Updated: Apr 28, 2006
In 1903, Robert Osgood (1873-1956), a US orthopedic surgeon, and Carl Schlatter (1864-1934), a Swiss surgeon, concurrently described the disease that now bears their names. Osgood-Schlatter disease (OSD) is one of the most common causes of knee pain in active adolescents.
OSD affects 20% of athletic adolescents, as compared with the frequency of 4.5% of age-matched nonathletic controls. The disease is bilateral in 20-50% of patients. Boys are affected more commonly than girls, with a male-to-female ratio of 3:1. Boys aged 10-15 years and girls aged 8-13 years typically are affected, coinciding with growth spurts.
In girls younger than 11 years and in boys younger than 13 years, the tibial tubercle consists of cartilaginous tissue. The secondary ossification center or apophysis of the tibial tubercle develops when girls are aged 8-12 years and when boys are aged 9-13 years. During this stage of skeletal development, the Osgood-Schlatter lesion may occur. The most commonly accepted theory is that repeated traction (traction apophysitis) on the anterior portion of this developing ossification center leads to multiple subacute fractures or tendinous inflammation, resulting in a benign self-limited disturbance manifested as pain, swelling, and tenderness.
By the end of the ensuing 2 stages of bony development (eg, epiphyseal and bony stages), the growth plates of the proximal tibia fuse in both males and females (usually when aged 14-18 y) and the OSD usually subsides.
During running, gymnastics, and other sports requiring repeated contractions of the quadriceps, an extra-articular osteochondral stress fracture or microavulsion occurs. The proximal area of the patellar tendon insertion separates, resulting in elevation of the tibial tubercle. During the reparative phase of this stress fracture, new bone is laid down in the avulsion space, which may result in a deviated and prominent tibial tubercle. When an individual with an injured tibial tubercle continues to participate in sports, more and more microavulsions develop, and the reparative process may result in a markedly pronounced prominence of the tubercle with longer-term cosmetic and functional implications. A separated fragment may develop at the patellar tendon insertion and may lead to chronic nonunion-type pain.
The physical examination is very specific with point tenderness over the tibial tubercle. Other physical examination findings may include the following:
The cause of OSD is unknown; however, theories suggest that this condition is a result of repeated knee extensor mechanism contraction that causes partial avulsions or microavulsions of the chondrofibroosseous tibial tubercle. OSD usually occurs in those involved in sports that require running and jumping.
Femur Injuries and Fractures
Knee Osteochondritis Dissecans
Patellofemoral Joint Syndromes
Pes Anserine Bursitis
Sinding-Larson-Johansson syndrome
Osteomyelitis
Tibia, fibula, or femur fracture
Tumor
Perthes disease
Quadriceps tendon avulsion
Patellofemoral stress syndrome
Chondromalacia patellae
Patellar tendonitis
Infectious apophysitis
Soft tissue malignancy
Accessory ossification centers
Long-term immobilization is contraindicated because it may result in increased knee stiffness in mild cases, thus predisposing the athlete to additional sports-related injuries.
If conservative treatment has failed, surgical excision of the united painful ossicle is recommended. Removal of ossicle fragmentation in immature patients with an unfused apophysis should be approached with caution, as a resultant recurvatum deformity may occur due to premature fusion of the tibial tubercle.
Tibial tubercle avulsions occasionally can occur due to the contracture of the extensor mechanism. Open reduction and internal fixation (ORIF) usually is recommended, depending on the size and displacement of the fragment as well as the phase of apophyseal closure. (See Osgood-Schlatter Disease in Orthopedic Surgery journal.)
An orthopedic consultation is recommended.
Cortisone injections are not recommended.
See Physical Therapy, Acute Phase.
The following regimen recommendations for patients with OSD are taken from Meisterling, Wall, and Meisterling:
The goal of rehabilitation is for the athlete to be able to return to his or her sport as quickly and safely as possible. The physical therapist and the physician determine when the athlete is ready to resume competition, depending on the findings of the clinical examination and functional testing. The pain may take up to 6-24 months to resolve. If an individual returns to activity too soon, he or she may worsen the condition. Athletes need to work on improving the flexibility and strength of the quadriceps and hamstring muscles throughout the course of rehabilitation to ensure that they are ready to return to sports.
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Short-term NSAIDs may be used for pain relief. Steroids are not recommended for use in this condition. NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase 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 with food q4-6h while symptoms persist; not to exceed 3.2 g/d
5-10 mg/kg/dose PO q6-8h; not to exceed 40 mg/kg/24h
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; may increase serum levels of digoxin
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal or hepatic insufficiency, or high risk of bleeding; ocular problems, granulocytopenia, and anemia may occur
B - Usually safe but benefits must outweigh the risks.
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain and inflammation. Small dosages initially are 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 for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>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
B - Usually safe but benefits must outweigh the risks.
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 cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
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; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Usually safe but benefits must outweigh the risks.
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
May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.
200-300 mg/d PO divided bid/qid
Not established
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
C - Safety for use during pregnancy has not been established.
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
After the pain has resolved (which may take 6-24 mo), the patient may return to play as tolerated. The patient may need to participate less frequently, run at a slower speed, or decrease jumping activities. Premedicating or relying on NSAIDs regularly before or after competition is not advised. An intensive rehabilitation program of stretching exercises helps to decrease the likelihood of developing pain with vigorous sports activity. OSD usually resolves by the time the adolescent is aged 18 years.
The most common long-term complications are pain on kneeling as an adult and the cosmesis of a bony prominence on the anterior knee. Less common complications are the persistence of a painful ossicle requiring surgical excision and a displaced avulsion of a tibial tubercle.
Activity modification and regular stretching and strengthening exercises provide the best prevention.
The prognosis is excellent. OSD usually resolves by the time the patient is aged 18 years, when the tibial tubercle apophysis ossifies. The likelihood for long-term sequelae increases in severe cases, in cases in which treatment is not sought, or in cases in which the patient demonstrates poor compliance with the physician's recommendations.
OSD is a self-limited illness that resolves as the patient approaches adulthood. For acute flare-ups, anti-inflammatory medications, ice, elevation, and rest are recommended. For prevention, the patient should engage in activity and sports as tolerated without development of knee pain. Regular daily stretching and strengthening exercises should be performed to help prevent OSD. Inform patients regarding the activities that aggravate the condition and regarding the self-limiting nature of the disease.
For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center, Arthritis Center, and Bone Health Center. Also, see eMedicine's patient education article Knee Pain.
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Bloom OJ, Mackler L, Barbee J. Clinical inquiries. What is the best treatment for Osgood-Schlatter disease?. J Fam Pract. Feb 2004;53(2):153-6. [Medline].
Demirag B, Ozturk C, Yazici Z, Sarisozen B. The pathophysiology of Osgood-Schlatter disease: a magnetic resonance investigation. J Pediatr Orthop B. Nov 2004;13(6):379-82. [Medline].
Epstein B. Common problems affecting adolescents - Osgood Schlatter disease: A common cause of knee pain. In: Iowa Health Book: Family Practice. Iowa City, Iowa: The University of Iowa; 1995.
Flowers MJ, Bhadreshwar DR. Tibial tuberosity excision for symptomatic Osgood-Schlatter disease. J Pediatr Orthop. May-Jun 1995;15(3):292-7. [Medline].
Meisterling R, Wall E, Meisterling M. Coping with Osgood-Schlatter disease. In: The Physician and Sports Medicine. Vol 26. New York, NY: McGraw-Hill; 1998.
Ross MD, Villard D. Disability levels of college-aged men with a history of Osgood-Schlatter disease. J Strength Cond Res. Nov 2003;17(4):659-63. [Medline].
Staheli L. 2nd ed. Fundamentals of Pediatric Orthopedics. Philadelphia, Pa: Lippincott-Raven; 1998:56, 123.
Tachdjian MO. Clinical Pediatric Orthopedics: The Art of Diagnosis and Principles of Management. Vol 1. Stamford, Conn: Appleton & Lange; 1997:107-108.
Wall E. Osgood-Schlatter disease: Practical treatment for a self-limiting condition. In: The Physician and Sports Medicine. Vol 26. New York, NY: McGraw-Hill; 1998.
OSD, tibial tubercle osteochondrosis, traction apophysitis, knee pain
Munisha Mehra Bhatia, MD, General Academic Pediatrics, Faculty Development Fellow, Children's Memorial Hospital of Northwestern University
Munisha Mehra Bhatia, MD is a member of the following medical societies: Ambulatory Pediatric Association and American Academy of Pediatrics
Disclosure: Nothing to disclose.
Janos P Ertl, MD, Clinical Assistant Professor, Department of Orthopedic Surgery, Chief of Orthopedic Trauma, University of California at Davis; Director of Amputee Clinic, Kaiser Hospital
Janos P Ertl, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, Hungarian Medical Association of America, Orthopaedic Trauma Association, and Sierra Sacramento Valley Medical Society
Disclosure: Nothing to disclose.
Gyorgy Kovacs, MD, Department of Orthopedic Surgery, Consulting Surgeon, GOC Clinic
Disclosure: Nothing to disclose.
Andrew L Sherman, MD, Associate Professor, Departments of Neurological Surgery, Orthopedics, and Rehabilitation, University of Miami Miller School of Medicine
Andrew L Sherman, MD 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, and American Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Marlene DeMaio, MD, Consulting Staff, Department of Orthopedic Surgery, Assistant Professor, Bone & Joint/Sports Medicine Institute, Naval Medical Center
Marlene DeMaio, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American College of Sports Medicine, American Orthopaedic Foot and Ankle Society, and American Orthopaedic Society for Sports Medicine
Disclosure: Nothing to disclose.
Jon Whitehurst, MD, Consulting Staff, Rockford Orthopedic Associates
Disclosure: Nothing to disclose.
William Jay Bryan, MD, Clinical Professor, Department of Orthopedic Surgery, Baylor University College of Medicine
William Jay Bryan, MD is a member of the following medical societies: Texas Orthopaedic Association
Disclosure: Nothing to disclose.
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