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Although the mechanical properties of cartilage are functions of the extracellular matrix, it is the chondrocyte that directs the synthesis and composition of the matrix. Though few in number, chondrocytes also mediate critical pathways of regeneration and growth by highly regulated signal transduction pathways that are now becoming better understood [2, 3]. However, cartilage neoplasms, especially the benign forms, are among the most common primary tumors of bone and illustrate the close association between radiologic and pathologic findings.

Perichondrium is a layer of dense fibrous tissue that covers cartilage in most locations except the articular surfaces. No neurovascular structures penetrate beyond the perichondrium. Consequently, all nutrition arrives by diffusion, limiting the thickness of cartilage surfaces to a few centimeters - a rule that manifests in even the largest animals.

As cartilage ages, it transforms from bluewhite to yellowish and opaque, which may be related to dehydration and age-related pigment deposits [4]. Cartilage is attached to the underlying bone by means of radial collagen fibers that penetrate from bone into the cartilage over a complex three-dimensional interface. However, the specialized collagen fibers of cartilage do not extend into subchondral bone. A specialized type of hyaline cartilage is also present in the epiphyseal plate growth plate.

Fibrocartilage is present in the temporomandibular and sternoclavicular joints and the annulus fibrosus of the intervertebral disk as well as the meniscus at the knee and the labrum of the shoulder. Finally, elastic cartilage is largely restricted to the external ear and a few other sites. All cartilage is ideally suited to resist compressive forces. However, the presence of type I collagen and elastin in fibrocartilage and elastocartilage, respectively, also allows these tissues to resist tension. Although the anatomy of cartilage differs somewhat depending on subtype, articular cartilage is the most common and best studied in terms of biochemical and histologic features.

Link ed. Horvai Fig. Hyaline cartilage, in young patients, can be seen in the articular surface and growth plate a and is usually a translucent blue-white rubbery material a. With aging, the articular surface becomes more opaque and yellow-white b. In articular cartilage, water is unevenly distributed such that the highest concentration is present at the articular surface [6].

The constant diffusion and tidal movement of water in and out of the cartilage matrix with joint compression allow nutrients to reach the chondrocytes. Proteoglycans are composed of high molecular weight proteins with carbohydrate side chains resulting in large, charged molecules that attract water thereby increasing their volume dramatically. In cartilage, type II collagen encoded by the COL2A1 gene predominates and confers the tensile stiffness and strength to the matrix [7, 8]. The expansive pressure of water within the matrix is opposed by the collagen cross-links that restrict expansion and result in a steady-state turgor pressure.

This turgor pressure is critical to maintain the viscoelastic properties of the matrix. Type II collagen is composed of three identical aI polypeptide chains to form a triple helix. The aI monomer is produced as a propeptide with large N- and C-terminal regions that are required for assembly in the chondrocyte. The aI trimers then associate in a staggered array via covalent cross-links that continue to accumulate over time with a concomitant increase in fiber strength.

Type II collagen is relatively resistant to degradation by most proteases; therefore, little collagen turnover is observed under normal circumstances, but specialized matrix metalloproteases MMPs are able to selectively target a single site on the aI helix [11]. MMPs, specifically MMP, play a significant role in degenerative joint disease, as discussed in greater detail below. Fibrocartilage is distinguished by the presence of smaller amounts of type I collagen, while all three types of cartilage also contain small amounts of other cartilage-specific collagens: collagen IX anchorin , collagen X chondrocalcin , and collagen XI.

Types IX and XI appear to play roles during fetal development [7, 8], decreasing in abundance during adult life. Types IX and XI collagens are present on the surface of chondrocytes and bind the cells to the surrounding matrix. Type X collagen is most prevalent in the growth plate and is necessary for endochondral ossification [5]. It is not typically found in articular cartilage except in osteoarthritis.

At the highest level of organization, multiple proteoglycans are noncovalently attached to a central hyaluronic acid moiety, stabilized by a small protein known as link protein. A proteoglycan is composed of a protein backbone to which long, sulfated, carbohydrate side chains are covalently attached at approximate right angles to the backbone. A single proteoglycan may be glycosylated with — such side chains. The resulting organization is similar to a bottle brush. The predominant proteoglycan in cartilage is Aggrecan, a amino acid protein with globular domains at the N- and C-terminal ends and a large intervening sequence that is densely glycosylated.

Chondrotoin sulfate and keratan sulfate are the most common carbohydrate side chains [12]. Chondrotoin sulfate is a glycosaminoglycan relatively specific to cartilage and is composed of approximately 25—30 sugar dimers N-acetylgalactosamine and glucuronic acid. Keratan sulfate is a repeating disaccharide of N-acetylglucosamine and galactose that is smaller 5—6 dimers and more widely distributed in the body than chondrotoin sulfate. As a result of the sulfated carbohydrate side chains, proteoglycans are highly charged, thereby attracting water and expanding in volume.

Unlike the more stable collagens, proteoglycans undergo continuous proteolytic cleavage during life with release of small fragments into the synovial fluid [5]. Chondrocytederived MMPs are responsible for this degradation. In the case of aggrecan, at least, the resulting shorter molecule becomes relatively more resistant to degredation so the process is somewhat self-limited. Chondrocytes also maintain a steady-state equilibrium by the synthesis of new aggrecan molecules, but this equilibrium is disturbed under pathologic conditions.

In addition to the above primary structural components, cartilage contains numerous other minor proteins that serve both structural and regulatory roles including other proteoglycans, fibronectin, galectin, as well as growth promoting and catabolic factors [5]. The articular cartilage may be divided into four zones superficial, transitional, deep, and calcified; Fig. The transition among the first three zones is somewhat arbitrary, but the deep and calcified zones are separated by a distinct front of mineralization known as the tidemark.

The tidemark is a unique histologic feature of articular cartilage and is not present in other hyaline cartilage. The organization Fig. Note the relative paucity of chondrocytes, typically with only a single cell in a lacuna Normal Histology Articular Cartilage The hyaline cartilage of diarthrotic articular surfaces is the most prevalent and best characterized of the cartilage subtypes. Microscopically, joint cartilage is composed of large Fig. The tidemark is a distinguishing feature of articular cartilage separating calcified from noncalcified zones.

For example, collagen fibers are oriented parallel to the surface in the superficial zone [6] and the chondrocytes tend to be elongated parallel to the surface Fig. This architecture is responsible for resisting the shear forces of joint movement at the surface. The transitional and deep zones show a radial arrangement of collagen fibers Fig. The latter areas are responsible for resistance to compressive forces. The calcified zone forms the attachment to the subchondral bone, and chondrocytes are enlarged but very sparse in this area.

Like other constituents, proteoglycan concentration varies within the articular cartilage such that it is lowest at the surface and greatest around chondrocytes in the deep zone [14], a feature which may be demonstrated by denser hematoxylin blue staining around lacunae Fig. However, under some circumstances, special histochemical stains, such as the cationic dyes Safrarin-O Fig.

The advantage of these stains is their relative selectivity for acidic polysaccharides. Safrarin-O reacts with both carboxylated and sulfated polysaccharides, while Alcian blue can be used selectively to stain both types pH 2. Although these dyes do offer increased specificity and likely stoichiometric binding to sulfate groups on chondrotoin sulfate or keratan sulfate [15], it should be remembered that histochemical methods are Fig.

Safrarin-O a stains acid polysaccharides both carboxylated and sulfated orange, while Alcian blue at pH 1. Chondrocytes continue to differentiate from the perichondrium. Unlike other types of connective tissue, cartilage is remarkable for its lack of blood vessels, nerves, inflammatory cells, or fibroblasts.

Chondrocytes are derived from immature mesenchymal cells that differentiate from somatic or visceral mesoderm during early fetal life Fig. Studies suggest that osteoblasts arise from the same precursor stem cell, but the hypovascular matrix of cartilage favors the differentiation of a chondrocyte [17]. Mesenchymal stem cells treated with a cocktail of transforming growth factor beta TGF-b , dexamethasone, and bone morphogenetic proteins BMPs result in cells that produce type II and type X collagen, although they do not completely recapitulate chondrogenesis during development [19, 20].

At the molecular level, several key regulatory proteins play roles in chondrocyte differentiation. The transcription factor Sox-9 appears to be a master regulator of chondrocyte differentiation from precursor cells. However, Sox-9 may not be lineage-specific, also driving the differentiation of osteoprogenitor cells [22]. Along with Sox-9, the transcription factors, RunX2 and Indian hedgehog Ihh , contribute to the regulation of chondrocyte maturation, and abnormal expression of all three proteins is thought to be important in the pathogenesis of some cartilage neoplasms [23].

Classically, chondrocytes have a round, pale eosinophilic cytoplasm and a small, hyperchromatic, central nucleus. The characteristic clear space lacuna identified on routine hematoxylin and eosin stained slides surrounding a chondrocyte is actually an artifact of processing. The clearing results from retraction of the matrix and cell away from one another during formalin fixation.

In vivo, the chondrocyte actually makes contact with a specialized layer of collagen-poor matrix. Unlike other mesenchymal cells, chondrocytes make few intercellular contacts. Cells in separate lacunae make no contact, but occasionally multiple cells may be present within a lacuna a finding referred to as cloning or nesting , and their cytoplasmic processes in such lacuna do form cell—cell contacts. Ultrastructurally, chondrocytes have abundant endoplasmic reticulum and Golgi but sparse mitochondria Fig.

Not only does the orientation of the chondrocytes Fig.

Online Cartilage Imaging Significance Techniques And New Developments

Superficial cells near articular surface a tend to have a fusiform spindled shape, while deeper chondrocytes b are round to polygonal with obvious cell processes 6 vary across zones of the articular surface described above , but superficial chondrocytes have more basal cell processes while deeper cells have more abundant endoplasmic reticulum and Golgi.

These differences may be related to the organization of collagen fibers in the different layers. Growth Plate In long bones, longitudinal growth is achieved by a primary ossification center known as the growth plate or physis Fig. In the functional growth plate, a specialized type of hyaline cartilage, which undergoes a highly regulated process of proliferation, mineralization, and apoptosis, is responsible for the growth. The maturing epiphyseal plate can be divided into zones reserve, proliferating, hypertrophied, and mineralization that correspond to stages of maturation of chondrocytes Fig.

The chondrocytes do not literally move through the matrix. Rather, they proliferate, hypertrophy, and undergo apoptosis in place while cartilage matrix is added and ultimately replaced by osteoid at the metaphyseal aspect of the growth plate. The net effect is longitudinal growth. The chondrocytes of the growth plate have abundant cytoplasm and prominent nuclei. In the proliferating zone, they are arrayed in regular, linear nests, a pattern that is pathognomonic of growth plate cartilage. As mentioned above, the cartilage contains collagen X chondrocalcin in a pericellular distribution, especially in the zone of mineralization.

Horvai Fibrocartilage The annulus fibrosus of the intervertebral disk represents the most prevalent fibrocartilage in the human body. Fibrocartilage is also found in the menisci of the knee and the labrum of the shoulder and hip joints. The annulus fibrosus Fig. Broad fascicles of collagen fibers alternate obliquely to compose the annulus. Microscopically, fibrocartilage is made up of a more fibrillar and eosinophilic matrix than hyaline cartilage. The chondrocytes tend to be fewer and smaller than hyaline cartilage and distributed in a more haphazard fashion Fig.

A trichrome stain, which stains collagen a deep blue while staining cytoplasm and other proteins red, is useful to demonstrate the extensive unidirectional arrangement of collagen Fig. Elastic Cartilage The cartilage of the external ear pinna , ligamentum flavum, and epiglottis are composed of elastic cartilage or elastocartilage. Elastic cartilage is typically more cellular than hyaline cartilage and the cells are haphazardly distributed, although the chondrocytes are similar in cytomorphology [13].

These fibers are best demonstrated using special histochemistry using sliver-based stains Fig. Pathology The pathology of cartilage includes congenital-developmental, degenerative, and neoplastic processes. A complete discussion of these entities is beyond the scope of this chapter, but selected entities that illustrate characteristic features, particularly as they relate to radiographic findings, are described below.

Osteoarthritis Fig. A Gomori trichrome stain highlights the abundant, directional collagen fibers with bright blue staining b Fig. However, the presence of abundant elastin fibers can be demonstrated by the black filaments using Verhoeff stain b of the articular cartilage with associated subchondral bone changes. Briefly, the articular surface shows cracks and fissures of the cartilage, ultimately leading to cartilage loss and exposure of the underlying subchondral bone.

Microscopically, depending on severity, the cartilage shows fissures and clefts, thinning, a decrease in proteoglycans, cloning of chondrocytes, and duplication of the tidemark Fig. The severity score ranging from 0 to 14 correlates reasonably well with biochemical metrics of osteoarthritis severity. The morphologic changes described and illustrated above represent changes to the matrix and chondrocytes at the cellular and molecular level. Virtually every component of articular cartilage is somehow affected during the process.

The major change in collagen is the degradation of type II collagen fibers by MMPs synthesized by the chondrocytes. The normally horizontally arranged fibers in the superficial zone are cleaved as a relatively early step in the process resulting in the fissures and clefts seen histologically. As previously mentioned, the collagen normally resists the swelling capacity of the water-rich proteoglycans, and destruction of the collagen network accounts for the increased hydration and hypertrophy of the articular cartilage early in the course of the disease. Furthermore, the chondrocytes produce a different balance of proteoglycans that recapitulates immature cartilage rich in chondrotoin sulfate with decreased keratan sulfate [26].

It is not entirely clear whether the altered composition contributes significantly to the mechanical changes in the matrix or if the net loss of proteoglycans is sufficient to account for the changes. Matrix metalloproteases MMPs , also synthesized by chondrocytes, play critical roles in the osteoarthritis phenotype. Grossly, clefts and destruction of the articular cartilage with exposed subchondral bone are hallmarks a. Nevertheless, certain cytokines and diffusible factors associated with other inflammatory conditions do exist in low concentrations within cartilage matrix possibly through diffusion from synovial or bone marrow origins.

Although initially thought to be an impermeable barrier, the osteochondral junction contains channels that allow the diffusion of materials. BMPs represent a second class of diffusible signals that stimulate chondrocytes to produce various matrix components. BMPs are regulated by a set of specific antagonists, which are often elevated at different stages of osteoarthritis further disturbing the balance of matrix production and destruction [28].

A number of interleukins, TNF-a, prostaglandins, and nitric oxide have been implicated in osteoarthritis pathogenesis [5]. MMP is found in highest concentration in the deep zone while aggrecanase is more widely distributed. Neoplasia Cartilage neoplasms are relatively rare and consist of a variety of intraosseous, extraosseous, and surface proliferations of chondrocytes and matrix.

With rare exceptions, the matrix of cartilage tumors is hyaline type. Most notably, neoplastic cartilage usually lacks the linear, zonal architecture of articular cartilage. Instead, most benign cartilage neoplasms grow as an aggregate of multiple tumor lobules. If mineralized, the osteoid corresponds to the ring-like calcifications seen radiographically Fig. The prototypical benign cartilage neoplasm is the enchondroma or simply chondroma. Grossly, an enchondroma consists of a well-circumscribed ovoid nodule of pale blue translucent cartilage, typically Depending on site, enchondromas may be quite cellular and even demonstrate atypia [30].

However, the most important finding supporting a benign diagnosis is a sharp margination between the tumor and the surrounding bone. Enchondromas may expand the cortex but spread through the cortex into soft tissues is incompatible with the diagnosis. The single most important pathologic feature that distinguishes chondrosarcoma from enchondroma is the presence of a permeative or infiltrative pattern in the former [30]. The matrix may be a gelatinous, viscid liquid myxoid rather than hyaline, likely due to abnormalities in matrix components and composition.

However, in high grade chondrosarcomas, the chondrocytes demonstrate marked cytologic atypia and mitotic activity Fig. References 1. The permeability of articular cartilage. J Bone Joint Surg Br. Karsenty G, Wagner EF. Reaching a genetic and molecular understanding of skeletal development.

Dev Cell. Tuan RS.

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J Bone Joint Surg Am. Senescent pigmentation of cartilage and degenerative joint disease. Arch Pathol. Cartilage in normal and osteoarthritis conditions.

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Best Pract Res Clin Rheumatol. Venn MF. Chemical composition of human femoral and head cartilage: influence of topographical position and fibrillation. Ann Rheum Dis. Eyre DR. The collagens of articular cartilage. Semin Arthritis Rheum. Articular cartilage collagen: an irreplaceable framework? Eur Cell Mater. ADAMTS proteinases: a multi-domain, multifunctional family with roles in extracellular matrix turnover and arthritis.

Arthritis Res Ther. Procollagen N-proteinase and procollagen C-proteinase. Two unusual metalloproteinases that are essential for procollagen processing probably have important roles in development and cell signaling. Matrix Biol. The new collagenase, collagenase-3, is expressed and synthesized by A. Horvai human chondrocytes but not by synoviocytes. A role in osteoarthritis. J Clin Invest. Roles of aggrecan, a large chondroitin sulfate proteoglycan, in cartilage structure and function. J Biochem. Bullough PG. In: Mills SE, editor. Histology for pathologists. Roughley PJ.

Articular cartilage and changes in arthritis: noncollagenous proteins and proteoglycans in the extracellular matrix of cartilage. Arthritis Res. Rosenberg L. Chemical basis for the histological use of safranin O in the study of articular cartilage. Stockwell R, Meachim G.

The chondrocytes. In: Freeman MA, editor. Adult articular cartilage. London: Pitman Medical; Bone marrow stromal stem cells: nature, biology, and potential applications. Stem Cells. In vitro chondrogenesis of bone marrow-derived mesenchymal progenitor cells. Exp Cell Res. Chondrogenic differentiation of mesenchymal stem cells from bone marrow: differentiationdependent gene expression of matrix components. Detailed examination of cartilage formation and endochondral ossification using human mesenchymal stem cells. Clin Exp Pharmacol Physiol. The influence of ferucarbotran on the chondrogenesis of human mesenchymal stem cells.

Contrast Media Mol Imaging. Osteo-chondroprogenitor cells are derived from Sox9 expressing precursors. Differential expression of runx2 and Indian hedgehog in cartilaginous tumors. Pathol Oncol Res. Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. Correlation of morphology with biochemical and metabolic data. Large and small proteoglycans of osteoarthritic and rheumatoid articular cartilage. Arthritis Rheum.

Human osteoarthritis synovial fluid and joint cartilage contain both aggrecanase- and matrix metalloproteinase-generated aggrecan fragments. Osteoarthritis Cartilage. Differential gene expression and regulation of the bone morphogenetic protein antagonists follistatin and gremlin in normal and osteoarthritic human chondrocytes and synovial fibroblasts.

Unni KK. Cartilaginous lesions of bone. J Orthop Sci. Horvai A. Cartilage-forming tumors. Bone and soft tissue pathology. Philadelphia: Saunders; Symptomatic osteoarthritis OA causes substantial physical and psychosocial disability [1]. Interestingly, the risk for disability defined as needing help walking or climbing stairs attributable to knee OA is as great as that attributable to cardiovascular disease and greater than that due to any other medical condition in elderly persons [1]. Like arthritis prevalence, the prevalence of arthritis-related disability is also expected to rise by the year , when an estimated Compounding this picture are the enormous financial costs that our nation bears for treating arthritis, its complications, and the disability that results from uncontrolled disease.

The balance is largely due to D. Thus, arthritis has become one of our most pressing public health problems — a problem that is expected to worsen in the next millennium with the increasing prevalence of this disease. This chapter delineates the characteristic symptoms and signs associated with cartilage loss and OA and how they can be used to make the clinical diagnosis with discussion of the role of imaging. The predominant symptom in most patients presenting with OA is pain. Over recent years a number of imaging-based studies have narrowed the discord between knowledge about structural findings on imaging and symptoms.

The remainder of the chapter focuses on what we know causes pain in OA and contributes to its severity, with a predominant focus on imaging findings. What Is OA? OA can be viewed as the clinical and pathological outcome of a range of disorders that result in structural and functional failure of synovial joints [5]. This highly prevalent disease occurs when the dynamic equilibrium between the breakdown and repair of joint tissues is overwhelmed [6].

The resulting progressive joint failure may cause pain, physical disability, and psychological distress [1], although many persons with structural changes consistent with OA are asymptomatic [7]. The reasons why there is this disconnect between disease severity and the level of reported pain and disability are largely unknown, although recent imaging studies are beginning to shed light on this.

Typically OA presents as joint pain. When symptomatic, especially so for the base of thumb joint, T. OA of the thumb carpo-metacarpal joint is a common condition that can lead to substantial pain, instability, deformity, and loss of motion [11]. In contrast, studies in Asian, black, and East Indian populations indicate a very low prevalence of hip OA [13]. The joint pain of OA is typically described as mechanical; that is, exacerbated by activity and relieved by rest. More advanced OA can cause rest and night pain leading to loss of sleep which further exacerbates pain.

Physical examination should include an assessment of body weight and body mass index, joint range of motion, the location of tenderness, muscle strength, and ligament stability. For lower limb joint involvement, this should include assessment of body mass and postural alignment in both standing and walking [15]. According to the ACR criteria for classification of hand OA unlike the hip and knee where radiographs enhance the sensitivity and specificity , X-rays are less sensitive and specific than physical examination in the diagnosis of symptomatic hand OA [16].

The usefulness of X-rays relates more importantly to the exclusion of other diagnostic possibilities rather than confirmation of osteoarthritic disease [17]. In clinical practice, the diagnosis of OA should be made on the basis of the medical history and physical examination, and the role of radiography is to confirm this clinical suspicion and rule out other conditions. When disease is advanced, it is visible on plain radiographs, which show narrowing of joint space, osteophytes, and sometimes changes in the subchondral bone. MRI can be used in infrequent circumstances to facilitate the diagnosis of other causes of joint pain that can be confused with OA osteochondritis dissecans, avascular necrosis.

Laboratory testing has little role in establishing the diagnosis of OA. Because OA is a noninflammatory arthritis, laboratory findings are expected to be normal. What Are the Diagnostic Criteria for Osteoarthritis? These are the criteria that are used in research studies and should be used to inform the diagnosis of OA in individuals, but not limiting the information gathering to these criteria and considering the wealth of other information that patients with OA may provide, which can help to either confirm or refute an OA diagnosis.

Also, ask about how the person is coping with pain and how well that is going. It is important to look for signs of psychological distress, e. Factors That Contribute to Pain The source of pain is not particularly well understood and is best framed in a biopsychosocial framework posits that biological, psychological, and social factors all play a significant role in pain in OA [19, 20]. From a biological perspective, neuronal activity in the pain pathway is responsible for the generation and ultimate exacerbation of the feeling of joint pain.

During inflammation, chemical mediators are released into the joint, which sensitize primary afferent nerves such that normally innocuous joint movements such as increased physical activity, high heeled shoes, and weather changes now elicit a painful response. This is the neurophysiological basis of allodynia, i.

This central sensitization phenomenon intensifies pain sensation and can even lead to pain responses from regions of the body remote from the inflamed joint, i. Pain has long been recognized as a complex sensory and emotional experience [21]. Each individual has a unique experience of pain influenced by their life experience and genotypic profile. The 13 biopsychosocial model is a very useful approach to understanding and assessing the experience of pain in persons with OA [23]. Constitutional factors that can predispose to symptoms include self-efficacy, pain catastrophizing, and the social context of arthritis social support, pain communication are all important considerations in understanding the pain experience.

Local Tissue Pathology The structural determinants of pain and mechanical dysfunction in OA are also not well understood but are believed to involve multiple interactive pathways. In broad terms, there are a number of tissues within the joint that contain nociceptive fibers, and these are the likely sources of pain in osteoarthritis. The subchondral bone, periosteum, periarticular ligaments, periarticular muscle spasm, synovium, and joint capsule are all richly innervated and are the likely source of nociception in OA.

In population studies, there is a significant discordance between radiographically diagnosed OA and knee pain [7]. While radiographic evidence of joint damage predisposes to joint pain, it is clear that the severity of the joint damage on the radiograph bears little relation to the severity of the pain experienced.

However, utilizing other imaging modalities such as magnetic resonance imaging MRI , significant structural associations, such as bone marrow lesions [24, 25], subarticular bone attrition [26], synovitis, and effusion [27, 28], have been related to knee pain. It remains unclear which of these local tissue factors predominate as until recently these analyses did not account for the fact that much of the structural change is collinear a person who has more severe disease will have worse structural change in multiple tissues including the bone, synovium, etc.

The different tissues within the joint and their respective contribution to symptoms are discussed below. Hyaline Articular Cartilage Articular cartilage is both aneural and avascular. As such, cartilage is incapable of directly generating pain, inflammation, stiffness, or any of the symptoms that patients with OA typically describe [30].

Hunter symptom sources in the joint are ignored. Some studies have suggested a relation between cartilage morphometry and lesions and the symptoms of OA [31]. It is important to note that this disease of the whole joint concurrently affects other tissues that do contain nociceptors. The studies that have demonstrated a relation of cartilage damage to pain have traditionally investigated the role of cartilage in predisposing to symptoms in isolation from other tissues and as such are fundamentally flawed.

A recent study suggested that areas of denuded cartilage are related to symptoms [32]. Again, the likely mechanism for symptom genesis is through secondary mechanisms such as: 1 exposing the underlying subchondral bone and the inherent symptom genesis from this structural alteration, 2 vascular congestion of subchondral bone leading to increased intraosseous pressure, and 3 synovitis secondary to articular cartilage damage with activation of synovial membrane nociceptors.

Subchondral Bone Periarticular bone changes associated with OA can be segregated into distinct patterns based on the anatomic location and pathogenic mechanisms. These alterations include progressive increase in subchondral plate thickness, alterations in the architecture of subchondral trabecular bone, formation of new bone at the joint margins osteophytes , development of subchondral bone cysts, and advancement of the tidemark associated with vascular invasion of the calcified cartilage. Of these lesions that which has the most supportive evidence for a role in symptom genesis is the bone marrow lesion Fig.

Lesions in the bone marrow play an integral if not pivotal role in the symptoms that emanate from knee OA and its structural progression [24]. Bone marrow lesions were found in of One likely source that remains underexplored is that of intraosseous hypertension. The pathophysiology remains unclear, although phlebographic studies in OA indicate impaired vascular clearance from bone and raised intraosseous pressure in the bone marrow near the painful joint [38—41].

What may subsequently cause pain is as yet unknown. Increased trabecular bone pressure, ischemia, and inflammation are all possible stimuli. Synovitis, Effusion The synovial reaction in OA includes synovial hyperplasia, fibrosis, thickening of synovial capsule, activated synoviocytes, and in some cases lymphocytic infiltrate B- and T-cells as well as plasma cells [42]. The site of infiltration of the synovium is of obvious relevance as one of the most densely innervated structures of the joint is the white adipose tissue of the fat pad, which also shows evidence of inflammation and can act as a rich source of inflammatory adipokines [43].

Semiquantitative scoring of peripatellar synovitis in OA ideally should be performed using T1w CE sequences and should include scoring of synovial thickness. Meniscus Fig. On noncontrast sequences such as this, the magnitude of synovitis is difficult to determine release of prostaglandins, leukotrienes, proteinases, neuropeptides, and cytokines [20, 44].

Analysis, Segmentation and Prediction of Knee Cartilage using Statistical Shape Models

Synovitis and effusion are frequently present in osteoarthritis and correlate with pain and other clinical outcomes Fig. Synovial thickening around the infrapatellar fat pad using noncontrast MRI has been shown on biopsy to represent mild chronic synovitis [45]. A semiquantitative measure of synovitis from the infrapatellar fat pad is associated with pain severity, and similarly change in synovitis is associated with change in pain severity [28].

This study assessed subjects male, female with at least one follow-up MRI. Mean synovitis score at baseline was 3. An increase of one unit in summary synovitis score resulted in a 3.

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Of the three locations for synovitis, changes in the infrapatellar fat pad were most strongly related to pain change 4. In an important caveat to this analysis, a recent study compared nonenhanced proton-density-weighted fat-suppressed PDFS sequences with T1-weighted T1w fat-suppressed FS contrast-enhanced CE sequences for semiquantitative assessment of peripatellar synovitis in OA [46]. If the meniscus does not cover the articular surface that it is designed to protect due to change in position, or if a tear leaves it unable to resist axial loading, it will not perform this role.

Meniscectomy is often accompanied by the onset of OA because of the high focal stresses imposed on articular cartilage and subchondral bone subsequent to excision of the meniscus. The studies that have explored the relationship between the meniscus and risk of disease progression in OA provide a clear indication of the risk inherent with damage to this vital tissue [55—57]. Each aspect of meniscal abnormality whether change in position or damage Fig.

Thus, the intact and functional meniscus is clearly important to the preservation of joint integrity and prevention of further joint damage. In contrast the meniscus plays a much smaller role in symptom genesis. An unfortunate consequence of the frequent use of MRI in clinical practice is the frequent detection of meniscal tears [58]. Degenerative lesions, described as horizontal cleavages, flap oblique , or complex tears or meniscal maceration or destruction are associated with older age and are almost universal in persons with osteoarthritis [58].

In the interests of preserving menisci, an important cautionary note: meniscal tears are nearly universal in persons with knee OA and are unlikely to be a cause of increased symptoms [59, 60]. The penchant to remove menisci is to be avoided, unless there are symptoms of locking or extension blockade, at which point surgical treatment often becomes necessary [61]. Various studies have investigated the role of muscle strength on joint integrity, and some have explored the impact on physical functioning. They found that in addition to factors such as age, reduced absolute quadriceps and hamstrings strength and poor proprioceptive acuity increased the likelihood of poor physical functioning as measured by the time to perform five repetitions of rising and sitting in a chair.

In addition to their exploration in observational studies, there is ample evidence from clinical trials demonstrating that muscle strengthening exercises result in improvements in pain, physical function, and quality of life in people with knee OA [64, 65]. Obesity is the single most important risk factor for development of severe OA of the knee and more so than other potentially damaging factors including heredity [66]. Even if it is usually accepted that mechanical loading contributes to joint destruction in overweight patients, recent advances in the physiology of adipose tissue add further D.

Hunter insights in understanding the relationship between obesity and osteoarthritis. Indeed, the positive association between overweight or obesity and osteoarthritis is observed not only for knee joints but also for nonweight-bearing joints, such as hands [67, 68]. Furthermore, if weight loss may prevent the onset of osteoarthritis, the loss of body fat is more closely related to symptomatic benefit than is the loss of body weight [69].

Local fat depots may play an important role in disease and symptoms genesis. Among these tissues, the synovium and infrapatellar fat pad appear to produce large amounts of adipokines [70]. Until recently, the fat pad, which is an extrasynovial but an intra-articular tissue, had been neglected. However, this adipose tissue is able to release growth factors, cytokines and adipokines [43].

Since obese individuals have higher concentrations of inflammatory markers, inflammation may contribute to functional limitation and disease progression in those with OA [71]. Besides direct effects on the joint, inflammatory mediators can affect muscle function and lower the pain threshold. Another source of joint pain in OA may be from the nerves themselves. Following joint injury in which there is ligamentous rupture, the nerves which reinnervate the healing soft tissues contain an overabundance of algesic chemicals such as substance P and calcitonin gene-related peptide.

An interesting observation of these new nerves was that their overall morphology was abnormal with fibers appearing punctate and disorganized [72, 73]. Since these phenomena are consistent with the innervation profiles described in nerve injury models, we speculate that injured joints may develop neuropathic pain post-trauma. Indeed, treatment of inflamed joints with the neuropathic pain analgesic gabapentin can also relieve arthritis pain [74].

Conclusion Though cartilage is aneural and avascular, it plays a central role in the pathophysiology of symptomatic OA, and cartilage abnormalities are directly associated with damage to other tissues within the joint that contain nociceptors. The pathophysiology of pain in OA is complex and similarly the symptomatic presentation in OA diverse and heterogeneous. Recent studies, particularly those with an emphasis on MRI, are providing unique insights into the relation between structure and symptom genesis.

The traditional predominant focus of imaging studies and preclinical investigation is cartilage. However, the subchondral bone, periosteum, periarticular ligaments, periarticular muscle spasm, synovium, and joint capsule are all richly innervated and are the likely source of nociception in OA. Attention to the many modulating factors that alter the experience of pain may improve the way we treat this disease. The effects of specific medical conditions on the functional limitations of elders in the Framingham Study.

Am J Public Health. Arthritis prevalence and activity limitations — United States, Yelin E, Callahan LF. The economic cost and social and psychological impact of musculoskeletal conditions. National Arthritis Data Work Groups [see comments]. Can we reduce disease burden from osteoarthritis?

Med J Aust. Nuki G. Osteoarthritis: a problem of joint failure [Review] [55 refs].

Significance, Techniques, and New Developments

Z Rheumatol. Collagens and cartilage matrix homeostasis [Review] [37 refs].

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Am J Epidemiol. Epidemiology of musculoskeletal impairments and associated disability. The prevalence of degenerative arthritis of the base of the thumb in post-menopausal women. J Hand Surg Br. Felson DT, Zhang Y. An update on the epidemiology of knee and hip osteoarthritis with a view to prevention [Review] [ refs]. Very low prevalence of hip osteoarthritis among Chinese elderly in Beijing, China, compared with whites in the United States: the Beijing osteoarthritis study.

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Ababneh , Jeffrey W. Cartilage imaging: significance, techniques, and new developments. Clinical, radiographic, molecular and MRI-based predictors of cartilage loss in knee osteoarthritis. Comparison of 1-year vs 2-year change in regional cartilage thickness in osteoarthritis results from participants from the Osteoarthritis Initiative. Related Papers. By clicking accept or continuing to use the site, you agree to the terms outlined in our Privacy Policy , Terms of Service , and Dataset License.

Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments
Cartilage Imaging: Significance, Techniques, and New Developments Cartilage Imaging: Significance, Techniques, and New Developments

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