Focal Cartilage Injuries Research Articles

Can We Really Trust MRI in Diagnosing Knee Injuries in Athletes?

AbstractThis review discusses the so frequent dilemma for a sports physician or orthopaedic surgeon to stand in front of a professional soccer or rugby player with a knee injury, showing clear clinical signs of a meniscus tear or possibly chondral injury, but with an magnetic resonance imaging (MRI) which has been reported as normal. When arthroscopy finally is undertaken after a lot of discussion and delay caused by the reportedly normal MRI, the clinical suspicion is verified. The opposite situation may of course also occur. A clinician usually refers to MRI when the clinical diagnosis is unclear. However, among professional clubs in the UK the referral to a tertiary specialist is in many cases accompanied with an already undertaken MRI. In this review, we demonstrate several illustrative cases, where MRI has led to unnecessary management delays. The review focuses on meniscus and focal cartilage injuries. We suggest a range of possible solutions, which may improve the situation. There are several controversies to be addressed. First, detailed communication between the clinician and radiologist are often hampered by formal procedures. A referral is sent to the Radiology Department and a radiographer will perform a routine MRI protocol. The referral question may not always point to the correct injury, and is depending on the experience of the clinician. Usually, the radiologist is not present during scanning and instead puts together a protocol and subsequently reports on the images without having seen the injured player. Secondly, the use of different routine protocols for investigation of different structures is often not known in detail by the clinician. Thirdly, there is often a lack of standardized reporting of exact location, size and severity of focal cartilage injury in relation to the patients sporting demands. Furthermore, the quality of healed cartilage in a treated focal defect is of course of vital interest for allowing return to sport. Last but not least, inability to verify dynamic instabilities and structural behaviour during movement of the injured knee decreases the clinical value of MRI when compared with arthroscopy for a number of common sport injuries of the knee.

The role of chondrocyte–matrix interactions in maintaining and repairing articular cartilage

Throughout life chondrocytes maintain the articular cartilage matrix by replacing degraded macromolecules and respond to focal cartilage injury or degeneration by increasing local synthesis activity. These observations suggest that mechanisms exist within articular cartilage that stimulate chondrocyte anabolic activity in response to matrix degradation or damage. An important cartilage anabolic factor, insulin‐like growth factor I (IGF‐I), appears to have a role in stimulating chondrocyte anabolic activity. Although IGF‐I is ubiquitous, its bioavailability is controlled by a class of secreted proteins, IGF binding proteins (IGFPBs). Of the six known IGFPBs, IGFBP‐3 is the most abundant in human articular cartilage. We recently found that with increasing age, articular chondrocytes increase their expression of IGFBP‐3. This observation led us to investigate the potential role of IGFBP‐3 in chondrocyte–matrix interactions. Using immunofluorescent staining and confocal microscopy we found that IGFBP‐3 accumulates with increasing age in the chondrocyte territorial matrix where it co‐localizes with fibronectin, but not with tenascin‐C or type VI collagen. Using purified proteins we demonstrated that IGFBP‐3 binds to fibronectin in a dose dependent manner, but not to tenascin‐C. In vitro studies showed that IGFBP‐3 alone inhibited chondrocyte synthetic activity while intact fibronectin alone significantly stimulated activity. When fibronectin and IGFBP‐3 were combined we found that the inhibitory activity of low concentrations of IGFPB‐3 was enhanced. These observations indicate that in mature articular cartilage IGF‐I is stored in the chondrocyte territorial matrix through binding to a complex of IGFPB‐3 and intact fibronectin. Storage of IGF‐I of the territorial matrix may help maintain a relatively constant level of available IGF‐I and the local increase in matrix synthesis following matrix damage may result from release of IGF‐I. This mechanism may have an important role in maintaining and repairing articular cartilage and failure of this mechanism may lead to progressive articular cartilage degeneration.