**3. Focal articular cartilage injury**

#### **3.1 Prevalence and natural history**

Chondral defects in the knee may be seen in up to 63% of knee arthroscopies(Curl, Krome et al. 1997). The prevalence of arthroscopically-detected full-thickness defects is 16%(Flanigan, Harris et al. 2010). Full-thickness focal lesions with an area of 1 cm2 to 2 cm2 are seen in approximately 5% of all knee arthroscopies in patients less than 40 years of age(Hjelle, Solheim et al. 2002; Aroen, Loken et al. 2004; Widuchowski, Widuchowski et al. 2007). In an exclusively athletic population, chondral pathology is more common than in the general population. The overall prevalence of full-thickness defects in this population is 36%(Flanigan, Harris et al. 2010). Further, the prevalence of full-thickness lesions is 59% in an asymptomatic group of professional basketball players and runners. The reasons for the increased prevalence in the athlete are multifactorial. Compared with the general population, athletes are 12 times more likely to develop osteoarthritis of the knee(Roos 1998; Drawer and Fuller 2001).

The natural history of the isolated chondral defect and to what degree the isolated defect may become symptomatic is incompletely understood(Buckwalter 1998). Full-thickness lesions may progress due to biomechanical overload with stress concentration around the rim of a defect(Guettler, Demetropoulos et al. 2004), subchondral bone structural changes(Minas and Nehrer 1997), and intra-articular inflammatory cytokine concentration elevations(Fraser, Fearon et al. 2003). Full-thickness defects obviate the shock-absorbing and load-transmitting function of articular cartilage(Minas 1999). The subchondral bone eventually bears the load (Figure 6). Subchondral bone overgrowth has been observed in patients undergoing autologous chondrocyte implantation (ACI), especially in more chronic, larger defects on the lateral femoral condyle(Henderson and LaValette 2005). The subchondral plate becomes sclerotic with vascular congestion and periarteriolar nociceptive fiber stimulation(Minas, Gomoll et al. 2009). The stiffer subchondral plate alters the biomechanical properties of the subchondral bone-articular cartilage interface, which increases shear forces with weight-bearing. Further, subchondral plate thickening and sclerosis due to tidemark advancement is a component of osteoarthritis(Radin and Rose

Fig. 5. 5a) Proteoglycan aggrecan molecule composed of chondroitin (CS) and keratan sulfate (KS) glycosaminoglycans, a protein core, and link protein attached to hyaluronic acid

(HA) chain; 5b) ECM structure of collagen fibrils intertwined in aggrecan molecules (reproduced with permission from Ulrich-Vinther M, et al: Articular cartilage biology, in *Journal of the American Academy of Orthopaedic Surgeons* 2003; 11: 423. Publisher AAOS)

likely to develop osteoarthritis of the knee(Roos 1998; Drawer and Fuller 2001).

Chondral defects in the knee may be seen in up to 63% of knee arthroscopies(Curl, Krome et al. 1997). The prevalence of arthroscopically-detected full-thickness defects is 16%(Flanigan, Harris et al. 2010). Full-thickness focal lesions with an area of 1 cm2 to 2 cm2 are seen in approximately 5% of all knee arthroscopies in patients less than 40 years of age(Hjelle, Solheim et al. 2002; Aroen, Loken et al. 2004; Widuchowski, Widuchowski et al. 2007). In an exclusively athletic population, chondral pathology is more common than in the general population. The overall prevalence of full-thickness defects in this population is 36%(Flanigan, Harris et al. 2010). Further, the prevalence of full-thickness lesions is 59% in an asymptomatic group of professional basketball players and runners. The reasons for the increased prevalence in the athlete are multifactorial. Compared with the general population, athletes are 12 times more

The natural history of the isolated chondral defect and to what degree the isolated defect may become symptomatic is incompletely understood(Buckwalter 1998). Full-thickness lesions may progress due to biomechanical overload with stress concentration around the rim of a defect(Guettler, Demetropoulos et al. 2004), subchondral bone structural changes(Minas and Nehrer 1997), and intra-articular inflammatory cytokine concentration elevations(Fraser, Fearon et al. 2003). Full-thickness defects obviate the shock-absorbing and load-transmitting function of articular cartilage(Minas 1999). The subchondral bone eventually bears the load (Figure 6). Subchondral bone overgrowth has been observed in patients undergoing autologous chondrocyte implantation (ACI), especially in more chronic, larger defects on the lateral femoral condyle(Henderson and LaValette 2005). The subchondral plate becomes sclerotic with vascular congestion and periarteriolar nociceptive fiber stimulation(Minas, Gomoll et al. 2009). The stiffer subchondral plate alters the biomechanical properties of the subchondral bone-articular cartilage interface, which increases shear forces with weight-bearing. Further, subchondral plate thickening and sclerosis due to tidemark advancement is a component of osteoarthritis(Radin and Rose

**3. Focal articular cartilage injury 3.1 Prevalence and natural history** 

1986; Burr and Radin 2003). With increasing defect size, these osteocartilaginous changes can only be more greatly accelerated(Flanigan, Harris et al. 2010).

Fig. 6. Well-shouldered, small full-thickness chondral defect with no contact on underlying subchondral bone (left); larger full-thickness defect exhibits subchondral bone contact by the opposing surface (reproduced with permission from The American Academy of Orthopaedic Surgeons in: Jones D and Peterson L: Autologous chondrocyte implantation, Lecture in *Journal of Bone and Joint Surgery, American* 2006; 88A(11): 2503. Publisher AAOS)

Fig. 7. International Cartilage Repair Society (ICRS) cartilage injury classification (reproduced from the ICRS Cartilage Injury Evaluation Package [www.cartilage.org], with permission from the ICRS).

## **3.2 Classification systems**

The two most commonly used classification systems for arthroscopic analysis of chondral defects in the knee are the Outerbridge system and the International Cartilage Repair Society (ICRS) system (Figure 7). The Outerbridge system grades defects I – IV(Outerbridge 1961). Grade 1 lesions exhibited softening or swelling of cartilage; Grades 2 and 3 both exhibit fragmentation and fissuring of cartilage, with Grade 2 being less than ½ inch and Grade 3 being greater than ½ inch diameter; Grade 4 defects exhibit subchondral bone exposure. The newer ICRS system(Brittberg and Winalski 2003) is advantageous as it

Management of Knee Articular Cartilage Injuries 111

Therefore, surgical correction of tibiofemoral malalignment to neutral or overcorrection is recommended in conjunction with most cartilage surgery (Figure 8). Thus, in addition to standard radiographic workup (extension standing anteroposterior [AP], Rosenberg view, lateral, and Mercer Merchant views), the full-length bilateral hip-to-ankle x-ray allows

Fig. 8. Left) Standing hip-to-ankle x-ray demonstrating mechanical axis of lower extremity (in medial compartment); Right upper) Rosenberg view (no evidence of OA); Right lower)

MRI is highly advantageous in imaging articular cartilage. This non-invasive modality avoids ionizing radiation, has superior sensitivity and specificity for articular cartilage, and allows for high contrast with proximate structures. Standard MRI sequences in imaging cartilage include conventional spin-echo (SE) and gradient-recalled echo (GRE), and fast SE sequences. The morphologic features of cartilage, evaluated with these standard techniques, can be semiquantitatively analyzed with the WORMS (whole-organ MRI score)(Peterfy, Guermazi et al. 2004). Also, the MOCART (magnetic resonance observation of cartilage repair tissue) has been demonstrated to be accurate, reliable, and reproducible in post-ACI assessment of cartilage restoration tissue(Marlovits, Singer et al. 2006). Fast SE sequences are included in the ICRS cartilage repair evaluation package for non-invasive assessment of cartilage following surgery. Fat-suppression techniques increase the contrast between articular cartilage and the

Rosenberg view after high tibial osteotomy.

**4.2 Magnetic resonance imaging (MRI)** 

calculation of mechanical axis of the limb and the necessary alignment correction.

accounts not only for lesion area (cm2), but also depth, while Outerbridge does not. Osteochondritis dissecans lesions can also be classified according to a similar ICRS-OCD system(Brittberg and Winalski 2003). This classification is based on lesion stability.
