In part one of this series, Chris Mallac explained the anatomy and complex biomechanics of the VMO and its role in relation to the patellofemoral joint. In part 2, he argues that regardless of cause and effect of the VMO on patellofemoral pain, VMO dysfunction in the presence of pain is very real, and thus exercises to rehabilitate the function of this muscle are necessary... MORE
Cartilage injuries of the knee – causes, diagnosis and treatment review
These are the current techniques for diagnosing and treating chondral injuries of the knee
Knee injuries are one of the most common causes of days off amongst sportspeople, especially in sports such as football, skiing, rugby and netball. Most injuries are self-limiting and can be adequately managed without surgery. Knee pain following such injuries can be caused by damage to extra-articular structures (ie, structures outside the knee joint itself), or intra-articular structures. Extra-articular structures include the medial or lateral collateral ligaments, the patellar tendon and retinacula, bursae and muscles or tendons adjacent to the knee. Intra-articular structures comprise the menisci (colloquially often called cartilages), the anterior and posterior cruciate ligaments and the articular cartilage (the true hyaline cartilage – the joint surface).
The term ‘cartilage’ with respect to knee injuries is sometimes used loosely and can be given different interpretations. For instance, a patient or athlete with a ‘damaged cartilage’ often has an injury to one of the menisci, while to the doctor ‘damaged cartilage’ is an injury to the joint lining articular cartilage. Meniscal injuries will be the subject of a future issue of SIB; in this article, we will discuss articular cartilage injuries and their management.
Cartilage is a specialised connective tissue and is present at several sites in the skeleton (for example ears, respiratory tract, intervertebral discs and lining of the surfaces of synovial joints). There are three main types of cartilage, namely, hyaline cartilage, fibrocartilage (the menisci are made of this) and elastic cartilage, which differ in structure and function. In the knee hyaline (articular) cartilage provides a smooth, white, glistening layer covering the femur, tibia and undersurface of the patella. The main functions of this hyaline cartilage are:
(1) to provide a sort of shock-absorbing structure which can withstand compression, tension and shearing forces, and dissipate load
(2) to provide an almost frictionless articulating surface.
Hyaline cartilage in the knee has to deal with repetitive mechanical forces that can sometimes reach 65 times body weight. It is well adapted for this through its biochemical and biophysiological properties: it is composed of a network of collagen fibres and a proteoglycan matrix within which lie cartilage cells. The collagen is responsible for the tensile strength while the proteoglycan matrix (consisting of 80% water) resists compressive forces.
The main problem with articular cartilage is that it lacks an arterial blood supply, venous and lymphatic drainage and derives its nutrition primarily from the synovial fluid and to some extent from the adjacent bone. This has implications with regard to healing since superficial lesions rely solely on very slow and unsatisfactory cell mitosis and regeneration for repair. Deeper lesions which, together with the articular cartilage involve the underlying bone, heal better because there is direct access of the repair cells in the bone to the cartilage defect. This type of repair, although better than that seen with superficial lesions, is far from ideal since the type of cartilage produced is not the original hyaline cartilage but ‘fibrocartilage’ which is not as well adapted to the mechanical forces generated on weight bearing. It is important to understand the difference between these two forms of repair as it forms the rationale behind the treatment options for such injuries.
Causes of injury
Most articular cartilage defects are caused by trauma. This can either be one single impact injury (with the edge of the patella, for example) or repeated micro trauma. A specific group of cartilage damage is ‘osteochondritis dissecans’ where a well-demarcated small area of cartilage and underlying bone loses its blood supply, dies and eventually fragments and separates into the knee joint.
The clinical picture
The presenting features of articular cartilage damage are non-specific. These include intermittent pain and swelling. The patient may also present with locking or giving way if the fragment has separated into the joint. On examination, there is usually muscle wasting /inhibition, a reduced range of movement and tenderness over the site of the damage which is most commonly the medial femoral condyle or the patella.
In cases of acute trauma, the patient may have a haemarthrosis (the rapid accumulation of blood in the knee). The fact that there is blood in the knee indicates that the cartilage defect is deep and goes down to bone. This is essentially a fracture in the knee and should always be included in the differential diagnosis of a haemarthrosis; the other main causes are an anterior cruciate ligament tear, a peripheral meniscal injury and a severe bone bruise.
Since all the above findings can be present in a number of knee pathologies, it can be quite difficult to confidently reach a clinical diagnosis on clinical findings only.
Plain x-rays will only show cartilage damage if it is associated with underlying bone injury and, even so, small lesions can easily be missed. Lesions appear as a line of demarcation around a small area of bone if the lesion is still attached and as a ‘crater’ or loose body if separation has occurred.
A much better investigation is MRI scanning. This will not only show the osteochondral lesion clearly but will also provide information about the surrounding bone, menisci and anterior cruciate ligament. However, MRI scanning still compares poorly to direct inspection of the joint surface at the time of an arthroscopy.
Arthroscopies are now common day-case operations where the inside of the knee is viewed with a camera and any necessary procedures undertaken through ‘keyhole’ scars. At arthroscopy, cartilage defects can be identified and treated. Arthroscopy will also provide the opportunity for the surgeon to examine the knee under anesthesia, inspect and probe all the articular surface, remove any loose bodies and inspect the menisci and the cruciate ligaments.
Chondral damage has been documented in up to 61.5% of knee arthroscopies for knee symptoms and it is estimated that 41,000 surgical procedures to repair cartilagenous defects are performed annually in the United States.
The outcome of the treatments available does not depend solely on the surgical intervention itself but also on the exact nature of the cartilage defect. Size, depth, location, associated pathologies and chronicity will all contribute to the outcome of surgery and have to be taken into account when comparing different treatments.
The goal of any intervention would be the formation of a durable repair tissue providing symptomatic relief, allowing high physical activity and delaying the option of replacement surgery.
The main treatment options available for cartilage damage of the knee are:
(1) Lavage and debridement
(2) Drilling and microfracture
(3) Paste, periosteal and perichondral grafting
(4) Autologous chondrocyte implantation
(5) Osteochondral autografts
(6) Osteochondral allografts
(7) Artificial matrices
Lavage and debridement
This involves ‘washing out’ the knee arthroscopically and removing any unstable articular cartilage flaps. The debridement of fibrillated or damaged cartilage may relieve symptoms in three ways. Firstly, it may help to relieve mechanical symptoms due to unstable cartilage flaps; secondly, it can decrease the synovitis (angry joint lining) and joint effusion induced by cartilage debris and finally the lavage itself may decrease the concentrations of intra-articular inflammatory mediators.
Some series report a satisfactory early outcome in 68% of patients with such treatment, but some patients’ symptoms may actually deteriorate following ‘wash outs’. Although this is a common procedure in many institutions, there is very limited scientific evidence supporting its use. It should not be the treatment of choice and should be seen as preparation for any future cartilage surgery.
Drilling and microfracture
During a knee arthroscopy the bone at the base of a cartilage defect can be either drilled using fine wires or punctured using fine bone picks. Drilling, which was popularised in the 1960s, is gradually being replaced by microfracture. The latter is simpler to perform, less traumatic and appears to yield better results.
Both these techniques involve penetration of the bone just beneath the cartilage defect in an attempt to replace the defect by fibrocartilage. The response to this is unpredictable and although the early appearance may be gratifying macroscopically, the repair tissue lacks the important biomechanical properties of the native hyaline cartilage and rapidly becomes fibrous and begins to deteriorate. These are nevertheless straightforward procedures that are the mainstay of treatment in most centres. They have little likelihood of harming and some chance of helping the patient and given the current data they are a reasonable first-line treatment option.
Osteochondral paste, periosteal and perichondral grafting
These techniques involve taking different tissues from around the knee and transplanting them
into the cartilage defect. Osteochondral paste is produced by morsellising a graft of cartilage and underlying bone taken from elsewhere in the knee. This paste is then placed in a microfractured defect. Up to 94% pain relief at two years has been reported in one study using this technique.
Periosteal and perichondral grafts are composed of the tissue lining the surface of bone and cartilage respectively. The advantage of such grafts is that they can be placed on large defects and it is believed that cells present in these grafts can give rise to cartilage resembling very closely the original hyaline cartilage. There have been encouraging results from animal models but this has yet to be borne clinically. These techniques remain largely experimental for the time being.
Autologous chondrocyte implantation
This is the area where much of the excitement and investment in the field has been focused. First described in clinical trials in 1994, this involves harvesting cells from the upper outer medial aspect of the femoral condyles during a preliminary arthroscopy. These biopsies are then enzymatically treated and the cartilage cells obtained cultured in vitro. The cultured cells are then reimplanted on to the cartilage defect at a second (open) procedure. The knee is opened, the defect debrided and the cultured cells implanted and secured with a periosteal graft taken from the tibia. This retaining graft is made watertight by adding fibrin glue over the sutured repair. The original results were encouraging with an excellent outcome in 88% of patients at 32 months. Biopsies of the resultant repair are described as ‘hyaline-like’ tissue.
This technique probably leads to a more durable repair than that produced by marrow-stimulation techniques such as microfracture. In centres with the necessary expertise, it is an ideal option for an isolated large cartilage defect in a high-demand patient.
Autogenous (patient’s own) osteochondral implanted grafts have shown early promise. This is mainly due to the encouraging clinical results and to the two new instrumentation systems available on the market. The ideal indications for this repair are full thickness traumatic focal defects or a localised degenerative change in symptomatic patients aged less than 40. Cylindrical 4.5-6.5mm osteochondral grafts are taken from non-weight bearing areas such as the femoral condyle peripheries and inserted into corresponding holes drilled at the site of the chondral defect. What worries most surgeons is the extent of the donor defects. Two recently published studies show 82.5% satisfaction at 18 months and 87% pain relief at two years. While no significant donor-site problems were recorded, the most common complication was persistent swelling which occurs in up to 45% of patients.
This involves transplanting cadaveric osteochondral fragments (from a deceased donor) so as to replace the cartilage defect. Disadvantages include donor availability, tissue treatment and handling, and the fear of disease transmission. The best results have been for large, isolated, post-traumatic defects in young individuals. Although allografts may offer the only alternative to replacement surgery in young patients, questions regarding immunogenicity, host reactions, mechanical properties, and long-term function remain unanswered.
Sterile artificial matrices
Several sterile artificial matrices which might support and toughen the repair fibrocartilage formed on the surface of joints have been studied. The synthetic scaffolds would provide the initial framework from which the healing process could progress. Such matrices include fibrinogen-based products, collagen gels, polylactic/polyglycolic meshes and hydrophylic polymers such as poly-ethyl-methacrylate/tetra-hydro-furfuryl-methacrylate. These techniques are still under investigation but have been overtaken by the previously described biological techniques.
Osteotomies around the knee
When articular defects are too large or advanced to be treated by the above methods, osteotomies around the knee may be used to delay the progression of generalised arthritis and joint replacement surgery. This involves breaking the femur or, more commonly, the tibia in a controlled manner so as to alter the alignment of the leg. These alignment changes result in a redistribution of forces in the knee. Thus an early degenerate compartment in the knee can be protected by realignment surgery and the shifting of forces to the rest of the knee. Osteotomies are the treatment of choice if there is obvious malalign-ment of the knee.
Cartilage injuries are common and can pose difficulties both in diagnosis and treatment. The prognosis of the resultant articular cartilage defects varies according to age, mechanism of injury, site, size, associated injuries and treatment received.
The variety of treatment options available implies that there is no single ideal, reliable and predictable option. The short- and medium-term results described for most of the treatments listed above are promising but clearly more long-term clinical results are needed.
If the progress achieved in the last decade is in any way a reflection of the future, it would be reasonable to have a more optimistic and exciting outlook. This is particularly the case now that industrial interest in cartilage repair has generated financial support for more detailed research that will include the use of growth factors, gene therapy and tissue engineering.