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Cartilage Injuries: Repair Options to Preserve Your Joint Health

Operative Management of Osteochondroses and Osteochondritis Dissecans

13 Apr 2026 10 min read 1 Views

Key Takeaway

Osteochondroses and osteochondritis dissecans (OCD) represent a complex spectrum of subchondral bone and articular cartilage pathologies. This comprehensive guide details the evidence-based operative management of OCD lesions across the knee, elbow, and ankle, alongside apophyseal conditions like Osgood-Schlatter and Freiberg disease. Emphasizing biomechanics, precise surgical indications, and step-by-step techniques—from arthroscopic drilling to osteochondral autograft transfer—this text provides orthopedic surgeons with critical protocols for optimizing joint preservation and functional recovery.

Introduction to Osteochondroses and Osteochondritis Dissecans

Osteochondroses encompass a diverse group of idiopathic conditions characterized by the derangement of normal enchondral ossification, primarily affecting the epiphyses and apophyses of skeletally immature patients. When this process involves the articular surface and subchondral bone, it is termed Osteochondritis Dissecans (OCD). The pathophysiology is multifactorial, involving repetitive microtrauma, localized ischemia, and genetic predispositions, culminating in subchondral bone necrosis, potential articular cartilage delamination, and subsequent joint incongruity.

This masterclass delineates the evidence-based operative management of the most clinically significant osteochondroses and OCD lesions, synthesizing decades of biomechanical research and surgical advancements. The focus remains strictly on joint preservation, restoration of articular congruity, and the mitigation of early-onset osteoarthritis.

Clinical Pearl: The critical determinant in the management of OCD is skeletal maturity. Juvenile OCD (open physes) possesses a robust healing potential and often responds to conservative management. Adult OCD (closed physes) or unstable juvenile lesions invariably require surgical intervention to prevent progressive joint deterioration.


Osteochondritis Dissecans of the Knee

The knee is the most frequent site for OCD, with the classic lesion located on the lateral aspect of the medial femoral condyle (LAME mnemonic).

Biomechanics and Pathoanatomy

The medial femoral condyle bears the brunt of weight-bearing forces during the stance phase of gait. Repetitive impingement of the tibial spine against the lateral aspect of the medial femoral condyle during internal tibial rotation is a primary biomechanical driver. As the subchondral bone fails, the overlying cartilage loses its structural support, leading to softening, fibrillation, and eventual separation (loose body formation).

Surgical Indications

  1. Failure of non-operative management (minimum 3–6 months of restricted weight-bearing) in a compliant skeletally immature patient.
  2. Clinical or radiographic signs of instability, including mechanical symptoms (catching, locking).
  3. MRI evidence of instability, defined by high T2 signal fluid interposing between the OCD fragment and the parent bone, or multiple subchondral cysts.
  4. Skeletally mature patients with symptomatic lesions.

Positioning and Setup

  • Anesthesia: General or regional anesthesia.
  • Positioning: Supine on the operating table. A lateral post or leg holder is utilized to allow full range of motion and valgus/varus stress.
  • Tourniquet: Placed proximally on the thigh, inflated only if visualization is compromised.

Step-by-Step Surgical Approaches

1. Arthroscopic Transarticular Drilling (For Intact, Stable Lesions)

The goal is to breach the sclerotic subchondral bone, stimulating angiogenesis and marrow-derived mesenchymal stem cell migration to facilitate healing.
* Diagnostic Arthroscopy: Assess the lesion using a tactile probe. An intact surface that softens upon probing indicates a stable, yet compromised, lesion.
* Drilling: Using a 0.062-inch Kirschner wire (K-wire) or a specialized microfracture awl, create multiple perforations (spaced 3–4 mm apart) through the articular cartilage into the subchondral bone.
* Depth: Penetrate approximately 10–15 mm to ensure access to vascularized cancellous bone. Fat droplets entering the joint confirm adequate depth.

2. Internal Fixation (For Unstable, Salvageable Lesions)

If the fragment is hinged or completely detached but structurally intact, in situ fixation is mandated.
* Bed Preparation: Hinge open the fragment. Debride the fibrous tissue at the base of the crater using a motorized shaver and curettes down to bleeding subchondral bone.
* Reduction: Anatomically reduce the fragment. Temporary fixation is achieved with smooth K-wires.
* Fixation: Secure the fragment using bioabsorbable pins (e.g., poly-L-lactic acid), headless compression screws, or Herbert screws. Bioabsorbable implants are preferred in pediatric populations to avoid a secondary removal surgery.
* Countersinking: Ensure all implants are countersunk at least 1–2 mm below the articular surface to prevent opposing "kissing" lesions on the tibial plateau.

3. Osteochondral Autograft Transfer System (OATS) / Mosaicplasty

Indicated for unsalvageable fragments or chronic craters.
* Harvest: Cylindrical osteochondral plugs are harvested from non-weight-bearing regions (e.g., the superolateral trochlea or intercondylar notch).
* Preparation: The recipient site is reamed to a matching diameter and depth.
* Implantation: The autograft plugs are press-fit into the defect, ensuring the articular cartilage is perfectly flush with the surrounding native cartilage.

Postoperative Protocol

  • Phase I (0–6 weeks): Strict non-weight-bearing (or touch-down weight-bearing for OATS). Continuous Passive Motion (CPM) is initiated immediately to nourish the articular cartilage.
  • Phase II (6–12 weeks): Progressive weight-bearing. Closed kinetic chain exercises begin.
  • Phase III (3–6 months): Return to light jogging and sport-specific drills, contingent upon radiographic evidence of bony incorporation.

Osteochondritis Dissecans of the Capitellum

Capitellar OCD is predominantly seen in adolescent overhead athletes (baseball pitchers) and gymnasts, driven by repetitive valgus overload and radiocapitellar compression.

Biomechanics and Pathoanatomy

During the throwing motion, the elbow experiences extreme valgus stress during the late cocking and early acceleration phases. This creates tensile stress medially (ulnar collateral ligament) and severe compressive and shear forces laterally at the radiocapitellar joint. The tenuous vascular supply to the capitellum renders it highly susceptible to avascular necrosis and subsequent fragmentation.

Surgical Warning: Capitellar OCD must be differentiated from Panner's disease. Panner's disease affects children under 10, involves the entire ossific nucleus, and is universally self-limiting. OCD affects adolescents (>10 years), involves localized subchondral defects, and frequently requires surgery.

Surgical Indications

  1. Persistent pain and loss of extension despite prolonged rest (cessation of throwing).
  2. Unstable lesions, capitellar flattening, or intra-articular loose bodies.
  3. Enlarging cystic changes on MRI.

Step-by-Step Surgical Approach: Arthroscopic Debridement and Microfracture

  • Positioning: Lateral decubitus or prone position with the arm draped over a bolster.
  • Portals: Standard anterolateral, anteromedial, and direct lateral (soft spot) portals.
  • Loose Body Removal: Thoroughly inspect the radiocapitellar joint and the olecranon fossa for loose bodies.
  • Debridement: Excise the unstable capitellar fragment. Unlike the knee, capitellar fragments are rarely amenable to internal fixation due to their small size and poor bone stock.
  • Microfracture: Use an arthroscopic awl to perforate the sclerotic base of the defect, creating bleeding bone to stimulate a fibrocartilage healing response.
  • Margin Plasty: Smooth the vertical edges of the surrounding healthy cartilage to prevent further delamination.

Postoperative Protocol

  • Immediate active and active-assisted range of motion (ROM) to prevent elbow stiffness.
  • Avoidance of valgus stress and weight-bearing on the upper extremity for 8–12 weeks.
  • Return to throwing is delayed until 4–6 months postoperatively, utilizing a structured interval throwing program.

Osteochondral Lesions of the Talus (OLT)

Historically termed OCD of the ankle, OLTs are almost exclusively traumatic in origin, resulting from severe inversion injuries.

Biomechanics and Pathoanatomy

  • Anterolateral Lesions (DIAL): Dorsiflexion and Inversion injuries. These are typically shallow, wafer-shaped, and highly symptomatic due to shear forces.
  • Posteromedial Lesions (PIMP): Plantarflexion and Inversion injuries. These are usually deeper, cup-shaped, and may be asymptomatic initially.

Surgical Indications

  1. Symptomatic lesions failing 3–6 months of conservative care (immobilization, NSAIDs).
  2. Acute displaced osteochondral fractures.
  3. Cystic lesions >1.5 cm in diameter.

Step-by-Step Surgical Approach: Arthroscopic Marrow Stimulation

  • Positioning: Supine with a thigh holder. Non-invasive ankle distraction is applied via a sterile strap.
  • Portals: Anteromedial and anterolateral portals. Care is taken to avoid the superficial peroneal nerve laterally and the saphenous nerve medially.
  • Debridement: The unstable cartilage is excised using a curette. The sclerotic base is debrided until punctate bleeding is visualized.
  • Drilling/Microfracture: A microfracture awl or K-wire is used to penetrate the subchondral plate at 3 mm intervals.
  • Adjuncts: For lesions >1.5 cm, consider OATS or Autologous Chondrocyte Implantation (ACI), which may require a medial malleolar osteotomy for perpendicular access to posteromedial lesions.

Postoperative Protocol

  • Immobilization in a neutral splint for 2 weeks to allow soft tissue healing.
  • Transition to a CAM boot with strict non-weight-bearing for 4–6 weeks.
  • Early ankle ROM exercises (dorsiflexion/plantarflexion) are encouraged to mold the regenerating fibrocartilage.

Osgood-Schlatter Disease (Tibial Tubercle Apophysitis)

Osgood-Schlatter disease is a traction apophysitis of the tibial tubercle, ubiquitous in active adolescents experiencing rapid growth spurts.

Biomechanics and Pathoanatomy

The patellar tendon inserts onto the secondary ossification center of the tibial tubercle. Repetitive eccentric contractions of the quadriceps (e.g., jumping, sprinting) transmit massive tensile forces across this apophysis. This microtrauma leads to partial avulsions, inflammation, and the formation of heterotopic ossicles within the distal patellar tendon.

Surgical Indications

Surgery is strictly contraindicated in skeletally immature patients due to the risk of premature physeal closure, which can result in genu recurvatum.
Indications for skeletally mature patients include:
1. Persistent, debilitating pain localized to a prominent tibial tubercle.
2. Radiographic confirmation of an ununited ossicle within the patellar tendon.
3. Failure of exhaustive conservative measures (activity modification, physical therapy, infrapatellar straps).

Step-by-Step Surgical Approach: Ossicle Excision (Ferciot Procedure)

  • Positioning: Supine with a tourniquet applied to the proximal thigh.
  • Incision: A longitudinal midline or slightly lateral incision over the distal patellar tendon and tibial tubercle.
  • Tendon Splitting: The paratenon is incised. A longitudinal split is made in the distal third of the patellar tendon, directly over the palpable ossicle.
  • Excision: The ununited ossicle is carefully shelled out using a scalpel and curettes.
  • Tubercle Plasty: If the tibial tubercle is excessively prominent, a rongeur or osteotome is used to resect the anterior prominence (tubercleplasty), ensuring the main insertion of the patellar tendon is not compromised.
  • Closure: The tendon is repaired with heavy absorbable sutures, and the paratenon is meticulously closed to prevent adhesions.

Pitfall: Over-resection of the tibial tubercle or aggressive detachment of the patellar tendon can lead to catastrophic extensor mechanism rupture. Dissection must remain strictly intralesional.

Postoperative Protocol

  • Weight-bearing as tolerated in a hinged knee brace locked in extension for 2 weeks.
  • Progressive ROM begins at week 2.
  • Strengthening of the quadriceps mechanism begins at 4 weeks, with a return to sports typically at 8–12 weeks.

Freiberg’s Infraction (Metatarsal Head Osteochondrosis)

Freiberg’s disease is an osteochondrosis of the metatarsal head, most commonly affecting the second metatarsal in adolescent females.

Biomechanics and Pathoanatomy

The second metatarsal is typically the longest and relatively rigidly fixed at its base. During the propulsive phase of gait, it absorbs maximum shear and compressive forces. Repetitive microtrauma, combined with a tenuous vascular supply to the metatarsal head, leads to subchondral collapse, flattening of the articular surface, and eventual joint incongruity.

Surgical Indications

  1. Smillie Stage III (central collapse), Stage IV (fragmentation), or Stage V (arthrosis) lesions.
  2. Intractable forefoot pain failing metatarsal pads, stiff-soled shoes, and activity modification.

Step-by-Step Surgical Approach: Dorsal Closing-Wedge Osteotomy (Gauthier’s Technique)

The objective of this procedure is to rotate the healthy, uninvolved plantar articular cartilage dorsally to articulate with the proximal phalanx, effectively bypassing the necrotic dorsal defect.
* Positioning: Supine. Ankle or calf tourniquet applied.
* Incision: A dorsal longitudinal incision over the affected metatarsophalangeal (MTP) joint.
* Exposure: The extensor tendons are retracted. The dorsal capsule is incised to expose the flattened metatarsal head.
* Debridement: Loose bodies and the necrotic dorsal cartilage are meticulously debrided.
* Osteotomy: A dorsal closing-wedge osteotomy is performed at the surgical neck of the metatarsal. The wedge size is dictated by the extent of the dorsal defect (typically 3–4 mm).
* Rotation and Fixation: The metatarsal head is rotated dorsally, closing the osteotomy site. This brings the pristine plantar cartilage into the functional joint space. Fixation is achieved using a threaded K-wire or a micro-fragment screw.

Postoperative Protocol

  • The patient is placed in a rigid postoperative shoe or short leg cast, restricted to heel-weight-bearing for 4–6 weeks.
  • Pins (if used) are removed at 4 weeks.
  • Aggressive MTP joint mobilization is initiated at 4 weeks to prevent severe stiffness, a common complication of forefoot surgery.

Conclusion

The operative management of osteochondroses and osteochondritis dissecans requires a profound understanding of joint-specific biomechanics, rigorous patient selection, and meticulous surgical execution. Whether performing an arthroscopic transarticular drilling for a juvenile knee OCD, or executing a complex intra-articular osteotomy for Freiberg's infraction, the orthopedic surgeon's paramount objective remains the restoration of articular congruity and the preservation of long-term joint function. Adherence to the evidence-based protocols outlined in this text ensures optimal outcomes in this challenging demographic.

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