blood vessels. This generates a blood clot, which facilitates the migration of bone marrow cells into the defect. Microfracture is generally performed as an arthroscopic procedure as a first- line treatment in patients with smaller (<2cm2

) isolated chondral defects. The

blood clot takes about eight weeks to convert to fibrous tissue and therefore needs to be protected. The fact that the repair tissue generated by microfracture is often fibrocartilage, which is not as durable as hyaline cartilage, has led some clinicians to question its role as a first-line treatment for high-demand athletes.

Osteochondral grafts: OATS/mosaicplasty Osteochondral grafting involves taking full-thickness cylindrical plugs of articular cartilage attached to subchondral bone from a non-weight- bearing area of the knee. These plugs are then inserted into matching holes that have been drilled in the chondral defect. This is completed during a single operation either arthroscopically or via a small arthrotomy. The plugs are comprised of hyaline cartilage, but the spaces around the plugs fill in with fibrocartilage, as does the donor site. The biggest problem with this technique is donor site morbidity, and consequently it is often limited to chondral defects less than 4cm2

the defect (many millions). The second stage involves trimming back the chondral defect so that all the edges are healthy cartilage and the underlying bone is exposed. The cultured cells are then reintroduced back into the defect and kept in place by a periosteal or collagen membrane; alternatively, the cells are seeded directly on to a membrane or matrix that is then secured in the defect. This is a fast- moving area in medicine, and new variations of the ACI technique emerge frequently. For a comprehensive outline

of indications, contraindications, techniques and outcomes of the various cartilage repair surgical options, readers are directed to the reference list (6–20).

REHABILITATION FOLLOWING CARTILAGE REPAIR

in size.

The benefit of this technique is that the grafts are mature subchondral plugs, so although it is not quite ‘plug and return to sport’, timescales are generally quicker than with other cartilage repair techniques.

Cell-based repair A new cell-based therapy for the treatment of cartilage defects called autologous chondrocyte implantation (ACI) was developed in the 1980s, and the results of the first human trial were published in 1994 (4). Currently ACI is the most widely researched cartilage repair technique. ACI is generally a two- stage procedure (5), although several European countries have started to perform the technique in a single arthroscopic procedure. The first stage involves an arthroscopic assessment of the chondral defect. A small sample of cartilage is harvested from a non- weight-bearing area of the femur. This sample is cultured for 3–6 weeks until there are sufficient chondrocytes to fill

18

Cartilage adaptation is slow compared with that of other soft tissues (Fig. 2). Over a period of 2 years, only 75% adaptation of cartilage tissue can be expected. This is highly relevant for the rehabilitation of chondral injuries and post-cartilage repair procedures. On the one hand, Wolff’s law dictates that ‘form follows function’ and physical demands need to be placed on the tissue for remodelling to occur. On the other hand, chondral tissue is slow to adapt to increasing loads and is often the weakest link in the tissue chain, so an element of protection against potentially damaging loads is necessary. There is therefore a delicate balance between exposing the repair tissue to sufficient loading in order to stimulate chondral matrix production and minimising the exposure to levels of loading that could lead to mechanical failure of the repair (Fig. 3). The primary rehabilitation goals for an athlete are the local adaptation and remodelling of the repair; a return to full function, including sport and exercise; and the prevention of re- injury and further degeneration in later life. In order to achieve these goals, an optimal environment is required that addresses mechanical, chemical and psychological issues. Although a direct evidence base for cartilage repair rehabilitation is sparse (21), there is an available underpinning scientific framework (22–26). The fundamental principle behind cartilage repair

limited

capacity for regeneration

asymptomatic athletes

++ ++ =

incidence and prevelance of lesions

impact

on sports participation

Figure 1: Cartilage is troublesome

60 50 40 30 20 10 0

muscle bone

ligament tissue

tendon cartilage

Figure 2: Speed of adaptation of various tissues of the body, as determined by the time to replace half of the cells of each tissue.

non specific diagnosis

? progression to OA

management is a significant challenge – especially for the athlete

ENCOURAGE

PREVENT

joint motion

intermittent partial loading

cartilage nutrition

structural adaptation

Figure 3: Function versus protection sportEX medicine 2009;39(Jan):17-21

reptitive friction

shearing stresses overload underload