesio Taping may improve neuromotor control of the patellofemoral joint by affecting the osseoligamentous structures through alteration of patellar tracking, improving proprioception, or a combination of these factors.^9,10
• Provide arch supports or orthotics to correct foot malalignments.

Recreational Therapy

The patient should avoid any exacerbating activity (eg, deep knee bends, stair climbing, running, hiking). Initiate a home therapy program of flexibility, strengthening, and proprioceptive exercises. In addition, eccentric loading activities may be initiated.

Medical Issues/Complications

Give special consideration to young patients in whom conservative therapy fails. In such cases, entertain the possibility of referred pain from the hip (eg, Legg-Calvé-Perthes disease, slipped capital femoral epiphysis).

Related eMedicine topics:
Legg-Calve-Perthes Disease
Slipped Capital Femoral Epiphysis

Surgical Intervention

Surgical intervention is not appropriate in the acute phase. Surgery should be reserved for those in whom a conservative course of treatment of 6 months' duration was unsuccessful.^9,12,13 Other more specific causes of anterior knee pain should be excluded first. Lateral retinacular release with or without medial capsular reefing may benefit active young adult patients who have not been helped by 12 months of nonoperative treatment and who have patellar tilt and/or subluxation.

Other Treatment

Analgesics, which may reduce pain, do not possess anti-inflammatory properties. Acetaminophen may be helpful for moderate pain; tramadol hydrochloride (HCl) may abort severe pain.¹⁴

Nonsteroidal anti-inflammatory drugs (NSAIDs) can aid in pain reduction and reduce the inflammatory component, which can be associated with this condition. In the acute phase, administer NSAIDs on a scheduled basis at sufficient doses to confer the anti-inflammatory benefits. Narcotics are not appropriate for this condition. For severe pain, corticosteroid injections may be beneficial.

Dietary food supplements may prove beneficial in a select group of patients. Glucosamine/chondroitin sulfate and hyaluronic acid may have the potential to provide the substrates used in regenerating the articular cartilaginous surfaces.¹⁵ To date, however, no scientific proof has been presented that this occurs, despite anecdotal reports that some people who take these supplements have reported decreased pain, decreased swelling, and improved joint mobility.

Potential future treatment may include viscosupplementation with an intra-articular injection. However, this is not a US Federal Drug Administration (FDA) – indicated treatment thus far, and future research needs to be undertaken. Hyaluronic acid may provide a scaffolding for rebuilding worn articular cartilage surfaces. 

Recovery Phase

Rehabilitation Program

Physical Therapy

If formal physical therapy was utilized in the acute phase, the patient should start to be weaned to a home therapy program. Activity may be advanced as tolerated in a slow, progressive manner. The patient should be sure to continue the following:

• Emphasize flexibility, strengthening, and proprioception exercises. Maintain eccentric loading activities.
• Use ice as needed for pain or inflammatory relief, especially following activity.
• Use a patellofemoral brace or McConnell taping as needed for activity.
• Use arch supports or orthotics, as needed.

Recreational Therapy

Advance activity as tolerated in a slow, progressive manner. One suggested approach may be to decrease the previous volume and intensity training by 50%, and then if symptoms do not return, to increase activity by 10% each week.

Surgical Intervention

Surgical intervention is usually not appropriate in the recovery phase. Surgery should be reserved for those in whom a 12-month trial of conservative therapy was unsuccessful.

Other Treatment (Injection, manipulation, etc.)

Analgesics (acetaminophen and tramadol HCl), as well as NSAIDs, should be continued for those with persistent pain; for those whose pain resolves, wean off these drugs. These medications may be continued on an as-needed basis for individuals with activity-related pain.

Intra-articular corticosteroid injections may be useful in recalcitrant cases. Corticosteroid injections should never be injected into the patellar tendon because of the predisposition for tendon rupture that is associated with this procedure.

Maintenance Phase

Rehabilitation Program

Physical Therapy

Flexibility, strengthening, and proprioception programs should be continued indefinitely. Arch supports and orthotics should also be continued indefinitely. Braces and taping, as well as ice, may be weaned as progress permits.

Recreational Therapy

Activity may be progressed as tolerated.

Surgical Intervention

Surgery may be useful for patients who have been compliant and in whom a 12-month trial of conservative therapy was unsuccessful. Surgery may completely resolve the patient's symptomatology, partially resolve the symptomatology, or may not change the symptomatology; rarely is the symptomatology exacerbated iatrogenically. Surgery is more successful when a specific diagnosis has been established and when clear surgical goals can be defined.

Surgical intervention includes arthroscopy for articular cartilage shaving, with or without lateral release of the retinaculum. Surgery may also include proximal or distal realignment. Open surgical procedures include patellar tendon transfer, or rarely, patellectomy.

Other Treatment

Analgesics (acetaminophen and tramadol HCl) and NSAIDs may be beneficial on an as-needed basis. Dietary supplements may be helpful on an individual basis. Corticosteroid injections may be beneficial for recalcitrant cases.

Medication

Analgesics may provide pain relief (acetaminophen for moderate pain, tramadol HCl for severe pain). NSAIDs may alleviate the pain, as well as reduce the inflammatory component. Narcotic medication is not indicated for this condition.

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or who have sustained injuries.

Acetaminophen (Tylenol, Panadol, Aspirin Free Anacin)

Provides pain relief. May be a first-line drug therapy, especially in those with contraindications to NSAID use. May use on a prn basis.

Dosing

Adult

325-650 mg PO q4-6h prn pain

Pediatric

<6 years: Not established
6-12 years: 325 mg, 1/2-1 tab PO 3-4 times/d prn pain
>12 years: Administer as in adults

Interactions

Rifampin can reduce the analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity can occur in patients with chronic alcoholism with various dose levels of acetaminophen; severe or recurrent pain or high or continued fever may indicate a serious illness.

Tramadol HCl (Ultram)

Inhibits ascending pain pathways, altering the perception of and response to pain. Also inhibits reuptake of norepinephrine and serotonin.

Indicated for moderate to moderately severe pain. This drug is generally not a first-line DOC, but it is a reasonable second-line DOC in those who do not have opioid dependency.

Dosing

Adult

50-100 mg PO q4-6h; maximum of 400 mg/d; adjust dose in those with a decreased creatinine clearance or who have cirrhosis to 50-100 mg PO q12h

For those aged >75 years, the maximum dosage is 300 mg/d

Pediatric

Not established

Interactions

Decreases carbamazepine effects significantly; cimetidine increases toxicity, risk of serotonin syndrome with coadministration of antidepressants

Contraindications

Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, opioids, acute alcohol intoxication

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in the presence of respiratory depression, increased intracranial pressure, head trauma, seizures, opioid dependency; not recommended in nursing mothers; can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in the presence of liver disease, myxedema, hypothyroidism, hypoadrenalism; development of tolerance or dependency with extended use may occur

Nonsteroidal Anti-inflammatory Drug (nsaid), Cox-2 Selective

COX-2 selective drugs are:

• Indicated for the relief of the signs and symptoms of osteoarthritis, rheumatoid arthritis in adults, and ankylosing spondylitis
• Indicated for the management of acute pain in adults
• Indicated for the treatment of primary dysmenorrhea
• Indicated to reduce the number of adenomatous colorectal polyps in familial adenomatous polyposis

Celecoxib (Celebrex)

A 4-[5-(4-methylphenyl)-3-(triflouromethyl)-1H-pyrazol-1-yl) benzenesulfonamide and a diaryl-substituted pyrazole. Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. Seek lowest dose for each patient.

Dosing

Adult

200 mg/d PO qd; alternatively, 100 mg PO bid

Pediatric

Not established

Interactions

CYP450 2C9 substrate; coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of the celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations

Contraindications

Documented hypersensitivity; treatment of perioperative pain in the setting of coronary artery bypass graft surgery (CABG)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in the presence of severe heart failure and hyponatremia because circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or laboratory results suggest liver dysfunction

Nonsteroidal Anti-inflammatory Drug (NSAID), Oral

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase 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. Many NSAIDs are currently on the market. In general, the mechanism of action of these agents is the same. No evidence exists that one NSAID is more efficacious than another; however, individual response may differ.

Flurbiprofen (Ansaid)

May inhibit the cyclooxygenase enzyme, which in turn inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Dosing

Adult

200-300 mg/d PO divided bid/qid

Pediatric

Not established

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

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

Ibuprofen (Ibuprin, Advil, Motrin)

First-line DOC for the reduction of pain and inflammation. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

10 mg/kg PO q6-8h; not to exceed 40 mg/kg/d

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of anticoagulation abnormalities or during anticoagulant therapy

Ketoprofen (Actron, Orudis, Oruvail)

For relief of mild to moderate pain and inflammation.

Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient response.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of anticoagulation abnormalities or during anticoagulant therapy

Naproxen (Naprelan, Naprosyn, Anaprox)

For the relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO, followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

2.5-5 mg/kg/dose PO; not to exceed 15 mg/kg/d

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

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

Precautions

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

Dietary Supplements

Dietary supplements may provide nutrients that may play a role in the formation of cartilage.

Glucosamine

Dietary supplement derived from crab shells. Hypothesized to provide the structural building blocks that are used in regenerating articular cartilage.

Dosing

Adult

1500 mg/d for a minimum of 6-8 wk; must be taken regularly

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity to shellfish (glucosamine is derived from crab shells)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Shellfish allergies

Chondroitin sulfate

Dietary supplement derived from bovine trachea. Hypothesized to provide the structural building blocks that are used to regenerate articular cartilage.

Dosing

Adult

1200 mg/d for minimum of 6-8 wk; must be taken regularly

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

None reported

Follow-up

Return to Play

Return to play or previous activity may be resumed when 80% of the strength of the uninjured knee (as measured by isokinetic testing) has been reached in the affected knee. If there has not been a significant loss of strength, the athlete may continue to play as symptoms allow. For those with loss of strength, continued play predisposes to injury secondary to guarding by the athlete.

Prevention

Prevention consists of correcting biomechanical imbalances. The patient should wear arch supports or orthotics for pes cavus or pronation of the foot. Promote flexibility, strengthening, and proprioceptive programs (particularly for the VMO).

Other preventative measures may be sport specific, depending upon the equipment being utilized. For example, with cycling, the seat height should be properly adjusted. For cyclists with femoral anteversion or tibial torsion, floating clips or shims on the pedals may prevent patellofemoral syndromes. For runners, proper shoe maintenance can prevent problems.

Moderation of frequency or intensity of activity can also prevent problems. When a new activity is initiated, it should be done in a slow, progressive manner. Intensity levels should not change drastically over relatively short time periods. Runners, in particular, often follow a 10% rule, in which distance or time is increased by 10% on weekly intervals.

Prognosis

Empiric treatment is successful in 80% of cases of patellofemoral joint syndrome. The treatment goal is to control the symptoms (ie, decrease the pain).

Education

Education consists of the clinician being able to describe the condition anatomically and biomechanically to the patient. Because the problem is primarily one of pain, educate athletes about flexibility, strengthening, and proprioceptive programs, as well as the importance of using the proper equipment.

Miscellaneous

Medicolegal Pitfalls

• The only medicolegal pitfall is misdiagnosis of the condition.

Special Concerns

• A special consideration in young patients is that knee pain can be referred from the hip. Those patients who fail to respond to treatment warrant radiography of the hip to rule out Legg-Calvé-Perthes disease or slipped capital femoral epiphysis.
• Additionally, pain and tenderness to palpation at the inferior pole of the patella may indicate apophysitis (Sinding-Larsen-Johansson disease).

Related eMedicine topics:
Legg-Calve-Perthes Disease
Slipped Capital Femoral Epiphysis

References

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2. Scuderi GR, ed. The Patella. New York, NY: Springer-Verlag; 1995:xii-351.

3. Wertheimer C. Patellofemoral mechanics as a cause of anterior knee pain. Your Patient and Fitness. 1995;9:19-23.

4. Eilert RE. Adolescent anterior knee pain. Pediatric Orthopedics. Philadelphia, Pa: Lippincott-Raven; 1991:499-515.

5. Ruffin MT 5th, Kiningham RB. Anterior knee pain: the challenge of patellofemoral syndrome. Am Fam Physician. Jan 1993;47(1):185-94. [Medline].

6. Pizzutillo PD. Osteochondroses. In: Sullivan JA, Grana WA, eds. The Pediatric Athlete. Park Ridge, Ill: American Academy of Orthopaedic Surgeons; 1990:224.

7. Walsh WM. Knee injuries. In: Mellion MB, Walsh WM, Shelton GL, eds. The Team Physician's Handbook. Philadelphia, Pa: Hanley & Belfus; 1990:414-39.

8. Hudson Z, Darthuy E. Iliotibial band tightness and patellofemoral pain syndrome: a case-control study. Man Ther. Feb 28 2008;epub ahead of print. [Medline].

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10. Cowan SM, Bennell KL, Hodges PW. Therapeutic patellar taping changes the timing of vasti muscle activation in people with patellofemoral pain syndrome. Clin J Sport Med. Nov 2002;12(6):339-47. [Medline].

11. [Best Evidence] Syme G, Rowe P, Martin D, Daly G. Disability in patients with chronic patellofemoral pain syndrome: a randomised controlled trial of VMO selective training versus general quadriceps strengthening. Man Ther. Jun 2009;14(3):252-63. [Medline].

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14. Weil EK. Pain and pyrexia. Residents' Edition Prescribing Reference. 5^th ed. New York, NY: Prescribing Reference, Inc; 1996:164-8.

15. Kelly GS. The role of glucosamine sulfate and chondroitin sulfates in the treatment of degenerative joint disease. Altern Med Rev. Feb 1998;3(1):27-39. [Medline]. [Full Text].

16. Freeman AJ, Jacobson NA, Fogg QA. Anatomical variations of the plantaris muscle and a potential role in patellofemoral pain syndrome. Clin Anat. Mar 2008;21(2):178-81. [Medline].

17. Liebensteiner MC, Szubski C, Raschner C, et al. Frontal plane leg alignment and muscular activity during maximum eccentric contractions in individuals with and without patellofemoral pain syndrome. Knee. Feb 21 2008;epub ahead of print. [Medline].

18. Vicenzino B, Collins N, Crossley K, et al. Foot orthoses and physiotherapy in the treatment of patellofemoral pain syndrome: a randomised clinical trial. BMC Musculoskelet Disord. Feb 27 2008;9(1):27. [Medline]. [Full Text].

Keywords

anterior knee pain, chondromalacia patella, patellalgia, patellar compression syndrome, patellofemoral dysfunction, patellofemoral pain syndrome, PFPS, peripatellar knee pain, retropatellar knee pain, global or generalized knee pain, joint line pain, posterior knee pain, patellar maltracking syndrome, miserable malalignment syndrome

Contributor Information and Disclosures

Author

Jane T Servi, MD, Consulting Staff, Northern Colorado Orthopedic Associates
Jane T Servi, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, and American Medical Society for Sports Medicine
Disclosure: Ferring Pharmaceuticals Honoraria Speaking and teaching

Medical Editor

Andrew L Sherman, MD, MS, Associate Professor of Clinical Rehabilitation Medicine, Vice Chairman, Chief of Spine and Musculoskeletal Services, Program Director, SCI Fellowship and PMR Residency Programs, Department of Rehabilitation Medicine, Leonard A Miller School of Medicine, University of Miami
Andrew L Sherman, 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 College of Sports Medicine, American Medical Association, American Paraplegia Society, American Spinal Injury Association, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

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