Conventional radiography is widely used to evaluate the long-term progression of osteoarthritis (OA) and is able to clearly depict the established hallmarks of OA, namely, joint space narrowing, subchondral sclerosis, subchondral cyst formation, and osteophytosis. Conventional radiography is limited by its inability to directly visualize articular cartilage, the tissue in which OA is thought to begin (1). Magnetic resonance imaging (MRI) offers the distinct advantage of detecting signal and morphologic changes in articular cartilage and is the most sensitive and accurate test for evaluating the articular cartilage noninvasively; MRI has been used to detect articular cartilage changes such as cartilage swelling (or “blistering”), surface fraying, fissuring, and varying degrees of cartilage thinning (2, 3). Cartilage-sensitive MRI techniques, such as spoiled gradient-echo (GE) or fast spin-echo (FSE) sequences, have been shown to have a significant correlation with arthroscopic grading scores (r = 0.705) and thus can be used in an effective, noninvasive evaluation of the knee joint (4–7).
At this time, however, little is known about how such cartilage lesions develop and what their natural progression is over time. The purpose of our study was to evaluate the rate of progression of cartilage loss associated with OA of the knee joint using MRI and to evaluate potential risk factors for more rapid cartilage loss. Ultimately, we wanted to determine the prognostic significance of cartilage defects and associated articular disorders identified on knee MRIs. To accomplish this, we performed a retrospective review of MRIs in 43 patients who had undergone repeat MRIs of the knee over a relatively short observation period of an average of 1–2 years.
- Top of page
- PATIENTS AND METHODS
The current study indicates that MRI is capable of detecting cartilage loss in a relatively short time. MRI can predict areas of articular cartilage that are prone to more rapid disease progression and can identify early lesions that may progress to further cartilage loss.
Comparison of the anterior, central, and posterior regions of the medial and lateral compartments demonstrated that changes in cartilage integrity are significantly more likely to occur in the central region of the medial tibiofemoral compartment; the central portion of the medial tibiofemoral compartment is prone to more rapid progression of cartilage loss. This may be the result of higher biomechanical loads in this compartment.
Studies of walking mechanics have shown that the knee is loaded asymmetrically. The medial tibiofemoral compartment of the knee is subject to significantly higher loads relative to the lateral compartment. In addition, the outcome of treatment for medial compartment OA has been related to the magnitude of the load on the medial compartment during walking (8–11). Harman et al have found that knees in a range of various alignments demonstrate articular cartilage wear patterns in the central to anterior regions of the medial tibial plateau (12). Furthermore, in conditions resembling the stance phase of a normal gait cycle, a computer model of the weight-bearing surfaces of the total knee found the central portion of the medial tibial plateau and the central/posterior portions of the lateral tibial plateau to be the initial contact points during loading of the knee (13). These studies corroborate our findings that cartilage lesions located in the central region of the medial compartment are prone to more rapid progression of cartilage loss than cartilage lesions in the anterior and posterior portions of the medial compartment.
There are several cartilage lesions identified by both arthroscopists and radiologists, with one lesion in particular generating much interdisciplinary (and intradisciplinary) debate. This is the MR grade 1 lesion, and many believe this lesion is difficult to diagnose with either MRI or arthroscopy. The results of our study, which demonstrate a relatively high rate of persistence or progression of grade 1 lesions, underscore the need for future clinical studies, advanced MRI, and histologic/arthroscopic correlation to better characterize these findings. There have already been substantial efforts made to better characterize this lesion, as described below.
The grade 1 lesion is a focus of signal heterogeneity within an intact cartilage surface, as defined within our MRI classification system and by others using similar classification systems (3, 7). The arthroscopic correlate to this lesion has been suggested to be cartilage “softening,” “swelling,” or “blistering,” which is also characterized as a grade 1 lesion in the arthroscopic grading scheme (14, 15). Histologically, grade 1 lesions are thought to represent anatomic aberrations, especially in the early changes of OA. Donohue et al showed that indirect blunt trauma to canine articular cartilage is able to produce ultrastructural changes, namely, the disruption of the collagenous network within the extracellular matrix, while the articular surface remains intact (16). More specifically, some authors believe that focal alterations in the network of collagen fibrils result in increased local hydration of cartilage, which is seen as aberrant signal intensity and disruption of the normal, laminar appearance on MRI (17, 18). They may represent microfissures that are below the spatial resolution of the standard MRI pulse sequences. They may also represent gross changes in composition in the extracellular matrix (e.g., breakdown of collagen, change in proteoglycan composition, or change in water content). In contrast, focal proteoglycan depletion in the articular cartilage of rat knees has been shown to be a less likely reason for grade 1 lesions (19).
Regardless of the etiology of these lesions, our study suggests that they are important given that 29 (38%) of 77 areas progressed to higher grade lesions (grades 2–6). Grade 1 signal heterogeneity lesions may represent actual articular cartilage derangement and may serve as predictors of future articular cartilage degeneration. Thus, detection of grade 1 lesions, using even the current MRI sequences, should warn of potential cartilage loss, and close attention should be directed to the affected articular cartilage on the followup studies. It is hoped that further development of high-resolution MRI sequences will elucidate the nature of these lesions, and that sodium MRI or gadolinium-enhanced MRI may characterize the biochemical changes (20). Recent work by Mosher et al, using a 3.0T magnet, demonstrated a significant increase in T2 relaxation of the transitional zone of patellar articular cartilage in symptomatic patients when compared with asymptomatic controls (21). Akella et al were able to correlate the loss of proteoglycan from the cartilage matrix with MRI signal alterations using a 4.0T magnet (22). Studies such as these are highly encouraging.
Despite the substantial proportion of grade 1 signal heterogeneity lesions that progressed, one-fourth of the lesions reverted to grade 0. The somewhat capricious nature of grade 1 lesions and the phenomenon of reversion may be explained as follows. Lesions were not seen on the followup study because of partial volume averaging. Grade 1 lesions seen at baseline represent artifacts of partial volume averaging or the magic angle phenomenon. To minimize this possibility, we confirmed the lesion presence on 2 contiguous slices and/or in an alternative imaging plane. Furthermore, the magic angle phenomenon is a less likely possibility since it is a homogeneous signal artifact (23, 24). Reversion to a smaller or lower grade lesion may, in fact, also represent repair and healing.
Indeed, a review of the literature indicates that detection of grade 1 lesions has been challenging at best. There appears to be a controversy between the use of MRI and arthroscopy, as to which is the optimal study for detection of grade 1 lesions. Some authors believe arthroscopy is best for this, while others believe MRI has a unique ability to detect subsurface lesions. For example, in a retrospective analysis of 63 patients, the sensitivity of MRI evaluation of grade 1 lesions (when compared with arthroscopy) was 14.3% despite the use of MRI machines with identical magnetic field strength (1.5T magnet) and similar cartilage-sensitive sequences (proton density FSE) (14). Similarly, a study of 320 patients who had experienced acute trauma, using MRI and arthroscopy, showed that MRI diagnosed only 14% of the grade 1 lesions (25). In contrast, MRI was able to detect between 75% and 94% of lesions characterized as cartilage erosions and 100% of full-thickness cartilage loss.
The discrepancy between MRI and arthroscopy seen with grade 1 lesions can be attributed to the fact that lesions without surface irregularities are inherently difficult to diagnose arthroscopically and, in fact, the authors of such studies have found that MRI can “overgrade” intracartilaginous lesions relative to arthroscopy (26). Furthermore, those investigators concede that the arthroscopic correlate to an MRI grade 1 lesion, which is referred to as cartilage softening or swelling, can be appreciated only by gentle palpation of the articular surface. This is an arthroscopic technique not normally used on the entire cartilage surface, resulting in a high rate of false-negative results. We also can presume that this palpation technique is prone to significant subjectivity. We do not know whether intracartilaginous signal abnormalities seen with MRI necessarily translate into altered mechanical properties. It is conceivable that early cartilage lesions may have stiffness similar to the adjacent normal cartilage, thus making them difficult to detect with the arthroscopic technique. MRI is likely to prove to be an invaluable tool, more sensitive than arthroscopy for evaluation of early cartilage changes and subsurface lesions.
The natural course of cartilage loss appears to be accelerated in the presence of meniscal tears. In our study, we found a strong relation between meniscal tears and lesions that progressed more rapidly. Dandy and Jackson, as well as Frankel et al, have demonstrated that meniscal abnormalities have led to enhanced chondromalacia as a result of abnormal articular forces created by such an alteration (27, 28). Photoelastic studies by Radin et al showed that the meniscus serves to protect articular cartilage by distributing load throughout the articular surface and preventing focal stress concentrations (29). The borderline influence of ACL tears on progression of cartilage derangements may be partially explained by the fact that nearly all torn ACLs were replaced, thus preventing rapid cartilage loss.
Limitations of this study include its retrospective design, limited clinical information, small sample size, varying ages of the patients, and population bias toward patients with chronic knee pain and dysfunction. Furthermore, the MRI readers were ultimately not blinded to the order of the studies, despite the best intentions (see Patients and Methods). Knowledge of the order may introduce bias in image interpretation as well as analysis of disease progression. Also, the sorting of lesion size into 2 different groups was perhaps too crude. Perhaps a more specific size measurement is needed, because we expect that cartilage lesion size would increase more rapidly in patients with a meniscal tear or ACL injuries. However, despite the small sample size and the absence of proper stratification of patient groups, we showed that MRI was able to detect progression of cartilage loss within a short observation period of 1–2 years. Furthermore, patients with arthritis who are enrolled in clinical trials may have to be randomized according to lesion location and the presence of meniscal or cruciate ligament tears.
Unlike conventional radiography, MRI can detect cartilage loss in patients with OA within a short observation period. Cartilage lesions such as focal signal heterogeneity, surface fraying, fissuring, thinning, and full-thickness cartilage loss can be identified and followed longitudinally. No specific lesion has a predilection for more rapid cartilage loss. Grade 1 lesions progress to a higher grade (grades 2–6) in ∼40% of the cases over the observation period, enhancing the importance of this early lesion. The cartilage lesions identified in the central region of the medial compartment are prone to more rapid progression of cartilage loss when compared with those in the anterior and posterior regions of the medial tibiofemoral compartment or the lateral tibiofemoral compartment. Lesions located in the anterior region of the lateral compartment showed significantly less cartilage degradation. Furthermore, meniscal (and possibly ACL) tears predispose knee articular cartilage to more rapid cartilage loss.