(B) Longitudinal ultrasonographic image of gthe medial joint line demostratesmedial meniscal extrusion (m) with displacement of the medial collateral ligament.
Role of Recent Magnetic Resonance Imaging Techniques in Evaluation and Early Detection of Articular Hyaline Cartilage Changes of Knee Joint in Suspected Osteoarthritis A thesis Submitted for partial fulfillment of MD Degree in Radiodiagnosis
By Mohammad Fouad Abd El Baki Allam MBBCh Faculty of Medicine El-Minia University
Supervisors
Prof. Adel Mohamed Samy Mohsen Professor of Radiodiagnosis, Faculty of Medicine El-Minia University
Prof. Ahmad Fathy Ahmad Ebeed El Gebaly Professor of Radiodiagnosis, Faculty of Medicine El-Minia University
Prof. Khaled Aboualfotouh Ahmad Professor of Radiodiagnosis, Faculty of Medicine Ain Shams University
Dr. Mohamed Farghaly Amin Assistant professor of Radiodianosis, Faculty of Medicine El-Minia University Faculty of Medicine El-Minia University 2015
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ACKNOWLEDGMENTS First and last, great thanks to ALLAH, without his help, this work could not have been accomplished. I wish to express my deep gratitude to Dr. Adel M. S. Mohsen, professor of Radiodiagnosis, Faculty of Medicine, El-Minia University for his kind supervision, encouragement and moral support all through the study. I wish to express my great appreciation also to Dr. Ahmad F. ElGebaly, professor of Radiodiagnosis, Faculty of Medicine, El-Minia University, who love nothing in our life more than teaching a resident at the view box, great thanks to his gracious supervision and moral support all through my work. Special acknowledgement is due to Dr. Khaled Aboualfotouh Ahmad professor of Radiodiagnosis, Faculty of Medicine, Ain Shams University, for his careful supervision, scientific support and great cooperation during the fulfillment of this work. My great thanks to Dr. Mohamed F. Amin, assistant professor of Radiodiagnosis, Faculty of Medicine, El-Minia University, who, as my teacher, interested me in musculoskeletal radiology, thanks to his scientific support and great help throughout the study I would like to thanks many unnamed technicians during collection of the study cases, for their kind and moral support. Lastly, my great thanks to all patients participating in this study.
Mohammad F. Allam
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List of Contents Contents Acknowledgments……………………………………...... Contents…………………………………………………. List of abbreviations…………………………………….. List of figures……………………………………………. List of tables……………………………………………... Introduction……………………………………………… Aim of the work…………………………………………. Review of literature……………………………………… - Anatomy and biomechanics of the knee joint……........ - Pathophysiology of osteoarthritis …….………………. - Imaging of knee osteoarthritis………...………..….. … Patients and methods…………………….………………. Results…………………………………………………… Case presentation………………………………………... Discussion……………………………………………….. Summary………………………………………………… Conclusions……………………………………………… References……………………………………………….. Arabic summary…………………………………………
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List of Tables Table (I) KL grading scale of osteoarthritis of knee joint Table (2) MRI sequence parameters used in the study Table (3) Comparison between cartilage loss in each KL score Table (4) Comparison between full-thickness cartilage loss in each KL score Table (5) Comparison of sum of BML in both groups Table (6) Comparison of quantitative joint features in both groups Table (7) Comparison non-quantitative joint features in both groups Table (8) Correlation of KL score to surface area cartilage loss Table (9) Correlation of PF cartilage scores to other joint features Table (10) Correlation of MFT cartilage scores to other joint features Table (11) Correlation of LFT cartilage scores to other joint features Table (12) Correlation of MFT BML scores to other joint features Table (13) Correlation of MFT osteophyte scores to other joint Features Table (14) Correlation between Lequesne index score and cartilage scores Table (15): Correlation between Lequesne score and different joint features other than articular cartilage
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List Of Figures Figure (1): AP and lateral radiograph of the knee Figure (2): 3D CT image of the knee Figure (3): Normal knee radiographic anatomy Figure (4): The tibial plateau Figure (5): Sunrise radiograph Figure (6): The dorsal patellar defect Figure (7): Molecular structure of hyaline cartilage matrix Figure (8): Normal articular cartilage Figure (9): Imaging of patellar hyaline cartilage Figure (10): Normal anterior cruciate ligament Figure (11): Normal posterior cruciate ligament Figure (12): MRI of the medial and lateral menisci Figure (13): The load-bearing knee joint in deep flexion Figure (14): MRI of the medial and lateral collateral ligaments Figure (15): Microscopic pathology of OA articular cartilage Figure (16): Skewed and parallel radioanatomic alignment of the medial tibial plateau Figure (17): Ultrasonographic features in OA Figure (18): CT arthrography of the knee Figure (19): Eight-point scale employed in WORMS for scoring articular cartilage Figure (20): Anatomic devision of knee joint Figure (21): MOAKS grading of the size of any cartilage loss Figure (22): MR PD FS arthrogra m Figure (23): Measurement of articular cartilage defect Figure (24): Scoring of osteophytes Figure (25): Effusion-synovitis Figure (26): Box plot of age distribution in studied groups Figure (27): Column chart of sex distribution in studied groups Figure (28): Box plot of Lequesne score value distribution in studied groups Figure (29): Scatterplot of ACL correlated to lateral posterior femoral osteophytes
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List Of Abbreviations
6
Introduction
7
Introduction Osteoarthritis (OA) is a slowly progressive degenerative disease characterized by a gradual loss of articular hyaline cartilage.
It is
considered as one of the most common cause of disability among the elderly population. It occurs when articular cartilage cannot maintain homeostasis in response to the forces acting on it. When homeostasis breaks down, there is a wide range of possible biologic responses which may be anabolic or catabolic involving the articular cartilage, bony articular surface and bone marrow, ligaments and synovium. Thus; OA is considered as a disease of the entire joint. (1) The knee joint is one of the most frequently affected joints by OA in the body; it is characterized by abundant thickness of articular cartilage easily assessed on imaging, compared with other joints as hip, spine and hands. Damaged cartilage does not heal or regenerate spontaneously, so early diagnosis at early stage of osteoarthritic process is necessary for prompt control of joint damage, preventing its progress and postpones the eventual disability. (1) In recent decades, magnetic resonance imaging (MRI) has become the most important modality for assessment of pathologic changes in knee cartilage. One of the major advantages of MRI is that it allows the manipulation of contrast to highlight different tissue types. The new surgical and pharmacologic options available to treat damaged cartilage, and the need to monitor these effects, have led to development of various MRI techniques that allow morphologic assessment of cartilage. Moreover; MRI can assess the entire joint when osteoarthritis is suspected, by studying cartilaginous and non-cartilaginous tissues in a whole-organ assessment. (2)
1
Aim Of The Work This study was aiming to evaluate the ability of MRI in early detection of pathological articular cartilage changes in clinically suspected knee OA. This study was also aimed to evaluate the role of recent semiquantitative MRI method in evaluating knee OA as a whole organ disease.
2
Review
3
Anatomy And Biomechanics Of The Knee Joint Knee joint is the largest and most complex joint in the body. It is described as a modified hinge joint throughout its range of motion with additional rotary component that occurs in locking and unlocking of the knee at the end of extension movement and at beginning of flexion movement from a fully extended state respectively. The bones of the knee joint do not interlock like other joints, as the articular surfaces are not mutually adapted to each other, so, the knee joint is considered as partly arthrodial but not completely so. (Figure 1). In all positions, the femur is kept in contact with tibia, with large areas of contact. The patella is kept in contact with femur in all positions. Ligaments, tendons, capsule, and menisci maintain the joint stability. (2, 4) The knee is a major weight-bearing joint in the body. Cartilage is the material inside the joint that provides shock absorption during weightbearing activities such as walking or stair climbing. (5) The knee joint is composed of three articulations: the medial and lateral femoro-tibial and patella-femoral articulations. Although they share a common joint capsule, these articulations are often referred to separately as the medial, lateral and patella-femoral compartments or joints. (6) The knee joint is composed of osseous and non-osseous structures; the non-osseous structures are divided into intra-articular and extra-articular ones.
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I- OSSEOUS STRUCTURES: The bony structures forming the knee joint are the medial and lateral femoral condyles, tibial plateau, and the patella. (Figure 2).
Figure 1: Anteroposterior (A) and lateral (B) radiographs of the knee in a boy aged 14 years. 1. Patella. 2. Cartilaginous growth plate. 3. intercondylar eminence. 4. Prolongation of proximal tibial epiphysis and growth plate forming the tibial tuberosity. Quoted from Ref No. 5.
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Figure 2: 3D CT image demonstrating various anatomical osseous components of the knee joint. Quoted from Ref No. 7. Femoral condyles: The femoral condyles are two rounded prominences at the lower end of the femur with anterior groove found between them termed trochlear or patello-femoral groove, the trochlear groove accommodates the patella and is generally V-shaped. Posteriorly, the condyles are separated by the intercondylar notch that accommodates the cruciate ligaments; and seen as Blumensaat line on lateral radiograph. (3) The lateral femoral condyle is wider than the medial and relatively flat along its anterior weight-bearing surface, while the medial femoral condyle is longer than the lateral and has a rounder contour of the distal surface. There is mild concavity in the flat distal articular surface of the
5
lateral femoral condyle termed lateral femoral condylar sulcus or recess. The medial condyle also has a condylar sulcus, but is located more anteriorly, as part of the medial margin of the trochlea. (3, 6) (Figure 3). Osseous irregularity may be seen at posteromedial femoral metaphysis at the adductor or medial gastrocnemius insertion, termed cortical desmoid. (3) Each femoral condyle flares into small protrusions or elevation called epicondyle. The medial epicondyle is a large convex eminence to which the medial collateral ligament of the knee joint is attached. The lateral epicondyle is smaller and less prominent than the medial; it gives attachment to the lateral collateral ligament of the knee joint. (3) The articular surface of the femoral condyles occupies their anterior, inferior, and posterior surfaces. Its anterior part is named the patellar surface and articulates with the patella. The lower and posterior parts of the articular surface constitute the tibial surfaces for articulation with the corresponding condyles of the tibia and menisci. (3)
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(B)
(A)
Figure 3: Normal knee radiographic anatomy. (A). Slightly oblique lateral radiograph, the medial compartment projects slightly lower and more anteriorly (short arrow). The concave medial tibial plateau (black arrowheads) project just below the straight lateral tibial plateau. The lateral condylar sulcus (long arrow). The Blumensaat line (white arrowheads). (B). Slightly oblique lateral radiograph with 40 degrees flexion. The mid-weightbearing surfaces of the femoral condyles (arrows) in contact with the tibial plateaus. The contact smaller than at extension especially the lateral condyle (white arrow). The femoral condylar sulci are seen (black arrowhead, medial; white arrowhead, lateral). Quoted from Ref. No. 6.
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Tibial plateau: The tibial plateau is the large expanded proximal tibial end, it act as bearing surface for body weight, which is transmitted through the femur. It consists of medial and lateral condyles with inter-condylar area in-between. Both condyles have articular facets on their superior surfaces that are separated by an irregular, non-articular inter-condylar area into medial and lateral facets; the medial facet is oval in shape, while the lateral is nearly circular. The lateral tibial plateau has a flat surface, while the medial plateau has a subtly concave surface. (Figure 3.A). The central portions of these facets articulate with the condyles of the femur, while their peripheral portions support the menisci of the knee joint, which intervene between the two bones. The rough-surfaced inter-condylar area between articular surfaces is narrow centrally where is an inter-condylar eminence (spine of tibia), the edges of which project slightly proximally as the lateral and medial inter-condylar tubercles. The eminence, with medial and lateral tubercles is thought to provide a slight stabilizing influence on the femur. The inter-condylar area widens behind and in front of the eminence as the articular surfaces diverge. The anterior inter-condylar area harbors a depression, antero-medially anterior to the medial articular surface, for attachment of anterior horn of medial meniscus. Behind this, a smooth area receives the anterior cruciate ligament. The anterior horn of lateral meniscus is attached anterior to the inter-condylar eminence, lateral to the anterior cruciate ligament. The posterior horn of the medial meniscus is attached to the posterior slope of the inter-condylar area. The posterior inter-condylar area inclines down and backwards behind the posterior horn of the lateral meniscus. A depression behind the base of the medial inter-condylar tubercle is for the posterior horn of the medial meniscus. The rest of the area
8
is smooth and provides attachment for the posterior cruciate ligament, spreading back to a ridge to which the capsule is attached. (3-6) (Figure 4). The anterior surfaces of the condyles are continuous with one another, forming a large, somewhat flattened area, this area is triangular, broad above and narrow below where it ends in a large oblong elevation, the tuberosity of the tibia, into which the patellar ligament is attached. (5) The medial condyle presents posteriorly a deep transverse groove, for the insertion of the tendon of the semimembranosus. Its medial surface is convex, rough, and prominent; it gives attachment to the tibial collateral ligament. The lateral condyle presents posteriorly a flat articular facet, nearly circular in form, directed downward, backward, and lateralward, for articulation with fibular head. The distal attachment of the ilio-tibial tract makes a flat but definite marking, termed Gerdy’s tubercle, on anterior aspect of lateral condyle just distal to the joint. This tubercle, which is triangular and facet-like, is usually palpable. (5)
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Figure 4: The tibial plateau. 1. Tibial tuberosity. 2. Attachment of anterior horn, lateral meniscus. 3. Lateral condyle. 4. Attachment of posterior horn, lateral meniscus. 5. Attachment of anterior horn, medial meniscus. 6. Attachment of anterior cruciate ligament. 7. Medial condyle. 8. Intercondylar eminence. 9. Attachment of posterior horn, medial meniscus. 10. Attachment of posterior cruciate ligament. Quoted from Ref. No. 5.
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Patella: The patella is a flat triangular bone, situated on the front of the knee joint (figure 5). It is usually regarded as a sesamoid bone, developed in the tendon of the quadriceps femoris. It is wider superiorly at its base with an apex inferiorly. It has anterior and posterior surfaces, three borders, and an apex, the posterior is the articular surface, which is divided by a vertical median ridge into a long lateral facet with shallow angle, and a short medial, which is more angulated. The odd facet is a frequent facet seen most medial and often sagittal in orientation. Several other facets described but not of imaging importance. The patella act to serves protection to the front of the knee joint, and increases the leverage of the quadriceps femoris by making it act at a greater angle. Bipartite and multipartite patella is a normal variant, located almost always at upper outer quadrant, although the osseous fragments may not appear to match the apparent defect, the articular cartilage is continuous over the defect. Dorsal patellar defect is another normal variant of unknown etiology, usually located in the superolateral aspect of the patella, the articular cartilage is intact over it, but in rare occasions, cartilaginous involvement coexists.
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(3-6)
(Figure 6).
Figure 5: Sunrise radiograph demonstrating the patellofemoral joint and the intercondylar sulcus and patella relationship. Quoted from Ref. No 8.
Figure 6:. The dorsal patellar defect on plain film (A) and gradient echo, T2*-weighted axial MR image (B). Note intact articular hyaline cartilage over the defect. Quoted from Ref. No. 9.
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Hyaline articular cartilage: Hyaline articular cartilage is the smooth glass-like surface tissue, lining the ends of the articular bones. A tissue with low friction and high capacity to bear load, cartilage serves the critical function of permitting movement of one bone against another. (10) Molecular composition of the hyaline cartilage: Hyaline cartilage is composed of specialized proteins and macromolecules that allow the tissue to function in the rigorous mechanical environments of articulating joints. Collagens and proteoglycans interact with a charged fluid environment to give articular cartilage its unique mechanical properties. The composition and structure of the tissue have a direct role in its function as a mechanical surface through regulation of its tensile, shear and compressive properties. (10) Though articular cartilage is a metabolically active tissue that maintains its extracellular matrix in a state of constant turnover, not all molecular components are reconstituted at the same rate and variations exist based on the spatial location within the tissue. Degradation and synthesis are concentrated in the regions immediately surrounding the chondrocysts. The turnover of collagen is estimated to be very slow (>100 years), whereas aggrecan turnover is more rapid, with a half-life of 8-300 days in rabbits. (10) Mature articular cartilage is composed primarily of water, approximately 70-80% by weight. The solid fraction of the tissue is primarily collagens (50-57%) and proteoglycans (15-30%), with the remaining balance including minor protein molecules and chondrocysts. This mix of collagens and proteoglycans form an integrated network that provides the basis for the mechanical properties observed in articular cartilage. (10)
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Water is the main fluid component in articular cartilage, most of water is contained in the molecular pore space of the extra-cellular matrix but also permeates throughout the entire tissue. Since cartilage has no vascularity, the chondrocysts obtain nutrients through diffusion from the joint space. As the primary carrier, interstitial fluid plays an important role in transporting both nutrient and waste within the tissue. Fluid permeating the cartilage matrix also has an important mechanical role. Compressive loading is a constant stressor of cartilage, and without a high water fraction, the tissue would breakdown much more quickly under constant use. Short periods of loading and unloading are needed to provide the required high pressure to maintain interstitial fluid flow. This mechanical compression of the cartilage cause rapid pressurization of the fluid in the tissue, which in turn supports the load. This mechanism allows for longevity of cartilage under repeated compression since loading is borne by fluid instead of a solid-solid interaction. In addition, the pressure loads applied to the cartilage creates mechanical, electrical and chemical signals that help direct the synthetic activity of the chondrocytes. As the body ages, however, the composition of the matrix changes and the chondrocytes lose their ability to respond to these stimuli. (10) Collagens: Collagens serve a primary role in the structure of the connective tissue throughout the body. They are comprised of repeating amino acid sequences
(glycine,
proline,
hydroxyproline,
etc.)
and
exhibit
a
characteristic triple helix structure. Collagen type II is the predominant collage type in articular cartilage, comprising over half the dry weight of the tissue. Collagen fiber orientation varies through the depth of the articular cartilage with the superficial zone containing tangentially arranged fibers, the deep zone containing radially oriented fibers and the middle zone having
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both an arcade-like structure and randomly oriented fibers that forms the transition between the other zones. Hyaline cartilage also contains other fibrillar and globular collagen types, such as type V, VI, IX and XI. While the definitive roles of these other collagen types are not fully known, they are believed to play a role in inter-molecular interactions as well as modulating the structure of collagen type II. (10) Proteoglycans: Proteoglycans are large macromolecules comprised of a protein core with attached polysaccharide chains (glycosaminoglycans). The primary proteoglycan in articular cartilage is aggrecan, which consists of a hyaluronana core with numerous glycosaminoglycan side chains. The dominant polysaccharides in this macromolecule are chondroitin and keratan sulfates in mature articular cartilage. The protein core contains several distinct globular and extended domains where glycosaminoglycans attach.
The conglomeration of
many proteoglycans
into
large
macromolecules is critical for proper functionality of cartilage tissue.
(10)
(Figure 7). The presence of carboxyl and sulfate groups gives the proteoglycan mesh a negative charge, which in turn gives the cartilage extracellular matrix a net negative charge known as a "fixed charge density". Because of this charge, the matrix imbibes fluid, swelling the tissue to maintain equilibrium. The swelling is balanced against the elastic restraint of the collagen network. (10)
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F igure 7: Molecular structure of hyaline cartilage matrix. This schematic diagram shows the relationship of proteoglycan aggregates to type II collagen fibrils and chondrocytes in the matrix of hyaline cartilage. A hyaluronan molecule forming a linear aggregate with many proteoglycan monomers is interwoven with a network of collagen fibrils. Quoted from Ref. No. 10.
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Gross features of the hyaline cartilage: The use of hyaline as a descriptor of cartilage derives from the appearance of articular cartilage, which ranges from glossy, slightly translucent white or bluish-white to a slightly yellowish-off-white tissue with advancing age. (11) The hyaline cartilage of both medial and lateral femoral condyles has not a uniform thickness; it is thicker over the posterior aspect of the femoral condyles than the central weight-bearing surfaces. Moreover; there is a focal thinning at the concave surfaced lateral femoral condylar sulcus than the rest of weight-bearing surface. The hyaline cartilage at lateral femoral condylar sulcus is normally measured less than 2 mm thickness. (3, 11)
(Figure 8). The tibial articular cartilage has a uniform thickness, it gradually
thins near the periphery, near the tibial spine and anteriorly. The medial compartment articular cartilage is slightly thinner than the lateral compartment. (3) (Figure 8). The patellar articular cartilage is the thickest articular hyaline cartilage in the body; it has a uniform thickness, and is measured 3- 4 mm in average, but can be as thick as 7 mm. (3, 11) (Figure 9).
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Figure 8: Normal articular cartilage. Sagittal fat-suppressed 3D SPGR MR image shows normal articular cartilage appears as bright signals. Quoted from Ref. No. 12.
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Figure 9: Imaging of patellar hyaline cartilage. Fat saturated gradient T1WI (A) and gradient echo. The articular cartilage appears hyperintense in contrast to hypointense joint fluid. Quoted from Ref. No 13.
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Motion of the knee and relationship of osseous structures: During flexion of the knee: 1. Initiating flexion requires slight medial rotation of tibia, produced by popliteus, to unlock the joint. 2. The patella slides downward on femur. The patello-femoral contact point moves proximally, the contact area broadens to cope with increase stress that accompany progressive flexion. 3. The femoral condyles roll backward on tibial condyles and menisci. The contact point is centered posteriorly, and is smaller than at extension especially at the lateral condyle. (3-6) In full flexion: 1. The posterior surfaces of femoral condyles articulate with posterior tibial condyles. 2. The highest lateral facet of patella is in contact with the anterior part lateral femoral condyle. 3. The odd patellar facet contacts the antero-lateral aspect of the medial femoral condyle. 4. The supporting ligaments are not taut, thus, rotation of the leg is allowed. (3, 5) During motion of extension: 1. The femoral condyles roll forward on tibial condyles and menisci. The area of articular contact enlarges progressively more than at flexion. 2. The lateral femoral condyle being shorter anteroposteriorly than medial, reaches full extension earlier than medial condyle. 3. The medial femoral condyle continues to slide after lateral stops, and rotates slightly medially on the tibial plateau and medial meniscus,
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and tightens the anterior cruciate ligament (ACL), collateral ligaments, and posterior capsular ligaments, turning the knee into a rigid pillar. 4. The patella slides upward on femur, the middle patellar facets contacts the lower half of femoral surface. When full extension of the knee is achieved, the lowest patellar facets are in contact with the femur. (3, 5)
II- INTRA-ARTICULAR NON-OSSEOUS STRUCTURES The intra-articular structures are the anterior cruciate ligament, posterior cruciate ligament, and the medial and lateral menisci. I. Anterior cruciate ligament (ACL): The anterior cruciate ligament (ACL) is intra-capsular, extrasynovial ligament, composed of longitudinally oriented bundles of collagen tissue arranged in fascicular subunits interspersed with fibro-fatty bands within larger functional bands. It originates from the posterior part of the medial surface of the lateral femoral condyle within the condylar notch, posterior to the longitudinal axis of the femoral shaft, it courses anteriorly, medially, and inferiorly (oriented more vertically compared with the intercondylar notch roof), to insert at the anterior aspect of the inter-condylar eminence, medial to the insertion of the anterior horn of the lateral meniscus in a depressed area anterolateral to the anterior tibial spine. The ACL is narrow medial to lateral, but much wider anterior to posterior, and thus is somewhat sheet-like. (5, 14) (Figure 10). The anterior cruciate ligament is a two-bundle ligament, consisting of a small anteromedial and a larger posterolateral bundle. The anteromedial
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bundle forms the anterior border of the ACL, and it is easily damaged. The femoral attachment of the ACL is smaller than tibial attachment site, making it more vulnerable to injury. The tibial attachment site is larger and fan-like, it is considered more secure than the femoral attachment site. The mean length of the ACL is 38 mm and width 11 mm. (14, 15) The anterior cruciate ligament is the primary stabilizer of the knee against anterior tibial subluxation. It remains taut through the range of knee motion. According to biomechanical tests by Noyes et al (1980).
(16)
, it
accounts for approximately 85% of the resistance to the anterior tibial translation when the knee is at 90 degrees flexion and neutral rotation. In addition, it has proprioceptive function as evidenced by the presence of mechanoreceptors in the ligament. These nerve endings may provide the afferent arc for postural changes of the knee through deformations within the ligament. Adachi et al. (2002)
(17)
found a positive correlation between
the number of mechanoreceptors and accuracy of the joint position sense, and recommended preserving ACL remnants during ACL reconstruction. (14, 17, 18)
II. Posterior cruciate ligament (PCL): The posterior cruciate ligament (PCL) is composed of two major parts, a large anterior portion that forms the bulk of the ligament and a smaller posterior portion that runs obliquely to the back of the tibia. It originates from a wide area in the lateral margin of the medial femoral condyle at the inter-condylar notch, it course in a posterior, lateral, and inferior direction to insert in a depression behind the inter-condylar region of the tibia below the joint line, with a slip usually blending with the posterior horn of the lateral meniscus. The posterior cruciate ligament (PCL) is round in cross-section, with mean length is 38 mm, and width is 13 mm.
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PCL is taut only in knee flexion (assuming that the ACL is intact). In extension, the PCL appears thick and curved with its apex posterior (Figure 11A). (14) In 70% of knees, a structure reinforces the PCL, extending from the posterior horn of the lateral meniscus to the femur, known as meniscofemoral ligament. (Figure 11). If it passes behind the PCL, it is known as the posterior meniscofemoral ligament (Wrisberg's ligament), and if it passes anteriorly, it is named the anterior meniscofemoral ligament (Humphrey's ligament). Rarely do both of these structures coexist, but in some instances they are quite large. (3, 14) The posterior cruciate ligament is the primary restraint against posterior tibial subluxation and accounts for 89% of the resistance to posterior translation of the tibia on the femur and that it acts as a check of hyperextension only after the anterior cruciate ligament has been ruptured. (14)
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Figure 10: Normal anterior cruciate ligament (ACL). Sagittal intermediate weighted MR image (ACL denoted by arrows). Note sheet-like appearance of ACL with linear bands of dark signal interspersed with fibrofatty bands of intermediate signal. IFP infra-patellar fat pad, TrML transverse meniscal ligament, pCap posterior capsule. Quoted from Ref. No. 19.
Figure 11: Normal posterior cruciate ligament (PCL) and meniscofemoral ligaments. (A) Sagittal PD image through the PCL shows the uniformly low signals and curved appearance of the PCL (black arrow), the anterior meniscofemoral ligament of Humphry (white arrow). (B) Coronal PD image shows the longitudinal extent of the posterior meniscofemoral ligament of Wrisberg (short black arrow) extends from posterior horn, lateral meniscus (long black arrow) to the medial femoral condyle, the distal aspect of PCL is visualized (P). The popliteo-fibular ligament (white arrow) extends from the fibular head to the popliteus tendon (round tail arrow). Quoted from Ref. No. 20.
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III. Menisci: The menisci are two medial and lateral crescentic, intra-capsular, fibro-cartilaginous laminae that cover one half to two thirds of the articular surface of the corresponding tibial plateau. They are composed of dense collagen fibers that have great elasticity and ability to withstand compression. (3, 5, 21) The medial meniscus is a C-shaped structure larger in radius than the lateral meniscus with the posterior horn being wider than the anterior and is borne to most of the weight applied to the meniscus. The lateral meniscus is more circular. (22) The peripheral edges of the menisci are convex, thick, and attached to the inner surface of the knee joint capsule, except where the popliteus is interposed laterally; these peripheral edges also are attached loosely to the borders of the tibial plateaus by the coronary ligaments. The inner edges are concave, thin, and unattached. The menisci are attached by their anterior and posterior roots to intercondylar area of the tibia. The menisci are avascular except their peripheral portions, which are vascularized by capillary loops from the fibrous capsule and synovial membrane. The inferior surface of each meniscus is flat, whereas the superior surface is concave serving to widen and deepen the tibial articular surfaces that receive the femoral condyles. (3,5) (Figure 12). Meniscal integrity is essential to the normal knee function. They are shock absorbers, joint lubricant (helping to distribute synovial fluid throughout the joint), and joint filler, preventing capsular and synovial impingement during movements. They aid in nutrition of the articular cartilage. They undoubtedly contribute to stability in all planes but are especially important rotary stabilizers. (5)
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Figure 12: MRI of the medial and lateral menisci. Coronal T1 weighted MRI shows: 1. Vastus medialis muscle. 2. Vastus lateralis muscle. 3. Femur. 4. Posterior cruciate ligament. 5. Medial meniscus. 6. Lateral meniscus. 7. Tibia. Quoted from Ref. No. 23.
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The menisci act primarily to redistribute the contact force across the tibio-femoral articulations. This function is achieved through a combination of structural properties of meniscal tissue, shape and attachments of the menisci. The main ligaments that attach the menisci to the tibia are insertional ligaments and deep medial collateral ligament. The meniscal attachment to the femur occurs through the meniscofemoral ligaments and deep medial collateral ligament as well. Additional attachments are driven from fascia covering the popliteus muscle and from the arcuate complex at the posterolateral corner of the knee. The menisci are attached to each other by anterior inter-meniscal ligament. The microstructure of the menisci shows that the collagen fibers are arranged predominately in circumferential orientation, which is directly correlated to the tissue ability to withstand tension. (21) When bearing load, the knee joint is subjected to axial compression. The compression force through the joint is distributed over an articulating contact area resulting in contact stresses (contact pressure). The average stresses are proportional to the load and inversely proportional to the contact area; this means that the larger the contact area over which the load is distributed, the less the contact stresses on the contact area. The geometry and the range of motion of the knee joint do not follow full conformity between the surfaces of contact, and so the possible contact area across the tibial plateau cannot be utilized to result in minimum contact pressure without the menisci. The medial compartment is more congruent than the lateral compartment because the medial femoral condyle articulates over a concave medial tibial plateau, whereas the lateral femoral condyle articulates over a flat or slightly convex lateral tibial plateau. (21)
27
Under no load, contact across the knee occurs primarily on the menisci. With increasing loads, the menisci cover between 59 and 71% of the joint contact surface area around the periphery of the tibial plateau, with direct bone-to-bone contact in the central areas, there is an increasing congruence of articulation and area of contact as well with increasing load, it occurs when the femoral condyles bear down onto the menisci, causing the menisci to extrude radially out of the joint, resulting in decrease in mean contact pressure on the articulating surfaces. In the absence of the menisci, the load is carried by a much smaller area of cartilage and so; the joint contact pressure is significantly increased. This may explain the prevalence of osteoarthritis following meniscectomy and the acceleration of degeneration of the meniscectomised, osteoarthritic joint. (21, 24) It is believed that the menisci move with the tibial plateau during flexion and extension. Yao J. et, al (2008) studied the meniscal displacement and cartilage-meniscus contact behavior in a full extension position and a deep knee flexion position and correlated the meniscal translation pattern with the tibiofemoral cartilage contact kinematics. They found that both medial and lateral menisci were translated posteriorly on the tibial plateau during deep knee flexion, and the lateral meniscal translation was greater than the medial one and the contact areas in deep flexion were approximately 75% those at full extension. (Figure 13). This may aid in better understanding of the mechanism of meniscal degeneration and osteoarthritis associated with prolonged kneeling and squatting. (25)
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Figure 13: The load-bearing knee joint in deep flexion. (a) The posterior horn of the medial meniscus is pushed against the posterior rim of the medial tibial plateau under femoral compression. (b) the posterior horn of the lateral meniscus has moved posteriorly off the lateral tibial plateau. Quoted from Ref. No. 25.
29
III-EXTRA-ARTICULAR SUPPORTING STRUCTURES Extra-articular structures that hold the knee together and give it stability include: medial capsulo-ligamentous complex, lateral supporting structures, and the extensor mechanism and retinacula.
I. Medial capsulo-ligamentous complex: Medial capsulo-ligamentous complex is highly complex structure; it has three layers (superficial, middle and deep layers) that vary from anterior to mid to posterior, with variable merging at different sites. It is considered the primary stabilizer of femorotibial joint in valgus motion and a secondary stabilizer to joint rotation. (26) Superficial Layer: The superficial layer consists primarily of the crural fascia, which is continuous with fascia overlying vastus medialis anteriorly and superiorly. The crural fascia envelops the sartorius muscle and tendon, which in turn contribute to this layer. The semitendinosus, and gracilis tendons, which lie immediately deep to sartorius and superficial fascia, blend with crural fascia and fibers of medial collateral ligament as they insert distally on tibia where they form pes anserinus together with sartorius tendon. (26, 27) Middle Layer:
30
The middle layer is formed from superficial fibers of the medial collateral ligament (MCL). (Figure 14). It is vertically oriented originating from the medial epicondyle and coursing slightly anteriorly to insert on tibia approximately 5 cm below joint line, it measures 12 cm length, 1-2 cm width, and 2-4 mm thickness. There is layer of fat, containing medial inferior genicular artery, lies between superficial MCL and the tibia. The superficial MCL merge with crural fascia anteriorly. Posteriorly, the superficial MCL has a posterior oblique component that extends from middle to deep layer and fuse with the deep layer forming the posterior oblique ligament, which attaches closely to posteromedial portion of the meniscus. The middle layer is reinforced by attachment of semimembranosus tendon, which inserts mainly to the postero-medial tibial plateau and give other attachment to middle and deep layers of medial supporting system. (26, 27) Deep layer: It is a layer of capsular thickening. It is made from the deep fibers of MCL at mid-knee and primarily from the joint capsule anteriorly and posteriorly. The capsule is thickened at mid-knee to form menisco-femoral and menisco-tibial (or coronary) ligaments. The menisco-femoral ligament originates from the outer superior aspect of body of medial meniscus and extends proximally in oblique direction to insert to either the superficial fibers of the MCL or directly to the femur. It measures 1-2 cm long. The menisco-tibial or coronary ligament is shorter (1 cm long), extends from
31
outer inferior aspect of body of medial meniscus to the tibia just distal to joint line and located slightly more posterior than meniscofemoral ligament. The deep layer is continuous anteriorly with the capsule along with the patello-meniscal ligament, which extends anteriorly from meniscus to patellar margin. The capsular layers fuse posteriorly with oblique fibers of superficial MCL without interposed fat, to form the posterior oblique ligament. Also the posterior capsule, but receives fibers from the semimembranosus and oblique popliteal ligament that envelops the posterior aspect of the femoral condyle. (26, 27) II. Lateral supporting structures: Lateral supporting system is a complex structure composed of combination of muscles, tendons, and ligaments, which contribute to lateral stability of the knee, it consists of three layers, superficial, middle, and deep layers.
Superficial Layer: The superficial layer is made of ilio-tibial tract (IT) anteriorly, and superficial portion of biceps femoris posterolaterally. The IT tract originates as a strong band of deep fascia composed of the fusion of aponeurotic coverings of, tensor fascia lata, gluteus maximus, and gluteus minimus muscles. It inserts to Gerdy tubercle at anterolateral tibia near tibial plateau as a main insertion, along with small other attachments to patella and patellar ligament. Ilio-tibial tract has additional insertion arms to the supracondylar tubercle of lateral femoral condyle, and to the intermuscular septum above the knee. (28) The biceps femoris has two heads (long and short), they are joined above knee, with main insertion site to the head and styloid process of the fibula.
32
There are several tendinous and fascial insertional components, including a portion that inserts on posterior edge of IT tract. (28) Middle Layer: The middle layer consists of lateral retinaculum anteriorly, and two ligamentous thickenings originating from lateral patella and attaching at the lateral intermuscular septum, and at the femoral insertion of posterolateral capsule and lateral head of gastrocnemius tendon. (28) Deep Layer: The deep layer forms the lateral part of knee joint capsule; it contains several thickenings that function as discrete structures, the most important ones are the lateral collateral ligament and the arcuate ligament complex. The lateral collateral ligament (LCL) attaches proximally at distal femur just proximal and posterior to lateral epicondyle, slightly proximal and anterior to sulcus for origin of popliteus tendon. It extends posterolaterally to insert on upper facet of fibular head, anterolateral to attachment of fabello-fibular and arcuate ligaments. (28) (Figure 14). The arcuate ligament, is Y-shaped ligament arises from fibular styloid process, just deep to fabello-fibular ligament, its lateral limb courses straight upward along the lateral knee capsule to reach lateral femoral condyle, while the medial limb crosses over the posterior surface of popliteal tendon and attaches to posterior knee capsule, the medial limb, along with the superior popliteo-meniscal fascicle, forms bowed roof of popliteal hiatus. Arcuate may be dominant when fabello-fibular is absent (or may contain fibers of fabello-fibular ligament). (28)
33
Figure 14: MRI of the medial and lateral collateral ligaments. Coronal T1 weighted MRI shows: 1. Vastus medialis muscle. 2. Femur. 3. Vastus lateralis muscle. 4. Posterior cruciate ligament. 5. Anterior cruciate ligament. 6. Medial collateral ligament (superficial fibers). 7. Lateral collateral ligament. 8. Medial meniscus. 9. Lateral meniscus. 10. Tibia. Quoted from Ref. No. 29.
34
III Extensor mechanism and retinacula: Extensor mechanism of the knee is composed of quadriceps muscle and tendon, patella, patellar tendon, and patellar retinacula. (30) Quadriceps: The quadriceps muscle consists of rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius. It has trilaminar tendon with interposed fat, the superficial lamina is formed from rectus femoris, the middle lamina from vastus lateralis and vastus medialis, and the deep lamina from vastus intermedius. Quadriceps tendon inserts on non-articular (anterior) portion of patella. (30) Patellar tendon: Patellar tendon is composed mainly of rectus femoris fibers that course over patella; it extends from inferior pole of patella to tibial tuberosity. It measures 5 cm length (equal to the height of the patella), 2-3 cm width, and 5-6 mm thickness. (30) Medial Retinaculum Complex: It is the medial stabilizer of patellofemoral joint, extending from the patella to vastus medialis. Medial retinacular complex can be divided into superior, mid, and inferior portions, which blend into one another. (A) Superior portion: Made of vastus medialis obliquus muscle and medial patello-femoral ligament. The vastus medialis obliquus is a muscular slip of vastus medialis; arises either from adductor magnus tendon or from adductor tubercle, it inserts at superior medial border of patella, with its aponeurosis being tightly adherent to underlying medial patello-femoral ligament. The medial patello-femoral ligament arises from adductor tubercle adjacent to MCL origin and inserts at medial border of patella. (26, 30)
35
(B) Mid portion: Thin fibers of superficial MCL fascia. (30) (C) Inferior portion: consists of patello-tibial ligament that arises from tibia at level of insertion of gracilis and semitendinosus, and inserts on inferior aspect of the patella and patellar tendon. (26, 30) Lateral Retinaculum: It is the lateral stabilizer of patello-femoral joint, extends from the lateral patella to vastus lateralis. It consists of three layers: A- Superficial: Iliotibial tract and its anterior expansion, supplemented posteriorly by superficial portion of biceps femoris and its anterior expansion. (30) (B) Mid: The retinaculum of quadriceps (vastus lateralis). (30) (C) Deep: Lateral part of joint capsule. (30)
36
Pathophysiology Of Osteoarthritis Osteoarthritis (OA) is the most common forms of arthritis; it is a progressively debilitating significant public health challenge and can be considered as one of the leading causes of disability in elders. This highly prevalent disease occurs when the dynamic equilibrium between the breakdown and repair of the synovial joint tissues become unbalanced. (31) When considering synovial joint is an organ; OA represents failure of that organ, and can be initiated by abnormalities arising in any of its constituent tissue. Early investigators tended to regard OA as an isolated disease of articular cartilage, but although cartilage loss is the prominent feature in the disease, OA is not exclusively a disorder of articular cartilage; the entire synovial joint organ is affected in OA, resulting in structural and functional organ failure. Multiple components of the joint are adversely affected by OA, including the peri-articular bone, synovial joint lining, adjacent
supporting
connective tissue elements and osteochondral
overgrowth (osteophytes). (32, 33) Articular cartilage is one of the few tissues of the musculoskeletal system that is incapable of regeneration, however, the cells of the cartilage and bone are structurally and functionally normal in OA, and if the inciting breakdown mechanism is reduced in early stages in the disease, the joint can restore the damaged tissue to normal. Thus, OA may not be considered exclusively as a degenerative joint disease, there are associated inflammatory articular changes in OA which are secondary process; they are caused by particulate and soluble breakdown products of cartilage and bone. (34)
37
Etiology and risk factors of osteoarthritis: Multiple theories exist regarding the etiology of primary OA; the widely accepted theory is chronic microtrauma that leads to disruption of the articular surface, fibrillation, subchondral cysts, and osteophyte formation. Genetic defect in articular cartilage synthesis contribute in etiology of primary OA. Secondary OA results from healing of major trauma or other predisposing events. (35) Development and progression of OA are best understood as resulting from excessive mechanical stress applied in the context of systemic susceptibility. The increased mechanical stress can be a subsequent of either local mechanical factors or increased joint loading, both of which can increase the likelihood of OA onset or progression. (34) Systemic susceptibility to OA is referred to some intrinsic risk factors that increase joint vulnerability to OA. (36) These factors include: 1. Older age, (majority of individuals over the age of 65 have radiographic and/or clinical evidence of OA), this is probably a consequence of cumulative biologic changes occur with aging such as alteration of cartilage extracellular matrix, cartilage thinning, weak muscle strength, poor proprioception, and oxidative damage, that make the joint less able to cope with adversity. 2. Female gender. The predilection for OA, being more prevalent in women than men, may be explained partly on the basis of the female knee being more mechanically vulnerable to OA. The
38
quadriceps strength is weaker in women than men, and this difference may play a role in increasing postural sway and decreasing joint stability.
(37)
The higher fat mass and lower muscle
mass in women may explain some of the gender difference in OA susceptibility. Other gender differences that have an impact on joint loading include pelvic dimensions, knee morphology, Q angle, and increased ligamentous laxity. (38-40) 3. Nutritional
factors,
particularly
those
that
function
as
antioxidants as selenium and some vitamins. 4. Genetic inheritance (positive family history increases risk). 5. Ethnicity. In general, research suggests some minority groups, as African-American and Hispanic individuals, may be at risk for poorer outcomes (such as pain and disability), compared to Caucasian Americans. But, these racial and ethnic differences in OA and its medical care are poorly understood and research is needed to examine biological, psychosocial, and lifestyle factors that may contribute to these disparities. (41, 42) On the other hand, local mechanical risk factors can facilitate the progression of OA.
(34)
In persons vulnerable to the development of knee
OA, these factors are: 1. Abnormal joint congruity. 2. Malalignment. Varus or valgus deformity is associated with accelerated structural deterioration in the compartment subjected to abnormally increased compressive stress. Varus malalignment has been shown to lead to a fourfold amplification of focal medial knee OA, whereas valgus malalignment has been shown
39
to predispose to two- to fivefold increase in lateral OA progression. Malalignment has consequences beyond the direct effects on cartilage, including alteration in other knee-related tissue which further propagates OA disease and lead to further malalignment, and it is vicious circle that is the major determinant of the rate of structural progression in knee OA.
(43,
44)
3. Occupation: The risk of development of knee OA is greater for men whose jobs required carrying, kneeling or squatting more than for those whose jobs did not require these physical activities. (45) 4. Muscle weakness particularly the quadriceps. (46) 5. Alteration in the structural integrity of the joint environment such as knee laxity which is considered as a potential risk factor for knee OA, it is suggested that increased laxity of knee OA may precedes and predispose to disease development. (47) The articular surface plays an essential role in load transfer across the joint and there is good evidence that conditions that produce increased load transfer and/or altered patterns of load distribution can accelerate the initiation and progression of OA. (48) Joint loading can be affected by: 1. Obesity: Obesity and overweight have long been recognized as potent risk factors for OA, especially of the knee. It is usually accepted that mechanical loading contributes to joint destruction in obese patients; recent advances in the physiology of adipose tissue add further insights in understanding the relationship between the obesity and OA. The positive association between obesity and OA is observed not only for knee joints but also for
40
non-weight bearing joints, such as hands. This is may be explained by understanding the role of extra-articular adipose tissue in OA related inflammatory process, through release of inflammatory mediators as cytokines and adipokines which occur in high concentration in obese patients.
(49-51)
2. Joint injury (either acutely as in sporting injury or after repetitive overuse such as occupational exposure), particularly an intraarticular fracture, meniscal tear requiring meniscectomy, and anterior or posterior cruciate ligament injury. (52, 53) The human knee is a complex joint having three compartments: the patellofemoral, and the medial and lateral tibiofemoral joints. The medial compartment is subjected to more stress than the lateral compartment, which may account, In part, for why OA affects the medial tibiofemoral compartment in men and women, 75% of knee OA affects the medial compartment as opposed to 25 % affecting the lateral compartment. (54) General pathological features in osteoarthritis: Generally, OA begins as fatigue fracture of the collagen meshwork followed by increased hydration of the articular cartilage, (as opposed to desiccated cartilage seen with aging). (35) Pathological and molecular changes in osteoarthritic cartilage include: •
Fibrillation of the cartilage with resultant weakening of type II collagen network and increased water contents, followed by deep clefts and regeneration/proliferation of chondrocytes.
41
•
Articular cartilage thins and is fissured in areas of maximum mechanical stress.
•
Proliferative osteochondral changes occur at the joint margins and in the femoral notch with formation of marginal and nonmarginal (central) osteophytes.
•
Incidental ACL tear or failure with a reported prevalence ranging from 20 to 35 %. ACL failure occurs as a result of alteration of femoral notch width and depth, and the presence of notch osteophytes. (55)
•
Increased subchondral plate thickness with development of subchondral bone cysts. This occurs in the region of the so-called tidemark, located at the junction of the articular hyaline cartilage and adjacent subchondral bone, where there is a remnant of calcified cartilage. As OA progresses, vascular invasion and advancement of this zone of calcified cartilage into the articular cartilage occur that further contributes to a decrease in articular cartilage thickness and may lead to modification of the contours of articulating surfaces. These changes make the subchondral bone less compliant; as a result, the remaining cartilage is subjected to greater stress, which accelerates further cartilage loss. (56)
•
Compression of weakened bone with variable degrees of collapse.
•
Loose bodies are followed by fragmentation of osteochondral surfaces.
•
Synovial hypertrophy which can cause joint pain by nerve stimulation.
42
•
Synovial fluid with subsequent increasing intraarticular pressure and stretching the joint lining, causing pain.
•
Increased levels of degrading enzymes including matrix metalloproteinases, collagenase, gelatinase, and stromelysin.
•
Loss of proteoglycans from the matrix into the synovial fluid.
•
Associated abnormalities include deformities, subluxations, ankylosis and loose bodies with catching and locking.
Gross pathologic features: •
The cartilage is degraded with fissured and/or ulcerated surface, and loss of surface sheen.
•
Subchondral geodes (cysts) containing variable amounts of debris.
•
Buttressing osteophytes to increase surface area.
•
Articular surface collapse. (56)
Microscopic Features •
Diminution
of
chondrocytes
in
superficial
zones
with
chondrocyte swelling that progress to cell death. The matrix chondrocytes demonstrate proliferation in clusters (brood capsules). (Figure 15). •
Diminished capacity of the chondrocyte to respond to anabolic stimuli and its capacity to remodel and repair the cartilage extracellular matrix.
•
Decreases in size and structural organization of aggrecan and diminution of its content in the extracellular matrix, with accumulation of advanced glycation end products. This can
43
enhance collagen cross-linking and likely is a significant contributing factor to the increase in cartilage stiffness and altered biomechanical properties that has been observed with aging. •
(57)
(Figure 15. c).
Loss of cartilage matrix ability to stain with Alcian blue or safranin O.
•
Neovascularity penetrates layer of calcified cartilage and new chondrocytes extend up from deeper layers. (Figure 15. b).
•
Hypertrophied synovium becomes folded into villous folds with variable infiltration of plasma cells, and lymphocytes. The effects
of
synovial
inflammation
likely
contribute
to
dysregulation of chondrocyte function in remodeling the cartilage extracellular matrix. (58) Pathological staging of articular cartilage damage: •
I: Edema.
•
II: Articular fissuring. (Figure 15. b).
•
III: "Crabmeat" changes, in the form of white fronds resemble crabmeat.
•
IV: Full thickness defect and subchondral erosions. (59)
44
Figure (15). Microscopic pathology of OA articular cartilage. The photomicrographs are taken from different areas of the same specimen: (a), early OA; horizontal fibrillation, (arrow); chondrocyte clusters, c. (b), moderate OA, vertical fissure, arrow; chondrocyte death, (open arrow); tidemark undulation and duplication, (arrow head); vascular penetration into cartilage, v; chondrocyte clusters, c. (c), advanced OA, with cartilage erosion; cartilage matrix disorganization; and chondrocyte clusters, c. Hematoxylin and eosin stain, magnification 40. Quoted from Ref. No 59.
45
Imaging Of Knee Osteoarthritis Imaging modalities of the knee joint: 1. Plain radiography. 2. Ultrasonography. 3. Computed tomography (CT) and CT arthrography. 4. Magnetic resonance imaging (MRI) and MR arthrography.
1. Plain radiography: Conventional radiography is the simplest and least expensive method for imaging knee joint affected by OA. It is used in clinical practice in patients to establish the diagnosis of OA and to monitor the progression of the disease. Radiographs clearly visualize bony features, including marginal osteophytes, subchondral sclerosis, and subchondral cysts that are associated with OA and provide an estimate of cartilage thickness and meniscal integrity by the interbone distance or joint space width. The radiographic definition of OA mainly relies on the evaluation of both osteophytes and joint space narrowing (JSN). Because osteophytes are considered specific for OA, develop at an earlier stage than JSN, and more easier to ascertain than other radiographic features, they represent the widely applied criterion to define the presence of OA.
(60, 61)
However,
assessment of OA severity mainly relies on JSN and subchondral bone lesions. In addition, progression of JSN is the most commonly used criterion for the assessment of OA progression. Traditionally, the progression of knee OA in clinical trials has been assessed by measuring changes in joint space width between the medial femoral condyle and medial tibial plateau, as the medial compartment is the most common site of involvement in knee OA. The severity of OA can be estimated using semi-quantitative scoring
46
system, including the most widely employed Kellgren and Lawrence (KL) grade classification.(62) (Table 1). The KL grade scoring system suffers from limitations based on the invalid assumptions that changes in radiographic features (such as osteophytes and JSN) are linear over the course of the disease and that the relationship between these features is constant. Bilateral weight bearing AP view of both knees in full extension (The extended knee radiograph) has been the conventional plain radiograph employed to image the tibio-femoral joint. It remains an accepted radiographic technique for characterizing the bony changes in OA such as osteophytes and subchondral sclerosis, but this technique is limited as a means by which to visualize reproducibly the radiographic joint space.
(63)
The sine qua non for accurate measurement of radiographic joint space width is a reproducible image of joint space. In majority of patients, with full extension of the knee in weight bearing extended knee radiograph, there is tibial plateau tilt that is skew and not parallel to a horizontal x-ray beam, this skewed radio-anatomic alignment of the tibial plateau can significantly precludes accurate measurement of
minimum joint space
width. (64, 65) (Figure 16A). Some authors demonstrated that individualized flexion of the knee to achieve superimposition of the anterior and posterior margins of the medial tibial plateau that was confirmed under fluoroscopy before image acquisition resulted in measurement of medial tibiofemoral joint space width in repeat AP radiographs that were significantly more reproducible that those obtained from concurrent extended knee radiographs. Since then, so-called parallel radio-anatomic alignment of the medial tibial plateau has been a goal of developers of alternative protocols for standardized knee radiography. (66) (Figure 16B).
47
Grade of Osteoarthritis
Description
0
No
1
osteoarthritis.
2 3 4
radiographic
findings
of
Minute osteophytes of doubtful clinical significance. Definite osteophytes with unimpaired joint space. Definite osteophytes with moderate joint space narrowing. Definite osteophytes with severe joint space narrowing and subchondral sclerosis.
Table 1: Kellgren-Lawrence grading scale of osteoarthritis of knee joint.
(B) (A) Figure (16) Skewed (A) and parallel (B) radioanatomic alignment of the medial tibial plateau. There is apparent displacement of anterior and posterior margins of medial tibial plateau in A. while B shows superimposition of the anterior and posterior margins of the plateau. Qouted from Ref. No. 63.
48
Various protocols for standardized radiographic examination of the knee include fluoroscopically and non-fluoroscopically assisted protocols. Semiflexed AP view is a fluoroscopically assisted protocol using a small degree of flexion (7-10o) in order to compensate for the normal sloping of the medial tibial plateau. The foot with is rotated internally or externally, as needed, to center the tibial spines beneath the femoral notch. The net result is more precise estimation of the joint space width than those obtained from extended knee view. (66) Lyon schuss view is an alternative fluoroscopically assisted PA view that use schuss position in which there is coplanar alignment of anterior aspect of the thigh, the patella, and tip of the great toe against the cassette, the degree of flexion is with greater (20-35o), and the x-ray beam is angled caudally to compensate for the effect of flexion on the orientation of tibial plateau relative to the horizontal plane. (67) Semiflexed metatarsophalangeal (MTP) view is an alternative nonfluoroscopically assisted view, it is a PA radiograph of both knees with standing so that the MTP joints of both great toes are directly beneath the front of the cassette, with knee flexed slightly until the patellae are in contact with the cassette directly above the MTP joints. The degree of flexion is small and fixed (7-10o) with 15o foot rotation. (68) Fixed-Flexion view is PA view requiring schuss position as in Lyon schuss view, with fixed degree of flexion (20-35o), 10o foot rotation and 10o caudal x-ray beam angulation. (69)
49
2. Ultrasonography: Ultrasonography of joints is well developed and become part of mainstream practice. It require higher frequency probes (>7.5 MHz) for superficial joints.
Ultrasonography has limitations for assessing joint
disease, particularly OA, because of limited sonographic window precluding visualization of most articular cartilage lesions and inability of ultrasonography to demonstrate intrinsic bone abnormalities, such as marrow lesions, cysts, and sclerosis. (70) It is recommended that the knee initially be imaged with the patient supine in neutral position or slightly flexed position for lateral and anterior images, then in prone position for posterior images. Maximal flexion aids to visualize the trochlear cartilage. Standard scans should include imaging in transverse and longitudinal planes of the supra-patellar region, infra-patellar region, and posterior knee medially and laterally. The knee also should be imaged longitudinally over the medial and lateral aspects of the joint. (71) In knee OA, ultrasonography can define the following signs: •
Synovial hypertrophy: Common finding visualized as either flattened, thickened synovium, or frond-like protrusions into the supra-patellar pouch or in lateral and medial recesses. Increased vascularity can be seen using color Doppler signals, and this has been shown to correlate with articular inflammatory changes.(72) (Figure 17A).
•
Effusion: Synovial fluid is easily detected in the suprapatellar pouch especially with dynamic maneuver or in lateral and medial recesses as they may be the only sites of synovial hypertrophy or effusion. (Figure 17A).
50
•
Osteophytes: Commonly seen around the medial and lateral joint line, either at femoral or tibial side of the joint. Other relatively common place is over the distal femoral condyles with full knee flexion. Osteophytes appear as a single or multiple characteristic irregularities of the bone profile, located at the edges of the joint surface. (73) (Figure 17B).
•
Cartilage pathology: Can be appreciated in the trochlea of the femur with full flexion of the knee. Changes such as thinning or irregularity in thickness, heterogeneity, and loss of clarity of the cartilage margins have been described.
(73)
(Figure
17C). •
Meniscal pathology: The peripheral superficial aspects of menisci can be visualized allowing some meniscal pathologic conditions to be seen such as cysts, extrusion and horizontal tears. Meniscal extrusion is a significant component of JSN associated with displacement of the collateral ligaments. (Figure 17B).
51
(A) (B)
(C) Figure (17) Ultrasonographic features in OA. (A) sagittal ultrasonographic image of the supra-patellar pouch demostrates the cortical (arrows) bone of the patella (p) and distal femur (f) and quariceps tenodn (d), hypoechoic synovial fluid (sf) and villous synovial hypertrophy (*). (B) Longitudinal ultrasonographic image of gthe medial joint line demostratesmedial meniscal extrusion (m) with displacement of the medial collateral ligament (arrows) and obvious osteophytes (*) at boyth sides of the joint. (C) Coronal image over the distal femur in full flexion shows pathologic cartilage band, with irregular thickness, increased echogenicity, and loss of clarity of the cartilage margins. Qouted from Ref. No. 70.
52
3. Computed tomography: Although radiograph is the first imaging tool in suspected OA, it suffer from inability to detect non-osseous pathologic changes seen in OA, the joint space can appear normal although there is cartilage pathology. CT was evaluated as an additive tool; it is superior to conventional x-ray in bony assessment, as it can appreciate bony changes in greater details, such as early small subchondral cysts and subtle osteophytosis, especially if osteophyte is located in posterior medial femoral condyle. However, hyaline cartilage and soft-tissue structures lack adequate tissue contrast in CT to be detected owing to volume averaging effect of adjacent large volume of bony structures. (74)
CT arthrography: CT arthrography represents an attempt made for better delineate cartilage lesions using intra-articular contrast, benefited from development of multiplaner capability of helical or multi-detector raw CT. CT arthrography can be performed using either a single (iodine) or double contrast (iodine and air) technique, however single contrast CT arthrography is easier to perform and less painful, in addition to poor air penetration into cartilage lesions compared with that of fluid. Dilution of the contrast material can be achieved with local anesthetics or saline to avoid beam hardening artifact. Nevertheless, the dilution mainly depends on the radiologist preference. (75, 76) The CT acquisition parameters include narrow collimation, low pitch value, and a high milliampere-second value to obtain high resolution isotropic multi-planar reformats. The reconstruction use bone algorithms, providing high spatial resolution images. Metallic artifacts usually remain mild on new generation CT scanners. (77)
53
The normal hyaline cartilage appears as a low attenuating structure, with no variation of its density, cartilage surface appears smooth and continuous. CT arthrography is an accurate method for evaluation of cartilage thickness benefited from high contrast between the low attenuating cartilage and high attenuating boundaries (the subchondral bone and contrast material filling the joint), it is more accurate in demonstrating cartilage thickness than non-contrast MRI including cartilage sensitive sequences as spoiled gradient recalled echo (SPGR) as shown by cadaveric studies on the ankle.
(77, 78).
When comparing CT arthrography with MR
arthrography, CT arthrography and MR arthrography are equally accurate in measuring the articular cartilage thickness, so CT arthrography is spared for non-availability of MR arthrography or in claustrophobic patients. (79) Focal surface cartilage lesions are well depicted with CT arthrography even with thin lesions, they appear as areas filled with the intra-articular contrast material with high image contrast and resolution leading to high degree of confidence in diagnosing such lesions and a high inter-observer reproducibility. (80) (Figure18).
Figure (18). CT arthrography of the knee, cleary shows filling of a chondral defect (arrow head) by contrast in lateral patelar facet. Qouted from Ref. No. 81.
54
4. Magnetic resonance imaging (MRI): Currently, MRI is the method of choice for non-invasive diagnosis of chondral lesions; it is the only non-invasive technique that allows the evaluation of surface lesions, subchondral changes, and the structure of the cartilage. MRI has added much to the understanding of all the joint tissues involved by OA. Whole organ MR imaging protocols are available in new MR machines to assess all tissues affected by OA, these protocols include morphologic and physiologic sequences. The current standard field strength is 1.5 tesla (1.5-T) imaging, and most of the studies establishing MR imaging for assessment of OA, including semiquantitative and quantitative parameters, were performed and concluded at this field strength, and although 1.5-T imaging is standard, 3.0-T MR imaging allow better evaluation of articular cartilage lesions of the knee joint. (82, 83) In addition to field strength, dedicated surface coil for the knee is important prerequisite to achieve good image quality and visualization of the joint tissues involved in OA. Currently, most surface coils are multichannel phased-array coils that give high signal to noise ratio (SNR) and allow parallel imaging which can provide short acquisition time by maintaining image quality. With parallel imaging, each of the coil channels provides image information separately, and then the information is fused to obtain one image. (84) Sequence protocols: Because different tissues are involved in OA, a number of different sequences have been tailored and developed for whole organ assessment of OA. The workhorse sequences for morphologic imaging of knee joint are fast spin echo (FSE) sequences, particularly fluid sensitive sequences that
55
have been found useful to assess cartilage, bone marrow, ligaments, menisci, and tendons. (84) Most experience and good results in morphologic imaging of the cartilage and subchondral pathology were gathered with: 1. Two-dimensional (2D) proton density (PD), intermediate weighted (IM), T2 weighted FSE. Additional fat suppression was found useful to visualize cartilage pathology better and to reduce chemical shift artifacts. 2. Three-dimensional (3D) fast low-angle shot (FLASH) gradient echo or spoiled gradient recalled echo (SPGR). 3. Other sequences that asses the morphology of the articular cartilage as 3D double-echo steady state sequence (DESS), driven equilibrium Fourier transform (DEFT) and steady-state free precision (SSFP) imaging. (84) 1. Intermediate- and T2-weighted fast spin echo sequences: The sequence frequently used for OA assessment in clinical practice is IM-weighted fat-suppressed (FS) fast spin echo (FSE) sequence; it is easy to use practically applicable, allowing good visualization of cartilage defects, the pattern of bone marrow edema, menisci, and tendons. The standard parameters used for this sequence are a repetition time (TR) of 3000 to 4000 milliseconds; an echo time (TE) of 30 to 60 milliseconds; and an echo train length of 8. This chosen TE range provides higher intrinsic contrast of the cartilage and it is less prone to magic angle effects than true PD-weighted pulse sequences obtained at shorter TE. (84) With IM- and T2-weighted FSE sequences, normal hyaline cartilage has intermediate signal intensity, and fluid is bright, allowing good contrast to identify surface abnormalities as well as pathologies of the cartilage matrix. Diagnostic efficacy of fast spin echo MRI including fat suppressed
56
IM-weighted FSE sequence in articular cartilage abnormalities in osteoarthritic knee was studied by Saadat and colleagues (2008)
(85)
using
3.0-T MR imaging and histology as standard of reference, they concluded that fat suppressed IM-weighted FSE sequence is useful in assessing cartilage thickness and surface lesions, but the changes in cartilage signals were found to be of limited value and not useful for characterizing the severity of cartilage degeneration and softening. (85) Multiple clinical studies have found IM- and T2-weighted FSE sequences have high sensitivity and specificity is assessing tissue abnormalities that may be related to OA. (85- 87) The diagnostic performance of cartilage lesions improve when different imaging planes are used. Bredella and colleagues (1999)
(88)
studied how the use of a combination of different imaging planes affects the detection and grading of articular cartilage defects in the knee. They found that the sensitivity of a sagittal T2-weighted FSE sequence was only 40% and the specificity was 100%. The sensitivity of a combination of axial and coronal fat-suppressed T2-weighted FSE sequences and sagittal T2weighted FSE sequence was 94%, specificity was 99%, and accuracy was 98%, using arthroscopy as a reference standard. (88) 2. Three-dimensional spoiled gradient-echo and fast low-angle shot sequences: 3D SPGR and FLASH sequences are among the most frequently used sequences, they are well suited for depicting the cartilage volume and, to some extent, the cartilage surface. Sequence parameters used to visualize cartilage are in the range of TR: 20 to 35 milliseconds, TE: 7 to 12 milliseconds, and flip angle: 12 to 30o; parameters need to be optimized according to the field strength. The bright signals of cartilage in the SPGR and FLASH images limits the visualization of internal pathology to some
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extent; fissures, for example, may not be well visualized. These gradientecho sequences are not suited for visualizing bone marrow pathology, ligaments, and tendons. They have been found useful, however, in segmenting cartilage for quantitative measurement of volume and thickness. (89)
When comparing SPGR with IM- and T2-weighted FSE sequences, similar overall diagnostic performance in detecting focal cartilage lesions is the result. 3D SPGR and FLASH sequences provide high spatial resolution but usually require fairly long imaging time, and motion artifacts can degrade image quality. These gradient-echo sequences also are very sensitive to susceptibility artifacts, a consideration after previous surgery and in particular after cartilage repair. (90) Water selective cartilage scan (WATS-c) and water selective fluid scan (WATS-f) are 3D T1-fast field echo with water excitation for cartilage imaging and 3D fast field echo with water excitation for fluid imaging respectively, they are alternative 3D gradient-echo sequences using water excitation technique for fat suppression instead of fat saturation, similar to the water excitation 3D FLASH scan. WATS-c and WATS-f are proved to be more helpful in characterizing high grade articular cartilage defects, than do fat suppressed PD. WATS-f sequence can shows articular surface lesions such as cartilage fissure and delamination more conspicuously than do WATS-c sequence, as WATS-f, being a fluid sensitive sequence, has good synovial fluid-to-cartilage contrast. (91, 92) Advantages of water excitation compared with the conventional fat saturation technique include: •
The acquisition time is significantly decreased (by up to 50%).
•
Greater signal-to-noise ratio and contrast-to-noise ratio.
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•
Better uniformity of fat suppression as water excitation technique is less sensitive to magnetic field inhomogeneity.
•
Reduction of foldover and metallic artifacts.
•
Better overall image quality with more conspicuousness of cartilage lesions. (91, 93)
3. Other sequences: A number of sequences have been developed to improve morphologic depiction of cartilage. These sequences include 3D doubleecho steady state sequence (DESS) which has shown good results in detecting cartilage lesions. This sequence utilizes mixed T1/T2*-weighting that provides high spatial resolution with the cartilage appearing more intermediate in signals. It is as useful as 3D FLASH in detecting cartilage surface lesions, and sensitive to cartilage softening. (94) In addition, the driven equilibrium Fourier transform (DEFT) and steady-state free precision (SSFP) imaging. DEFT imaging makes use of a much higher cartilage-to-fluid contrast; the signal of synovial fluid is higher than in SPGR sequences, and the signal of cartilage is higher than in T2weighted FSE sequences. It is similar to SPGR and IM-weighted FSE sequences in detection of cartilage defects with high sensitivity but with relatively low specificity. (90) Steady-state free precision (SSFP) imaging has been described as an efficient, high signal method for obtaining 3D images and may be useful for depicting cartilage, because cartilage signals is higher than in conventional sequences. SSFP-based techniques show higher signal-to-noise ratio and contrast-to-noise ratio than SPGR. (95) Although DEFT, SSFP, and 3D-DESS sequences have demonstrated successful results for detecting chondral lesions, these are not widely used in most clinical settings, they show variable reported sensitivities and
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specificities for the evaluation of chondral defects in different study settings. (96)
Quantitative imaging of molecular composition and cartilage matrix: In addition to assessing cartilage pathology, thickness, and volume, recent studies have shown the potential of MR imaging parameters to reflect changes in the biochemical composition of cartilage with early OA. These techniques include T2 quantification, T1rho quantification, and delayed gadolinium-enhanced MR imaging of cartilage (dGEMRIC).
These
techniques allow characterization of the cartilage matrix and, quality before morphologic damage occurs. (97-99) T2 quantification: T2 is an MR relaxation time reflecting interactions between water molecules and between water and surrounding macromolecules; increased interaction results in decreased T2. T2 is affected by many physiologic and pathophysiologic processes that relate to the state of cartilage. T2 is sensitive to changes in hydration or, nearly equivalently, collagen concentration, and orientation of the highly organized anisotropic arrangement of collagen in the extracellular matrix. (100, 101) The signal intensity of normal cartilage in T2 map varies with depth from the articular surface. Regional and zonal differences in density and structural organization of the type II collagen matrix are primarily responsible for this variation in cartilage T2. Near the bone cartilage interface, densely packed collagen fibrils are preferentially aligned perpendicular to the subchondral cortex. In this region termed the radial zone, the high density and anisotropic orientation of collagen fibrils provides efficient T2 relaxation, leading to low signal intensity on proton density or T2 weighted images. Closer to the articular surface, less fibril
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anisotropy and oblique orientation of the collagen matrix in the transitional zone lead to gradual increase in T2 relaxation time and thus a relative increase in signal intensity on T2 weighted images. At the articular surface, collagen fibers are oriented parallel to the articular surface, it is too thin to resolve on routine clinical MR imaging. (102) T2 maps of osteoarthritic cartilage are heterogeneous, with elevated T2 values associated with cartilage damage due to relative increased hydration. There does not appear to be a linear relationship between T2 and OA grade. Several studies have shown that T2 can be used to differentiate normal from mildly degenerated tissue, but cannot be used to differentiate between mild and more sever grades of OA. The current interpretation of the T2 changes is that a loss of collagen anisotropy with early damage produces an initial rise in cartilage T2; with further cartilage degradation there is an increase in T2 heterogeneity but no further elevation in T2. As such, it may ultimately be that cartilage T2 values will be useful to identify individuals with sites of early disruption of the collagen matrix, but may be inappropriate as a marker for radiologically observable disease progression. (102)
T1rho quantification: T1rho (T1ρ) is spin-lattice relaxation in the rotating frame and is similar to T2 relaxation except that there is an additional radiofrequency (RF) pulse applied after the magnetization is tipped into transverse plane. The magnetization becomes aligned or “spin-locked” with the applied RF field. The signal decay is exponential with a time constant, T1ρ, and is typically calculated from multiple images by changing the duration of the spin-locking pulse. In liquids, T1, T2, and T1ρ relaxation times may be similar, but in tissue these values are typically different (T2< T1ρ 66%. The marrow signal within the osteophytes was not scored.
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2. Articular cartilage Two separate cartilage scores were performed in each of the subregions excluding the subspinous region using simple ruler measurements: -
The first score was for the size of area affected that harbor any cartilage loss (either partial or full thickness loss).
-
The other was for the full thickness cartilage damage regardless of its morphology.
Each articular cartilage subregion was assessed using both scoring systems and graded as follow: 0: none, 1: 75% of region of cartilage surface area. The study used PD SPAIR, 3D WATSc and multiple fast field echoe (mFFE) sequences for cartilage evaluation.
Figure (23):. Simple ruler measurement of hyaline cartilage defect.
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3. Osteophytes The present study scored the osteophytes for their protuberance size and how far they extend from the joint, rather than their total volume, the largest osteophyte was scored within a given location, 12 specific locations were assessed for osteophyte scoring:. 1. Medial trochlea (axial/sagittal plane). 2. Lateral trochlea (axial/sagittal plane). 3. Central medial femoral condyle (coronal plane). 4. Central lateral femoral condyle (coronal plane). 5. Central medial tibia (coronal plane). 6. Central lateral tibia (coronal plane). 7. Posterior peripheral and posterior central margins of medial femoral condyle (axial/sagittal plane). 8. Posterior peripheral and posterior central margins of lateral femoral condyle (axial/sagittal plane). 9. Medial margin of the patella (axial plane). 10. Lateral margin of the patella (axial plane). 11. Superior margin of the patella (axial plane). 12. Inferior margin of the patella (axial plane). For posterior medial and posterior lateral femoral condyles, the larger osteophyte for either peripheral or central location was scored. Osteophyte grading was: Grade 0 = none; Grade 1 = small; Grade 2 = medium; Grade 3 = large.
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Figure (24). Scoring of osteophytes. A. Grade 1 osteophyte medial femur. B. Grade 2 osteophyte lateral femur. C. Grade 3 osteophyte lateral femur quoted from Ref. No. 115. 4. Hoffa’s synovitis and effusion- synovitis Synovitis induced Hoffa’s fat pad signal changes, were assessed for presence of diffuse hyperintense signal on T2/PD-fat suppressed sequences within the fat pad. Hoffa-synovitis score was performed on sagittal images giving a single score for the degree of hyperintensity. Hoffa's synovitis score was based on size: 0 = normal; 1 = mild, 2 = moderate, 3 = severe. Effusion-synovitis was scored on axial T2/PD-fat suppressed sequences for presence of fluid equivalent signal within the joint cavity that represent a composite of effusion and synovial thickening. Scoring of effusion excluded any paraarticular cysts or ganglia. It was graded regarding its size and associated capsular distension: Grade 0: physiologic amount, Grade 1: small fluid in retro-patellar space, Grade 2: medium size with minimal convexity in supra-patellar bursa, Grade 3: large amount distending the joint capsule.
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Figure (25). Effusion-synovitis. A. Grade 0. B. Grade 1. C. Grade 2. D. Grade 3 quoted from Ref. No. 115.
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5. Meniscus The meniscus position change which is termed subluxation or extrusion was scored; the medial meniscus was scored for medial extrusion on coronal image relative to medial tibial margin excluding any osteophytes and for anterior extrusion on sagittal image relative to medial tibial margin excluding any osteophytes, the scoring was performed where extrusion is maximum. The lateral meniscus was also scored for lateral extrusion on coronal image relative to lateral tibial margin excluding any osteophytes and for anterior extrusion on sagittal images excluding any osteophytes, scoring was performed where extrusion is maximum. Grading for extrusion: Grade 0: < 2 mm; Grade 1: 2-2.9 mm, Grade 2: 3-4.9 mm; Grade 3: > 5 mm. The meniscal morphologic changes in both medial and lateral menisci were scored at the anterior, body and posterior horn as presence or absence (Y/N) of the following morphologic features: 1) Signal (not extending through meniscal surface): Y/N. 2) Vertical tear (includes radial and longitudinal tears): must extend to both the femoral and tibial surfaces as high signal on at least two slices. Y/N. 3) Horizontal and radial tear: must extend from the periphery of the meniscus to either a femoral or tibial surface on at least two slices. Y/N. 4) Complex tear: as defined by high signal that extends to both the tibial and femoral surfaces and ≥ 3 points on those surfaces). Y/N. 5) Root tear (posterior horn): Y/N. 6) Partial maceration: as defined by loss of morphological substance of the meniscus, with or without associated increased signal in the remaining meniscal tissue. Y/N.
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7) Complete maceration: No meniscal substance was visible. Y/N. 8) Meniscal cyst: Y/N. 9) Meniscal hypertrophy is defined as definite increase in meniscal volume in given subregion when compared to normal: Y/N. The scoring was performed using PD fat-suppressed images in both coronal and sagittal planes
6. Ligaments The definite complete tear of the anterior cruciate ligament was recorded as either present or absent, whereas partial tears were scored as “normal” according to MOAKS. Score: normal = 0, complete tear = 1. The associated BML/cyst at site of ACL insertion or origin and ACL repair as well were scored as presence or absence Y/N. The posterior cruciate Ligament score: normal 0, complete tear = 1. The associated BML/cyst at site of insertion or origin was also scored as presence or absence Y/N. The patellar tendon score: 0: no signal abnormality, 1: signal abnormality present.
7. Peri-articular features The study scored the presence or absence of the following periarticular abnormality: 1. Pes anserine bursitis. 2. Ilio-tibial band signals. 3. Popliteal cyst. 4. Infra-patellar bursal fluid signal. 5. Pre-patellar bursal fluid signal. 6. Ganglion cyst.
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7. Loose bodies. Statistical analysis Results of MOAKS scoring system were recorded, tabulated and statistically analyzed. Descriptive statistics were done for all data. Data were represented as means ± standard deviations (SD) or numbers and percent [N (%)]. Comparison between different groups was done using Mann Whitney test and chi-square test where appropriate. Correlation analysis between MOAKS joint features with each other and with Lequesne pain index score was done. Spearman correlation coefficient (r) was assessed: r value < 0.2 was considered very low and probably meaningless. r = ≥ 0.2 < 0.4 was considered low correlation that might warrant further investigation. r = ≥ 0.4 < 0.6 was considered reasonable correlation. r = ≥ 0.6 < 0.8 was considered high correlation. r = ≥ 0.8 was considered very high correlation. Statistical analyses were performed using the MegaStat system for Windows (version 10.0; MHHE Institute, Orris, JB). P value
