Cartilage Injuries of the Knee

Trauma (blunt impacts, fractures, traumatic patellar dislocation, polytraumatic injuries)

Axial malalignment of the knee

Partial or total meniscectomy

Instability (ACL, PCL, etc.)

Osteochondritis dissecans

Osteoarthritis

Rheumatoid arthritis, lupus, gout, psoriasis, etc.

Genetic factors

Obesity

Cartilage tumours

Microtrauma

Iatrogenic (surgery, infiltration, medicaments, etc.)

ACL anterior cruciate ligament, PCL posterior cruciate ligament

Cartilage injuries in sportsmen are thought to be caused by mechanical injury in the context of a blunt trauma or ligament disruption (i.e. anterior cruciate ligament – ACL). Blunt injury can also cause bone oedema [3]. The key point on cartilage injuries is the degree of cell death and matrix disruption. Chondrocytes die as a direct consequence of trauma. Matrix disruption derives from the inability of the remaining chondrocytes to maintain the matrix. In the acute setting, just 2 % of traumas lead to a chondral defect, but on medial to long term, it could be developed on 20 % of cases.

The natural history of these lesions is not well-known. As we do not know which lesions become symptomatic and what governs the evolution of symptoms, it is difficult to determine the effect of interventions on that natural history [4]. This is particularly important in smaller lesions. In larger lesions, the tendency appears to be for the lesion to enlarge over time, becoming more symptomatic as it becomes bigger.

The most common locations for chondral lesions are the patella (36 % of total) and medial femoral condyle (34 %). They rarely occur in isolation; 37 % of cases have a medial meniscal tear and 36 % occur alongside an anterior cruciate ligament injury [5–7].

Most studies and most surgeons use the Outerbridge classification to categorize these lesions [8], but other options have been proposed (Table 11.2) including that of the International Cartilage Repair Society (ICRS) which we will use in this chapter. In the past, the great majority of lesions were treated non-surgically, but many options now exist for the management of osteochondral lesions, from non-invasive treatments to the most recent biological strategies (Tables 11.3 and 11.4). The main objectives of the treatment are pain relief and improvement of function.

Table 11.2

Classifications of cartilage lesions

Grade	Modified Outerbridge	ICRS (International Cartilage Repair Society)	ICRS
0	Normal cartilage	Intact cartilage	Intact cartilage
I	Softening and swelling	Chondral softening or blistering with intact surface	Superficial affection (soft indentation, fissures, cracks)
II	Fragmentation and fissures in area less than 0.5 in. in diameter	Superficial ulceration, fibrillation or fissuring less than 50 % of depth of cartilage	Lesion less than half the thickness of articular cartilage
III	Fragmentation and fissures in area larger than 0.5 in. in diameter	Deep ulceration, fibrillation, fissuring or chondral flap more than 50 % of cartilage without exposed bone	Lesion more than half the thickness of articular cartilage
IV	Exposed subchondral bone	Exposed subchondral bone	Exposed subchondral bone

ICRS International Cartilage Repair Society

Table 11.3

Operative interventions capable of covering a knee cartilage defect completely

Refixation of detached cartilage fragments

With reabsorbable pins

With screws

With fibrin glue

With osteochondral plugs

Cartilage reparative strategies

Aggressive debridement (spongialisation): removal of the subchondral plate to expose cancellous bone

Bone marrow stimulation techniques: drilling, microfractures, abrasion arthroplasty (gentle superficial burring of the subchondral plate)

Cartilage restorative techniques

Transplantation of fresh osteochondral allografts

Transplantation of osteochondral autografts (plugs-mosaicplasty)

Autologous chondrocyte implantation (ACI) and matrix-induced autologous chondrocyte implantation (MACI)

Table 11.4

Indications for the different knee cartilage repair/restorative techniques

Technique	Advantages	Disadvantages	Indications
Bone marrow stimulation	No donor site morbidity Arthroscopic procedure	Fibrocartilage	Lesion size <4 cm²; age <40 years; focal contained lesions in the femoral condyles
Transplantation of fresh osteochondral allograft	No size limitation Hyaline cartilage	Arthrotomy Graft availability High cost Prolonged return to sports	Large uncontained lesions and lesions with bone and cartilage loss
Transplantation of osteochondral autograft (plugs-mosaicplasty)	Mature hyaline cartilage Primary bone healing Fast recovery	Technically difficult Donor site morbidity	Femoral lesions <2.5 cm²
Autologous chondrocyte implantation (ACI) and matrix-induced autologous chondrocyte implantation (MACI)	No size limitation Hyaline-like cartilage	Arthrotomy High reoperation rate High cost Prolonged rehabilitation	Chondral lesions >2 cm²

Choice of management strategy must take into consideration the demands and expectations of the patient as well as the size, depth and location of the defect, the degree of chronicity and any concomitant intra-articular, extra-articular or general conditions. Previous treatments and injuries should be addressed before starting the treatment [9].

As the population ages, and sporting injuries become more common, the prevalence of symptoms related to cartilage injuries are increasing. The challenge we face as orthopaedic surgeons is that the potential of cartilage to regenerate is virtually non-existent, in contrast to other tissues we encounter such as bone [10]. As a result, a number of approaches have been proposed to address chondral injuries. Despite this, there is limited evidence that any surgical procedure significantly alters the natural history of these lesions. While bone marrow techniques such as microfracture continue to play a role, recent techniques such as osteochondral auto- or allograft, techniques based on the stimulation or growth of chondrocytes such as ACI (autologous chondrocyte implantation) or MACI (matrix-induced ACI) and even genetic techniques are becoming more available for clinical use and it is likely that the indications for these techniques will expand in the coming years [11].

The purpose of this chapter is to determine how to diagnose and manage an osteochondral injury and to summarise the different options which are available in clinical use today [12, 13].

11.2 Physiology of Articular Cartilage

Hyaline articular cartilage is a hypocellular and viscoelastic tissue. It covers bone in synovial joints, providing a low-friction surface, with a coefficient of friction even lower than that of ice on ice [14]. Hyaline cartilage is a specialized tissue, with specific architecture to provide an excellent vehicle for transmission of forces with little friction while being resistant to injury. The key of the tissue architecture is in the cartilage matrix, formed by chondrocytes.

The cartilage can be divided in four zones: superficial, middle, deep and tidemark layer. Superficial layer is mainly composed of collagen with minimal proteoglycans, oriented parallel to the joint surface, and contains a high concentration of water concentration, which decreases the friction. The chondrocytes in this layer are flat or disc-shaped.

The middle layer has oblique collagen fibers, with increased proteoglycan content and a lower concentration of water. This matrix is produced by round chondrocytes. No progenitors exist in this layer.

The vertical disposition of collagen type II in the deep layer confers special resistance to compression forces. These fibers are attached to the calcified layer known as the tidemark, which is a barrier to nutrient diffusion [15].

Proteoglycans give a negative charged environment within articular cartilage and incorporate water in non-weight-bearing situations. On weight-bearing, water leaves the matrix. When the cartilage is damaged, loss of proteoglycans and water alter the normal mechanical properties and joint function.

In general, articular cartilage is unable to heal. The absence of an intrinsic source of new chondrocytes and the fact of being an avascular tissue are the main reasons. The density of chondrocytes and their ability to divide decrease with ageing. Despite this, lesions in which subchondral bone is affected tend to heal, at least clinically. This repair of the chondral surface is determined by the mobilization of cells of subchondral bone marrow, including multipotential cells and chondroblasts [16].

11.3 Clinical Presentation and Physical Examination

There are no pathognomonic symptoms of knee cartilage defects. Consequently, it is necessary to conduct a thorough assessment including symptoms, examination and imaging studies to identify a cartilage lesion as the cause of symptoms [17].

Any type of impact leading to increased force transmission through the articular surface can cause alterations in the ultrastructure of the cartilage. Accumulation of microtrauma or high-energy trauma can lead to macroscopic cartilage damage [18].

Many cartilage lesions can be asymptomatic [19], especially those which are small or away from weight-bearing areas in the knee joint. As lesions become larger, they tend to become more symptomatic. Symptoms are more frequent in those lesions affecting the patellofemoral joint and weight-bearing surfaces of tibiofemoral compartments.

Hyaline cartilage has no sensory innervation, in contrast with the rich innervation of the subchondral bone. When a cartilage defect is full-thickness, contact with the subchondral plate leads to pain. Overload on the defect can lead to enlargement of the injury and increasing symptoms. Breakdown products of the defect produce synovitis, with effusion, liberation of enzymes, pain and increased degradation of the cartilage. If cartilage repair occurs, new tissue is produced to fill the defect, with relief of symptoms and delay of development of osteoarthritis.

Most of patients with osteochondral lesions suffer repetitive episodes of swelling and pain with loading. Pain is typically associated with weight bearing and is located in the area where the defect is. In tibiofemoral defects, pain is usually located at the joint line and it is associated with weight bearing. Posterior defects are more symptomatic in knee flexion. Trochlear defects are associated with crepitus and large effusions while these symptoms are not so frequent in condylar defects. This sign can be useful to differentiate trochlear defects of patellofemoral pain syndrome, where swelling usually is not present. Unless there is a concomitant meniscal tear, mechanical symptoms are not a common feature of chondral defects [17]. Other symptoms can be present as catching, locking and popping, especially if there are loose bodies in the joint.

Physical examination should be focused to identify where the painful lesion is (femoral condyle, patellofemoral joint, etc.), to confirm if the symptoms are related to the presence of the lesion, and to rule out concomitant pathologies which may affect results of chondral surgery or require treatment in themselves [20].

Most symptomatic lesions are painful with palpation, weight-bearing or overload manoeuvres. Standing analysis (and full-length radiographs of the lower limb) should be performed to rule out any malalignment, including rotational deformity. Gait, muscle power, flexibility and contractures should also be evaluated.

Ligament injuries have to be ruled out, as instability has been demonstrated to lead to inferior results in cartilage restoration techniques [21]. Anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), collateral ligaments and both posterolateral and posteromedial corners should be examined (see Chaps. 1, 8 and 9). Attention should be paid to the medial patellofemoral ligament (MPFL) in patellofemoral defects, as it can be insufficient as a consequence of a traumatic patellar dislocation. Some specific manoeuvres as Wilson’s test can be performed if an osteochondral defect or osteochondritis dissecans of the medial femoral condyle is suspected [22].

11.4 Imaging Diagnosis

11.4.1 Radiography and CT

A standard study of knee cartilage lesions should include an AP (anteroposterior) radiograph in full extension (to evaluate femorotibial compartments), AP in 45° of flexion or Rosenberg view (to assess the joint space in flexion), lateral view, and sunrise or Mercer-Merchant view (for the patellofemoral compartment). All AP and lateral views should be performed standing. A standard full-leg radiograph should be obtained to study the mechanical and anatomic axis [18], as normal alignment is necessary for success in cartilage restoration techniques. An osteotomy may be performed in presence of abnormal axis.

Radiographs (Fig. 11.1) provide good information about cartilage surfaces but they are more useful in more advanced stages of cartilage lesions or osteoarthritis [17]. Computed tomography (CT) provides good information about the bony characteristics of the joint. Another potential advantage of using CT is that it provides imaging at different flexion angles or muscle contraction states, which can be helpful in assessing patellofemoral mechanics. CT arthrogram may be helpful and is more accurate than arthroscopy to determine the presence of subchondral bone cysts [14].

Fig. 11.1

Anteroposterior (left) and lateral (right) radiographs of an osteochondral lesion with loose bodies in the medial femoral condyle of the knee

11.4.2 Magnetic Resonance Imaging (MRI)

MRI studies are the most accurate test for assessing cartilage in the knee (Fig. 11.2). It is indicated when an intra-articular pathology (i.e. pain, swelling or mechanical symptoms) is present, despite relatively normal weight-bearing radiographs.

Fig. 11.2

Two lateral images of an MRI of a knee with a chondral lesion

Gradient-echo sequences are able to differentiate articular cartilage from the articular fluid. T2-weighted sequences are better to discriminate subchondral bone oedema from the cartilage surface. Newer MRI techniques, such as T1rho mapping, T2-mapping, sodium imaging and delayed gadolinium-enhanced MRI of cartilage are becoming more and more frequent in the clinical setting and provide useful information about cartilage ultrastructure, morphology, biology and metabolism [18].

While there are many sequences described for cartilage, the most important detail is to be able to discriminate between healthy and affected cartilage. It is important to review all sequences and all slices (axial, sagittal and coronal). Bone oedema is a sign of mechanical overload and its extension is usually correlated with pain and symptoms [23]. It is also important to know the state of the ligaments and extra-articular soft tissues.

11.5 Non-operative Treatment

Conservative treatment is the first line of treatment for all chondral defects. Despite this, the presence of symptomatic loose bodies is an indication for surgical treatment to retrieve them, even if the defect is not being treated [17].

Physical measures such as weight loss, exercise and bracing can be helpful in the initial stages of the treatment. Obesity is an independent risk factor for symptomatic arthritis of the knee and isolated weight loss decreases symptoms [24]. Muscle imbalance, especially quadriceps weakness, is a contributing factor to symptomatic osteoarthritis, and strengthening can be helpful to partially relieve symptoms. However, high-level activities and those including impact and torsion are not recommended, because they can increase symptoms [25]. Bracing can be helpful in cases of a ligament deficit or to offload unicompartmental lesions [26].

Pharmacologic treatment includes painkillers, non-steroidal anti-inflammatory drugs (NSAIDs), chondroitin and glucosamine. Steroids and viscosupplementation can be useful for the management of the pain in mid-term, but they have no effect on the natural history of the defect.

11.6 Predictors of Outcome Following Cartilage Injury and Treatment

Prior to surgery, a full evaluation of the state of the ligaments and menisci, bone oedema and any extra-articular pathology has to be performed. Several factors may adversely affect the natural course of the injury and the results of surgery (Table 11.5).

Table 11.5

Conditions influencing prognosis and post-operative results

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