Chondral defects

Briefly, the acetabulum and femoral head are covered by hyaline articular cartilage, a specialized low-friction tissue that distributes joint loads across congruent surfaces of the hip. This structure enables near-frictionless motion while transmitting high compressive forces to subchondral bone. This cartilage transitions into the labrum at the chondrolabral junction, forming a functional unit that contributes to load distribution and joint stability 1. Integrity of this region is essential because disruption of either the labrum or adjacent cartilage alters force transmission and increases focal stress at the rim 2.

Chondral defects are focal or regional areas of damage to the articular cartilage covering the femoral head or acetabulum. The acetabular cartilage (particularly near the peripheral chondrolabral junction, where articular cartilage transitions into the acetabular labrum) is most frequently affected 1. Lesions range from cartilage softening to delamination, unstable flaps, or full-thickness loss with exposure of the subchondral bone 1,3. Chondral defects frequently coexist with labral tears, particularly in FAIS where repetitive shear at the chondrolabral junction produces combined injury patterns 1. In dysplasia, cartilage injury is more often related to increased contact stress and instability rather than impingement 2.

A purely chondral lesion is confined to articular cartilage, whereas an osteochondral lesion also involves the underlying subchondral bone. This distinction is important because articular cartilage is avascular, aneural, and alymphatic with very low chondrocyte mitotic activity and limited access to progenitor cells, resulting in minimal intrinsic capacity for structural repair after injury, whereas involvement of subchondral bone allows access to marrow-derived repair elements that can partially contribute to healing (typically fibrocartilaginous rather than hyaline repair). Progressive cartilage loss may therefore represent a transition from a focal mechanical lesion toward more generalized joint degeneration 4,5.

Most chondral lesions within the hip preservation field are secondary to abnormal joint mechanics rather than primary cartilage disease 2, the most important of which is femoroacetabular impingement syndrome (FAIS).

As previously described in previous sections, in the cam morphology, an aspherical femoral head-neck junction enters the acetabulum during flexion and internal rotation, producing shear stress at the anterosuperior acetabular rim. Repetitive contact leads to separation of cartilage from subchondral bone and characteristic delamination injury 2.

Other etiologies include:

• Pincer morphology, where focal overcoverage leads to rim impingement and labral-cartilage injury, typically via compression rather than shear 2.
• Acetabular dysplasia or instability, which reduces contact area and increases joint contact stress, predisposing to cartilage overload 1.
• Trauma, including dislocation or direct impact, which can produce focal chondral or osteochondral injury 1.
• Degenerative joint disease, where cartilage loss becomes diffuse and progressive rather than focal 4.

Hip morphology therefore strongly determines both location and pattern of cartilage injury.

It is very essential to properly describe the defect morphology using appropriate depth, stability, and structural configuration descriptors. See the following table for examples:

The Outerbridge classification grades cartilage degeneration from normal (grade 0), to softening and superficial fibrillation (grade I), partial-thickness fragmentation or fissuring (<1.5 cm, grade II), larger partial-thickness defects (>1.5 cm, grade III), and full-thickness cartilage loss with exposed subchondral bone (grade IV) 6.

Whereas Hip-specific systems such as the Beck classification further characterizes acetabular injury patterns seen in FAIS, ranging from normal cartilage (grade 0), surface wear (grade 1), partial-thickness damage (grade 2), and delamination at the chondrolabral junction (grade 3), to full-thickness cartilage loss with exposed bone (grade 4), thereby better reflecting the typical shear-based failure mechanism in the hip 2. These systems are descriptive tools and should not replace understanding of the underlying mechanical failure 7.

In summary, for a hip arthroscopist, the key principle is that cartilage damage is not an isolated finding but a manifestation of underlying mechanical pathology]. Failure to address contributing abnormalities such as cam morphology, instability, or dysplasia risks persistent abnormal loading and progression of cartilage loss. Conversely, extensive full-thickness cartilage loss may indicate a joint in which arthroscopic preservation strategies have limited durability.