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Osgood-Schlatter Disease

  • Author: James R Gregory, MD; Chief Editor: Craig C Young, MD  more...
 
Updated: Aug 16, 2015
 

Background

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 a common causes of knee pain in active adolescents.

OSD is a traction phenomenon resulting from repetitive quadriceps contraction through the patellar tendon at its insertion upon the skeletally immature tibial tubercle. This occurs in preadolescence during a time when the tibial tubercle is susceptible to strain. The pain associated will be localized to the tibial tubercle and occasionally the patellar tendon itself.  A similar process can occur at the patella-patellar tendon junction, which is referred to as Sinding-Larsen-Johansson syndrome (the adolescent equivalent of jumper's knee).[1] (See the images below.)

Radiograph of a patient who is skeletally mature. Radiograph of a patient who is skeletally mature. Note that the tibial tubercle is enlarged and there is an ossicle. A bursa was overlying this.
Image courtesy of John T. Killion, MD; OSA Pediatr Image courtesy of John T. Killion, MD; OSA Pediatric Orthopaedics
Image courtesy of John T. Killion, MD; OSA Pediatr Image courtesy of John T. Killion, MD; OSA Pediatric Orthopaedics

OSD is a very common cause of knee pain in children aged 8-15 years. This condition can have a prolonged course and cause loss of time from athletics. However, it is rarely a cause of permanent impairment or disability. (See Etiology and Prognosis.)

Because of a lack of a precise etiology and therefore definition, some practitioners may find differentiating OSD from avulsion fractures of the tibial tubercle to be difficult. In general if the patient is unable to ambulate, an acute avulsion fracture of the tibial tubercle is more likely. OSD patients typically can ambulate, albeit with pain. (See Physical Examination and Differentials.)

The onset of OSD is usually gradual, with patients commonly complaining of pain in the tibial tubercle and/or patellar tendon region after repetitive activities. Typically, running or jumping activities that significantly stress the patellar tendon insertion upon the tibial tubercle aggravate the patient's symptoms. They may even have waxing and waning of symptoms that correspond to variations in their athletic seasons.  A sudden onset of pain with no antecedent symptoms in the region of the tibial tubercle should alert the clinician to assess for a possible acute tibial tubercle avulsion rather than OSD. (See History.)

OSD is a self-limiting condition. In a study by Krause et al, 90% of patients treated with conservative care were relieved of all of their symptoms approximately 1 year after onset of symptoms.[2] After skeletal maturity, patients may continue to have problems kneeling.  This typically is due to tenderness over an unfused tibial tubercle ossicle or a bursa that may require resection.[3] Minimal association seems to exist between residual anterior knee pain after OSD and patellar stability, as was noted in the Krause study. The authors also noted no cases of recurvatum from premature closure of the proximal tibial physis. (See Prognosis.)

Development of Osgood-Schlatter disease

The insertion of the patellar tendon at the tibial tubercle consists of cartilaginous tissue in girls younger than age 11 years and in boys younger than age 13 years. The secondary ossification center, or apophysis, of the tibial tubercle develops when girls are aged 10-12 years and when boys are aged 12-14 years. (During this stage of skeletal development, the Osgood-Schlatter lesion may occur.) (See Etiology.)

By the end of the ensuing 2 stages of bony development (eg, epiphyseal and bony stages), the primary growth plate of the proximal tibia and the secondary ossification center of the tibial tubercle fuse in males and females (usually when aged 14-18 y), and the OSD usually subsides.

The most commonly accepted theory regarding the development of OSD is that repeated traction (traction apophysitis) on the anterior portion of the developing ossification center leads to multiple subacute microavulsion fractures and/or tendinous inflammation, resulting in a benign, self-limited disturbance manifested as pain, swelling, and tenderness.

The most common long-term ramifications of OSD 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.

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Etiology

The cause of Osgood-Schlatter disease (OSD) is unknown; however, theories suggest that this condition is a result of repeated knee extensor mechanism contraction that causes partial microavulsions of the chondrofibro-osseous tibial tubercle. This proposed pathophysiology is supported by the repetitive runner, jumper athletic patient population OSD occurs most commonly.

During running, jumping, 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.

In a magnetic resonance imaging (MRI) study of 20 patients with OSD, the patellar tendon was noted to attach more proximally and in a broader area to the tibia in patients with OSD.[4] Approximately 50% of patients with OSD relate a history of precipitating trauma.

Histologic studies support a traumatic etiology.

Risk factors

Risk factors for OSD include the following:

  • Age: female 8-12 years & male between 12-15 years
  • Male sex (3:1)
  • Rapid skeletal growth
  • Repetitive sprinting and jumping sports
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Epidemiology

Incidence

One study found that Osgood-Schlatter disease (OSD) affected approximately 21% of athletic adolescents surveyed, as compared with a frequency of 4.5% in age-matched nonathletic controls.[5]

One Finnish study found that OSD affected 13% of athletes.

Sex predilection

OSD occurs more frequently in boys, with a male-to-female ratio of 3:1.

Age predilection

OSD usually is seen in the adolescent years, after a patient has undergone a rapid growth spurt the previous year.

Girls who are affected are typically aged 10-11 years but can range from age 8-12 years.

Boys who are affected are typically aged 13-14 years but can range from age 12-15 years.

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Prognosis

The prognosis in Osgood-Schlatter disease (OSD) is excellent. OSD is usually self-limiting and resolves by the time the patient is aged 18 years, when the tibial tubercle apophysis ossifies. In approximately 10% of patients, however, the symptoms continue unabated into adulthood despite all conservative measures.[6] This may be from residual enlargement of the tuberosity or from ossicle formation in the patellar tendon.

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.

In the study by Krause et al, 90% of patients treated with conservative care were relieved of all of their symptoms approximately 1 year following symptom onset.[2]

In some cases, however, discomfort may persist for 2-3 years until the tibial growth plate closes.

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Patient Education

Inform patients about activities that aggravate Osgood-Schlatter disease and about the self-limiting nature of the condition. For patient education information, see the Foot, Ankle, Knee, and Hip Center, the Arthritis Center, and the Osteoporosis and Bone Health Center, as well as Knee Pain.

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Contributor Information and Disclosures
Author

James R Gregory, MD Assistant Professor, Department of Orthopedic Surgery and Rehabilitation, University of Oklahoma Health Sciences Center

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

J Andy Sullivan, MD Clinical Professor of Pediatric Orthopedics, Department of Orthopedic Surgery, University of Oklahoma College of Medicine

J Andy Sullivan, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, Oklahoma State Medical Association, Pediatric Orthopaedic Society of North America

Disclosure: Nothing to disclose.

Acknowledgements

Andrew K Chang, MD Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center

Andrew K Chang, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Thomas M DeBerardino, MD Associate Professor, Department of Orthopedic Surgery, Consulting Surgeon, Sports Medicine, Arthroscopy and Reconstruction of the Knee, Hip and Shoulder, Team Physician, Orthopedic Consultant to UConn Department of Athletics, University of Connecticut Health Center

Thomas M DeBerardino, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, and American Orthopaedic Society for Sports Medicine

Disclosure: Arthrex, Inc. Grant/research funds Other; Arthrex, Inc. Consulting fee Speaking and teaching; Genzyme Biosurgery. Inc. Grant/research funds Other; Musculoskeletal Transplant Foundation Grant/research funds Other; Histogenics Grant/research funds None

Janos P Ertl, MD Assistant Professor, Department of Orthopedic Surgery, Indiana University School of Medicine; Chief of Orthopedic Surgery, Wishard Hospital

Janos P Ertl, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Hungarian Medical Association of America, and Sierra Sacramento Valley Medical Society

Disclosure: Nothing to disclose.

Gyorgy Kovacs, MD Consulting Surgeon, Department of Orthopedic Surgery, GOC Clinic

Disclosure: Nothing to disclose.

David B Levy, DO, FACEP, FAAEM Chairman, Department of Emergency Medicine, St Elizabeth Health Center; Associate Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine

David B Levy, DO, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Informatics Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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: Academic Pediatric Association and American Academy of Pediatrics

Disclosure: Nothing to disclose.

Albert W Pearsall IV, MD Associate Professor, Department of Orthopedic Surgery, University of South Alabama College of Medicine; Director, Section of Sports Medicine and Shoulder Service, Department of Orthopedic Surgery, University of South Alabama Medical Center

Disclosure: Nothing to disclose.

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, University of Miami, Leonard A Miller School of Medicine

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 Medical Association, and Association of Academic Physiatrists

Disclosure: Pfizer Honoraria Speaking and teaching

Mark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

References
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  3. Weiss JM, Jordan SS, Andersen JS, Lee BM, Kocher M. Surgical treatment of unresolved Osgood-Schlatter disease: ossicle resection with tibial tubercleplasty. J Pediatr Orthop. 2007 Oct-Nov. 27(7):844-7. [Medline].

  4. Demirag B, Ozturk C, Yazici Z, Sarisozen B. The pathophysiology of Osgood-Schlatter disease: a magnetic resonance investigation. J Pediatr Orthop B. 2004 Nov. 13(6):379-82. [Medline].

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  8. EHRENBORG G. The Osgood-Schlatter lesion. A clinical study of 170 cases. Acta Chir Scand. 1962 Aug. 124:89-105. [Medline].

  9. EHRENBORG G. The Osgood-Schlatter lesion. A clinical and experimental study. Acta Chir Scand Suppl. 1962. Suppl 288:1-36. [Medline].

  10. Ducher G, Cook J, Spurrier D, Coombs P, Ptasznik R, Black J, et al. Ultrasound imaging of the patellar tendon attachment to the tibia during puberty: a 12-month follow-up in tennis players. Scand J Med Sci Sports. 2010 Feb. 20(1):e35-40. [Medline].

  11. Ducher G, Cook J, Lammers G, Coombs P, Ptazsnik R, Black J, et al. The ultrasound appearance of the patellar tendon attachment to the tibia in young athletes is conditional on gender and pubertal stage. J Sci Med Sport. 2010 Jan. 13(1):20-3. [Medline].

  12. Pihlajamäki HK, Mattila VM, Parviainen M, Kiuru MJ, Visuri TI. Long-term outcome after surgical treatment of unresolved Osgood-Schlatter disease in young men. J Bone Joint Surg Am. 2009 Oct. 91(10):2350-8. [Medline].

  13. Binazzi R, Felli L, Vaccari V, Borelli P. Surgical treatment of unresolved Osgood-Schlatter lesion. Clin Orthop Relat Res. 1993 Apr. 202-4. [Medline].

  14. Eun SS, Lee SA, Kumar R, Sul EJ, Lee SH, Ahn JH, et al. Direct bursoscopic ossicle resection in young and active patients with unresolved Osgood-Schlatter disease. Arthroscopy. 2015 Mar. 31 (3):416-21. [Medline].

  15. Orava S, Malinen L, Karpakka J, Kvist M, Leppilahti J, Rantanen J, et al. Results of surgical treatment of unresolved Osgood-Schlatter lesion. Ann Chir Gynaecol. 2000. 89(4):298-302. [Medline].

  16. Trail IA. Tibial sequestrectomy in the management of Osgood-Schlatter disease. J Pediatr Orthop. 1988 Sep-Oct. 8(5):554-7. [Medline].

 
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Radiograph of a patient who is skeletally mature. Note that the tibial tubercle is enlarged and there is an ossicle. A bursa was overlying this.
Radiograph of a patient who is skeletally immature. The tubercle is elongated and fragmented
Image courtesy of John T. Killion, MD; OSA Pediatric Orthopaedics
Image courtesy of John T. Killion, MD; OSA Pediatric Orthopaedics
 
 
 
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