Important for:. Consists of:. Collagen provides tensile strength and durability, however, proteoglycans are also important. For example, if you inject papain an enzyme that digests the protein cores of proteoglycans into the ears of a rabbit, after a few hours the ears will loose their stiffness and droop. Three types of cartilage - extracellular matrix differs in terms of concentration of collagen and elastin fibers.
Copyright R. Hyaline cartilage. Bluish-white in life d. In adult, mainly found lining outer wall of respiratory system and on surfaces of bone joints where it is called Articular cartilage.
Undergoes calcification in bone formation and also as part of aging process. Elastic cartilage. Example - external ears c. Fibrous cartilage fibrocartilage.
This tissue acts to support softer tissues and also is important in the formation and healing of endochondral bines such as the long bones of the arm and leg.
The qualities of the different types of cartilage depend on differences in the concentration of collagen and elastin fibers in the extracellular matrix and on the proteoglycan molecules that these fibers are associated with.
Cartilage is devoid of blood vessels. Articular hyaline cartilage and fibrocartilage do not have a perichondrium. More information on cartilage:. Hyaline cartilage is the most common cartilage in the body. It is bluish-white and translucent. Important in the formation of long bones of the body in embryo and during growth.
In adult, mainly found lining the respiratory passages such as trachea. Dominant component of extracellular matrix is collagen fibers.
Other components are sulfated proteoglycans and hyaluronic acid. Main tissue components. Rich in collagen. Contains fibroblasts that secrete the materials for the collagen fibers.
Inner layer next to cartilage matrix contains cells that are thought by some to be fibroblasts and by others to be undifferentiated mesenchyme cells. In either case, these cells can differentiate to form chondroblasts. Secrete extracellular matrix, but are not yet rigidly embedded in that matrix. These cells reside in small spaces within the matrix that are called lacunae.
May be more than one cell in a lacuna. Living chondrocytes have an eliptic shape. Organelle systems in cytoplasm are typical of cells that secrete. Chondrocytes in hyaline cartilage that are grouped together are called isogenic groups. Similar to hyaline cartilage except,. No isogenic groups 4. An irregular, dense, fibrous tissue with thinly dispersed, encapsulated chondrocytes.
No perichondrium, so it blends with adjacent connective tissue. Most easily seen in articular disks such as the intervertebral disks. Also found where tendon connects to bone. Shows resistance to compression, durability and high tensile strength. As the embryo develops, mesenchymal cells will aggregate into closely knit clusters and differentiate into chondroblasts. These cells will begin to secrete collagen and mucopolysaccharide matrix containing chondroitin sulfate.
The matrix secretion will cause the chondroblasts to be pushed apart. As this occurs, the cartilage cells will undergo divisions. This will result in small clusters of chondroblasts within the developing matrix which will also start to secrete matrix and be pushed away from each other. This sort of growth of cartilage is termed interstitial growth due to the fact that the extracellular matrix is secreted into spaces between the cells.
Growth of cartilage can also be appositional , that is a layer of chondroblasts can lay down matrix at the outer edge of a mass of cartilage. As the cartilage continues to grow, the central regions become more rigid due to various secretory products and the cells in this region become embedded in rigid matrix and take on the characteristics of mature chondrocytes.
The outer edge of the cartilage mass becomes invested with additional mesenchymal cells that differentiate into fibroblasts to form a specialized connective tissue covering for the cartilage known as perichondrium. Chondroblasts that differentiate from mesenchyme cells at the inner edge of the perichondirum also secrete matrix causing appositional growth of the cartilage mass. Similar histogenesis can result in elastic external ear or fibrous cartilage intervertebral discs in other parts of the body.
Bone is one of the hardest substances in the body. You might look at it and think of it as dead, mineralized material. It's important to realize that bone is a living tissue composed of cells and their associated extracellular matrix. Two distinct layers. External layer very fibrous, while internal layer is more cellular and vascularized. Some of the collagen fibers penetrate the calcified bone matrix and bind the periosteum to the bone.
Cells of this connective tissue play important roles in bone histogenesis and in the healing of fractures. Lines the internal surfaces of bone. Important roles of the periosteum and endosteum are nutrition of bone cells and provision of osteoblasts for bone histogenesis and repair.
This matrix is composed of glycoproteins and collagen. In areas where these cells occur, they are located on the surfaces of forming bone and are not yet embedded in the extracellular matrix. These cells have cytoplasmic processes that bring them into contact with neighboring osteoblasts, as well as nearby osteocytes.
Ultrastructure shows organelle systems typical of secretory cells. These cells are osteoblasts that have become embedded in calcified bone matrix. They reside in lacunae within the matrix and are in contact with neighboring osteocytes via cytoplasmic processes that extend through small tunnels called canaliculi. Contacting cytoplasmic processes form gap junctions. This communication between osteocytes is important in the tranfer of nutrients to these cells and wastes out of them since they may be far removed from blood capillaries.
The cells are flattened and their internal organelles exhibit the characteristics of cells that have reduced synthetic activity.
Endochondral - cartilage template formed that is replaced by bone e. Intramembranous - direct formation of bone structure with no cartilagenous template e. In the embryo, osteoblasts are derived from mesenchymal cells. These cells either aggregate where bones are to form intramembranous bone formation and lay down the matrix that will later become calcified, or they migrate into pre-existing cartilage "models " of the presumptive bone and replace the cartilage with a calcareous matrix endochondral bone formation.
Long bone growth is also endochondral in nature. Osteoblasts are different than the chondroblasts that begin the histogenesis of cartilage and should not be confused with them.
As the primordial bone matrix is layed down, the osteoblasts become entrapped in lacunae within the matrix and are then known as mature osteocytes. As bone is being formed, there is also localized removal of the bone matrix by another set of connective tissue cells known as osteoclasts. These cells are thought to differentiate from monocytes and are responsible, in part, for the internal architecture of bones in that they excavate localized portions of the forming bone and make passageways for such things as blood vessels nerves.
A third population of cells involved in bone formation are the cells of the marrow. These are the stem cells for blood cells and all their progeny see Blood below.
Mesenchymal cells aggregate and begin to secrete matrix that is characterized by bundles of collagenous fibers. The secreted osteoid matrix has a high affinity for calcium salts, that are brought into the area of bone formation by the circulatory system. These deposit within and on the matrix to form calcified bone. As this calcification takes place, the mesenchymal cells undergo morphological changes. They loose the appearance of mesenchymal cells and round up becoming true osteoblasts.
The osteoblasts become oriented in epithelial-like layers along the forming bone. The osteoblasts and the collagen and other components of the intercellular matrix form the organic osteoid framework of the bone.
As a strand of matrix is invested with inorganic salts it forms a spicule of bone. In addition to the depth-dependent macromolecules in cartilage proteoglycans and collagen fibers , many other molecular concentrations in cartilage are depth-dependent. A recent study quantitatively analyzed extractable proteins in human lateral tibial cartilage, by first applying a non-targeted mass spectrometry approach iTRAQ: isobaric tags for relative and absolute quantitation and subsequently by analyzing protein distribution using a targeted multiple reaction monitoring mass spectrometry.
The unique distribution patterns of 70 ECM proteins were identified in the lateral tibial plateau, revealing groups of proteins with a preferential distribution to the superficial, intermediate or deep regions of articular cartilage. Since the primary function of a synovial joint is load bearing and facilitation of mechanical motion, the biomechanical properties of articular cartilage are the ultimate measure of its health. Articular cartilage prevents direct contact between bones and other parts of the joint, thus protecting the relatively brittle bone from frictional wear and the softer tissues of the joints from abrasion.
Through deformation, articular cartilage distributes the forces exerted on the bone to a greater contact area. Known as load processing , this reduces contact stresses between the bones and protects the bones from fatigue. Because of the unique molecular and morphological structures of articular cartilage, the biomechanical properties of cartilage in joints are both poroviscoelastic and depth-dependent. The sulfated parts of the GAG molecules are highly negatively charged, and through electrostatic repulsion cause the proteoglycan bottlebrush structure to expand and straighten into a rigid form that takes up a large molecular domain with a highly negative fixed charge density FCD.
The counter- and co-ions cloud the negative fixed charges and become electrostatically bound to the proteoglycan molecule Figure 1. This causes a greater ionic concentration in the ECM with respect to the external environment, causing water influx of the tissue, which generates an outward osmotic stress known as the Donnan osmotic swelling pressure. Collagen fibrils have an extremely high tensile modulus, individually found to be MPa, 93 but can reach values of several GPa, 94,95 depending on their environment.
The collagen fibrils provide the required structural resistance to swelling pressures, but although strong in tension they provide little resistance to compression due to the high length-to-width ratio. When a load is applied to the cartilage surface, the force is distributed across the contact area, generating pressure stress and resulting in tissue compression.
Different strain-rate regimes can be approximated by different mechanical models, and conversely, for any given regime, several models may yield very similar numerical results. The poroelastic model of articular cartilage can be qualitatively encapsulated as follows. Because water is incompressible, compression can only occur as a result of an outflow of water from the tissue.
The solid matrix of the ECM is a porous—permeable material that allows the flow of interstitial fluid. The frictional interaction between the pore walls and interstitial fluid generates large shear forces that dampen the outflow of water through the tissue.
This is accompanied by load sharing between the fluid and the solid components of the ECM. The load is initially borne by the fluid component in the form of the hydrostatic excess pore pressure HEPP. The HEPP initially increases, reaches a maximum, and then slowly decays as the load is transferred to the solid components of the ECM in the form of electrostatic and osmotic interactions.
The viscous dampening of the flow of interstitial fluid is crucial to both the physiology and biomechanics of articular cartilage. Biomechanically, it provides load-carrying capacity through the slow transient response to load. Physiologically, the dampening provides protection for the chondrocytes and ECM, and even represents a major factor in controlling the metabolic behavior of chondrocytes and ECM maintenance.
The poroelastic model provides a highly realistic physicochemical picture of cartilage compression. However, under many commonly used loading conditions e. Similar to the poroelastic model, viscoelastic response to a step stress or strain is time dependent and not instantaneous. In general, viscoelasticity is theoretically modeled using a spring—dashpot system to represent the elastic solid and fluid interstitial water phases, respectively. Several works have attempted to theoretically model the biomechanical behavior of cartilage using the viscoelastic model.
Similar to the pure poroelastic model, the compressive response of cartilage in the biphasic model was dependent upon the viscous fluid efflux from the porous—permeable solid phase of the ECM.
The triphasic model considered a three-phase ECM consisting of a porous—permeable solid phase, fluid phase, and an additional ionic phase counter-ion and co-ion species. The creep response Figure 1. As the tissue compresses, water is rapidly forced out of the ECM. Tissue volume and the molecular volume of aggrecan domains decrease, while the FCD and the concentration of counter-ion and co-ion species increase, causing increasing intermolecular repulsion and interstitial swelling stress.
The tissue deformation and water exudation slow down as the repulsive and swelling stresses slowly reach an equilibrium with the external load. In a stress—relaxation experiment Figure 1. As the tissue is compressed, water is forced out from the tissue. The reduction of water content leads to a time-dependent decrease in the interstitial stress as the tissue relaxes. The interstitial mechanisms involved in stress—relaxation are subtly different to those in the creep response, in that the relaxation process involves interstitial molecular rearrangement.
The reorganization occurs since the fibrils closest to the compressed surface are more compacted than the deeper fibrils, 96 which generates a gradient pressure within the tissue that eventually equalizes.
An interesting feature of stress—relaxation is that the peak stress is highly dependent upon the rate of compression Figure 1. Since the shear stress from the solid—fluid interaction limits the fluid flow, a higher displacement rate creates a higher interstitial pressure peak. The differences in peak loading stress govern stress redistribution between the ECM and the subchondral bone.
For perspective, the pressure of 20 MPa is approximately times the air pressure in the tires supporting an automobile, although automobile tires utilize a significantly larger surface area.
The close association between proteoglycan aggregates, interwoven collagen fibrils and interstitial fluid provides the compressive resilience to cartilage through negative electrostatic repulsion forces. Using fluorescence-labeled chondrocyte nuclei as intrinsic markers, Schinagl et al. This depth dependence of articular cartilage is the reason that, when articular cartilage is compressed externally either in vitro or in vivo , the surface regions of the tissue undergo compression before the deeper zones do Figure 1.
A change in the depth dependence of GAG concentration, which is related to the FCD, has been suggested to alter the depth dependence of the biomechanical behavior. The properties of articular cartilage discussed in the last several sections are generic in nature, i. In addition to variations within a single joint, cartilage from different types of joints in the same animal may vary because of the different load-bearing patterns of the different joints.
Likewise, cartilage from the same kind of joint in different animal species might also vary as a consequence of variations in their mechanics e. Since different species have a different distribution of applied stress in their joints, the properties of articular cartilage should be considered different between species.
The development of a synovial joint can be divided into two stages. Initially, early limb buds develop from the somatopleural mesoderm of the embryo. The contiguous mesenchyme condensations in the early limb buds undergo chondrification, and then separate by transverse bands of relatively flattened cells, which is known as an interzone. The band of CDexpressing cells could only present in the intermediate layer.
Subsequently, the interzone cavitates to form the joint cavity, followed by the morphogenesis of an interlocking structure. Following cavitation, the skeletal elements undergo morphogenesis Figure 1. The adult knee tibiofemoral joint is probably the most studied joint in osteoarthritis research, both because of the high incidence of osteoarthritis associated with this joint and because of its easy surgical access.
As shown in Figure 1. Different surfaces of cartilage within the knee have different modes of contact and motion e. Figure 1. The cross-sectional slices from anterior to posterior directions the coronal planes reveal clearly the significant topographical site to site variations of both lateral and medial tibial plateaus, which likely provides effective load dissipation.
In canine tibia, cartilage around the central region not covered by the meniscus is thicker than the periphery covered by the meniscus. Cartilage thickness also varies from the anterior to posterior direction.
Topographical variations have been found in many properties of tibial and condyle cartilage, including thickness, shear modulus, birefringence, water content, sulphated-GAG content, and collagen content. Even with the progress of age, there are site-specific changes in water and collagen content in asymptomatic cartilage. Cartilage from the adult shoulder joint a ball and socket joint between the scapula and the humeral head has also been studied in many biomedical studies, which in animal models is probably due to its availability as a spare tissue.
Compared with knee cartilage, humeral cartilage has much simpler contours, which has be used as a classical three-layer model of articular cartilage in a number of studies. A peculiar graphical pattern can be formed on the intact surfaces of many joints, by using a sharp pin to prick the surface of articular cartilage and coating the cartilage surface with a layer of India ink. This pattern clearly represents some type of surface anisotropy of articular cartilage over the joint, which could be the anisotropy of molecular structure as well as biomechanical nature.
Some have considered the pattern to reflect the directions of the surface fibers, which could represent the stress patterns on the surface of any joint. Incidentally, the collagen fibers in symphysis fibrocartilage also tend to follow the stress lines. Osteoarthritis is a progressively degenerative joint disease with a massive socioeconomic burden, as it is the leading cause of disability. This imbalance is characterized by ECM degradation, tissue loss, joint space narrowing, subchondral bone sclerosis, and osteophyte formation.
Osteoarthritis can be classified into two types: primary and secondary. There is little difference in their clinical symptoms, pathogenesis, and treatment, but there are differences in their triggers. Repetitive use of the joints over five or six decades may result in degeneration of articular cartilage in a large percentage of the senior population. Secondary osteoarthritis usually has an identifiable cause, such as trauma e.
Secondary osteoarthritis tends to strike at an earlier age. The molecular mechanisms underlying the pathogenesis of osteoarthritis are still not fully understood and there is no widespread agreement. Some recent studies relate osteoarthritis pathogenesis to the re-initiation of the transient chondrocyte phenotype as seen in terminal differentiated growth-plate chondrocytes and the upregulation of collagenase matrix metalloproteinase MMP MMPpromoted methylation in osteoarthritic cartilage, in part, may drive the chondrocyte hypertrophy.
Although osteoarthritis is not classified as an inflammatory joint disease, several inflammatory components e. In addition, nitric oxide NO can be spontaneously produced by osteoarthritis-affected cartilage to cause catabolic effects, including inhibiting PGE2 synthesis as well as activating MMPs. Along with the progressive loss of articular cartilage, osteoarthritis is characterized by increased subchondral bone sclerosis with thickening of cortical plate and formation of osteophytes, which at some stages can be diagnosed as bone bruises and edema via medical imaging.
Like cartilage, the subchondral bone of osteoarthritis patients releases high levels of alkaline phosphatase, osteocalcin, osteopontin, IL-6, IL-8, and progressive ankylosis protein homolog, PG, and insulin growth factor The current gold standard for diagnosing and measuring clinical efficacy in osteoarthritis is radiographic joint space narrowing. The elevated presence of biochemical biomarkers measured from the serum, urine, and synovia of osteoarthritis patients is often accompanied by cartilage degradation and subchondral bone turnover, such as cartilage oligomeric matrix protein, c -terminal telopeptide of type II collagen, helical fragments Helix-II and Coll , Coll NO2 , amino-terminal type II procollagen propeptide, carboxy-terminal type II procollagen propeptide, chondroitin sulfate epitope CS , HA, n -terminal type I collagen telopeptides, c -terminal type I collagen CTX I or serum CTX I, amino-terminal procollagen propeptide of type I collagen, carboxy-terminal procollagen propeptide of type I collagen, osteocalcin, urinary total pyridinoline, bone sialoprotein, and MMP The aims of osteoarthritis management are to educate patients about the disease, to alleviate pain, and to improve joint function.
Osteoarthritis should be managed on an individual basis and commonly requires a combination of treatment options. The recommended hierarchy of treatments consists of non-pharmacological treatments first, then drugs, and then, if necessary, surgery. The non-pharmacological approach includes education, weight loss e. Surgery may include arthroscopic debridement and lavage, osteotomy, joint replacement, allografts, autografts, autologous chondrocyte transplantation, and tissue-engineered cartilage transplantation.
The latter has received significant attention and is currently focused on selecting the seed cells e. MSCs and recreating the natural physical environment e. Osteoarthritis in humans has been extensively studied clinically. Since articular cartilage is avascular and aneural, a diagnosis of primary osteoarthritis is not made until a patient experiences pain in the joint, which signals later-stage disease. The main focus for human osteoarthritis research is to find a way to diagnose the disease early and accurately.
The best-known human imaging project during the recent years is the Osteoarthritis Initiative OAI , which is a multi-center observational study of human osteoarthritis sponsored by the National Institutes of Health in the USA.
The OAI data are available publically on the internet. Many correlational studies have been published using various parts of the OAI data.
In addition to studies on human osteoarthritis, a large number of different domestic animals have been used in osteoarthritis studies. This is because no disease can be induced ethically in the human; the only alternative for the entire biomedical community is to study the cellular and animal models of the human disease, in order to gain better insights that could be used to produce guidelines for human treatment.
Primary osteoarthritis progresses slowly over several decades. It is the most common form of osteoarthritis and increases in prevalence and severity with the age in both human and non-human animals. Post-traumatic osteoarthritis can be reproduced by mechanical insult or by surgery. Since articular cartilage has a limited capacity for repair, the physiological response to the resulting tissue damage rarely restores a normal articular surface.
Similarly, any changes in the cartilage structure caused by abnormal loading in a stable joint, or even by degradative enzymes in the synovium, can lead to the development of osteoarthritis.
The assessment of animal models of osteoarthritis traditionally depends on the histological analysis of articular cartilage. Recent advances have seen the emergence of many other effective analyses, such as biomarkers and imaging, for monitoring the progress of osteoarthritis.
Although there is a perceived advantage in using naturally occurring models of osteoarthritis e. Dunkin—Hartley guinea pigs with a slower onset and progression similar to human osteoarthritis, many investigators have utilized fast-advancing animal models first reported by Magnuson in In , Paatsama published a thesis describing the degradation of canine articular cartilage associated with a cranial cruciate ligament rupture.
In addition to cartilaginous changes, Radin and Rose showed alterations in the sub-chondral bone and the calcified zone of cartilage after application of repetitive sub-impact loads to the patellofemoral joint. Responses to traumatic injury were also studied using a direct impact applied to the patella using a "drop tower" type of apparatus in order to produce high-energy damage similar to that seen in human injuries. Intra-articular injections of many proteolytic enzymes such as trypsin, papain, and collagenase have also been used to trigger model osteoarthritis in mice, rats, and rabbits.
However, the mechanisms responsible for cartilage degradation in these models, particularly those in which papain or trypsin was injected, may deviate significantly from those that normally occur in the human disease. Chemically induced osteoarthritis models use intra-articular injection of sodium iodoacetate to study acute cartilage toxicity and degradation and joint pain; however, this has many limitations as a model of osteoarthritis.
However, it does provide an in vivo model of rapid cartilage degradation mirroring some of the events observed in vitro in organ culture screening studies. In contrast to in vivo animal studies concentrating on the outcomes of post-traumatic joints and progression of osteoarthritis, many in vitro models have been used to study the effect of cell death and specific degradative mechanisms in well-defined loading and culture environments.
For example, to investigate the potential use of imaging as a diagnostic tool for osteoarthritis, purified collagenase, trypsin, or chondroitinase ABC , have been used to digest bovine patellar cartilage in order to generate spatial and temporal changes in the cartilage matrix.
Similar changes in structure and collagen network were observed in proteoglycan-depleted tissue and correlated directly with the loss of compressive strength. As an alternative to enzymatic cleavage, many studies have used in vitro explant injury models to study the molecular mechanisms of chondrocyte death and matrix degradation in injured cartilage. The relatively low compressive moduli and the compression-induced stiffening in the superficial zone are closely related to cell death following a blunt impact or repeated mechanical insults.
This was well demonstrated in vitro in a study of chondrocyte necrosis, where chondrocyte death occurred only in the superficial zone when two cartilage disks were positioned articular-surface-to-articular-surface and subjected to 1. Some aspects of cartilage repair can also be examined in vitro by osteochondral models, such as defects of different depths created using a dermal biopsy punch and a scalpel.
Thibault et al. These studies indicated that acute injury in articular cartilage can induce an upregulation of reactive oxygen species and pro-inflammatory cytokines. These are important areas of research, since the prevention of cell death and the inhibition of matrix-degrading enzymes in the injured joint are significant for the prevention of posttraumatic osteoarthritis. Together, these in vitro explant models provide effective systems to study biomechanical and mechanobiological factors involved in initiating cartilage injury; biochemical factors associated with cell death and matrix degradation; and gene regulation critical for the advance of post-traumatic osteoarthritis.
Yang Xia, Konstantin I. Momot, Zhe Chen, Christopher T. The right human knee is shown. The subchondral bone plate arrowheads form relatively thin strata beneath the hyaline articular cartilage tissue. The section was stained with basic fuchsine and toluidine blue O. Reproduced from Osteoarthritis Cartilage , 10 , E. Hunziker, T. Quinn, H. The lines represent the orientation of the collagen fibers; the ovals represent the chondrocytes in cartilage not to scale.
Reproduced with permission from Poole et al. Helical collagen molecules form from three polypeptide chains, and these associate laterally to form collagen fibrils with a characteristic banded structure. The sulfate groups are highly negatively charged and cause the aggrecan to spread out. Reproduced with permission from themedicalbiochemistrypage LLC. These repulsive forces cause the aggregate to assume a stiffly extended conformation, occupying a large solution domain.
B Applied compressive stress decreases the aggregate solution domain left , which in turn increases the charge density and thus the intermolecular charge repulsive forces right Reproduced with permission from Mow et al. A faster displacement rate creates a higher interstitial pressure peak, while loading slowly could cause the tissue to reach equilibrium without experiencing a spike in interstitial stress.
Arrows and circles indicate tracking of cell nuclei. Reproduced from Osteoarthritis Cartilage , 9 , S. Chen, Y. Falcovitz, R. Schneiderman, A. Maroudas, R. Sah, Depth-dependent compressive properties of normal aged human femoral head articular cartilage: relationship to fixed charge density, —, Copyright with permission from Elsevier.
Within an initial mesenchymal condensation, an unknown trigger stimulates wnt14 expression at the site of incipient joint formation. Gdf5 is thereafter expressed and the cells take on an elongated morphology and significantly reduce SOX9 and collagen type II expression. Bone morphogenetic protein BMP antagonists chordin and noggin are expressed in the interzone cells and act to stabilize joint-inducing positional cues.
The interzone adopts a three-layered structure in the case of long bone elements that undergoes separation or cavitation on mechanically induced synthesis of hyaluronan. The morphogenesis of the functional joint organ results in articular cartilage lining the ends of skeletal elements, which are bathed in synovial fluid, produced by a synovial membrane, and encased within a fibrous capsule.
Reproduced from Curr. Khan, S. Redman, R. Williams, G. Dowthwaite, S. Oldfield, C. Archer, Copyright with permission from Elsevier. The variations in the cartilage thickness and topographical directions are significant. Reproduced from Arthrosc. A consideration in the orientation of autologous cartilage grafts, —, Copyright with permission from Elsevier. A The non-loaded control; B loaded explants subjected to 1.
Dead cells red were located near the articular surface of loaded explants Reproduced with permission from Chen et al. Gray , P. Williams and L. CDC Morb. Marieb and K. Benjamin and E. Evans , J. Martini , M. Timmons and R.
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Hyaline cartilage is the most widespread cartilage type and, in adults, it forms the articular surfaces of long bones, the rib tips, the rings of the trachea, and parts of the skull. This type of cartilage is predominately collagen yet with few collagen fibers , and its name refers to its glassy appearance. In the embryo, bones form first as hyaline cartilage before ossifying as development progresses. Hyaline cartilage is covered externally by a fibrous membrane, called the perichondrium, except at the articular ends of bones; it also occurs under the skin for instance, ears and nose.
Hyaline cartilage is found on many joint surfaces. It contains no nerves or blood vessels, and its structure is relatively simple. If a thin slice of cartilage is examined under the microscope, it will be found to consist of cells of a rounded or bluntly angular form, lying in groups of two or more in a granular or almost homogeneous matrix. These cells have generally straight outlines where they are in contact with each other, with the rest of their circumference rounded.
They consist of translucent protoplasm in which fine interlacing filaments and minute granules are sometimes present. Embedded in this are one or two round nuclei with the usual intranuclear network. Fibrous cartilage has lots of collagen fibers Type I and Type II , and it tends to grade into dense tendon and ligament tissue.
White fibrocartilage consists of a mixture of white fibrous tissue and cartilaginous tissue in various proportions. It owes its flexibility and toughness to the fibrous tissue, and its elasticity to the cartilaginous tissue.
It is the only type of cartilage that contains type I collagen in addition to the normal type II. Fibrocartilage is found in the pubic symphysis, the annulus fibrosus of intervertebral discs, menisci, and the temporal mandibular joint.
Elastic or yellow cartilage contains elastic fiber networks and collagen fibers. The principal protein is elastin. Elastic cartilage is histologically similar to hyaline cartilage but contains many yellow elastic fibers lying in a solid matrix.
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