Diagnosis of osteoarthritis: MRI of articular cartilage

The MRI image of articular cartilage reflects the totality of its histological structure and biochemical composition. Articular cartilage is hyaline, which does not have its own blood supply, lymphatic drainage and innervation. It consists of water and ions, type II collagen fibers, chondrocytes, aggregated proteoglycans and other glycoproteins. Collagen fibers are strengthened in the subchondral layer of the bone, like an anchor, and run perpendicular to the joint surface, where they diverge horizontally. Between the collagen fibers are large proteoglycan molecules with a significant negative charge, which intensively attracts water molecules. Cartilage chondrocytes are located in even columns. They synthesize collagen and proteoglycans, as well as inactive enzymes that break down enzymes and enzyme inhibitors.

Histologically, three layers of cartilage have been identified in large joints such as the knee and hip. The deepest layer is the junction of cartilage and subchondral bone and serves as an anchoring layer for an extensive network of collagen fibers extending from it to the surface in dense bundles connected by numerous cross-linking fibrils. This is called the radial layer. Toward the articular surface, the individual collagen fibers become finer and are bundled together into more regular and compact parallel arrays with fewer cross-links. The middle layer, the transitional or intermediate layer, contains more randomly organized collagen fibers, most of which are obliquely oriented to resist vertical loads, pressures, and shocks. The most superficial layer of articular cartilage, known as the tangential layer, is a thin layer of tightly packed, tangentially oriented collagen fibers that resists the tensile forces exerted by compressive loading and forms a watertight barrier to interstitial fluid, preventing its loss during compression. The most superficial collagen fibers of this layer are arranged horizontally, forming dense horizontal sheets on the articular surface, although the fibrils of the superficial tangential zone are not necessarily connected to those of the deeper layers.

As noted, within this complex cellular network of fibers are located aggregated hydrophilic proteoglycan molecules. These large molecules have negatively charged SQ and COO" fragments at the ends of their numerous branches, which strongly attract oppositely charged ions (usually Na ⁺ ), which in turn promotes osmotic penetration of water into the cartilage. The pressure within the collagen network is enormous, and the cartilage functions as an extremely efficient hydrodynamic cushion. Compression of the articular surface causes a horizontal displacement of the water contained in the cartilage, since the collagen fiber network is compressed. The water is redistributed within the cartilage so that its overall volume cannot change. When the compression after joint loading is reduced or eliminated, the water moves back, attracted by the negative charge of the proteoglycans. This is the mechanism that maintains a high water content and thus a high proton density of cartilage. The highest water content is observed closer to the articular surface and decreases towards the subchondral bone. The concentration of proteoglycans is increased in the deep layers of cartilage.

Currently, MRI is the main imaging technique for hyaline cartilage, performed mainly using gradient echo (GE) sequences. MRI reflects the water content of cartilage. However, the amount of water protons contained in cartilage is important. The content and distribution of hydrophilic proteoglycan molecules and the anisotropic organization of collagen fibrils affect not only the total amount of water, i.e. the proton density, in cartilage, but also the state of the relaxation properties, namely T2, of this water, giving cartilage its characteristic "zonal" or stratified images on MRI, which some researchers believe correspond to the histological layers of cartilage.

On very short echo time (TE) images (less than 5 ms), higher resolution images of cartilage typically show a two-layer image: the deep layer is located closer to the bone in the pre-calcification zone and has a low signal, since the presence of calcium greatly shortens the TR and does not produce an image; the superficial layer produces a medium- to high-intensity MP signal.

In intermediate TE images (5-40 ms) the cartilage has a three-layered appearance: a superficial layer with low signal; a transition layer with intermediate signal intensity; a deep layer with low MP signal. In T2-weighting the signal does not include the intermediate layer and the cartilage image becomes homogeneously low intensity. When low spatial resolution is used, an additional layer sometimes appears in short TE images due to oblique cut artifacts and high contrast at the cartilage/fluid interface, this can be avoided by increasing the matrix size.

In addition, some of these zones (layers) may not be visible under certain conditions. For example, when the angle between the cartilage axis and the main magnetic field changes, the appearance of the cartilage layers may change, and the cartilage may have a homogeneous image. The authors explain this phenomenon by the anisotropic property of collagen fibers and their different orientation within each layer.

Other authors believe that obtaining a layered image of cartilage is not reliable and is an artifact. Researchers' opinions also differ regarding the intensity of signals from the obtained three-layer images of cartilage. These studies are very interesting and, of course, require further study.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ]

Structural changes in cartilage in osteoarthritis

In the early stages of osteoarthritis, degradation of the collagen network in the superficial layers of cartilage occurs, leading to surface fraying and increased permeability to water. As some of the proteoglycans are destroyed, more negatively charged glycosaminoglycans appear, which attract cations and water molecules, while the remaining proteoglycans lose their ability to attract and retain water. In addition, the loss of proteoglycans reduces their inhibitory effect on the interstitial flow of water. As a result, the cartilage swells, the mechanism of compression (retention) of fluid "does not work" and the compressive resistance of the cartilage decreases. The effect of transferring most of the load to the already damaged hard matrix occurs, and this leads to the fact that the swollen cartilage becomes more susceptible to mechanical damage. As a result, the cartilage is either restored or continues to deteriorate.

In addition to damage to proteoglycans, the collagen network is partially destroyed and is no longer restored, and vertical cracks and ulcers appear in the cartilage. These lesions can extend down the cartilage to the subchondral bone. The decay products and synovial fluid spread to the basal layer, which leads to the appearance of small areas of osteonecrosis and subchondral cysts.

In parallel with these processes, the cartilage undergoes a series of reparative changes in an attempt to restore the damaged articular surface, which include the formation of chondrophytes. The latter eventually undergo enchondral ossification and become osteophytes.

Acute mechanical trauma and compressive load can lead to the development of horizontal cracks in the deep calcified layer of cartilage and detachment of cartilage from the subchondral bone. Basal splitting or delamination of cartilage in this way can serve as a mechanism of degeneration not only of normal cartilage under mechanical overload, but also in osteoarthrosis, when there is joint instability. If the hyaline cartilage is completely destroyed and the articular surface is exposed, then two processes are possible: the first is the formation of dense sclerosis on the bone surface, which is called eburnation; the second is damage and compression of trabeculae, which on X-ray images looks like subchondral sclerosis. Accordingly, the first process can be considered compensatory, while the second is clearly a phase of joint destruction.

The increase in cartilage water content increases the proton density of the cartilage and eliminates the T2-shortening effects of the proteoglycan-collagen matrix, which has a high signal intensity in areas of matrix damage on conventional MRI sequences. This early chondromalacia, which is the earliest sign of cartilage damage, may be visible before even minor thinning of the cartilage occurs. Mild thickening or "swelling" of the cartilage may also be present at this stage. Structural and biomechanical changes in the articular cartilage are progressive, with loss of ground substance. These processes may be focal or diffuse, limited to superficial thinning and fraying, or complete disappearance of the cartilage. In some cases, focal thickening or "swelling" of the cartilage may be observed without disruption of the articular surface. In osteoarthritis, focal increased signal intensity of cartilage on T2-weighted images is often observed, confirmed arthroscopically by the presence of superficial, transmural, and deep linear changes. The latter may reflect deep degenerative changes, beginning mainly as detachment of cartilage from the calcified layer or tide line. Early changes may be limited to the deep layers of cartilage, in which case they are not detectable on arthroscopic examination of the articular surface, although focal sparseness of the deep layers of cartilage may lead to involvement of adjacent layers, often with proliferation of subchondral bone in the form of a central osteophyte.

There are data in foreign literature on the possibility of obtaining quantitative information on the composition of articular cartilage, for example, on the content of the water fraction and the diffusion coefficient of water in cartilage. This is achieved using special programs of the MR tomograph or with MR spectroscopy. Both of these parameters increase with damage to the proteoglycan-collagen matrix during cartilage damage. The concentration of mobile protons (water content) in cartilage decreases in the direction from the articular surface to the subchondral bone.

Quantitative assessment of changes is also possible on T2-weighted images. By pooling data from images of the same cartilage obtained with different TEs, the authors assessed T2-weighted images (WI) of cartilage using a suitable exponential curve from the obtained signal intensity values for each pixel. T2 is assessed in a specific area of cartilage or displayed on a map of the entire cartilage, in which the signal intensity of each pixel corresponds to T2 at this location. However, despite the relatively large capabilities and relative ease of the above-described method, the role of T2 is underestimated, partly due to an increase in diffusion-related effects with increasing TE. T2 is mainly underestimated in chondromalacia cartilage, when water diffusion is increased. Unless special technologies are used, the potential increase in T2 measured with these technologies in chondromalacia cartilage will slightly suppress diffusion-related effects.

Thus, MRI is a very promising method for detecting and monitoring early structural changes characteristic of articular cartilage degeneration.

Morphological changes in cartilage in osteoarthritis

Evaluation of morphological changes in cartilage depends on high spatial resolution and high contrast from the joint surface to the subchondral bone. This is best achieved using fat-suppressed T1-weighted 3D GE sequences, which accurately reflect local defects identified and verified both at arthroscopy and in autopsy material. Cartilage can also be imaged with magnetization transfer by image subtraction, in which case articular cartilage appears as a separate band with high signal intensity, clearly contrasting with the adjacent low-intensity synovial fluid, intra-articular fat tissue and subchondral bone marrow. However, this method produces images half as slowly as fat-suppressed T1-weighted images, and is therefore less widely used. In addition, local defects, surface irregularities and generalized thinning of articular cartilage can be imaged using conventional MR sequences. According to some authors, morphological parameters - thickness, volume, geometry and surface topography of cartilage - can be quantitatively calculated using 3D MRI images. By summing the voxels that make up the 3D reconstructed image of cartilage, the exact value of these complexly related structures can be determined. Moreover, measuring the total cartilage volume obtained from individual slices is a simpler method due to smaller changes in the plane of a single slice and is more reliable in spatial resolution. When studying whole amputated knee joints and patellar specimens obtained during arthroplasty of these joints, the total volume of articular cartilage of the femur, tibia and patella was determined and a correlation was found between the volumes obtained by MRI and the corresponding volumes obtained by separating the cartilage from the bone and measuring it histologically. Therefore, this technology can be useful for dynamic assessment of cartilage volume changes in patients with osteoarthritis. Obtaining the necessary and accurate sections of articular cartilage, especially in patients with osteoarthritis, requires sufficient skill and experience of the physician performing the examination, as well as the availability of appropriate MRI software.

Measurements of total volume contain little information about widespread changes and are therefore sensitive to local cartilage loss. Theoretically, cartilage loss or thinning in one area could be balanced by an equivalent increase in cartilage volume elsewhere in the joint, and the measurement of total cartilage volume would not show any abnormality, so such changes would not be detectable by this method. Subdividing the articular cartilage into discrete small regions using 3D reconstruction has made it possible to estimate the cartilage volume in specific areas, particularly on force-bearing surfaces. However, the accuracy of the measurements is reduced because very little subdivision is performed. Ultimately, extremely high spatial resolution is necessary to confirm the accuracy of the measurements. If sufficient spatial resolution can be achieved, the prospect of mapping cartilage thickness in vivo becomes possible. Cartilage thickness maps can reproduce local damage during osteoarthritis progression.