Find information on thousands of medical conditions and prescription drugs.

Osteochondritis dissecans

Osteochondritis dissecans is when a loose piece of bone and cartilage separates from the end of the bone because of a loss of blood supply and insuffecient amounts of calcium. The loose piece may stay in place or slide around making the joint stiff and unstable. Osteochondritis Dissecans most commonly effects the knees or ankles. If a serious injury occurs in this area, the bone around it will supply it with as much calcium as possible to try and fix the loose piece of bone. This often results in a calcium build up around the loose piece. This build up is surgically removed most of the time. more...

Occipital horn syndrome
Oculocutaneous albinism,...
Oculopharyngeal muscular...
Olivopontocerebellar atrophy
Omenn syndrome
Ondine's curse
Opportunistic infections
Oppositional defiant...
Optic atrophy
Optic neuritis
Oral leukoplakia
Orthostatic intolerance
Osgood-Schlatter disease
Osteitis deformans
Osteochondritis dissecans
Osteogenesis Imperfecta
Osteopetrosis, (generic...
Ovarian cancer

This is a minor disease, however it is very rare. It commonly occurs in boys and young men from 10-20 years of age while they are still growing. As girls become more active in sports, it is becoming more common among them as well.


To determine whether your pains are Osteochondritis Dissecans, you can have an MRI to show whether the loose piece of bone is still in place. In specific cases if caught early enough, a harmless dye will be injected into your blood stream to show where the calcium will most likely continue to build up. Doing this makes the removal process much easier.


[List your site here Free!]

Fate of the osteochondral fragments in osteochondritis dissecans after Legg-Calve-Perthes' disease
From Journal of Bone and Joint Surgery, 9/1/02 by Rowe, Sung Man

The treatment of osteochondritis dissecans after Legg-Calve-Perthes' disease has not been clearly determined. It may be either by simple observation or surgical removal of the osteochondral fragment. We studied the evolution of the lesion in 13 children and reviewed 92 hips reported in the literature. In our patients ten showed a tendency towards spontaneous healing, one required drilling + grafting to obtain fusion, and in two there was separation into the joint. These loose bodies were in the acetabular fossa and caused no symptoms. On reviewing the literature, we found only four cases of hips with loose bodies from osteochondritis dissecans. These were lying in the inferomedial capsule and were also asymptomatic. Treatment of osteochondritis dissecans after Legg-Calve-Perthes' disease should therefore be conservative unless the fragment interferes with the mechanics of the hip.

J Bone Joint Surg [Br] 2002;84-B:1025-9. Received 6 February 2002; Accepted 19 March 2002

Osteochondritis dissecans (OCD) after Legg-CalvePerthes' disease (LCPD) is rare. It was first described by Haas.1 In 1982, Catterall 2 found that only 54 cases had been reported in the literature. Osterman and Lindholm 3 and Kamhi and MacEwen 4 took the view that OCD after LCPD was more common than had been previously estimated. Several reports described OCD as occurring in up to 4% of patients with LCPD. 5-8 The treatment of this lesion has not been defined and has varied between simple observation and surgical removal of the fragment.5,9-13 We sug gest a form of treatment for this lesion, based upon our experience of 13 patients and a review of the literature. This includes seven which have already been reported by us,8 but with further follow-up, and 92 hips (87 children) reported in 28 previously published papers. 1-7,9-29

Patients and Methods

Of 578 children (619 hips) who had LCPD diagnosed between 1973 and 1998, 13 had OCD. All the affected children were boys; in three the LCPD was bilateral. They were followed for a mean of 16 years (3 to 22) for LCPD, and 13 years (2 to 19) for OCD. Their mean age was 8.83 years (7 to 11.5) when LCPD was diagnosed, and 11.67 (7.67 to 15.92) when OCD became apparent. Plain radiography and CT were performed to determine the natural history and the fate of the osteochondral fragments (Tables I and II).


The incidence of OCD after LCPD was 2.1% in our series. LCPD was classified in terms of severity into two groups according to the classification of Salter and Thompson;30 two were in Salter group A (Catterall groups 1 and 2) and 11 were in Salter group B (Catterall groups 3 and 4).30 Treatment for these 13 hips consisted of an abduction brace in seven, femoral osteotomy in three, and no treatment in three. The hips were assessed radiologically according to the classifications of Mose 23 (good in eight, fair in two, poor in three) and Stulberg and Cooperman 31 (I and II in nine, III and IV in four) (Table I). Using serial radiography, we observed the development of the lesion. A radiolucent area was formed initially in the dome of the capital epiphysis followed by multiple tiny ossific nuclei, which gradually enlarged and coalesced to form a small osteochondral fragment with a distinct margin (Figs 1 and 2).

There were no symptoms of internal derangement suggestive of OCD in ten patients. Three complained of intermittent pain in the hip and a limp. One of these underwent exploration and it was thought that the symptoms arose not from the OCD but from the deformed femoral head. The mean interval of time between the onset of LCPD and the development of OCD was 2.83 years (1 to 5). The best radiological view of the lesion was the anteroposterior (AP) in nine of the hips and the lateral in four. The mean size of the osteochondral fragment was 15 x 7 mm (10 to 26 x 4 to 10). No special treatment was given, except in one patient in which the lesion was drilled and grafted (Table II).

The state of the osteochondral fragments at final followup suggested that there had been spontaneous healing in seven and that healing was occurring in three. Healing after drilling and bone grafting was seen in one and separation of the fragment into the joint in two. In these latter two no treatment was required since the fragment lay in the acetabular fossa and did not interfere with function (Fig. 3).


Reviewing the literature, 1-7,9-29 we found that 87 cases (92 hips) with OCD after LCPD had been reported in 28 articles (Table III). The current series includes seven cases which we reported in 1989(8) with further follow-up, and six new cases. By combining the available information on the total of 105 hips some observations may be made. OCD can occur in the epiphysis of the femoral head in patients with LCPD, but reports on the incidence of this lesion have been rare. Kamhi and MacEwen4 reported seven cases in 200 patients with LCPD, Katz and Siffert7 ten cases in 450 patients and Bowen et al5 reported 14 children (15 hips) with OCD in a series of 465 patients. In our study, 13 cases of OCD were seen in 619 hips giving an incidence of 2.1%.

Our group of patients conformed to the pattern which has been previously described.4,5,8,10,28 The pathogenesis of OCD has been discussed by several authors. Catterall2 stated that clefts are formed in the fibrocartilaginous tissue of the epiphysis during the healing process of LCPD. The free cartilage fragment may ossify to become OCD. He also proposed that ossification occurs after the invasion by granulation tissue of the fibrocartilaginous area in the superior part of the epiphysis suggesting that, when the centres of ossification do not coalesce, an area of OCD may form. It was suggested by Ratliff26,27 that osteochondritis is the result of an unhealed necrotic fragment persisting into adult life. With serial radiography we observed the sequential development of OCD. A radiolucent area first forms in the dome of the femoral epiphysis. Multiple tiny osseous nuclei then appear and coalesce forming a small osteochondral fragment with distinct margins. This observation corresponds to Catterall's theory.

Kamhi and MacEwen4 reported that the lesion can remain silent for many years and that separation of the osseous fragment from its bed is rare. Of the 92 hips described in the literature, there was information concerning symptoms for 63; 19 were asymptomatic, 25 caused intermittent pain and 19 caused catching or locking of the hip. In our group 10 of the 13 hips were asymptomatic. Conservative management is usual for this lesion in the absence of interference with the mechanics of the hip.4

Surgical removal of the fragment had been considered for hips with symptoms of locking or catching which usually develop in cases of incomplete separation. Osterman and Lindholm3 considered that removal of the fragment would lead to incongruity of the joint and an increased risk of osteoarthritis. They advised against its removal unless interfered with movement.

With regard to the fate of the osteochondral fragment, we wished to know how often it separated from its bed and entered the joint and how often it healed spontaneously. Reviewing the literature, we found such information for 66 of the 92 hips. The fragment remained in situ without displacement in 40, was in situ with partial separation in 22 and completely separated into the joint and four. The fragments in these four hips, however, were lying in the inferomedial corner of the joint and were not symptomatic (Table III). In our group, the fragment remained in situ in 11 hips and separated completely into the joint in two. In these two it remained in the acetabular fossa and was asymptomatic.

Only three publications described spontaneous healing of the osteochondral fragment.3,5,7 In our group, we followed the patients until a mean age of 24 years and observed spontaneous healing in seven hips and progression towards healing in three. From all the well-documented cases, the 66 in the literature and our 13, we were only able to find six examples of complete separation of the fragment into the joint.

We conclude that separation of osteochondral fragments is not common in OCD after LCPD and that the six patients in whom a loose body separated from the femoral head, suffered no symptoms as a result. We recommend that supervised neglect, with interval observation, is the preferred management for these patients.

No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.


1. Haas A. Umbau von Perthes'scher Krankheit in osteochondritis dissecans. Zentralbl F Chir 1937;64:2873-5.

2. Catterall A. Current problems in orthopaedics: Legg-Calve-Perthes disease: clinical features. Edinburgh, etc: Churchill Livingstone, 1982;34-63.

3. Osterman K, Lindholm T'S. Osteochondritis dissecans following Perthes' disease. Clin Orthop 1980:152:247-54.

4. Kamhi E, MacEwen GD. Osteochondritis dissecans in Legg-CalvePerthes disease. J Bone Joint Surg [Am] 1975;57-A:506-9.

5. Bowen JR, Kumar VP, Joyce JJ, Bowen JC. Osteochondritis dissecans following Perthes' disease: arthroscopic-operative treatment. Clin Orthop 1986;209:49-56.

6. Brotherton B, McKibbin B. Perthes' disease treated by prolonged recumbency and femoral head containment: a long-term appraisal. J Bone Joint Surg [BrI 1977;59-B:8-14.

7. Katz JF, Siffert RS. Osteochondritis dissecans in association with Legg-Calve-Perthes disease. Int Orthop 1979;3:189-95.

8. Rowe SM, Kim HS, Yoon TR. Osteochondritis dissecans in Perthes' disease. Report of 7 cases. Acta Orthop Scand 1989;60:545-7.

9. Freehafer AA. Osteochondritis dissecans following Legg-CalvePerthes disease: a report of one case. J Bone Joint Surg [Am] 1960;42-A:777-82.

10. Goldman AB, Hallel T, Salvati EM, Freiberger RH. Osteochondritis dissecans complicating Legg-Perthes' disease: a report of 4 cases. Radiology 1976;121:561-6.

11. Grossbard GD. Hip pain during adolescence after Perthes' disease. J Bone Joint Surg [Br] 1981;63-B:572-4.

12. Jenkins SA, Snowball LAH. Osteochondritis dissecans of the hip. J Bone Joint Surg [Br] 1958;40-B:827.

13. Woodward AH, Decker JS. Osteochondritis dissecans following Legg-Perthes' disease. Southern Med J 1976;69:943-4,8.

14. Brailsford JF The radiology of bones and joints. Ed. 5. Baltimore, The Williams and Wilkins Co., 1953. (Quoted in Freehafer AA. Osteochondritis dissecans following Legg-Calve-Perthes disease. J Bone Joint Surg [Am] 1960;42-A:777-82).

15. Edgren W. Coxa plana. Acta Orthop Scand (Sup) 1965;85.

16. Evans DL. Legg-Calve-Perches disease. J Bone Joint Surg fBr] 1958;40-B:168-81.

17. Freund E. Osteochondritis dissecans of the head of the femur: partial idiopathic aseptic necrosis of the femoral head. Arch Surg 1939;39:323-52.

18. Goff CW, Shutkin NM, Hersey MR. Legg-Calve-Perthes disease and related osteochondroses of youth. Springfield, Illinois: Charles C. Thomas, 1954. (Quoted in Stillman BC. Osteochondritis dissecans and coxa plant. J Bone Joint Surg [Br] 1966;48-B:64-81).

19. Gossling HR, McArthur R. Osteochondritis dissecans of the hip as a sequela to Legg-Calve-Perches disease: 11 congres international de Chirugie Orthopedique, pp.807-34, Mexico, 1969. (Quoted in Katz JF, Siffert RS. Osteochondritis dissecans in association with Legg-CalvePerthes disease. Int Orthop (SICOT) 1979;3:189-98).

20. Halle] T, Salvati EA. Osteochondritis dissecans following LeggCalve-Perches disease: report of 3 cases. J Bone Joint Surg [Am] 1976;58-A:708-11.

21. Mindell ER, Sherman MS. Late results in Legg-Perches disease. J Bone Joint Surg [Am] 1951;33-A: 1-23.

22. Morris ML, McGibbon KC. Osteochondritis dissecans following Legg-Calve-Perthes' disease. J Bone Joint Surg [Br] 1962;44-B:5624.

23. Mose K. Legg-Calve-Perthes disease. Universtetsforlaget 1. Aarhus 1964. (Quoted in Katz JF, Siffert RS. Osteochondritis dissecans in association with Legg-Calve-Perches disease. Inter Orthop (SICOT) 1979;3:189-95).

24. Pantazopoulos TH, Matsoukas J, Gavras M, Nikiforidis P, Hartofilakidis-Garofalidis G. Osteochondritis dissecans following coxa plana. Acta Orthop Scand 1972;43:532-8.

25. Petrie PWR. Osteochondritis of the hip following Perthes disease. J Bone Joint Surg [Br] 1970;52-B:799.

26. Ratliff AHC. Pseudocoxalgia: a study of late results in the adult. J Bone Joint Surg [Br] 1956;38-B:498-9.

27. Ratliff AHC. Osteochondritis dissecans following Legg-Calve-Perthes disease. J Bone Joint Surg [Br] 1967;49-B:108-11.

28. Stillman BC. Osteochondritis dissecans and coxa plans: review of the literature with a personal case report. J Bone Joint Surg [Br] 1966;48-B:64-81.

29. Wood JB, Klassen RA, Peterson HA. Osteochondritis dissecans of the femoral head in children and adolescents: a report of 17 cases. J Pediatr Orthop 1995;15:313-6.

30. Salter RB, Thompson GH. Legg-Calve-Perches disease: the prognostic significance of the subchondral fracture and a two-group classification of the femoral head involvement. J Bone Joint Surg [Am] 1984;66-A:479-89.

31. Stulberg SD, Cooperman DR. The natural history of Legg-CalvePerthes disease. J Bone Joint Surg [Am] 1981;63-A: 1094-8.

Sung Man Rowe, Eun Sun Moon, Taek Rim Yoon, Sung Taek Jung, Keun Bae Lee, Jae Joon Lee

From Chonnam National University Hospital, Gwangju, Korea

S. M. Rowe, MD, PhD, Professor

E. S. Moon, MD, PhD, Professor

T. R. Yoon, MD, PhD, Associate Professor

S. T. Jung, MD, PhD, Assistant Professor

K. B. Lee, MD, PhD, Assistant Professor

J. J. Lee, MD, Chief Resident

Department of Orthopedics, Chonnam National University Hospital, Hakdong 8, Gwangju, Korea.

Correspondence should be sent to Dr S. M. Rowe.

Copyright British Editorial Society of Bone & Joint Surgery Sep 2002
Provided by ProQuest Information and Learning Company. All rights Reserved

Return to Osteochondritis dissecans
Home Contact Resources Exchange Links ebay