Cartilage Problems in Sports

General Principles

•
Functions to decrease joint friction and distribute load across the joint; also referred to as hyaline cartilage
•
Composition: Water (65%–80%), collagen (10%–20%, predominantly type II), proteoglycans (10%–15%, aggrecan is most responsible for the hydrophilic property), and chondrocytes (5%) ( Fig. 57.1 )

Figure 57.1

Composition and structure of articular cartilage.
•
Viability: Articular cartilage is avascular, and chondrocytes are nourished via diffusion from synovial fluid.
•
Structure: Organized into three primary layers—superficial, middle, and deep; the tidemark separates these layers from the calcified cartilage and subchondral bone (see Fig. 57.1 ).
•
Location: Articular surfaces, ribs, and nasal septum

•
Functions in direct tendon and ligament insertions and helps in the healing of articular cartilage lesions
•
Composition: Primary collagen is type I collagen. Fibrocartilage is not as durable as hyaline articular cartilage.
•
Location: Tendon/ligament junction with bone, menisci, and annulus fibrosis of the intervertebral disc

•
Healing is enhanced by motion of the involved joint.
•
Deep lesions: Cross the tidemark and penetrate the subchondral bone; vascularity from the subchondral bone promotes fibrocartilage healing (type I collagen) rather than the preferred articular cartilage.
•
Superficial lesions: Do not penetrate the subchondral bone and therefore have no intrinsic healing potential secondary to the avascular nature of articular cartilage

•
Cartilaginous prominence adjacent to the physis
•
Site of tendon attachments before skeletal maturity
•
Secondary ossification centers develop later with eventual osseous fusion.
•
Traction apophysitis: Repetitive microtrauma caused by the pull of attached tendons; results in partial avulsion and inflammation of the apophysis; common in active children and adolescents; excessive force may result in avulsion fracture of the apophysis.
•
Osteochondrosis: General term for disorders affecting one or more ossification centers in children; encompasses conditions such as traction apophysitis and avascular necrosis

•
History should focus on the nature of injury and symptoms of the involved joint.
•
Acute injuries typically result in focal chondral or osteochondral injuries, as opposed to the more generalized nature of degenerative lesions.
•
These injuries may not be initially identified and are occasionally diagnosed after the persistence of symptoms.
•
Chronic symptoms may also be secondary to various osteochondroses.

•
Few, if any, physical examination tests are specific for the evaluation of articular cartilage injury.
•
A complete examination of the involved joint should be conducted.

•
Imaging studies are essential for the evaluation of cartilage injuries.
•
Plain radiographs: Useful in ruling out fractures and identifying various osteochondroses and osteochondral lesions such as osteochondritis dissecans (OCD); also beneficial in identifying intra-articular loose bodies, assessing limb alignment, and evaluating joint space
•
Computed tomography (CT): Helpful in assessing cartilage lesions with associated osseous involvement
•
Magnetic resonance imaging (MRI): Gold standard for the evaluation of articular cartilage; can identify subchondral edema; focal chondral defects may be underestimated ( Table 57.1 ). Newer MRI techniques such as delayed gadolinium-enhanced MRI of cartilage can identify proteoglycans, while the measurement of T2 relaxation times are sensitive to collagen architecture.

TABLE 57.1

CARTILAGE SIGNAL INTENSITIES ON MRI

T1-Weighted Images T2-Weighted Images

Hyaline cartilage Gray Gray

Fibrocartilage Dark Dark

	T1-Weighted Images	T2-Weighted Images
Hyaline cartilage	Gray	Gray
Fibrocartilage	Dark	Dark

Description: Localized, full-thickness loss of articular cartilage with exposed subchondral bone ( Fig. 57.2 )

Figure 57.2

Hip anatomy and femoroacetabular impingement.

(Arthroscope image from Miller M, Cole B. Textbook of Arthroscopy . Philadelphia: Saunders, Elsevier; 2004.)
Mechanism of injury: Typically, a direct blow to the greater trochanter; forces are transferred to the articular surfaces of the femoral head and acetabulum.
Presentation: History of injury with failure of full recovery, catching or locking with vague hip and groin pain
Physical examination: Nonspecific
Differential diagnosis: Avascular necrosis, femoroacetabular impingement (FAI), hip dysplasia, degenerative arthritis, labral pathology, and femoral neck stress fracture
Diagnostics: Radiographs are helpful in evaluating joint space and ruling out other conditions. MRI may demonstrate localized defect or subchondral edema. MRI arthrography has higher detection rates.
Treatment: Arthroscopic chondroplasty, drilling, or microfracture for localized lesions; excision of unstable or loose fragments to alleviate mechanical symptoms (see Fig. 57.2 )
Prognosis and return to sport: Return to sport when symptoms allow after debridement or excision of fragments. Chondral reparative procedures such as microfracture require partial weight bearing for 6–8 weeks; early range of motion encouraged

Description: Abnormal contact between the femoral head–neck junction and acetabulum; results in injury to the articular cartilage and labrum; may be a cause of chronic hip pain in athletes; two types defined based on the primary location of pathology:
- •
  CAM type: Femoral deformity; “pistol grip” deformity of the femoral head with decreased head–neck offset and asphericity, leading to abutment of this region with the normal acetabulum
- •
  Pincer type: Acetabular deformity; increased acetabular retroversion leading to abutment of the normal femoral head–neck junction on the acetabular rim
- •
  Mixed type: Combined deformity of femoral head and acetabulum, most common (up to 80%)

Mechanism of injury: Etiology unknown; combination of static factors and dynamic factors (see Table 57.2 )

TABLE 57.2

FACTORS INVOLVED IN FEMOROACETABULAR IMPINGEMENT

Type of Factor
Dynamic	A. Decreased offset and asphericity of femoral head–neck ratio (CAM-type lesion) B. Acetabular overcoverage C. Extra-articular impingement
Static	A. Undercoverage of hip (dysplastic hip) B. Femoral anteversion C. Femoral valgus