BONE CELLS

Osteoblasts

Osteoblasts are responsible for the synthesis of the organic components of bone matrix (type I collagen, proteoglycans, and glycoproteins). Deposition of the inorganic components of bone also depends on the presence of viable osteoblasts. Osteoblasts are exclusively located at the surfaces of bone tissue, side by side, in a way that resembles simple epithelium (Figure 8–3). When they are actively engaged in matrix synthesis, osteoblasts have a cuboidal to columnar shape and basophilic cytoplasm. When their synthesizing activity declines, they flatten, and cytoplasmic basophilia declines.

Some osteoblasts are gradually surrounded by newly formed matrix and become osteocytes. During this process a space called a lacuna is formed. Lacunae are occupied by osteocytes and their extensions, along with a small amount of extracellular noncalcified matrix.

During matrix synthesis, osteoblasts have the ultrastructure of cells actively synthesizing proteins for export. Osteoblasts are polarized cells. Matrix components are secreted at the cell surface, which is in contact with older bone matrix, producing a layer of new (but not yet calcified) matrix, called osteoid, between the osteoblast layer and the previously formed bone (Figure 8–3). This process, bone apposition, is completed by subsequent deposition of calcium salts into the newly formed matrix. Quiescent osteoblasts (not producing bone matrix) become flattened. However, they easily revert to the cuboidal shape typical of the active synthesizing state.

Osteocytes

Osteocytes, which derive from osteoblasts, lie in the lacunae (Figure 8–3) situated between lamellae (L. diminutive of lamina, leaf) of matrix. Only one osteocyte is found in each lacuna. The thin, cylindrical matrix canaliculi house cytoplasmic processes of osteocytes. Processes of adjacent cells make contact via gap junctions, and molecules are passed via these structures from cell to cell. Some molecular exchange between osteocytes and blood vessels also takes place through the small amount of extracellular substance located between osteocytes (and their processes) and the bone matrix. This exchange can provide nourishment for a chain of about 15 cells.

When compared with osteoblasts, the flat, almond-shaped osteocytes exhibit a significantly reduced rough endoplasmic reticulum (Figure 8–1) and Golgi complex and more condensed nuclear chromatin. These cells are actively involved in the maintenance of the bony matrix, and their death is followed by resorption of this matrix. Osteocytes are long-living cells.

MEDICAL APPLICATION

The fluorescent antibiotic tetracycline interacts with great affinity with recently deposited mineralized bone matrix. Based on this interaction, a method was developed to measure the rate of bone apposition—an important parameter in the study of bone growth and the diagnosis of bone growth diseases. Tetracycline is administered twice to patients, with an interval of 5 days between injections. A bone biopsy is then performed, and the sections are studied by means of fluorescence microscopy. The distance between the two fluorescent layers is proportional to the rate of bone apposition. This procedure is of diagnostic importance in diseases such as osteomalacia, in which mineralization is impaired, and osteitis fibrosa cystica, in which increased osteoclast activity results in removal of bone matrix and fibrous degeneration.

Osteoclasts

Osteoclasts are very large, branched motile cells. Dilated portions of the cell body (Figure 8–4) contain from 5 to 50 (or more) nuclei. In areas of bone undergoing resorption, osteoclasts lie within enzymatically etched depressions in the matrix known as Howship's lacunae. Osteoclasts are derived from the fusion of bone marrow-derived mononucleated cells.

In active osteoclasts, the surface-facing bone matrix is folded into irregular, often subdivided projections, forming a ruffled border. Surrounding the ruffled border is a cytoplasmic zone—the clear zone—that is devoid of organelles, yet rich in actin filaments. This zone is a site of adhesion of the osteoclast to the bone matrix and creates a microenvironment between the cell and the matrix in which bone resorption occurs (Figure 8–5).

The osteoclast secretes collagenase and other enzymes and pumps protons into a subcellular pocket (the microenvironment referred to above), promoting the localized digestion of collagen and dissolving calcium salt crystals. Osteoclast activity is controlled by cytokines (small signaling proteins that act as local mediators) and hormones. Osteoclasts have receptors for calcitonin, a thyroid hormone, but not for parathyroid hormone. However, osteoblasts have receptors for parathyroid hormone and, when activated by this hormone, produce a cytokine called osteoclast stimulating factor.

Ruffled borders are related to the activity of osteoclasts.

BONE MATRIX

Inorganic matter represents about 50% of the dry weight of bone matrix. Calcium and phosphorus are especially abundant, but bicarbonate, citrate, magnesium, potassium, and sodium are also found. X-ray diffraction studies have shown that calcium and phosphorus form hydroxyapatite crystals with the composition Ca₁₀(PO₄)₆(OH)₂. However, these crystals show imperfections and are not identical to the hydroxyapatite found in the rock minerals. Significant quantities of amorphous (noncrystalline) calcium phosphate are also present. In electron micrographs, hydroxyapatite crystals of bone appear as plates that lie alongside the collagen fibrils but are surrounded by ground substance. The surface ions of hydroxyapatite are hydrated, and a layer of water and ions forms around the crystal. This layer, the hydration shell, facilitates the exchange of ions between the crystal and the body fluids.

MEDICAL APPLICATION

In the genetic disease osteopetrosis, which is characterized by dense, heavy bones ("marble bones"), the osteoclasts lack ruffled borders, and bone resorption is defective.

The organic matter in bone matrix is type I collagen and ground substance, which contains proteoglycan aggregates and several specific structural glycoproteins. Bone glycoproteins may be responsible for promoting calcification of bone matrix. Other tissues containing type I collagen are not normally calcified and do not contain these glycoproteins. Because of its high collagen content, decalcified bone matrix intensely binds stains for collagen fibers.

The association of minerals with collagen fibers is responsible for the hardness and resistance of bone tissue. After a bone is decalcified, its shape is preserved, but it becomes as flexible as a tendon. Removal of the organic part of the matrix—which is mainly collagenous—also leaves the bone with its original shape; however, it becomes fragile, breaking and crumbling easily when handled.

PERIOSTEUM & ENDOSTEUM

External and internal surfaces of bone are covered by layers of bone-forming cells and connective tissue called periosteum and endosteum.

The periosteum consists of an outer layer of collagen fibers and fibroblasts (Figure 8–6). Bundles of periosteal collagen fibers, called Sharpey's fibers, penetrate the bone matrix, binding the periosteum to bone. The inner, more cellular layer of the periosteum is composed of fibroblastlike cells called osteoprogenitor cells, with the potential to divide by mitosis and differentiate into osteoblasts. Autoradiographic studies demonstrate that these cells take up [³H]thymidine, which is subsequently encountered in osteoblasts. Osteoprogenitor cells play a prominent role in bone growth and repair.

The endosteum (Figure 8–6) lines all internal cavities within the bone and is composed of a single layer of flattened osteoprogenitor cells and a very small amount of connective tissue. The endosteum is therefore considerably thinner than the periosteum.

The principal functions of periosteum and endosteum are nutrition of osseous tissue and provision of a continuous supply of new osteoblasts for repair or growth of bone.

TYPES OF BONE

Gross observation of bone in cross section shows dense areas without cavities—corresponding to compact bone—and areas with numerous interconnecting cavities—corresponding to cancellous (spongy) bone (Figure 8–7). Under the microscope, however, both compact bone and the trabeculae separating the cavities of cancellous bone have the same basic histological structure.

In long bones, the bulbous ends—called epiphyses (Gr. epiphysis, an excrescence)—are composed of spongy bone covered by a thin layer of compact bone. The cylindrical part—diaphysis (Gr. diaphysis, a growing between)—is almost totally composed of compact bone, with a small component of spongy bone on its inner surface around the bone marrow cavity. Short bones usually have a core of spongy bone completely surrounded by compact bone. The flat bones that form the calvaria have two layers of compact bone called plates (tables), separated by a layer of spongy bone called the diploë.

Microscopic examination of bone shows two varieties: primary, immature, or woven bone and secondary, mature, or lamellar bone. Primary bone is the first bone tissue to appear in embryonic development and in fracture repair and other repair processes. It is characterized by random disposition of fine collagen fibers, in contrast to the organized lamellar disposition of collagen in secondary bone.

Primary Bone Tissue

Primary bone tissue is usually temporary and, except in a very few places in the body (eg, near the sutures of the flat bones of the skull, in tooth sockets, and in the insertions of some tendons), is replaced in adults by secondary bone tissue.

In addition to the irregular array of collagen fibers, other characteristics of primary bone tissue are a lower mineral content (it is more easily penetrated by x-rays) and a higher proportion of osteocytes than in secondary bone tissue.

Secondary Bone Tissue

Secondary bone tissue is usually found in adults. It characteristically shows collagen fibers arranged in lamellae (3–7 m thick) that are parallel to each other or concentrically organized around a vascular canal. The whole complex of concentric lamellae of bone surrounding a canal containing blood vessels, nerves, and loose connective tissue is called a haversian system, or osteon (Figures 8–6 and 8–8). Lacunae containing osteocytes are found between, and occasionally within, the lamellae. In each lamella, collagen fibers are parallel to each other. Surrounding each haversian system is a deposit of amorphous material called the cementing substance that consists of mineralized matrix with few collagen fibers.

In compact bone (eg, the diaphysis of long bones), the lamellae exhibit a typical organization consisting of haversian systems, outer circumferential lamellae, inner circumferential lamellae, and interstitial lamellae (Figures 8–6 and 8–9).

Inner circumferential lamellae are located around the marrow cavity, and outer circumferential lamellae are located immediately beneath the periosteum. There are more outer than inner lamellae.

Between the two circumferential systems are numerous haversian systems, including triangular or irregularly shaped groups of parallel lamellae called interstitial (or intermediate) lamellae. These structures are lamellae left by haversian systems destroyed during growth and remodeling of bone (Figure 8–10).

Each haversian system is a long, often bifurcated cylinder parallel to the long axis of the diaphysis. It consists of a central canal surrounded by 4–20 concentric lamellae (Figure 8–11). Each endosteum-lined canal contains blood vessels, nerves, and loose connective tissue. The haversian canals communicate with the marrow cavity, the periosteum, and one another through transverse or oblique Volkmann's canals (Figure 8–6). Volkmann's canals do not have concentric lamellae; instead, they perforate the lamellae. All vascular canals found in bone tissue come into existence when matrix is laid down around preexisting blood vessels.

Examination of haversian systems with polarized light shows bright anisotropic layers alternating with dark isotropic layers (Figure 8–11). When observed under polarized light at right angles to their length, collagen fibers are birefringent (anisotropic). The alternating bright and dark layers are due to the changing orientation of collagen fibers in the lamellae. In each lamella, fibers are parallel to each other and follow a helical course. The pitch of the helix is, however, different for different lamellae, so that at any given point, fibers from adjacent lamellae intersect at approximately right angles (Figure 8–6).

Because bone tissue is constantly being remodeled, there is great variability in the diameter of haversian canals. Each system is formed by successive deposits of lamellae, starting inward from the periphery, so that younger systems have larger canals. In mature haversian systems, the most recently formed lamella is the one closest to the central canal.

HISTOGENESIS

Bone can be formed in two ways: by direct mineralization of matrix secreted by osteoblasts (intramembranous ossification) or by deposition of bone matrix on a preexisting cartilage matrix (endochondral ossification).

In both processes, the bone tissue that appears first is primary, or woven. Primary bone is a temporary tissue and is soon replaced by the definitive lamellar, or secondary, bone. During bone growth, areas of primary bone, areas of resorption, and areas of secondary bone appear side by side. This combination of bone synthesis and removal (remodeling) occurs not only in growing bones but also throughout adult life, although its rate of change in adults is considerably slower.

Intramembranous Ossification

Intramembranous ossification, the source of most of the flat bones, is so called because it takes place within condensations of mesenchymal tissue. The frontal and parietal bones of the skull—as well as parts of the occipital and temporal bones and the mandible and maxilla—are formed by intramembranous ossification. This process also contributes to the growth of short bones and the thickening of long bones.

In the mesenchymal condensation layer, the starting point for ossification is called a primary ossification center. The process begins when groups of cells differentiate into osteoblasts. Osteoblasts produce bone matrix and calcification follows, resulting in the encapsulation of some osteoblasts, which then become osteocytes (Figure 8–12). These islands of developing bone form walls that delineate elongated cavities containing capillaries, bone marrow cells, and undifferentiated cells. Several such groups arise almost simultaneously at the ossification center, so that the fusion of the walls gives the bone a spongy structure. The connective tissue that remains among the bone walls is penetrated by growing blood vessels and additional undifferentiated mesenchymal cells, giving rise to the bone marrow cells.

The ossification centers of a bone grow radially and finally fuse together, replacing the original connective tissue. The fontanelles of newborn infants, for example, are soft areas in the skull that correspond to parts of the connective tissue that are not yet ossified.

In cranial flat bones there is a marked predominance of bone formation over bone resorption at both the internal and external surfaces. Thus, two layers of compact bone (internal and external plates) arise, whereas the central portion (diploë) maintains its spongy nature.

The portion of the connective tissue layer that does not undergo ossification gives rise to the endosteum and the periosteum of intramembranous bone.

Endochondral Ossification

Endochondral (Gr. endon, within, + chondros, cartilage) ossification takes place within a piece of hyaline cartilage whose shape resembles a small version, or model, of the bone to be formed. This type of ossification (Figures 8–13 and 8–14) is principally responsible for the formation of short and long bones.

Endochondral ossification of a long bone consists of the following sequence of events. Initially, the first bone tissue appears as a hollow bone cylinder that surrounds the mid portion of the cartilage model. This structure, the bone collar, is produced by intramembranous ossification within the local perichondrium. In the next step, the local cartilage undergoes a degenerative process of programmed cell death with cell enlargement (hypertrophy) and matrix calcification, resulting in a three-dimensional structure formed by the remnants of the calcified cartilage matrix (Figure 8–15). This process begins at the central portion of the cartilage model (diaphysis), where blood vessels penetrate through the bone collar previously perforated by osteoclasts, bringing osteoprogenitor cells to this region. Next, osteoblasts adhere to the calcified cartilage matrix and produce continuous layers of primary bone that surround the cartilaginous matrix remnants. At this stage, the calcified cartilage appears basophilic, and the primary bone is eosinophilic. In this way the primary ossification center is produced (Figure 8–13). Then, secondary ossification centers appear at the swellings in the extremities of the cartilage model (epiphyses). During their expansion and remodeling, the primary and secondary ossification centers produce cavities that are gradually filled with bone marrow.

In the secondary ossification centers, cartilage remains in two regions: the articular cartilage, which persists throughout adult life and does not contribute to bone growth in length, and the epiphyseal cartilage, also called the epiphyseal plate, which connects the two epiphyses to the diaphysis (Figures 8–15 and 8–16). The epiphyseal cartilage is responsible for the growth in length of the bone, and it disappears in adults, which is why bone growth ceases in adulthood.

The closure of the epiphyses follows a chronological order according to each bone and is complete at about 20 years of age. Through x-ray examination of the growing skeleton, it is possible to determine the "bone age" of a young person, noting which epiphyses are open and which are closed. Once the epiphyses have closed, growth in length of bones becomes impossible, although widening may still occur.

Epiphyseal cartilage is divided into five zones (Figure 8–16), starting from the epiphyseal side of cartilage: (1) The resting zone consists of hyaline cartilage without morphological changes in the cells. (2) In the proliferative zone, chondrocytes divide rapidly and form columns of stacked cells parallel to the long axis of the bone. (3) The hypertrophic cartilage zone contains large chondrocytes whose cytoplasm has accumulated glycogen. The resorbed matrix is reduced to thin septa between the chondrocytes. (4) Simultaneous with the death of chondrocytes in the calcified cartilage zone, the thin septa of cartilage matrix become calcified by the deposit of hydroxyapatite (Figures 8–15 and 8–16). (5) In the ossification zone, endochondral bone tissue appears. Blood capillaries and osteoprogenitor cells formed by mitosis of cells originating from the periosteum invade the cavities left by the chondrocytes. The osteoprogenitor cells form osteoblasts, which are distributed in a discontinuous layer over the septa of calcified cartilage matrix. Ultimately, the osteoblasts deposit bone matrix over the three-dimensional calcified cartilage matrix (Figures 8–17, 8–18, 8–19, and 8–20).

In summary, growth in length of a long bone occurs by proliferation of chondrocytes in the epiphyseal plate adjacent to the epiphysis. At the same time, chondrocytes of the diaphyseal side of the plate hypertrophy; their matrix becomes calcified, and the cells die. Osteoblasts lay down a layer of primary bone on the calcified cartilage matrix. Because the rates of these two opposing events (proliferation and destruction) are approximately equal, the epiphyseal plate does not change thickness. Instead, it is displaced away from the middle of the diaphysis, resulting in growth in length of the bone.

Mechanisms of Calcification

There is still no generally accepted hypothesis to explain the events occurring during calcium phosphate deposition on bone matrix.

It is known that calcification begins by the deposition of calcium salts on collagen fibrils, a process induced by proteoglycans and high-affinity calcium-binding glycoproteins. The deposition of calcium salts is probably accelerated by the ability of osteoblasts to concentrate them in intracytoplasmic vesicles and to release these vesicles, when necessary, to the extracellular medium (matrix vesicles).

Calcification is aided, in some unknown way, by alkaline phosphatase, which is produced by osteoblasts and is present at ossification sites.

BONE GROWTH & REMODELING

Bone growth is generally associated with partial resorption of preformed tissue and the simultaneous laying down of new bone (exceeding the rate of bone loss). This process permits the shape of the bone to be maintained while it grows. Bone remodeling (bone turnover) is very active in young children, where it can be 200 times faster than the rate in adults. Bone remodeling in adults is a dynamic physiological process that occurs simultaneously in multiple locations of the skeleton, not related to bone growth.

Cranial bones grow mainly because of the formation of bone tissue by the periosteum between the sutures and on the external bone surface. At the same time, resorption takes place on the internal surface. Because bone is an extremely plastic tissue, it responds to the growth of the brain and forms a skull of adequate size. The skull will be small if the brain does not develop completely and will be larger than normal in a person suffering from hydrocephalus, a disorder characterized by abnormal accumulation of spinal fluid and dilatation of the cerebral ventricles.

Fracture Repair

MEDICAL APPLICATION

When a bone is fractured, bone matrix is destroyed and bone cells adjoining the fracture die. The damaged blood vessels produce a localized hemorrhage and form a blood clot.

During repair, the blood clot, cells, and damaged bone matrix are removed by macrophages. The periosteum and the endosteum around the fracture respond with intense proliferation producing a tissue that surrounds the fracture and penetrates between the extremities of the fractured bone (Figure 8–21).

Primary bone is then formed by endochondral and intramembranous ossification, both processes contributing simultaneously to the healing of fractures. Repair progresses in such a way that irregularly formed trabeculae of primary bone temporarily unite the extremities of the fractured bone, forming a bone callus (Figure 8–21).

Stresses imposed on the bone during repair and during the patient's gradual return to activity serve to remodel the bone callus. If these stresses are identical to those that occurred during the growth of the bone—and therefore influence its structure—the primary bone tissue of the callus is gradually resorbed and replaced by secondary tissue, remodeling the bone and restoring its original structure (Figure 8–21). Unlike other connective tissues, bone tissue heals without forming a scar.

INTERNAL STRUCTURE OF BONES

Despite its hardness, bone is capable of changes in its internal structure in response to the various stresses to which it is subjected. For example, the positions of the teeth in the jawbone can be modified by lateral pressures produced by orthodontic appliances. Bone is formed on the side where traction is applied and is resorbed where pressure is exerted (on the opposite side). In this way, teeth move within the jawbone while the alveolar bone is being remodeled.

METABOLIC ROLE OF BONE TISSUE

The skeleton contains 99% of the total calcium of the body and acts as a reservoir of calcium and phosphate ions. The concentration of calcium ions in the blood and tissues is quite stable because of a continuous interchange between blood calcium and bone calcium.

Bone calcium is mobilized by two mechanisms, one rapid and the other slow. The first is the simple transfer of ions from hydroxyapatite crystals to interstitial fluid—from which, in turn, calcium passes into the blood. This purely physical mechanism takes place mainly in spongy bone. The younger, slightly calcified lamellae that exist even in adult bone (because of continuous remodeling) receive and lose calcium more readily. These lamellae are more important for the maintenance of calcium concentration in the blood than are the older, greatly calcified lamellae, whose role is mainly that of support and protection.

The second mechanism for controlling blood calcium level depends on the action of hormones on bone. Parathyroid hormone promotes osteoclastic resorption of the bone matrix with the consequent liberation of calcium. This hormone acts primarily on osteoblast receptors. The activated osteoblasts stop producing bone and start the secretion of an osteoclast-stimulating factor.

Another hormone, calcitonin, which is synthesized mainly by the parafollicular cells of the thyroid gland, inhibits matrix resorption. Calcitonin has an inhibitory effect on osteoclast activity.

MEDICAL APPLICATION

Because the concentration of calcium in tissues and blood must be kept constant, nutritional deficiency of calcium results in decalcification of bones; decalcified bones are more likely to fracture and are more transparent to x-rays.

Decalcification of bone may also be caused by excessive production of parathyroid hormone (hyperparathyroidism), which results in increased osteoclastic activity, intense resorption of bone, elevation of blood Ca²⁺ and PO₄^3– levels, and abnormal deposits of calcium in several organs, mainly the kidneys and arterial walls.

The opposite occurs in osteopetrosis (L. petra, stone), a disease caused by a defect in osteoclast function that results in overgrowth, thickening, and hardening of bones. This process produces obliteration of the bone marrow cavities, depressing blood cell formation with consequent anemia and frequent infections that may be fatal.

Effects of Nutritional Deficiencies on Bone Tissue

Bone is very sensitive to nutritional factors during growth. Deficiency of calcium leads to incomplete calcification of the organic bone matrix, due either to the lack of calcium in the diet or to the lack of the steroid prohormone vitamin D, which is important for the absorption of Ca²⁺ and PO₄^3– by the small intestine.

Calcium deficiency in children causes rickets, a disease in which the bone matrix does not calcify normally and the epiphyseal plate becomes distorted by the normal strains of body weight and muscular activity. Ossification processes at this level are consequently hindered, and the bones not only grow more slowly but also become deformed.

Calcium deficiency in adults gives rise to osteomalacia (osteon + Gr. malakia, softness), which is characterized by deficient calcification of recently formed bone and partial decalcification of already calcified matrix. Osteomalacia should not be confused with osteoporosis. In osteomalacia, there is a decrease in the amount of calcium per unit of bone matrix. Osteoporosis, frequently found in immobilized patients and in postmenopausal women, is an imbalance in skeletal turnover so that bone resorption exceeds bone formation.

Hormones Acting on Bone Tissue

In addition to parathyroid hormone and calcitonin, several other hormones act on bone. The anterior lobe of the pituitary synthesizes growth hormone, which stimulates the liver to produce somatomedins. This, in turn, has an overall effect on growth, especially on the epiphyseal cartilage. Consequently, lack of growth hormone during the growing years causes pituitary dwarfism; an excess of growth hormone causes excessive growth of the long bones, resulting in gigantism. Adult bones cannot increase in length when stimulated by an excess of somatomedins because of the lack of epiphyseal cartilage, but they do increase in width by periosteal growth. In adults, an increase in growth hormone causes acromegaly, a disease in which the bones—mainly the long ones—become very thick.

The sex hormones, both male (androgens) and female (estrogens), have a complex effect on bones and are, in a general way, stimulators of bone formation. They influence the time of appearance and development of ossification centers and accelerate the closure of epiphyses.

Precocious sexual maturity caused by sex hormone-producing tumors retards bodily growth, since the epiphyseal cartilage is quickly replaced by bone (closure of epiphysis). In hormone deficiencies caused by abnormal development of the gonads, epiphyseal cartilage remains functional for a longer period of time, resulting in tall stature. Thyroid hormone deficiency in children, as in cretinism, is associated with dwarfism. Recent evidence indicates that the central nervous system participates in the regulation of bone formation during bone remodeling in adult mice. This regulatory mechanism involves the hormone leptin produced by adipose tissue and may thus explain the observation that bones of obese people have an increased mass, containing a higher concentration of calcium.

Bone Tumors

Although bone tumors are uncommon (0.5% of all cancer deaths), bone cells may escape the normal controls of proliferation to become benign (eg, osteoblastoma, osteoclastoma) or malignant (eg, osteosarcoma) tumors. Osteosarcomas show pleomorphic (Gr. pleion, more, + morphe, form) and mitotically active osteoblasts associated with osteoid. Most cases of this aggressive malignant tumor occur in adolescents and young adults. The lower end of the femur, the upper tibia, and the upper humerus are the most common locations. In addition to the tumors originating from bone cells, the skeleton is often the site of metastases from malignant tumors originating in other organs. The most frequent bone metastases are from breast, lung, prostate, kidney, and thyroid tumors.

JOINTS

Joints are regions in which bones are capped and surrounded by connective tissues that hold the bones together and determine the type and degree of movement between them. Joints may be classified as diarthroses, in which there is free bone movement, or synarthroses (Gr. syn, together, + arthrosis, articulation), in which very limited or no movement occurs. There are three types of synarthroses, based on the type of tissue uniting the bone surfaces: synostosis, synchondrosis, and syndesmosis.

In synostosis (syn + osteon + Gr. osis, condition), bones are united by bone tissue and no movement takes place. In older adults, this type of synarthrosis unites the skull bones, which, in children and young adults, are united by dense connective tissue.

Synchondroses (syn + chondros) are articulations in which the bones are joined by hyaline cartilage. The epiphyseal plates of growing bones are one example, and in the adult human, synchondrosis unites the first rib to the sternum.

As with synchondrosis, a syndesmosis permits a certain amount of movement. The bones are joined by an interosseous ligament of dense connective tissue (eg, the pubic symphysis).

Diarthroses (Figures 8–22 and 8–23) are joints that generally unite long bones and have great mobility, such as the elbow and knee joints. In a diarthrosis, ligaments and a capsule of connective tissue maintain the contact at the ends of the bone. The capsule encloses a sealed articular cavity that contains synovial fluid, a colorless, transparent, viscous fluid. Synovial fluid is a blood plasma dialysate with a high concentration of hyaluronic acid produced by cells of the synovial layer. The sliding of articular surfaces covered by hyaline cartilage (Figure 8–22) and having no perichondrium is facilitated by the lubricating synovial fluid, which also supplies nutrients and oxygen to the avascular articular cartilage.

The collagen fibers of the articular surface cartilage are disposed as gothic arches, a convenient arrangement to distribute the forces generated by pressure in this tissue (Figure 8–24).

The resilient articular cartilage is also an efficient absorber of the intermittent mechanical pressures to which many joints are subjected. A similar mechanism is seen in intervertebral disks (Figure 8–25). Proteoglycan molecules, found isolated or aggregated in a network, contain a large amount of water. These matrix components, rich in highly branched hydrophilic glycosaminoglycans, function as a biomechanical spring. When pressure is applied, water is forced out of the cartilage matrix into the synovial fluid. When water is expelled, another mechanism that contributes to cartilage resilience enters into play. This is the reciprocal electrostatic repulsion of the negatively charged carboxyl and sulfate groups in the glycosaminoglycan molecules. These charges are also responsible for separating the glycosaminoglycan branches and thus creating spaces to be occupied by water. When the pressure is released, water is attracted back into the interstices of the glycosaminoglycan branches. These water movements are brought about by the use of the joint. They are essential for nutrition of the cartilage and for facilitating the interchange of O₂, CO₂, and other molecules between the synovial fluid and the articular cartilage.

The capsules of diarthroses (Figure 8–22) vary in structure according to the joint. Generally, however, this capsule is composed of two layers, the external fibrous layer and the internal synovial layer (Figure 8–26).

The synovial layer is formed by two types of cells. One resembles fibroblasts and the other has the aspect and behavior of macrophages (Figure 8–27). The fibrous layer is made of dense connective tissue.

MEDICAL APPLICATION

Obesity imposes significant strain on the articular cartilage, accelerating its degeneration. Joint problems are far more frequent in obese individuals.

REFERENCES