GC230 Knee Sport Injuries: Part 4
Knee sport injuries Part 4 covers posterior cruciate ligament (PCL) injuries and posterolateral corner injuries, including their mechanisms, clinical assessment, and management principles.
This lecture — Knee Sport Injuries Part 4 — focuses entirely on articular cartilage injury of the knee. It sits within a six-part lecture series on Knee Sports Injuries (GC 230) by Professor WP Yau. While Parts 1–3 cover ligament and meniscal injuries, Part 4 zeroes in on the unique biology of articular cartilage and why it heals so poorly, the classification and management of traumatic cartilage defects, osteochondritis dissecans (OCD), and osteochondral fractures.
Why This Lecture Matters Clinically and for Exams
Articular cartilage is avascular, aneural, and alymphatic — meaning it cannot mount a normal inflammatory healing response. This single biological fact underpins everything in this lecture: why cartilage injuries are hard to diagnose clinically, why they progress to osteoarthritis if untreated, why different surgical strategies exist (marrow stimulation, grafting, cell-based therapy), and why prognosis differs between children and adults.
Learning Objectives (derived from slides) [1]:
- Understand the anatomy and biology of articular cartilage
- Classify traumatic articular cartilage injury (Modified Outerbridge)
- Know the treatment ladder for cartilage lesions
- Recognise, stage, and manage osteochondritis dissecans (OCD)
- Identify and manage osteochondral fractures
Core Concepts: Anatomy and Biology of Articular Cartilage
Articular cartilage is aneural, avascular, and alymphatic. — This is the single most important biological fact in this lecture. [1]
| Property | Consequence |
|---|---|
| Aneural | Cartilage injuries are painless unless they involve subchondral bone or cause synovitis/effusion → patients may present late |
| Avascular | No blood supply → cannot mount normal inflammatory response → very limited self-repair capacity; no haematoma → no callus |
| Alymphatic | No lymphatic drainage → inflammatory mediators, if present, are not efficiently cleared |
| Component | Details |
|---|---|
| Cells | Chondrocytes — the only cell type; sparse, isolated in lacunae, low metabolic rate |
| ECM | Type II collagen (tensile framework), proteoglycans & GAGs (compressive resistance via osmotic swelling), water (~65-80% of wet weight, trapped by proteoglycans) |
The articular surface of a synovial joint is covered with hyaline cartilage, which provides low friction, high resilience, and high compressive stiffness. [1]
- Biomechanical role: load distribution, shock absorption, minimization of wear
- However, cartilage has a relatively low tensile strength, making it more susceptible to injury under shear and tensile load. [1]
First-principles explanation: The collagen-proteoglycan matrix is optimized for compression (water is incompressible and trapped by GAGs). Under shear or tension, the collagen network must resist alone — and Type II collagen is less stiff than Type I — hence cartilage fails more easily under these forces. This is why pivoting sports injuries and tangential impacts damage cartilage.
Traumatic Articular Cartilage Injury
In young athletic individuals, articular cartilage pathology is usually traumatic in origin. In older individuals, the articular cartilage lesions are often degenerative in nature. [1]
Around 60% of patients having knee arthroscopy suffer from articular cartilage pathology. [1]
This is extremely common — if you put a camera in a symptomatic knee, more than half the time you will find cartilage damage.
- Mechanical knee pain — worsened by weight-bearing, twisting; often vague and difficult to localise
- Knee effusion — because damaged cartilage debris irritates the synovium, causing reactive synovitis and effusion
Why is the pain 'mechanical'?
Articular cartilage itself is aneural, so pain arises from the subchondral bone (once exposed), synovial irritation from debris, or altered joint mechanics. "Mechanical" pain = related to loading/movement rather than inflammatory rest pain.
- MRI — gold standard non-invasive test; can grade the depth of cartilage loss and detect subchondral bone oedema
- Diagnostic arthroscopy — direct visualisation; allows simultaneous treatment
This is the standard classification system for articular cartilage lesions, used both on MRI and arthroscopy. [1]
| Grade | Description | Key Points |
|---|---|---|
| Grade 0 | Intact cartilage | Normal |
| Grade 1 | Chondral softening or blistering with intact surface | Surface not breached; "chondromalacia" |
| Grade 2 | Superficial ulceration, fibrillation, or fissuring < 50% depth | Partial-thickness, superficial |
| Grade 3 | Deep ulceration, fibrillation, fissuring, or chondral flap > 50% depth without exposed bone | Partial-thickness, deep; flap may cause mechanical symptoms |
| Grade 4 | Full-thickness wear with exposed subchondral bone | Most severe; bone exposed → pain and risk of OA |
Exam Discriminator
Students often confuse Grade 3 and Grade 4. The critical distinction: Grade 3 = > 50% depth but bone is NOT exposed. Grade 4 = bone IS exposed. If a question asks "what grade involves exposed subchondral bone?" the answer is always Grade 4.
Treatment of Articular Cartilage Injury
Patient should be offered an initial trial of non-operative treatment. Surgery is indicated only if non-operative treatment fails to relieve patients' symptoms. [1]
- Activity modification — avoid high-impact loading
- Weight reduction — reduces joint contact forces
- Muscle-strengthening exercise — especially quadriceps; dynamic stabilisation reduces peak cartilage stress
For partial-thickness cartilage lesions (Outerbridge grade 1 to 3) and small-sized grade 4 lesion (e.g., < 1 cm), the mainstay of surgical treatment is arthroscopic debridement. [1]
| Technique | Indication (Outerbridge Grade & Size) | Mechanism | Advantages | Disadvantages |
|---|---|---|---|---|
| Arthroscopic debridement | Grades 1–3; small Grade 4 ( < 1 cm) | Remove unstable flaps, smooth surface | Simple, symptom relief | Does not regenerate cartilage |
| Marrow stimulation (microfracture / subchondral drilling / abrasion) | Grade 4, lesion < 2 cm | Breach subchondral bone plate → pluripotent MSCs flow out → fibrocartilage formation | Simple, inexpensive; 60–70% symptom improvement | Fibrocartilage deteriorates over time; not true hyaline cartilage |
| Osteochondral transplantation (autograft / allograft) | Grade 4, lesion 1–4 cm | Transplant intact osteochondral plug with viable chondrocytes | > 80% return to sport; 80–100% survivorship short-term, > 80% at 10 years | Donor site morbidity (autograft); disease transmission risk (allograft); graft size limitation |
| Autologous chondrocyte implantation (ACI) | Grade 4, lesion > 2 cm | Two-stage: harvest → culture/expand chondrocytes → implant with/without scaffold | 80–90% good/excellent results | Expensive; two operations required |
Deep Dive on Each Technique
The subchondral bone plate is breached by either abrasion, subchondral drilling or microfracture. The purpose is to breach the subchondral bone plate and allow the pluripotent stem cells within the bone marrow to flow out and fill the cartilage defect, resulting in fibrocartilage formation. [1]
Why fibrocartilage, not hyaline cartilage? The mesenchymal stem cells that emerge from the marrow differentiate into fibroblast-like cells producing predominantly Type I collagen (fibrocartilage) rather than Type II collagen (hyaline). Fibrocartilage is mechanically inferior — less resilient, higher friction, and it wears down over years. This explains the functional decline with longer follow-up.
An osteochondral graft is harvested and transplanted into the damaged area. [1]
- Autograft: harvested from non-weight-bearing/less-weight-bearing donor area of the same knee (e.g., superolateral trochlea margin). Advantage: no immunological rejection. Disadvantage: limited by donor area size and creates a new defect at the donor site.
- Allograft: from a fresh cadaveric size-matched femoral condyle. Advantage: can address larger defects. Disadvantage: risk of disease transmission, limited availability.
The transplanted osteochondral graft contains viable chondrocytes, and the damaged cartilage is replaced by the intact chondral component of the osteochondral graft. [1]
It is a two-staged operation. In the first-stage surgery, a small amount of articular cartilage is harvested from the patient. The chondrocytes in the harvested cartilage are cultured and expanded in a laboratory. In the second-stage surgery, the chondrocytes are implanted into the cartilage damage, with or without the use of a periosteum graft or an artificial scaffold. [1]
Why two stages? Chondrocytes need to be expanded in number — the initial harvest yields too few cells. Laboratory culture over 4–6 weeks multiplies them sufficiently to fill the defect.
| Lesion Characteristic | First-line | Second-line if fails |
|---|---|---|
| Grade 1–3 (partial thickness) | Non-operative → arthroscopic debridement | — |
| Grade 4, < 1 cm | Arthroscopic debridement | — |
| Grade 4, < 2 cm | Marrow stimulation (microfracture) | Osteochondral transplantation |
| Grade 4, 1–4 cm | Osteochondral transplantation | ACI |
| Grade 4, > 2 cm | ACI | Osteochondral allograft |
Size Thresholds — High Yield for MCQ
Microfracture: < 2 cm. Osteochondral transplantation: 1–4 cm. ACI: > 2 cm. Note the overlap zone (1–2 cm and 2–4 cm) where more than one option is valid — the exam will test the "best" option for a given size.
Osteochondritis Dissecans (OCD)
OCD is the most common cause of loose bodies in the knee joint in individuals aged 12 to 19 years old. [1]
In OCD, an area of subchondral bone becomes necrotic and degenerative changes usually occur in the cartilage overlying it. During the course of the disease, unless spontaneous healing occurs or surgical intervention is performed, the necrotic bone and the cartilage overlying it gradually separate from adjacent bone and cartilage and become a loose body, leaving a crater behind. [1]
Think of it as a patch of bone "dying" under the cartilage surface. The overlying cartilage, which depends on the subchondral bone for structural support (and some nutrient diffusion from below), degenerates. Eventually the fragment separates — like a piece of plaster falling off a ceiling.
Etiology is unclear. Proposed theories include ischemia, repetitive microtrauma, familial predisposition, endocrine imbalance, epiphyseal abnormalities, osteochondral fracture. [1]
- Twice more often in males than in females
- Age 10 to 50 years old
- Bilateral in 30% of patients
- Most OCD in the knee joint occur in the medial femoral condyle (specifically the lateral aspect of the medial femoral condyle)
Young patient before physeal closure: good prognosis if treatment is given promptly. Adult patient: poor prognosis. [1]
Why? Children with open physes have better vascularisation of the subchondral bone and greater regenerative capacity. Once the physis closes, revascularisation potential drops dramatically.
Symptoms:
- Vague and aching discomfort in the knee
- History of injury is present in 40–60% of patients
- +/- locking symptoms (if a fragment has become a loose body)
Signs:
- Quadriceps wasting (disuse atrophy from pain-limited activity)
- Effusion
- Joint line tenderness +/- tenderness over the lesion
- Reduced range of motion
- Wilson's sign — internally rotating the proximal tibia with gradual extension of the knee from 90° flexion → the medial tibial spine impacts the OCD lesion on the lateral aspect of the medial femoral condyle → pain. The pain is relieved by external rotation of the tibia (moves the spine away from the lesion).
Wilson's Sign — Classic Exam Question
Wilson's sign is specific for OCD of the medial femoral condyle. Know the manoeuvre: internal rotation of tibia + gradual extension from 90° flexion → pain. Relief with external rotation confirms it. The examiners love this.
- X-ray — may show a well-defined osteochondral fragment
- MRI — determines stability of the lesion, presence of fluid behind fragment
- Arthroscopy — definitive assessment of cartilage surface integrity and fragment stability
What the OCD triad shows: XR and MRI circles on a femoral-condyle osteochondral lesion, then arthroscopy with a probe on damaged cartilage — stage by stability across all three modalities. [1]
This staging system correlates X-ray, MRI, and arthroscopic findings — know all three modalities for each stage. [1]
| Stage | X-ray | MRI | Arthroscopy |
|---|---|---|---|
| Stage I | No visible fragment | Thickening of articular cartilage; low signal change | No definable fragment; irregularity and softening of cartilage |
| Stage II | Visible fragment that remains attached to the bone | Articular cartilage is breached; low signal rim behind fragment (fibrous attachment) | Articular cartilage is breached; definable fragment; not displaceable |
| Stage III | Non-displaced fragment without attachment | Articular cartilage is breached; high signal change behind fragment (synovial fluid between fragment and subchondral bone) | Articular cartilage is breached; definable fragment; displaceable but attached by some overlying cartilage |
| Stage IV | Displaced fragment | Loose body | Loose body |
MRI Signal Behind Fragment — Key Discriminator
Stage II vs Stage III on MRI: Low signal rim = fibrous attachment = stable (Stage II). High signal = fluid = unstable (Stage III). This distinction determines whether you can manage conservatively or need surgery.
OCD Treatment — Stage-by-Stage
The aim is to prevent detachment of the lesion and promote healing.
- A short period of non-operative treatment with activity modification can be attempted
- If symptoms persist despite non-operative management, surgical intervention in the form of multiple drilling should be performed to promote revascularization of the necrotic subchondral bone and healing of the cartilage flap
Why drilling? Creating channels through the subchondral bone allows new blood vessels to reach the necrotic area, promoting revascularisation and bone healing — similar in principle to marrow stimulation but the goal here is to save the existing fragment, not fill a defect.
The aim is to prevent dislodgement of the cartilage flap. Prompt surgical intervention should be offered to stabilize the flap and promote healing.
- If the fragment is fixable, it should be reduced and fixed with implants (e.g., biodegradable pins)
- If the fragment is not fixable, it should be removed. Cartilage repair surgery (e.g., marrow stimulation) should be performed to allow regeneration of a smooth articulating surface.
The aim is to prevent/slow down the development of secondary osteoarthritis through surgical intervention.
- The loose body should be removed and the lesion should be debrided
- Cartilage repair surgery (e.g., marrow stimulation, autologous chondrocyte implantation, osteochondral grafting) should be performed
- Prognosis is age-dependent: young patients with open physis → good prognosis; older adolescents and adults → poor prognosis
| Stage | Stability | Primary Aim | Treatment |
|---|---|---|---|
| I | Stable | Prevent detachment, promote healing | Activity modification → drilling if symptoms persist |
| II | Stable | Prevent detachment, promote healing | Activity modification → drilling if symptoms persist |
| III | Unstable | Prevent dislodgement | Fixation (biodegradable pins) if fixable; removal + cartilage repair if not |
| IV | Loose body | Prevent/slow OA | Remove loose body + cartilage repair (microfracture / ACI / osteochondral graft) |
Osteochondral Fracture
An osteochondral fracture refers to a condition in sports medicine where there is damage to both the cartilage and the underlying bone. The osseous component is often a thin sleeve of bone. High degree of suspicion is required for making the diagnosis using X-ray. [1]
High Yield
Osteochondral fractures occur in around 40% of patients who suffer from acute patellar dislocation. [1] If a question describes acute patellar dislocation with ongoing mechanical symptoms (locking, catching), think osteochondral fracture.
The bony component is often very thin ("thin sleeve of bone"), making it nearly invisible on plain films. You need a high index of suspicion — look for small flecks of bone within the joint on AP and lateral views.
- CT and MRI are helpful in identifying the site where the fracture arises and telling the size of the cartilage fragment
- If the fragment is large → reduction and internal fixation (to reduce the chance of early osteoarthritis)
- If the fragment is small and comminuted → arthroscopic removal (if the patient suffers from symptoms of locking)
From Part 1 [2]: The general management principle applies here — definitive management depends on whether the injured tissue can heal and whether it can restore normal function if allowed to heal. Articular cartilage, being avascular, has extremely limited healing capacity, which is why the surgical threshold is lower for symptomatic cartilage lesions compared to, say, MCL tears.
From Maksim Surgery Notes [3]: OA knee is the long-term consequence of untreated cartilage injury. The 2025 MCQ Q48 [4] tested that knee replacement is an effective and evidence-supported treatment for OA knee (not arthroscopic debridement, not glucosamine, not paracetamol alone). This connects to the Part 4 teaching that untreated Grade 4 lesions and OCD Stage IV progress to secondary OA.
Exam Intelligence
| Trap | Correct Answer |
|---|---|
| "Cartilage can heal if given enough time" | No — cartilage is avascular and has very limited self-repair; fibrocartilage at best with marrow stimulation |
| "Microfracture produces hyaline cartilage" | No — it produces fibrocartilage (Type I collagen), which deteriorates over time |
| "OCD most commonly affects the lateral femoral condyle" | No — most common site is the medial femoral condyle |
| "ACI is a single-stage procedure" | No — it is a two-staged operation |
| "Osteochondral fracture is easy to see on X-ray" | No — the osseous component is often a thin sleeve; high degree of suspicion needed |
| Confusing Outerbridge Grade 3 vs 4 | Grade 3 = > 50% depth without exposed bone; Grade 4 = exposed subchondral bone |
| "Non-operative management is never appropriate for OCD" | Wrong — Stage I and II can be initially managed with activity modification |
| "Wilson's sign involves external rotation" | No — Wilson's sign involves internal rotation of the tibia with extension from 90°; pain is relieved by external rotation |
- Marrow stimulation vs ACI: Size threshold. If lesion < 2 cm → marrow stimulation. If > 2 cm → ACI. Both are for Grade 4 lesions.
- Autograft vs allograft osteochondral transplantation: Autograft = donor site morbidity, size limitation. Allograft = disease transmission risk, no size limitation.
- OCD Stage II vs III on MRI: Low signal rim behind fragment = fibrous attachment = stable = Stage II. High signal = fluid = unstable = Stage III.
High Yield Summary
-
Articular cartilage
- is aneural, avascular, alymphatic → very limited healing capacity → early intervention matters.
-
Modified Outerbridge Classification
- Grade 0 (normal) → Grade 4 (exposed bone). Remember: Grade 3 ≠ exposed bone.
-
Treatment ladder by size for Grade 4 lesions
- < 1 cm debridement → < 2 cm microfracture → 1–4 cm osteochondral transplant → > 2 cm ACI.
-
Microfracture
- = fibrocartilage (NOT hyaline) = deteriorates over time.
-
ACI
- = two-stage procedure; best for large ( > 2 cm) Grade 4 defects.
-
OCD
- most common cause of loose bodies in the knee in teens (12–19). Most common site = medial femoral condyle. Wilson's sign = internal rotation + extension → pain. Staging I–IV dictates treatment: stable (I/II) = activity modification ± drilling; unstable (III) = fixation or removal + repair; loose body (IV) = remove + cartilage repair.
-
Osteochondral fracture
- occurs in ~40% of acute patellar dislocation. Hard to see on X-ray ("thin sleeve of bone"). Large fragment = ORIF. Small fragment = arthroscopic removal.
-
Prognosis
- Young patients with open physes do much better than adults in OCD.
Active Recall - Knee Sport Injuries Part 4: Cartilage Injury
GC230 Knee Sport Injuries: Part 3
Knee sport injuries (Part 3) covers posterior cruciate ligament (PCL) injuries, posterolateral corner injuries, and multi-ligament knee injuries, focusing on their mechanisms, diagnosis, and surgical management in athletes.
GC230 Knee Sport Injuries: Part 5
Knee sport injuries Part 5 covers posterior cruciate ligament (PCL) injuries, characterized by disruption of the PCL typically due to a posterior-directed force on the proximal tibia, resulting in posterior knee instability.