Osteochondritis dessicans

osteochondritis dessicans of knee

1. Osteochondritis Dessicans Dr Pratik Dhabalia Resident in Orthopedics Dr DY Patil Hospital, Navi Mumbai

2. INTRODUCTION Konnig in 1888 first coined the term osteochondritis dessicans . Pathological condition characterized by separation of a segment of articular cartilage together with subchondral bone either partially or completely from the joint surface.

3. SITES INVOLVED KNEE JOINT (75%) – Posterolateral portion of medial condyle - Lateral femoral condyle - medial facet of patella - tibial condyle - trochlea 2. ANKLE JOINT – Dome of talus 3. ELBOW – Capitellum 4. FEMORAL HEAD 5. WRIST JOINT

4. Rarely, might involve - shoulder joint : humeral head and glenoid - Scaphoid - Navicular

5. ETIOLOGY Its precise etiology still remains controversial. Various causative factors have been postulated. 1. Repetitive trauma has been implicated in a number of studies. Fairbanks has postulated that repetitive impingement of the tibial spine on the medial condyle. Also more common in athletes and high impact sporting population. It is postulated that repetitive trauma predispose to subchondral fracture and later on the classic appearance of OCDs. 2. Similarly an association between lateral femoral condyle osteochondritis and lateral discoid meniscus has been reported.

6. 3. Another view suggests vascular insufficiency as a factor but histological studies have found only necrosis and no evidence of infarction. 4. Defect of ossification may also lead to this condition. These defects when subjected to repetitive trauma may give rise to lesions. This theory may explain the lesions occurring in other parts of the joint apart from the medial femoral condyle. 5. Patients with a hereditary condition called multiple epiphyseal dysplasia have been quoted to be predisposed to osteochondritis

7. CLASSIFICATION There are two forms of OCDs : on the presence and absence of physeal closure respectively Adult onset OCD Juvenile OCD (Rare before 10 years)

8. CLINICAL FEATURES Male to female ratio is 3:1. Most cases are unilateral. Bilateral involvement is more in Juvenile form than adult form Usually occurs at 4 th decade of age Symptoms: The clinical presentation depends on the stage of the disease. In earlier stages there is diffuse pain and effusion In the later stages the pain increases in severity with localized tenderness over the medial femoral condyle. Locking and giving way In the presence of loose bodies these symptoms are more constant. In all stages the symptoms are aggravated by activity.

9. Physical Examination: There may be an effusion with diffuse tenderness on the femoral condyles in the earlier stages. Later tenderness is well defined on the medial femoral condyle. Quadriceps atrophy – Long-standing lesions. Patients with lesion on the lateral aspect of the medial femoral condyle may walk with the leg externally rotated to avoid abutment. In such patients if the knee is slowly extended from 90° flexion with the tibia internally rotated there may be sharp pain at approximately 30° flexion, which is relieved by external rotation. This is known as “Wilson sign”

10. INVESTIGATIONS PLAIN RADIOGRAPHS: Anteroposterior, lateral and skyline view and tunnel view. Rules out other abnormalities. Does not give information about the stability of lesion 2. MRI: Imaging modality of choice for OCDs. Gives excellent anatomical details Helps in assessment of stability and viability of lesion Differentiation from other conditions

11. 3. Computed tomography (CT) scan Details of the bony architecture but cartilage imaging is suboptimal 4. Bone scans Used both to diagnose and for follow up of treated patients 5. Diagnostic arthroscopy Gold standard for diagnosing the stability and extent of these lesions

12. De Smet and colleagues have proposed four criteria for instability in adults Guhl et al. have given the following arthroscopic classification of osteochondritic lesions

13. Differential Diagnosis Chondral separation osteochondral fracture Osteonecrosis accessory centers of ossification Hereditary epiphyseal dysplasia

14. MANAGEMENT The treatment modality depends on the age of the patient, Location and stability of the lesion. Usually Juvenile OCD responds well to conservative management adult OCD rarely does so. Juvenile OCD: Conservative Management In a patient with open physis and at least 1 year before fusion of the physis with a stable OCD can be treated conservatively. Rest & Ice fomentation There are two schools of thought. One emphasizes nonweight bearing with range of movement for 6 months to 1 year. This is to maintain cartilage health. The other method is immobilization in a cast till complete healing of the lesion. Both modalities have given good results in the specific subset of patients with reported rate of healing from 50–75%.

15. Surgical management Juvenile OCD patients not relieved by conservative treatment lasting 6 months to 1 year, less than 1 year for maturity and unstable lesions warrant operative treatment. Stable and non-detached lesions can be managed with drilling. Drilling could be extraarticular through the joint cartilage ( transarticular ); the former being preferred. For unstable but nondetached lesions some form of fixation is needed in the form of screws like bioabsorbable devices The only disadvantage of screws is the need for a second surgery for implant removal.

16. ADULT OCD: Conservative management Little role Rest and analgesics Nil weight bearing Ice fomentation

17. Surgical management The modalities can be divided into excision, Internal fixation, restorative techniques For small lesions - can be safely excised and cartilage margins stabilized. For larger stable lesions - Internal fixation is an option with a good subchondral bone stock, partially detached lesions and detached lesions less than 2–3 cm2 . Lesions without subchondral bone are not amenable to internal fixation. Special care should be taken to bury the fixation devices below the level of articular cartilage. If needed the bed of lesion can be freshened and cancellous bone grafting done to replace the bone stock and promote healing.

18. Restorative techniques include marrow stimulation with microfracture, autologous osteochondral autograft or allograft or autologous chondrocyte implantation . These techniques are used for detached lesions greater than 2–3 cm2 not amenable to fixation, lesions without sufficient subchondral bone and cases which have failed conservative or fixation techniques

19. a. Marrow Stimulation with Microfracture It involves debriding the nonviable cartilage and creating microfractures in the subchondral bone to allow marrow contents to flow into the crater. A stable fibrocartilage forms in a few weeks. This is applicable in smaller defects in low demand patients without loss of subchondral bone.

20. b. Autologous Osteochondral Grafting It involves debriding nonviable cartilage with subchondral bone and replacing the same with osteochondral graft harvested from a nonarticulating portion of the knee preferably from the lateral trochlea. Pegs of osteochondral graft can also be used to fix large lesions, which are unstable and not detached. This method is limited by the amount of graft that can be harvested but it does not involve risk of disease transmission.

21. c. Allograft For larger defects and earlier failed surgeries allografts provide the best alternative. Various studies have shown good results with reformation of hyaline like cartilage. However disease transmission remains a risk.

22. d. Autologous Chondrocyte Implantation This procedure requires two surgeries. Chondrocytes harvested from the healthy cartilage are cultured. At 6 weeks the defect is debrided and covered with a periosteal patch harvested from anterior tibia. The cultured chondrocytes are then injected under the periosteal patch. Stable hyaline like cartilage has been found to form after a few months.