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The Bone Essay

The skeletal system includes the osseous tissues of the body and the connective tissues that stabilize or interconnect the individual bones. The bone is a dynamic tissue. Throughout the lifespan, bone adjusts to the physiologic and mechanical demands placed on it by the processes of growth and remodeling. Bone serves the organism at multiple levels: As a system, bones permit the organism to locomote effectively and to maintain posture by bearing loads without deformation, by providing rigid attachment sites for muscles and acting as a system of levers to amplify small movements.

As an organ, bones protect the viscera and house the hemopoietic tissue (red marrow). As a tissue, bones serve as a reservoir of readily mobilizable calcium, an ion vital for many metabolic processes including cell motility, excitability, secretion, phagocytosis, intermediary metabolism, respiration, and reproduction. Bones (or osseous material) serve a number of diverse purposes in the human anatomy. In addition to providing structure, leverage, protection, and support for the organs of the body, bones also house marrow, which produces blood cells.

Within the bones are also stored the calcium deposits which the body may access, via resorption, when needed. Additionally, bones detoxify the system, by removing heavy metals, such as lead and arsenic, as well as other toxins, from the bloodstream. The skeletal system provides structural support for the entire body. Individual bones or groups of bones provide a framework for the attachment of soft tissue and organs. Delicate tissues and organs are often surrounded by skeletal elements.

The ribs protect the heart and lungs, the skull encloses the brain, the vertebrae shield the spinal cord, and the pelvis cradles delicate digestive and reproductive organs. Red blood cells and other blood elements are produced within the bone marrow that fills the internal cavities of many bones. The calcium salts of bone represent a valuable mineral reserve that maintains normal concentrations of calcium and phosphate ions in body fluids. In addition, fat cells within marrow cavities store lipids that represent an important energy reserve.

The bones of the skeleton function as levers that direct and modify the forces generated by skeletal muscles. The movements produced range from the delicate motion of a fingertip to powerful changes in the position of the entire body. Osseous tissue contains specialized cells, cell products, and a fluid matrix. The distinctive solid, stony nature of bone results from the deposition of calcium salts within the matrix. Crystals of calcium phosphate account for almost two-thirds of the weight of the bone.

The majority of bone mineral occurs in the form of hydroxylated calcium phosphate crystals Ca 10 [PO 4 ] 6 [OH]2 ) referred to as hydroxyapatite. The remaining third is dominated by collagen fibers, with osteocytes and proteoglycans contributing only around 2 percent. Calcium phosphate crystals are very strong, but inflexible. They can withstand compression, but the crystals are likely to shatter when exposed to bending, twisting, or sudden impacts. Collagen fibers are extremely tough, but quite flexible. They can easily tolerate stretching, twisting, and bending, but when compressed they simply bend out of the way.

In bone, the collagen fibers provide an organic framework for the formation of mineral crystals. The combination has properties intermediate between those of collagen and those of pure mineral crystals. When you examine sections of bone taken from different sites, you find two different architectural arrangements. Dense, or compact bone is relatively solid, whereas spongy, or cancellous bone resembles a network of bony shafts separated by marrow spaces. In both types of bone the individual bone cells, or osteocytes, reside within small pockets called lacunae.

These lacunae are found between narrow sheets of calcified matrix, know as lamellae. Individual lamellae range between 4um and 12um in thickness. Small channels radiate through the matrix, interconnecting lacunae and linking them to nearby blood vessels. These canaliculi contain cytoplasmic extensions of the osteocytes and their extensions provide a route for the diffusion of nutrients and waste products. Microscopic organization of bone tissue can be divided into two bone types. Primary or woven bone is bone which is produced de novo by intramembranous or endochondral ossification.

It has a highly irregular arrangement. Woven bone is weaker than lamellar bone due to the random organization of collagen fibers and greater number of osteocytes. Secondary or lamellar bone is highly organized mature bone. The collagen framework and mineralized matrix are arranged in lamellae or layers; collagen fibers of each lamella run in opposite helical directions to those in adjacent lamellae, thereby increasing the strength of the microscopic unit. Lamellar bone exists in three forms: osteonal, circumferential, and intersitial.

First, osteonal lamellar bone or the Haversian system is 200mm cylindrical units comprised of 15-20 lamellae surrounding a 50mm neurovascular canal called the Haversian canal. Osteocytes contained in lacunae are located between lamellae and are interconnected by canaliculi. Haversian canals are joined by perpendicular vascular channels called Volkmanns canals. Endosteum lines the Haversian and Volkmann canals. In long bones, osteons run parallel to the long axis of the bone. Second, Circumferential lamellar bone are large scale lamellae adjacent to the preinstall and endosteal surfaces of a long bone.

Third, Interstitial lamellar bone are remnants of old Haversian systems that have been cut by remodeling units. Lamellar bone exists in two macroscopic arrangement based on its degree of porosity: Compact (cortical) bone or spongy (cancellous, trabecular) bone. In compact bone the microscopic units are arranged in tightly packed parallel columns with very little space intervening (10% porosity), creating the illusion of a solid mass. This type of bone forms the outer shell of the skeletal elements and thus often is referred to as cortical bone. Cortical bone provides the strength to resist weight-bearing forces in the long bone.

In contrast, spongy bone is composed of irregularly branching trabeculae (struts or plates) surrounded by a great deal of space (50-90% porosity). Spongy bone is located in the epiphyseal ends of long bones and predominates in short and irregular bones of the skeleton. The open array of spicules/trabeculae serves to distribute forces from the joint surface to the diaphysial cortex and permit a certain degree of deformation for shock and absorption. The composition of bone consists of cells including osteoblast, osteocytes, and osteoclasts, bone lining cells, the extracellular matrix, and the periosteum and endosteum.

Osteoblasts are derived from osteoprogenitor cells, which are like stem cells for the bone, which are mesenchymal in origin. The fully differentiated osteoblasts produce and secrete the organic components or proteins of the matrix (collagens, proteoglycans, and glycoproteins) called osteoid. Since these are gene products, they need protein producing machinery to complete their function. Once the cell is surrounded by osteoid, the matrix mineralizes (the exact trigger for mineralization is still under investigation) and the osteoblast advances to the next maturity level, the ostoecyte.

They initiate mineralization of osteoid material, possibly by modulating electrolyte fluxes between the extracellular fluid volume and osseous fluid. Osteoblasts are in contact with one another and with mature osteocytes through cellular processes. Contact is maintained following mineralization. Histologically, osteoblasts appear basophilic due to the high concentration of rough endoplasmic reticulum. Osteoblasts are located on bone and calcified cartilage. They are connected by numerous gap junctions, facilitating electrical/chemical communication between cells.

The detection of mechanical signals and translation into a biological response is termed mechanotransduction and involves signal transduction between osteocytes and cells at the bone surface as described below: Osteoblast precursors most likely reach the bone by migration of progenitors from neighboring connective tissue. A major product of the bone-forming osteoblast is type I collagen. This polymeric protein is initially secreted in the form of a precursor, which contains peptide extensions . the propeptides are proteolytically removed.

Further extracellular processes results in mature three-chained type I collagen molecules, which then assemble themselves into a collagen fibril. Individual collagen molecules become interconnected by the formation of pyridinoline cross-links, which are unique to bone. Osteoblasts are essential for the mineralization of bone through the process of deposition of hydroxyapatite. They do this by regulating the concentrations of calcium and phosphate to promote its formation. Osteoblasts express high amounts of alkaline phosphatase, an enzyme which is anchored to the external surface of the plasma membrane.

Osteocytes are fully embedded in mineralized matrix and reside in chambers called lacunae. They maintain bone and comprise 90% of all cells in the mature skeleton. They originate as osteoblasts that have been trapped within osteoid formed by surrounding osteoblasts forming the lacuna. Compared with osteoblasts, osteocytes are smaller and have fewer numbers of organelles, although they do have a significant number of rough endoplasmic reticulum and have a prominent nucleus and nucleoli, therefore are not as active in matrix production.

They maintain the cytoplasmic extensions of the osteoblasts, creating a large canalicular system. They communicate with each other and with cells on the bone surface via multiple extensions of their plasma membrane that run along the canaliculi; osteoblasts, in turn, communicate with cells of the bone marrow stroma which extend cellular projections onto endothelial cells inside the sinusoids. This system may transport biophysical data to cells within and at the surface of the bone. They are directly stimulated by calcitonin and inhibited by PTH.

Gap junctions located between osteocyte cell processes physically connect the cells to one another. The continuity between cells allows for the transfer of nutrients, hormones, wastes, and mechanical messages in an otherwise inhospitable environment. They sense the need for growth or destruction of bone and send messages to other cells to make or destroy it. Osteoclasts are multinucleated cells with abundant mitochondria, lysosomes, and free ribosomes derived from the monocyte/macrophage cell family and function to reabsorb bone tissue. They act in opposition to osteoblasts.

These cells play an important role in remodeling and calcium homeostasis. Osteoclasts attach to the bone surface by their ruffled borders and digest away the inorganic matrix with acids and the organic matrix with enzymes. Recognition and adherence to the bone surface is mediated via intracellular contractile proteins attached to integrinsXthis leads to the formation of a apical clear zone and a ruffled border. Vacuolar proton-ATPase pumps then localize to this ruffled border and act with intracellular carbonic anhydrase II to lower the pH of the extracellular bone compartment, thus forming a resorption pit.

The resulting depression and seat for the osteoclast is known as a Howships lacuna. The lowered pH increases the solubility of hydroxyapatite crystals, and the exposed organic matrix is then digested by lysosomal enzymes. Histologically, osteoclast exhibit acidophillic cytoplasm due to abundance of mitochondria, which are needed for operation of proton pumps at the ruffled border. Osteoclasts cannot attach to the unmineralized collagenous layer that covers the surface of normal bone. Therefore, other cells, perhaps the lining cells, secrete collagenase, which removes this matrix before osteoclasts can attach to bone.

Bone-lining cells are narrow, flattened cells that differentiate from osteoblasts and cover the unmineralized collagen matrix. Their function is to encase the bone surface and moderate site-specific mineralization or resorption on activation by PTH. Both ostoeblasts and osteoclast are derived from precursors originating in the bone marrow. The precursors of osteoblasts are multipotent mesenchymal stem cells, which also give rise to bone marrow stromal cells, chondrocytes, muscle cells, and adipocytes, whereas the precursors of osteoclasts are hematopoietic cells of the monocyte/macrophage lineage.

Whereas osteoclast precursors reach bone from the circulation, osteoblast precursors most likely reach bone by migration of progenitors from neighboring connective tissue. The development and differentiation of osteoblasts and osteoclasts are controlled by growth factors and cytokines produced in the bone marrow microenvironment as well as adhesion molecules that mediate cell-cell and cell-matrix interactions. Several systemic hormones as well as mechanical signals also exert potent effects on osteoclast and osteoblast development and differentiation.

Although many details remain to be established concerning the operation of this network, a few themes have emerged. First, several of the growth factors and cytokines control each others production in a cascade fashion and , in some instances, form positive and negative feedback loops. Second, there is extensive functional redundancy among them. Third, some of the same factors are capable of influencing the differentiation of both osteoblasts and osteoclasts.

Fourth, systemic hormones influence the process of osteoblast and osteoclast formation via their ability to control the production and or action of local mediators. The only factors capable of initiating osteoblastogenesis from uncommitted progenitors are bone morphogenetic proteins (BMPs). BMPs stimulate the transcription of the gene encoding an osteoblast-specific transcription factor, known as osteoblast specific factor 2 (osf2) or core binding factor a1 (cbfal1). In turn, cbfal1 activates osteoblast-specific genes such as osteopontin, bone sialoprotein, type 1 collagen, and osteocalcin.

In addition to cbfa1, BMP-4 induces a homeobox-containing gene, distal-less 5, which also seems to act as a transcription factor, probably as a heterodime with another homeobox-containing protein. Distal-less 5 regulates the expression of osteoblast-specific genes such as osteocalcin and alkaline phosphatase as well as mineralization. In addition to growth factors, bone cells produce proteins that modulate the activity of growth factors either by binding to them and thereby preventing interaction with their receptors, by competing for the same receptors, or by promoting the activity of a particular factor.

Cytokines are capable of influencing the differentiation of osteoblasts as well. Thus, receptors for these cytokines are expressed on a variety of stromal/ osteoblastic cells, and ligand binding induces progression toward a more mature osteoblast phenotype, characterized by increased alkaline phosphatase and osteocalcin expression, and a concomitant decrease in proliferation. In addition to autocrine, paracrine, and endocrine signals, cell-cell and cell-matrix interactions are also required for the development of osteoclasts and osteoblasts.

Such interactions are mediated by proteins expressed on the surface of these cells and are responsible for contact between osteoclast precursors with stromal/osteoblastic cells and facilitation of the action of paracrine factors anchored to the surface of cells that are required for bone cell development. Adhesion molecules are also involved in the migration of osteoblast and osteoclast progenitors from the bone marrow to sites of bone remodeling as well as the cellular polarization of osteoclasts and the initiation and cessation of osteoclastic bone resorption.

The extracellular matrix consists of inorganic and organic components (osteoid). The organic components can be further divided into fibers and ground substances. Fibers account for approximately 90% of the organic portion of the matrix and serve as the framework for the deposition of inorganic materials. The fibrous scaffold is composed mostly of type I collagen. The remaining 10% of the organic matrix consists of an amorphous ground substance comprised of small proteoglycans (decorin and biglycan) and glycoproteins (osteocalcin, osteopontin, osteonectin).

These molecules have many functions that possibly, yet not conclusively, include adhesion between the matrix and cells, initiation of calcification, and control of cell proliferation. The inorganic matrix includes salts of calcium, phosphate, magnesium, carbonate, hydroxyl, chloride, fluoride, citrate, and sodium. The majority of bone mineral occurs in the form of hydroxylated calcium phosphate crystals referred to as hydroxyapatite. The hardness afforded by the mineral provides bone with resistance to compression while the toughness of the collagen provides bone with resistance to tensile stresses.

When these components are combined, bone is able to withstand the majority of imposed bending stresses during life. The periosteum is a layer of tissue lining the external surface of all bones while the endosteum lines the internal surfaces of bone including microscopic channels. The periosteum consists of two layers: an outer dense ct (fibrogenic) layer and an inner bone cell (osteogenic) layer. The endosteum consists of a single osteogenic layer. The periosteum isolates the bone from surrounding tissues, provides a route for circulatory and nervous supply, and actively participates in bone growth and repair.

The outer fibrous layer of the periosteum is primarily composed of type I collagen. Some fibers from the outer layer extend into the mineralized matrix of bone binding the structures to one another and providing a molecular link between bone and ultimately, the connective tissue sheaths of muscle. These fibers that cross into bone matrix are called Sharpeys fibers. Near articulations, the periosteum becomes continuous with the collagen fibers of the joint capsule. The fibers of tendons intermingle with those of the periosteum, attaching skeletal muscles to the bones they move.

Inside the bone, a cellular endosteum lines the marrow cavity. This layer covers the trabeculae of spongy bone and lines the inner surfaces of the central canals. The endosteum is especially active during the growth of bone and whenever repair or remodeling is underway. The endosteal lining is not a complete epithelium, and the matrix is occasionally exposed. At these sites are found osteoclasts. Acids secreted by osteoclasts dissolve the bony matrix and release the stored minerals. This process, called osteolysis, is important in the regulation of calcium and phosphate concentrations in body fluids.

The osteogenic layer and the endosteum consist of a single layer of osteoblasts. Upon completion of bone formation, osteoblasts that have not been incorporated in lacunae either become inactive bone-lining cells (also called surface osteocytes and inactive osteoblasts) of the periosteum/endosteum or they disappear entirely. Bone-lining cells of the peri/endosteum can be reactivated as occurs in fracture repair and certain pathologies. Human bones are mostly preformed from hyaline cartilage, some from condensed mesenchyme, usually at 6 weeks of gestation.

This cartilage model is gradually invaded by vascular buds, which bring in osteoprogenitor cells that differentiate into osteoblasts and form primary centers of ossification at around 8 weeks. The cartilage model grows through appositional growth (new bone is applied to the surface of existing bone leading to an increase in width of bone) and interstitial growth (growth and replacement by bone of deeper layers of epiphyseal growth plate, pushing the epiphysis and its overlying articular cartilage away from the metaphysis and diaphysisXleads to increased length of bone).

Ossification thus spreads to replace the cartilage model with bone. Marrow is formed by the resorption of the central cancellous bone and invasion of myeloid (blood cell) precursor cells, brought in by capillary buds. Secondary centers of ossification develop at the ends of bone, to form epiphyseal centers of ossification, which allow increase in length until the bones adult dimensions are obtained. During the developmental stage, the epiphyses enjoy a rich arterial supply composed of an dpiphyseal artery, metaphyseal arteries, nutrient arteries, and perichondral arteries.

In immature long bones there are 2 growth plates: 1) horizontal (the physis) and 2) spherical. Physeal cartilage is classified into zones according to growth and function. In the reserve zone, there is no evidence of cellular proliferation or active matrix production. There is decreased oxygen tension. Cells here store lipids, glycogen and proteoglycan aggregates for later growth. Therefore, diseases such as lysosomal storage diseases can affect this zone. In the proliferative zone, the cartilage cells undergo division and actively produce matrix, and the longitudinal growth occurs with chondrocytes forming columns.

The oxygen tension here is increased, and there is also increased proteoglycan in the surrounding matrix which inhibits calcification. Defects in this zone occur in achondroplasia. The hypertrophic zone can be subdivided into three zones: maturation, degeneration, and provisional calcification. Here the cartilage cells are greatly enlarged, they have clear cytoplasm as a result of the glycogen accumulated, and the matrix is compressed into linear bands between the columns of hypertrophied cells.

The cartilage cells accumulate calcium in mitochondria, then die, releasing calcium from matrix vesicles. Sinusoidal vessels bring osteoblasts, which use the cartilage as a template for bone formation. In the Metaphysis, osteoblasts from progenitor cells accumulate on cartilage bars formed by physeal expansion. Mineralization of primary spongiosa occurs, forming woven bone which is remodeled to form secondary spongiosa and a cutback zone at the metaphysis. Cortical bone is formed when physeal and intramembranous bone are remodeled in response to stress along the periphery of growing long bone.

The periphery of the Physis has 2 main components: the groove of Ranvier which allows chondrocytes to travel to the periphery of the growth plate, resulting in lateral growth, and the perichondrial rind of LaCroix with is dense fibrous tissue that anchors and supports the physis. Circulating hormones regulate the pattern of growth by changing the relationship between osteoblast and chondrocyte activity. Growth hormone, produced by the pituitary gland, and thyroxine, from the thyroid gland, maintain normal activity at the epiphyseal plates until roughly the time of puberty.

But when sexual hormone production increases, bone growth accelerates dramatically. Under this hormonal timulus the osteoblasts can produce bone faster than the cartilages can expand and the epiphyseal plates narrow and eventually ossify. The overall effect is a period of sudden growth that ends as the individual reaches sexual and physical maturity. The location of the plate can still be detected as a distinct epiphyseal line that remains after epiphyseal growth has ended. The flat bones of the skull, the mandible, and the clavicle ossify at least partly by intramembranous ossification.

This occurs without a cartilage model, and occurs by aggregation of layers of connective tissue cells at the site of future bone formation, and their differentionation into osteoblasts. The osteoblasts then form a center of ossification which expands by appositional growth which is where new cartilage is formed at cartilage surface by cells derived from chondroblasts of perichondrium. Once the skeleton has reached maturity, regeneration continues in the form of a periodic replacement of old bone with new at the same location.

This process is called remodeling and is responsible for the complete regeneration of the adult skeleton every 10 years. Osteoblasts and osteoclasts bring about remodelling in a coordinated fashion and their activities are regulated by genetic factors, systemic factors (eg hormones or drugs) and local tissue factors (eg cytokines and growth factors). Many of the signals can act directly on osteoblasts or osteoclasts, but the development of osteoclasts relies on signals which come from cells of the osteoblast lineage. Osteoclast precursors, for example, must come in contact with receptors on the osteoblast before they can proceed to maturity.

The evolution of a single basic multicellular unit (BMU) through successive stages of cancellous or Haversian remodelling is itself highly regulated and ordered. In Figure 3, the BMU is shown travelling left to right as it excavates a trench across the surface. It originates where a blood vessel arborises over a bone surface and is directed to remove a region of bone that is too old to carry out its function, or in need of repair due to microdamage. This direction tends to be largely mechanical in the metaphyses of long bones, and primarily metabolic (for calcium regulation etc) in the axial skeleton.

The BMU progresses beyond this target as part of the stochastic component of remodelling. progression is sustained by the continued recruitment of new pre-osteoclasts (Pre Oc) which need to be precisely targeted to the apex of the cutting cone adjacent to lining cells covering the bone that is about to be resorbed. Termination occurs when the supply of Pre Oc is turned off, but osteoblast recruitment continues until the trench is refilled. Not only is the evolution of a BMU highly ordered, but the thickness of bone resorbed (erosion depth) and replaced (the wall thickness) during remodelling is also highly regulated.

The wall thickness in osteons averages 75 mm and in cancellous bone 40 mm, with a small variation in the general population. For example, the coefficient of variation in wall thickness among young adults is only about 12%. The period of remodelling lasts between 2-8 months, but the lifespan of a typical osteoclast nucleus is only about 16 days, so continual recruitment and turnover of new preosteoclasts is required to sustain BMU progression. Because remodelling is occurring at a specific skeletal site, signals controlling BMU activity must originate from the BMU itself, or adjacent cells (such as bone lining cells).

So, how does the BMU regulate the depth to which it resorbs the old bone? It has been suggeted that osteoclast precursor recruitment determines the rate and forward advance of the BMU, but that nuclear turnover and osteoclast apoptosis determines the extent of lateral excavation as indicated in Figure 4. Each osteoclast undergoes apoptosis after about 12 days. This event may, itself, be linked to release of cytokines or factors involved in recruitment and targeting of osteoclast progenitor cells (OPC). The timing of apoptosis, however, determines the depth of erosion (E. De).

Just as the BMU provides signalling molecules such as cytokines to direct the recruitment and activity of new osteoclasts, the activity of the BMU is also thought to regulate the recruitment and arrival of osteoblast precursors. The linking of osteoclastic activity with subsequent bone formation is the phenomenon known as “coupling”. One possible coupling mechanism has been proposed and suggests that transforming growth factor (TGF) is laid down in the bone matrix in association with its binding protein.

This inactivates the matrix-bound protein and protects the peptide against the low pH environment beneath the osteoclast. As the pH rises outside the ruffled border of the osteoclast, the binding protein releases the peptide which may then stimulate the proliferation and recruitment of osteoblast precursors in the local environment of the BMU. The amount of bone formation may then be regulated in a concentration-dependent manner determined by the amount of bone resorbed. The average lifespan of human osteoclasts is about 2 weeks, while the average lifespan of osteoblasts is 3 months.

After osteoclasts have eroded to a particular distance, either from the central axis in cortical bone or to a particular depth from the surface in cancellous bone, they die and are quickly removed by phagocytes. Osteogenesis requires a continual source of minerals, especially calcium salts. During embryological development the necessary minerals are obtained from the mothers bloodstream. From infancy to adulthood, the diet must provide adequate amounts of calcium and phosphate, and the individual must be able to absorb and transport these minerals to the sites of bone formation.

Vitamin D plays an important role in normal calcium metabolism by stimulating the absorption and transport of calcium and phosphate ions. This vitamin can be obtained from the diet or manufactured by epidermal cells exposed to the ultraviolet radiation in sunlight. Deficiency of vitamin D results in poorly mineralized bone which leads to deformity; a condition known as rickets in children and osteomalacia in adults. In the vitamin D deficient state, there is a reduction in the absorption of calcium and phosphate, leading to a compensatory secondary hyperparathyroidism.

An initial increase in bone resorption is able to maintain normal serum calcium levels but continued deficiency exacerbates the secondary hyperparathyroidism causing loss of phosphate and decreased ability to maintain serum calcium levels. Vitamins A and C are also essential for normal bone growth and remodeling. Vitamin C is required for the proper function of type I collagen. Deficiency of vitamin C result in slowing of bone growth and repair due to impaired extracellular matrix production. Deficiency leads to defects in collagen growth and repair, and impaired hydroxylation of collagen peptides.

Hormones such as growth hormones, thyroid hormones, sex hormones, and those involved with calcium metabolism are also essential to normal skeletal growth and development. In the adult, osteocytes in lacunae maintain the surrounding matrix, continually removing and replacing the calcium salts. But osteoclasts and osteoblasts also remain active, even after the epiphyseal plates have closed. Normally their activities are balances, and as on osteon forms through the activity of osteoblasts, another is destroyed by osteoclasts. The turnover rate for bone is quite high, and up to 18% of the mineral components are removed and replaced each year.

Every part of every bone may not be affected as there are regional and even local differences in the rate of turnover. For example, spongy bone in the head of the femur may be replaced two or three times each year, whereas the compact bone along the shaft remains largely untouched. Building and demolishing almost one-fifth of the skeleton each year represents a substantial commitment of energy. Osteoblast sensitivity to electrical events has been suggested as the mechanism that controls the internal organization and structure of bone. Whenever a bone is stressed, the mineral crystals generate minute electrical fields.

Osteoblasts are apparently attracted to such fields, and one in the area they begin to produce bone. This may explain why the trabeculae of spongy bone are aligned with the stresses applied to the skeletal element, and why the trabecular structure changes when the applied forces increase or decrease. Similar factors affect the shapes of the bony surfaces. For example, bumps and ridges on the surface of a bone mark the site where tendons attach. If the muscle becomes more powerful, the corresponding ridge enlarges to withstand the increased force.

Heavily stressed bones become thicker and stronger, whereas bones not subjected to ordinary stresses will become thin and brittle. Regular exercise is therefore important as a stimulus that maintains normal bone structure. The bones of the skeleton are more than just racks to hang muscles on. They are also important mineral reservoirs. Calcium ion concentrations must be closely controlled to prevent damage to essential physiological systems. Even small variations from normal concentrations will have some effect on cellular operations. Larger changes can cause a clinical crisis.

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