Osteochondritis in Children

Osteochondrosis/osteochondritis is a family of orthopedic diseases of the joint that occur in children and adolescents and in rapidly growing animals, particularly pigs, horses, and dogs. 

They are characterized by interruption of the blood supply of a bone, in particular to the epiphysis,[1] followed by localized bony necrosis,[2] and later, regrowth of the bone.[3] This disorder is defined as a focal disturbance ofendochondral ossification and is regarded as having a multifactorial etiology, so no one thing accounts for all aspects of this disease.[1]


The ultimate cause for these conditions is unknown, but the most commonly cited etiologic factors are rapid growth, heredity, trauma (or overuse), anatomic conformation, and dietary imbalances; however, only anatomic conformation and heredity are well supported by scientific literature. The way that the disease is initiated has been debated. 

Although failure of chondrocyte differentiation, formation of a fragile cartilage, failure of blood supply to the growth cartilage, and subchondral bone necrosis all have been proposed as the starting point in the pathogenesis, recent literature strongly supports failure of blood supply to growth cartilage as most likely.

Osteochondrosis in pigs has been shown to be a condition responsive to supplementation with the essential trace element boronand may be a manifestation of boron deficiency.

These conditions nearly all present with an insidious onset of pain referred to the location of the bony damage. 

Some, notably Kienbock's disease of the wrist, may involve considerable swelling,[4] and Legg-Calvé-Perthes disease of the hip causes the victim to limp.[5] The spinal form, Scheuermann's disease, may cause bending, or kyphosis of the upper spine, giving a "hunch-back" appearance.[6]


Human osteochondrosis



In humans, these conditions may be classified into three groups:

Spinal: Scheuermann's disease (of the interspinal joints) which is a curve in the thoracic spine.[6]

Panner's disease (of the capitulum of the elbow), and 

Freiberg's infraction (of the second or third metatarsal of the foot and less frequently the first or fourth; sometimes called Freiberg's Infraction or Freiberg's disease)[7]
Non-articular: This group includes Sever's disease (of the calcaneus, or heel), and 

Kienbock's disease of the hand, and other conditions not completely characteristic of the osteochondrosis, 


 The prognosis for these conditions is very variable, and depends both on the anatomic site and on the time at which it is detected. 

In some cases of osteochondrosis, such as Sever's disease and Freiberg's infraction, the involved bone may heal in a relatively normal shape and leave the patient asymptomatic.[8] 

On the contrary, Legg-Calvé-Perthes disease frequently results in a deformed femoral head that leads to arthritis and the need for joint replacement.[5]


Osgood–Schlatter disease

Osgood–Schlatter disease or syndrome (also known as tibial tubercle apophyseal traction injury) is an irritation of the patellar ligament at the tibial tuberosity.[1]

Sinding–Larsen–Johansson syndrome is an analogous condition involving thepatellar tendon and the lower margin of the patella bone, instead of the upper margin of the tibia.

The condition occurs in active boys and girls aged 9–16[2] coinciding with periods of growth spurts. It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. It has been suggested the difference is related to a greater participation by boys in sports and risk activities than by girls.[citation needed]

The condition is usually self-limiting and is caused by stress on the patellar tendon that attaches the quadriceps muscle at the front of the thigh to the tibial tuberosity. Following an adolescent growth spurt, repeated stress from contraction of the quadriceps is transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple subacute avulsion fractures along with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump which can be very painful when hit.

The syndrome may develop without trauma or other apparent cause; however, some studies report up to 50% of patients relate a history of precipitating trauma.

Intense knee pain is usually the presenting symptom that occurs during activities such as running, jumping, squatting, and especially ascending or descending stairs and during kneeling. 

The pain is worse with acute knee impact. The pain can be reproduced by extending the knee against resistance, stressing the quadriceps, or striking the knee. 

Pain is mild and intermittent initially. In the acute phase the pain is severe and continuous in nature. Impact of the affected area can be very painful. Bilateral symptoms are observed in 20–30% of patients.

The symptoms usually resolve with treatment but may recur for 12–24 months before complete resolution at skeletal maturity, when the tibial epiphysis fuses. 

In some cases the symptoms do not resolve until the patient is fully grown. In approximately 10% of patients the symptoms continue unabated into adulthood, despite all conservative measures.[4]

The condition is named after Robert Bayley Osgood and Carl B. Schlatter who described the condition independently in 1903.

25 year old male with Osgood-Schlatter disease.
Male with Osgood-Schlatter disease



Diagnosis is made clinically,[5] and 

treatment is conservative with RICE (Rest, Ice,Compression, and Elevation), 

and if required acetaminophen (paracetamol),ibuprofen and/or Co-Codamol or stronger if in 'acute phase' & (the pain is severe and continuous in nature). 

The condition usually resolves in a few months, with a study of young athletes revealing a requirement of complete training cessation for 1 week (on average) and gradual resumption of full training by 1 months.[3]

Bracing or use of an orthopedic cast to enforce joint immobilization is rarely required and does not necessarily give quicker resolution. 

Sometimes, however, bracing may give comfort and help reduce pain as it reduces strain on the tibial tubercle.[6]

Surgical excision may rarely be required in skeletally mature patients.[4] 

In chronic cases that are refractory to conservative treatment, surgical intervention yields good results, particularly for patients with bony or cartilaginous ossicles. 

Excision of these ossicles produces resolution of symptoms and return to activity in several weeks. Removal of all loose intratendinous ossicles associated with prominent tibial tubercles is the procedure of choice, both from the functional and the cosmetic point of view.[7]

 According to one study, in the great majority of young adults, the functional outcome of surgical treatment of unresolved Osgood-Schlatter disease is excellent or good, the residual pain intensity is low, and postoperative complications or subsequent reoperations are rare.[8]

After symptoms have resolved, a gradual progression to the desired activity level may begin. In addition, predisposing factors should be evaluated and addressed. 

Commonly quadriceps and/or hamstring tightness is present and should be addressed with stretching exercise.

After being clinically diagnosed the patient should rest for at least 3 days and must try not to use the knee as hard for about 1–2 weeks without any physical activities. 

If the disease continues to a certain extent where the patient cannot move the joint then they should seek medical advice right away as although this is very rare it can be severely limiting for the patient's sporting future if it does occur. The Strickland Protocol has shown a positive response in patients with a mean return to sport in less than 3 weeks.[9]

Paul Scholes and Mark Winterburn are two sportsmen who have recovered from this condition.[10] The French tennis player,Gaël Monfils, wears patella bands in an attempt to combat the condition.[11]

[]References^ Nowinski RJ, Mehlman CT (1998). "Hyphenated history: Osgood-Schlatter disease". Am J. Orthop. 27 ): 584–5.PMID 9732084.

  1. ^ Yashar A, Loder RT, Hensinger RN (1995). "Determination of skeletal age in children with Osgood-Schlatter disease by using radiographs of the knee". J Pediatr Orthop 15 (3): 298–301. DOI:10.1097/01241398-199505000-00006.PMID 7790482.
  2. a b Kujala UM, Kvist M, Heinonen O (1985). "Osgood-Schlatter's disease in adolescent athletes. Retrospective study of incidence and duration". Am J Sports Med 13 (4): 236–41.DOI:10.1177/036354658501300404PMID 4025675.
  3. a b Gholve PA, Scher DM, Khakharia S, Widmann RF, Green DW (2007). "Osgood Schlatter syndrome". Curr. Opin. Pediatr. 19 (1): 44–50.DOI:10.1097/MOP.0b013e328013dbea.PMID 17224661.
  4. ^ Cassas KJ, Cassettari-Wayhs A (2006). "Childhood and adolescent sports-related overuse injuries". Am Fam Physician 73 (6): 1014–22. PMID 16570735.
  5. ^ Engel A, Windhager R (1987). "[Importance of the ossicle and therapy of Osgood-Schlatter disease]" (in German).Sportverletz Sportschaden 1 (2): 100–8. DOI:10.1055/s-2007-993701PMID 3508010.
  6. ^ O. Josh Bloom and Leslie Mackler (February 2004). "What is the best treatment for Osgood-Schlatter disease?".Journal of Family Practice 53 (2). PDF version
  7. ^ Hariri, S.; York, S. C.; O'Connor, M. I.; Parsley, B. S.; McCarthy, J. C. (2011). "Career Plans of Current Orthopaedic Residents with a Focus on Sex-Based and Generational Differences". The Journal of Bone and Joint Surgery 93 (5): e16. DOI:10.2106/JBJS.J.00489.PMID 21368070.
  8. ^ Strickland JM, Coleman NJ, Brunswic M and Kocken R. (2008). "Osgood-Schlatter's Disease: An active approach using massage and stretching"Presentation at the European Congress of Sports Science Conferenceappendix1ISSN 1536-7290.
  9. ^ Simply the best. Guardian. 18 May 2008
  10. ^ Gael could miss French Open. Sky Sports. 21 April 2009