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]

Articular: Legg-Calvé-Perthes disease (or, avascular necrosis of the femoral head in the hip),

Köhler's disease (of thetarsal navicular bone of the foot),

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,

such as Osgood-Schlatter's disease (of the tibial tubercle) and Osteochondritis dissecans.[7]


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.


Male with Osgood-Schlatter disease


Diagnosis is made clinically,[5] and

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

Apply Body oils + Pain-relieving gels like Brugel, Voveron etc

Pain Killers

Gradual resumption of sports.

Bracing or POP orthopedic cast give quicker resolution.

Surgical excision may rarely be required in skeletally mature patients.

Healthy eating, Hot Cold sponging bag


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:10.1177/036354658501300404. PMID 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-2007-993701. PMID 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 Conferenceappendix1. ISSN 1536-7290.

  9. ^ Simply the best. Guardian. 18 May 2008

  10. ^ Gael could miss French Open. Sky Sports. 21 April 2009