INTRODUCTION AND ETIOLOGY
Osteochondritis dissecans (OCD) of the knee represents a focal, idiopathic alteration of subchondral bone with the potential for secondary disruption of the adjacent articular cartilage. If left untreated, progressive destabilization of the osteochondral fragment can lead to premature osteoarthritis. The condition presents in two distinct clinical entities dictated by skeletal maturity: Juvenile Osteochondritis Dissecans (JOCD) in patients with open physes, and Adult Osteochondritis Dissecans (AOCD) in skeletally mature individuals.
The precise etiology of OCD remains highly controversial and is widely considered multifactorial. Prevailing theories include:
* Repetitive Microtrauma: The most widely accepted theory, positing that repetitive mechanical loading leads to subchondral stress fractures. Subsequent interruption of the interosseous blood supply to the subchondral area of the epiphysis prevents normal bone remodeling, leading to focal avascular necrosis.
* Ischemia: Vascular watershed areas within the developing epiphysis may predispose the subchondral bone to localized ischemic events.
* Mechanical Factors: Alterations in the mechanical axis of the lower extremity heavily influence lesion development. There is a strong association between medial condylar lesions and a varus mechanical axis, whereas lateral condylar lesions are frequently associated with a valgus axis.
* Other Proposed Factors: Familial predisposition, endocrine imbalances, epiphyseal abnormalities, accessory centers of ossification, and congenitally abnormal subchondral bone.
Clinical Pearl: The classic location for an OCD lesion in the knee is the lateral aspect of the medial femoral condyle (often remembered by the mnemonic "LAME"). This area is subjected to significant shear forces during tibial internal rotation, particularly when the tibial spine impinges against the condyle.
CLINICAL PRESENTATION AND PHYSICAL EXAMINATION
OCD of the knee occurs twice as often in males as in females, with peak incidence in adolescents and young adults. It is exceedingly rare in patients younger than 10 years or older than 50 years.
Symptomatology
The clinical picture varies significantly based on the stability of the lesion.
* Stable Lesions: The most common symptom is a vague, poorly localized, aching discomfort in the knee, frequently exacerbated by exercise. Approximately 80% of juvenile patients report symptoms for an average of 14 months prior to initial presentation. A history of antecedent trauma is reported in 40% to 60% of cases.
* Unstable Lesions: Once the lesion becomes partially or completely separated, mechanical symptoms predominate. Patients report catching, locking, and popping, which can closely mimic meniscal derangement. If complete separation occurs, the patient may palpate a mobile loose body within the joint capsule.
Physical Examination Findings
A meticulous physical examination is paramount to rule out concomitant intra-articular pathology.
* Gait: The patient may exhibit an externally rotated gait to avoid contact between the medial femoral condyle and the medial tibial spine.
* Palpation: Joint line tenderness or highly localized tenderness directly over the medial femoral condyle when the knee is flexed to 90 degrees.
* Wilson Sign: A classic, though not universally present, provocative test. The knee is flexed to 90 degrees, the tibia is internally rotated, and the knee is slowly extended. Pain at approximately 30 degrees of flexion that is relieved by external rotation of the tibia is considered a positive Wilson sign, indicative of a medial condyle lesion.
* Other Findings: Mild to moderate effusion (massive effusions are rare unless a loose body is actively causing synovitis), limitation of terminal extension, quadriceps atrophy, and a positive McMurray sign.
DIAGNOSTIC IMAGING AND STAGING
Radiographic Evaluation
Standard radiography remains the initial diagnostic modality. Routine anteroposterior (AP), lateral, and skyline (Merchant) views should be obtained.
* The Notch (Tunnel) View: Because the lesion most commonly resides on the inner aspect of the medial femoral condyle, a posteroanterior flexion weight-bearing view (notch/tunnel view) is often the most revealing.
* Bilateral Comparison: OCD is bilateral in approximately 30% of patients. Comparison radiographs are mandatory in juvenile and adolescent patients to differentiate true OCD from bilateral anomalous ossification centers. Anomalous centers typically cause transient symptoms and resolve spontaneously within 6 to 12 months.
Magnetic Resonance Imaging (MRI)
MRI is the gold standard for assessing fragment size, attachment, viability, and stability. It is also critical for identifying associated ligamentous and meniscal injuries. Currently, a spoiled gradient-echo sequence using fat suppression and three-dimensional acquisition is considered the optimal technique for evaluating articular cartilage integrity.
MRI Signs of Instability:
1. A high-signal intensity line (fluid) interposing between the fragment and the crater on T2-weighted or STIR images.
2. Focal cystic areas beneath the lesion.
3. A high-signal intensity line breaching the articular cartilage.
4. A focal articular cartilage defect.
Surgical Warning: The absence of a high-signal intensity zone at the interface of the fragment and the parent bone is the most reliable MRI sign of lesion stability. Do not aggressively debride or attempt to fixate a lesion that demonstrates complete MRI stability, particularly in a juvenile patient.
Scintigraphy and Computed Tomography (CT)
Technetium-99m bone scans can track healing activity and predict treatment outcomes. Sequential single-photon emission CT (SPECT) scans obtained at 8-week intervals are highly sensitive for monitoring revascularization. If CT is utilized to assess the osseous architecture of the crater, it should be reformatted in the coronal and sagittal planes.
Staging Systems
Table 1: Dipaola et al. MRI and Arthroscopic Staging System
* Stage I:
* Arthroscopy: Irregularity and softening of articular cartilage; no definable fragment.
* MRI: Thickening of articular cartilage; low signal changes.
* Radiography: Compression lesion; no visible fragment.
* Stage II:
* Arthroscopy: Articular cartilage breached; definable fragment not displaceable.
* MRI: Articular cartilage breached; low signal rim behind fragment indicating fibrous attachment.
* Radiography: Fragment attached.
* Stage III:
* Arthroscopy: Articular cartilage breached; definable fragment, displaceable but attached by some overlying cartilage.
* MRI: Articular cartilage breached; high signal changes behind fragment indicating synovial fluid between fragment and underlying subchondral bone.
* Radiography: Nondisplaced fragment without attachment.
* Stage IV:
* Arthroscopy: Loose body.
* MRI: Loose body.
* Radiography: Displaced fragment.
Table 2: Cahill Scintigraphic Staging System
* Stage 0: Normal radiographic and scintigraphic appearance.
* Stage I: Lesion visible on plain radiographs, bone scan normal.
* Stage II: Increased uptake in the area of the lesion on bone scan.
* Stage III: Increased isotopic uptake in the entire femoral condyle.
* Stage IV: Uptake in the tibial plateau opposite the lesion (kissing lesion).
PROGNOSTIC FACTORS AND INDICATIONS FOR SURGERY
Primary prognostic factors include patient age (status of the physes), lesion progression, size, stability, the amount of subchondral bone attached to the fragment, and the location of the lesion relative to the primary weight-bearing axis.
Non-Operative Management:
Indicated primarily for JOCD (open physes) with stable lesions (Stage I or II). Treatment consists of activity modification, protected weight-bearing, and immobilization for 6 to 12 weeks, followed by a gradual return to activity once radiographic healing is evident.
Indications for Surgical Intervention:
1. Failure of non-operative management in JOCD after 3 to 6 months.
2. AOCD (closed physes) regardless of stability, as spontaneous healing is exceedingly rare.
3. Unstable lesions (Stage III) or detached loose bodies (Stage IV) in any age group.
4. Lesions larger than 2 cm in diameter or those involving the primary weight-bearing zone.
SURGICAL MANAGEMENT: STEP-BY-STEP APPROACHES
1. Preoperative Planning and Positioning
- Anesthesia: General or regional anesthesia.
- Positioning: The patient is placed supine on the operating table. A tourniquet is applied to the proximal thigh. The leg is placed in a standard leg holder or positioned over a lateral post to allow for full, unencumbered flexion and extension, which is critical for accessing posterior condylar lesions.
- Diagnostic Arthroscopy: Standard anterolateral and anteromedial portals are established. A thorough diagnostic sweep is performed. The lesion is carefully probed to assess for ballotability, cartilage softening, and breaches in the articular surface.
2. Subchondral Drilling (For Stable, Intact Lesions)
The goal of drilling is to breach the sclerotic subchondral bone, creating vascular channels that allow marrow elements to migrate into the lesion, thereby stimulating revascularization and osteogenesis.
- Transarticular Drilling:
- Indicated for lesions accessible via standard portals.
- Using a 0.062-inch Kirschner wire (K-wire) or a specialized microfracture awl, multiple perforations are made directly through the intact articular cartilage into the subchondral bone.
- Drill depth should be approximately 10 to 15 mm to ensure penetration of the sclerotic base.
- Holes are spaced 3 to 4 mm apart.
- Retroarticular Drilling:
- Indicated for JOCD where preservation of the pristine articular cartilage is desired, or for lesions difficult to access transarticularly.
- Requires intraoperative fluoroscopy.
- A guide pin is advanced from the extra-articular epicondylar region, aiming for the center of the OCD lesion under fluoroscopic guidance.
- The pin is advanced until it reaches the subchondral bone of the lesion, taking extreme care not to breach the articular cartilage.
3. Fixation of Unstable Lesions (Stage II and III)
If the fragment is ballotable or partially detached but possesses sufficient subchondral bone for healing, internal fixation is mandated.
- Bed Preparation: The fragment is gently hinged open like a trapdoor. The fibrous tissue at the base of the crater and on the undersurface of the fragment is meticulously debrided using a motorized shaver and curettes down to bleeding subchondral bone.
- Bone Grafting: If a significant osseous defect exists after debridement, autologous cancellous bone graft (often harvested from the proximal tibia or distal femur) is packed into the crater.
- Reduction and Fixation: The fragment is anatomically reduced. Fixation can be achieved using:
- Bioabsorbable Pins/Darts: Advantageous as they do not require a second surgery for removal. However, they provide less compression than screws.
- Headless Metallic Compression Screws (e.g., Herbert screws): Provide superior compression. They must be countersunk below the articular cartilage to prevent kissing lesions on the tibia. Removal may be required once healing is confirmed.
- The fixation devices are placed perpendicular to the lesion interface to maximize compression.
Pitfall: Failure to adequately debride the fibrous interface between the fragment and the crater is the leading cause of non-union following OCD fixation. The bed must bleed prior to reduction.
4. Salvage and Cartilage Restoration (Stage IV)
When the fragment is completely detached, fragmented, devoid of subchondral bone, or deemed unsalvageable, it must be excised. The resulting defect is then managed based on its size and patient demands.
- Microfracture: Indicated for small defects (< 2 cm²). The calcified cartilage layer is removed, and the subchondral bone is perforated to stimulate a fibrocartilage healing response.
- Osteochondral Autograft Transfer System (OATS / Mosaicplasty): Indicated for moderate defects (1 to 3 cm²). Cylindrical osteochondral plugs are harvested from non-weight-bearing areas (e.g., the periphery of the trochlea) and press-fit into the defect, restoring hyaline cartilage.
- Autologous Chondrocyte Implantation (ACI) or Osteochondral Allograft: Indicated for massive defects (> 3 cm²). ACI requires a two-stage procedure (harvest, expansion, and reimplantation), while allografts provide immediate structural restoration of both bone and cartilage using donor tissue.
POSTOPERATIVE REHABILITATION PROTOCOLS
Postoperative rehabilitation is dictated by the specific surgical intervention performed.
Following Drilling or Fixation:
* Phase I (0-6 weeks): The patient is restricted to non-weight-bearing or touch-down weight-bearing with crutches. A hinged knee brace is locked in extension for ambulation but unlocked multiple times daily for continuous passive motion (CPM) or active-assisted range of motion (ROM) to nourish the cartilage.
* Phase II (6-12 weeks): Progressive weight-bearing is initiated based on radiographic evidence of healing. Closed kinetic chain exercises are introduced to restore quadriceps and hamstring strength.
* Phase III (3-6 months): Progression to full weight-bearing. Introduction of light jogging and sport-specific drills once the patient achieves 80% strength compared to the contralateral limb and demonstrates complete radiographic union.
* Return to Play: Typically requires 6 to 9 months, contingent upon complete resolution of symptoms, full ROM, and MRI or radiographic confirmation of osseous integration.
Following Cartilage Restoration (OATS/ACI):
Protocols are significantly more conservative, often requiring strict non-weight-bearing for 6 to 8 weeks and delaying return to high-impact sports for 9 to 12 months to allow for complete graft incorporation and maturation.
