**1.6 Mechanism of articular cartilage injury**

182 Modern Arthroscopy

although articular cartilage had a well-defined glycolytic system, oxygen use was considerably lower in articular cartilage than in other tissues. This difference subsequently was found to be related to the spares cell (*sic*) population rather than to a lack of metabolic activity per cell. Nevertheless, articular cartilage chondrocytes rely principally on the

Chondrocytes synthesize and assemble the cartilaginous matrix components and direct their distribution within the tissue. These synthetic and assembly processes are complex. They involve synthesis of proteins; synthesis of glycosaminoglycan chains, and their addition to the appropriate cores; and secretion of the completed molecules into the extra-cellular

Chondrocytes are responsible for the synthesis, assembly and sulfation of the proteoglycan molecule. However, in normal tissue, in repair and degradation processes proteoglycans of articular cartilage are continually being broken down and released from the cartilage. This activity is a normal event in the maintenance of the tissue and can occur at an accelerated rate. The rate of catabolism can be affected by soluble mediators and by various types of

Collagen is much more stable than the proteoglycan components. However, the collagen network is subject to metabolism, and in osteoarthritic or injured cartilage the collagen turnover increases, but as yet little is known about the mechanism of collagen breakdown

 The source of nutrients for articular cartilage is somewhat of an enigma. Because the tissue is avascular in adult life most investigators believe that nutrients diffuse through the matrix, either from the surrounding synovial fluid or from underlying bone (Mankin

The articular cartilage of diarthrodial joints is subject to high loads applied statically and repetitively for many decades. Thus, the structural molecules, which include collagens and proteoglycans must be organized into a strong, fatigue-resistant and tough solid matrix capable of sustainig the high stresses and strains developed within the tissue (Soltz and Ateshian, 2000). The solid matrix is porous and permeable, and very soft. Water, 65 to 80 percent of the total weight of normal articular cartilage, resides in the microscopic pores. This water may be caused to flow through the porous-permeable solid matrix by a pressure gradient or by matrix compaction. The biomechanical properties of articular cartilage therefore are understood best when the tissue is viewed as biphasic material composed of a

Although it is porous, the solid phase of the cartilage has low permeability due largely to a high frictional resistance to fluid flow. This causes a high interstitial fluid pressurization in the fluid phase, which contributes more then 90 percent of the load transmission function of cartilage (Soltz and Ateshian, 2000). The high pressurization of the fluid phase and the Low permeability of the solid phase establish both the stiffness and the visco-elastic properties of

anaerobic pathway for energy production (Oegema and Thompson, 1989).

matrix (Guilak et al, 1997).

(Mankin et al, 2005b).

et al, 2005b).

joint loading (Mankin et al, 2005b).

**1.4 Biomechanics of articular cartilage** 

**1.5 Local transmission of load** 

cartilage (Felson et al, 2000).

solid phase and a fluid phase (Soltz and Ateshian, 2000).

Direct blunt trauma, indirect impact loading, or torsional loading of a joint can damage articular cartilage and the calcified cartilage-subchondral bone region without disrupting the surrounding soft tissue. Examples of direct blunt trauma to articular cartilage of the knee include a shoe kick, knees colliding in games such as football and rugby, and falling on a hard surface. Examples of indirect impact and torsional loading include a blow to a bone that forms the subchondral part of a joint, and severe twisting of a joint that is loaded (Williams and Wilkins, 1998).

### **1.7 Age related chondral lesions**

Clinical experience suggests that there are age-related differences in the risk and patterns of articular surface injuries. High energy bone or joint trauma causes intra-articular osteochondral fractures in people of all age, but older people and people with more osteopenic bone tend to have more severely comminuted fractures (Buckwalter et al, 1993; Buckwalter and Lane, 1996). Chondral fractures associated with participation in sports generally occur in skeletally mature people, whilst osteochondral fractures associated with participation in sports typically occur in skeletally immature people or young adults. This difference may result from age-related changes in the mechanical properties of the articular surface, including the uncalcified cartilage, the calcified cartilage zone, and the subchondral bone (Buckwalter et al, 1993; Buckwalter and Lane, 1996). That is, age-related alteration in the articular cartilage matrix decreases the tensile stiffness and strength of the superficial zone, and the calcified cartilage zone. The subchondral bone region minimizes fully following completion of skeletal growth, presumably creating a marked difference in mechanical properties between the uncalcified cartilage and the calcified cartilagesubchondral bone region (Williams and Wilkins, 1998).

#### **1.8 Response of articular cartilage to blunt impact**

Articular cartilage can withstand single or multiple moderate and occasionally high impact loads. However, a number of studies have addressed the effects of either a single excessive high-impact force causing injury to the cartilage without a break in the surface, or repetitive below-trauma threshold loads causing an accumulation of damage to the cartilage by repeated application of the load. Both can lead to chondrocyte death, matrix damage, fissuring of surface, injury to underlying bone, and thickening of the tide mark region. At a certain threshold of impact loading, the cartilage may be sheared off the subchondral bone (Mankin et al, 2005).

Excessive impact or torsional joint loading causes three types of articular cartilage injury: chondral damage without visible tissue disruption; disruption of articular cartilage alone (chondral fractures and flaps); and disruption of articular cartilage and subchondral bone (osteochondral fractures) (Buckwalter et al, 1988). Intensity and rate of loading, muscle contractions that affect the transmission of force to the articular surface, age, and genetically determined differences in articular cartilage may influence the type of articular surface injury in a given individual (Buckwalter et al, 1988).

Traumatic Chondral Lesions of the Knee Diagnosis and Treatment 185

further from the subchondral bone into more superficial cartilage, with subsequent increasing incidence of partial thickness chondral injuries (Johnson-Nurse et al, 1985; cited by Speer et al, 1991). In a multicentral study conducted in the USA, between 1991 and 1995, Walton found the prevalence of chondral injuries in 31,516 knee arthroscopies to be 19,827 (63 %). A total of 53,569 hyaline cartilage lesions were found during these 19,827 arthroscopies, an average of 2.7 lesions per knee. The average age of the patient with lesions was 43 years. More male than female patients had lesions (61.6 and 38.4 percent, respectively). The lesions consisted of osteochondritis dissecans (0.7 %), articular fractures (1.3 %), grade I lesions (9.7 %), grade II lesions (28.1 %), grade III lesions (41.0 %), and grade IV lesions (19.2 %). Grade III lesions were the most common in patients over 30 years of age. The most common locations for grade III lesions were patella and medial femoral condyle. The medial femoral condyle was the most common location for single grade IV lesions. The patella and

lateral femoral condyle were the next two most common sites (Walton et al, 1997).

Although there are several different classification systems for the description of articular cartilage damage, each has certain limitations and deficiencies that can lead to confusion (Noyes and Stabler, 1989). Some systems combine the surface appearance of the articular cartilage lesion and the depth of involvement under a single description category, and then make no distinction as to the depth of involvement (Noyes and Stabler, 1989). According to the Outerbridge classification Grade II and III are identical in appearance (fragmentation and fissuring). The classification does not specify the extent of involvement from surface to bone in either stage. Rather, the distinction between the grades is based on the diameter of involvement (Noyes and Stabler, 1989). In the classification system of Bentley there is no category reserved for lesions with an intact surface. Furthermore, grades I, II and III all described as fibrillation or fissuring, and the distinction between grades is based on the area of damage (Noyes and Stabler, 1989). Ficet and Hangerford distinguished between closed (grade I) and open (grade II) lesions, but do not separate lesions within each category according to severity. Grade I describes varying degrees of softening from simple to pitting oedema. Grade II distinguishes between fissures and ulcerations, but either can be superficial and localized or can extend to subchondral bone (Noyes and Stabler, 1989). The classification systems of Casscells and Insall both describe lesions that become more extensive as one moves from grade I to grade IV. Casscell's system makes no allowance for a lesion without surface changes (Noyes and Stabler, 1989). Insall's system is problematic because the specification for grade II (Fissuring) and grade III (fibrillation) are somewhat qualitative and may or may not be applied similarly by observers (Noyes and Stabler, 1989). Although according to Noyes and Stabler (1989) Goodfellow differentiates between surface degeneration and basilar degeneration, the terms fasciculation I, blister, and fasciculation II, under the general category of basilar degeneration, can cause some confusion. Most other authors seem to use the term fasciculation when referring to disruption of an intact surface

The Outerbridge classification system (Outerbridge, 1961) was originally designed to classify chondromalacia patellae. Over the years it has been extrapolated for use in

**1.12 Grading of articular cartilage lesions** 

(Noyes and Stabler, 1989).

**1.12.1 Outerbridge classification** 

#### **1.9 Healing of articular cartilage**

More than a century ago articular cartilage was documented as lacking regenerative power; it had been observed that wounds in articular cartilage healed with fibrous tissue and fibrocartilage (Chen et al, 1999). As cartilage is avascular its reparative process differs significantly from the three-phase response of necrosis, inflammation and repair that occurs in vascularized tissue. Cartilage undergoes the initial phase of necrosis in response to injury, but there is less cell death, given its relative insensitivity to hypoxia (Chen et al, 1999). The second phase, inflammation, is largely absent as this response is primarily mediated by the vascular system. No fibrin clot or network is developed to act as a scaffold for the in growth of repair tissue, and no mediators or cytokines are released to stimulate cellular migration and proliferation. The third phase, repair, is also severely limited due to the lack of a preceding inflammatory response and recruitment of undifferentiated mesenchymal cells that normally proliferate and modulate the repair response. The burden of repair thus falls on the existing chondrocytes in a process termed intrinsic repair (Chen et al, 1999).

#### **1.10 Role of chondrocytes in healing**

Chondrocytes near the injured part may proliferate and form clusters or clones and synthesize new matrix, but the chondrocytes do not migrate into the lesion. The new matrix they produce remains in the immediate region of the chondrocytes, and their preoperative and synthetic activity fails to provide new tissue to repair the damage. This repair phase is initially brisk. It is, however, limited in scope and duration, disappearing within a matter of weeks (Mankin et al, 2005). Results from experimental studies of injuries limited to cartilage clearly demonstrate the inability of chondrocytes to repair cartilage defects. The results also show that limited experimental injuries to normal articular surfaces in normal synovial joints generally do not progress to full thickness loss of cartilage (Mankin et al, 2005).

#### **1.11 Incidence of articular cartilage injuries**

The incidence of articular cartilage injuries to the knee, determined arthroscopically, has been most frequently reported as part of a large series of assessment for haemarthrosis. Noyes et al (1980) reported a 20 percent incidence, Gillquist et al (1977) a 10 percent occurrence, and DeHaven (1980) a 6 percent incidence of chondral or osteochondral injuries. In a review of 1,000 knee arthroscopies Hjelle et al (2002) reported chondral or osteochondral occurrence in 61 percent of the patients, but focal chondral or osteochondral defects were found in 19 percent of the patients. With the increasing age of the patients the incidence of articular cartilage injury increased. Characteristic injury depth patterns have been found to be associated with the degree of skeletal maturity (Hopkinson et al, 1985 and Johnson-Nurse et al, 1985; cited by Speer et al, 1991). In children and adolescents osteochondral fractures are more frequent than full-thickness or partial-thickness chondral injuries. It has been suggested that the bond between articular cartilage and subchondral bone is stronger than the bone itself. With increasing age and skeletal maturity the basal layers of articular cartilage become calcified and the tide mark develops. This provides a plan of weakness through which separation may occur. Full thickness chondral lesions are most frequently seen in patients in their 30s. Beyond this age the plane of weakness moves

More than a century ago articular cartilage was documented as lacking regenerative power; it had been observed that wounds in articular cartilage healed with fibrous tissue and fibrocartilage (Chen et al, 1999). As cartilage is avascular its reparative process differs significantly from the three-phase response of necrosis, inflammation and repair that occurs in vascularized tissue. Cartilage undergoes the initial phase of necrosis in response to injury, but there is less cell death, given its relative insensitivity to hypoxia (Chen et al, 1999). The second phase, inflammation, is largely absent as this response is primarily mediated by the vascular system. No fibrin clot or network is developed to act as a scaffold for the in growth of repair tissue, and no mediators or cytokines are released to stimulate cellular migration and proliferation. The third phase, repair, is also severely limited due to the lack of a preceding inflammatory response and recruitment of undifferentiated mesenchymal cells that normally proliferate and modulate the repair response. The burden of repair thus falls on the existing chondrocytes in a process termed

Chondrocytes near the injured part may proliferate and form clusters or clones and synthesize new matrix, but the chondrocytes do not migrate into the lesion. The new matrix they produce remains in the immediate region of the chondrocytes, and their preoperative and synthetic activity fails to provide new tissue to repair the damage. This repair phase is initially brisk. It is, however, limited in scope and duration, disappearing within a matter of weeks (Mankin et al, 2005). Results from experimental studies of injuries limited to cartilage clearly demonstrate the inability of chondrocytes to repair cartilage defects. The results also show that limited experimental injuries to normal articular surfaces in normal synovial joints generally do not progress to full thickness loss

The incidence of articular cartilage injuries to the knee, determined arthroscopically, has been most frequently reported as part of a large series of assessment for haemarthrosis. Noyes et al (1980) reported a 20 percent incidence, Gillquist et al (1977) a 10 percent occurrence, and DeHaven (1980) a 6 percent incidence of chondral or osteochondral injuries. In a review of 1,000 knee arthroscopies Hjelle et al (2002) reported chondral or osteochondral occurrence in 61 percent of the patients, but focal chondral or osteochondral defects were found in 19 percent of the patients. With the increasing age of the patients the incidence of articular cartilage injury increased. Characteristic injury depth patterns have been found to be associated with the degree of skeletal maturity (Hopkinson et al, 1985 and Johnson-Nurse et al, 1985; cited by Speer et al, 1991). In children and adolescents osteochondral fractures are more frequent than full-thickness or partial-thickness chondral injuries. It has been suggested that the bond between articular cartilage and subchondral bone is stronger than the bone itself. With increasing age and skeletal maturity the basal layers of articular cartilage become calcified and the tide mark develops. This provides a plan of weakness through which separation may occur. Full thickness chondral lesions are most frequently seen in patients in their 30s. Beyond this age the plane of weakness moves

**1.9 Healing of articular cartilage** 

intrinsic repair (Chen et al, 1999).

of cartilage (Mankin et al, 2005).

**1.11 Incidence of articular cartilage injuries** 

**1.10 Role of chondrocytes in healing** 

further from the subchondral bone into more superficial cartilage, with subsequent increasing incidence of partial thickness chondral injuries (Johnson-Nurse et al, 1985; cited by Speer et al, 1991). In a multicentral study conducted in the USA, between 1991 and 1995, Walton found the prevalence of chondral injuries in 31,516 knee arthroscopies to be 19,827 (63 %). A total of 53,569 hyaline cartilage lesions were found during these 19,827 arthroscopies, an average of 2.7 lesions per knee. The average age of the patient with lesions was 43 years. More male than female patients had lesions (61.6 and 38.4 percent, respectively). The lesions consisted of osteochondritis dissecans (0.7 %), articular fractures (1.3 %), grade I lesions (9.7 %), grade II lesions (28.1 %), grade III lesions (41.0 %), and grade IV lesions (19.2 %). Grade III lesions were the most common in patients over 30 years of age. The most common locations for grade III lesions were patella and medial femoral condyle. The medial femoral condyle was the most common location for single grade IV lesions. The patella and lateral femoral condyle were the next two most common sites (Walton et al, 1997).

#### **1.12 Grading of articular cartilage lesions**

Although there are several different classification systems for the description of articular cartilage damage, each has certain limitations and deficiencies that can lead to confusion (Noyes and Stabler, 1989). Some systems combine the surface appearance of the articular cartilage lesion and the depth of involvement under a single description category, and then make no distinction as to the depth of involvement (Noyes and Stabler, 1989). According to the Outerbridge classification Grade II and III are identical in appearance (fragmentation and fissuring). The classification does not specify the extent of involvement from surface to bone in either stage. Rather, the distinction between the grades is based on the diameter of involvement (Noyes and Stabler, 1989). In the classification system of Bentley there is no category reserved for lesions with an intact surface. Furthermore, grades I, II and III all described as fibrillation or fissuring, and the distinction between grades is based on the area of damage (Noyes and Stabler, 1989). Ficet and Hangerford distinguished between closed (grade I) and open (grade II) lesions, but do not separate lesions within each category according to severity. Grade I describes varying degrees of softening from simple to pitting oedema. Grade II distinguishes between fissures and ulcerations, but either can be superficial and localized or can extend to subchondral bone (Noyes and Stabler, 1989). The classification systems of Casscells and Insall both describe lesions that become more extensive as one moves from grade I to grade IV. Casscell's system makes no allowance for a lesion without surface changes (Noyes and Stabler, 1989). Insall's system is problematic because the specification for grade II (Fissuring) and grade III (fibrillation) are somewhat qualitative and may or may not be applied similarly by observers (Noyes and Stabler, 1989). Although according to Noyes and Stabler (1989) Goodfellow differentiates between surface degeneration and basilar degeneration, the terms fasciculation I, blister, and fasciculation II, under the general category of basilar degeneration, can cause some confusion. Most other authors seem to use the term fasciculation when referring to disruption of an intact surface (Noyes and Stabler, 1989).

#### **1.12.1 Outerbridge classification**

The Outerbridge classification system (Outerbridge, 1961) was originally designed to classify chondromalacia patellae. Over the years it has been extrapolated for use in

Traumatic Chondral Lesions of the Knee Diagnosis and Treatment 187

Fig. 4. Outerbridge system for grading chondral defects (Kocheta and Tomes, 2004)

classifying chondral lesions throughout the body (Noyes et al, 1977). The accuracy and reproducibility of this classification system was addressed by Cameron et al, (2003) when they determined the intraobserver reliability, interobserver reproducibility and the accuracy of the system for grading chondral lesions in knees viewed arthroscopically. They compared the results obtained by using the system with observations at arthrotomy of six cadaveric donors. The accuracy rate ranged from 22 to 100 percent, with lower grade lesions diagnosed with less accuracy than higher-grade lesions (Cameron et al, 2003). The Outerbridge grading system is given in table.1 and figure 4.
