CONTENTS:

1) Introduction 2) Composition 3) Function 4) Classification 5) Development 6) Mineralization of bone 7) Bone histology 8) Scanning electron microscopic appearance 9) Bone remodeling 10) Ageing and bone tissue 11) Clinical consideration 12) Conclusion 13) Refrences

INTRODUCTION: Bone is that living tissue that makes up the body skeleton and is one of the hardest substance in the human body. It possesses a certain degree of toughness and elasticity. It provides shape and size to the body, site for the attachment of muscles and tendon , which are essential for locomotion. Protects the vital organ of the body. Bone serve as the storage site for the minerals and the marrow for the development and storage of blood cells. COMPOSITION: Bone is the connective tissue composed of cells, fibres, and ground substance. The intercellular substance consists of organic and inorganic substances. Organic part consists of collagenous and non collagenous components. The inorganic part of bone is made of bone minerals. FUNCTION: SUPPORT It forms a supporting framework, giving shape & rigidity to the body. LOCOMOTION It forms a system to which the voluntary muscles are attached. PROTECTION It serves to protect the soft & delicate tissues of the body. E.g. skull protects the brain. MANUFACTURING OF BLOOD CELLS RBC are manufactured in red bone marrow which is situated in spongy tissue at the ends of long bones.

CLASSIFICATION 1. Macroscopic appearance of cut surface : Compact bone Trabecular bone 2. Development origin : Intramembranous Intracartilaginous

3. Regions of long bone:

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 Diaphysis Metaphysis Epiphysis 4. Organisation of collagen fibres Woven fibred bone Parallel fibred bone 5. General microstructure Non lamellar bone Lamellar bone 6. Disposition of lamellae Circumferential Osteonic Interstitial 7. Types of osteons Primary Secondary 8. General terms Surface bone Interstitial bone

9. Classification based on shape Long bones Short bones

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DEVELOPMENT: Bone formation occurs by three main mechanism: 1) Endochondral formation 2) Intramembranous formation 3) Sutural formation

1. ENDOCHONDRAL FORMATION: Occurs at the extremeties of all long bones, vertebrae, and ribs & at the articular extremeties of mandible and skull base. In embryonic development condensation of mesenchymel cells occurs. Cartilage cells differentiate from these mesenchymal cells & a perichondrium forms around the periphery giving rise to a cartilage model that eventually is replaced by bone. o CARTILAGE DEVELOPMENT: At site embryo shows outgrowth of mesoderm covered by ectoderm. Mesenchymal cells in this site condense differentiate into chondroblast & cartilage matrix forming CARTILAGE MODEL. It begins in second month of development. Model is surrounded by perichondrium. Perichondrium is made up of an 2) Outer fibrous layer

1) Inner chondrogenic layer

Growth of cartilage occurs by two ways:

1) Interstitial growth in which there is increase in length of cartilage . 2) Appositional growth in which there is increase in width of the cartilage. As the differentiation of cartilage moves towards metaphysis, cells organized into longitudinal columns which are divided into three zones.

a) ZONE OF PROLIFERATION: In this zone cells are small and flat and constitute a sourse of new cells.

b) ZONE OF HYPERTROPHY AND MATURATION : The is the broadest zone. Chondrocyte hypertrophy & in early stage secrete type II collegen. Proteoglycans are secreted. Increase in size & cell secretion increases the size of the cartilage model. In maximum size type X collagen & non collagenous
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protein are secreted. Then there breakdown of proteoglycan which create a matrix environment receptive for mineral deposition. c) ZONE OF PROVISIONAL MINERALIZATION: Begins after formation of matrix vesicles. Vesicles contain alkaline phosphatase, calcium adinottriphosohate, proteoglycan, which bind to calcium & inorganic phosphate. o FORMATION OF BONE COLLAR: Chondrocytes in the midregion hypertrophy. Some of these hypertrophied cells burst, thereby releasing there contents, which changes the Ph of the matrix. This change in the Ph triggers calcification. Once the cartilage calcifies, other chondrocytes die because adequate nutrition does not reach them via the matrix. The lacunae of these cells become empty and form small cavities. The nutrient artery then penetrates the perichondrium and bone through the nutrient foramen. This stimulates the osteoprogenitor cells in perichondrium to form osteoblasts which then lay down a thin shell of compact bone k/a periosteal bone collar. The perichondrium is now k/a the periosteum. Formation of Periosteal Bud:

Perivascular cells with blood vessels invade in the middle of the module. Perivascular cells along with blood vessels forms periosteal bud. Periosteal capillaries grow into the cartilage model and initiate the development of PRIMARY SSIFICATION CENTRE , a region where bone tissue will replace most of the cartilaginous tissue. Perivascular cells give rise to osteoblast and deposit bone matrix which form cancellous bone with

remnants of calcified cartilage it is called mixed spicules. Bone matrix entraps osteoblasts to form osteocytes. Network of mixed spicules collectively termed primary spongiosa. o FORMATION OF MEDULLARY CAVITY: Space created by vascular system develop red bone marrow. Osteoclasts remove the core of mineralized cartilage & surrounding bone, so that cartilage activity gets limited to extremeties of bone. Process occurs at some rate as cartilage formation. It open up a medullary cavity in centre of shaft. Hematopoietic stem cells enter the medullary cavity giving rise to myeloid tissue. Two ends of bone are still composed entirely of cartilage.

Midsection is called diaphysis, cartilaginous end is called epiphysis. Hence primary centre of ossification is the diaphyeal centre of ossification.

2. INTRAMEMBRANEOUS OSSIFICATION: In this type of ossification bone develops directly within the soft connective tissue. It was first to recognized when early anastomosis observed that the fontanelles of fetal and new born skull were filled with a connective tissue membrane, that was replaced gradually by bone during development. FORMATION OF BONE MATRIX WITHIN THE FIBROUS MEMBRANE:

At the site when bone develop, there is initially loose mesenchyme, which appear widely separated, pale staining, stellate cells with interconnecting cytoplasmic processes. Mesenchymel cells proliferate and condense, some of these cells divide into capillaries. These cells differentiate into osteoblasts, when they are surrounded by bone matrix it is called osteocytes.

Then it start exihibiting alkaline phosphate activity. First small mass of newly formed bone matrix is an irregular shaped spicule. Concurrent with an increase in vascularity at these sites of condensed mesenchyme, osteoblasts differentiate and begin to produce bone matrix. FORMATION OF THE WOVEN BONE:

Bony spicules lengthens into larger anastomosing structure called trabeculae. They extend in radial pattern. These trabeculae encloses local blood vessels. This early membranous bone is termed as woven bone. External to woven bone is periosteum.

As the mesenchymal cells differentiate into osteoblasts, they start exhibiting alkaline phosphatase activity. This sequence of events occurs at multiple sites within each bone of cranial vault, maxilla, body of mandible, and midshaft of long bones. Once begun, Intramembranous bone formation proceeds rapidly. This first embryonic bone is termed woven bone.

At first the woven bone takes the form of radiating spicules and trabecules, but progressively they fuse into thin bony plates. In the cranium more than one plate fuse to form a single bone. Early plates of Intramembranous bone are structurally unsound, not only because of poor fibers orientation and mineralization but also because many islands

of soft tissue remain with in plates. Woven bone of the early embryo and fetus turnover rapidly. As fetal bone begins to assume their adult shape, continued proliferation of soft

connective tissue between adjoining bones brings about the formation of sutures and fontanelles. From early fetal development to full expression of the adult skeleton a continual slow transition occurs from woven bone to lamellar bone. This transition is rapid during late fetal development and the first year of life. Early transition stage involves the formation of primary osteons deposited around the blood vessels in the connective tissue. The primary osteons tend to be small, with lamellae that are neither numerous nor well delineated. Woven bone is characterized by intertwined collagen fibrils oriented in many directions, showing wide inter fibrillar spaces. Collagen fibers in lamellar bone, however are generally thicker and arranged in ordered sheets consisting of aligned and closely packed fibrils. Just as in the case of calcified cartilage, matrix vesicles are believed to be implicated in the initiation of mineral deposition during intramembranous bone formation. The relative importance of matrix vesicles versus secreted noncollagenous proteins in the control of initial events in mineralization remains unclear, and both may be implicated, independently or in succession

3. SUTURAL BONE GROWTH: Suture play an important role in skull growth and face. They are fibrous joint between bones; however they allow only limited movement. At the suture outer layer split and the outermost leaf run across the gap of the suture. The inner most leaf together with the osteogenic layer of the periosteum, runs down through the suture along with the corresponding layer of the other bone involved in the joint. The osteogenic layer of the suture is called as cambium, and the inner leaf, the capsule. Between these two layers is a loose cellular and vascular tissue.

MINERALIZATION OF BONE:

Blood and presumably tissue fluid are super saturated in bone salts but mineralisation doesnt take place in all the tissues under normal condition. This indicates that there are certain factors that cause deposition of calcium and phosphate in them, the knowledge of which is still obscure.

Mineralization : It denotes formation of mineral. Its a process which involves impregnation of mineral in a tissue in an organized manner.

Calcification : Complete formation of a calcified tissue by formation of organic matrix & its subsequent mineralization. Its a chemical activity of laying down Capo4 crystals without organization.

Ossification Includes both production of bone forming cells & following deposition of organic bone matrix.

Hydroxyapatite crystals Are found in the areas where there is a need for high mechanical strength, hardness. Like in bone, Dentin. They don't normally occur in soft tissue.

The mineralization process is based on 2 mechanisms: 1. Booster Mechanism 2. Seeding mechanism

And it is explained with the help of 3 Theories: 1. Booster Theory 2. Seeding Theory 3. Matrix Vesicle Theory A. Boosters Mechanism: According to this theory due to the concentration/action of the enzymes the concentration of the calcium and phosphate ions which are building stones of mineralization increases to such a level that would lead to their precipitation. There are 4 theories which explain this mechanism of mineralization:

B. Robinsons alkaline phosphatase theory. C. Cartiers theory. D. White and Hers theory. E. pH of cartilage explaining mineralization Robinsons Phosphatase theory: F. Normal level of Alkaline po4ase 0.5 3.5 Bodzanskys unit. Alkaline PO4ase is present in cell membrane of hard tissue forming cell, organic matrix of hard tissue form cells , in matrix vesicle. The main function of alkanline phosphatase is hydrolysis of organic phosphatsae and release of inorganic phosphate ion at an alkaline pH. According to him Alkaline phosphatase increases the local concentration of Inorganic phosphatase. Due to increase in concentration there is precipitation of calcium phosphate occurs which gets converted into Apatite. This mechanism is c/a Booster Mechanism G. According to him the presence of alkaline phosphatase releases the ions which take part in mineralization and increases their concentration to such a level that their precipitation is seen. H. Objections: Alkaline phosphatase is present even in tissues which do not calcify.for eg: kidney. Cartiers theory:

I. According to him there are 2 types of substances, one which inhibit and one which induce the process, so with proper control of their concentrations the mineralization takes place. J. Inducer: Adenosine triphosphate K. Inhibitor: Pyrophosphates

L. White and Hers theory. M. White and Hers made surprising discovery that bone and especially dentin still possessed possibility of splitting phosphate easters even on removing and destroying all the enzymes. Purified collagen seems to behave like ATPase. pH of cartilage explaining mineralization:
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 One of the oldest suggestion for mechanism of mineralisation is that pH of cartilage is higher then that of other tissues which would favor ppt of calcium phosphate. SEEDING MECHANISM: N. It refers to a presence of a seeding or nucleating substance which acts a mould (or) template on which the crystals are deposited, the seeding substance resemble apatite crystals. O. Seeding Theory : It was made on account of the shortcomings of the booster theory, and the experimental studies revealed collagen to act as a seed, with apetite crystals forming on the collagen fibers. This process is known as epitaxy The possible seeding substances are: a. COLLAGEN :
P. Collagen is found in abundance in dentin , bone , cementum. Q. Gilmer et al observed seeding capacity of collagen & stated that only those fibers

showing 640 banding are mineralized in vitro. This indicated that, the group responsible for seeding is not in Tropocollagen (which was thought earlier) , but is formed by combination of collagen molecule

b. CHONDROITIN SULPHATE: It is a glycosamino glycan. It is said that inhibit mineralization of soft tissue. However some workers says the combination of chondroitin sulphate that with collegen leads to rise of local factors that inititiate mineralization. However it is still unproved.

c. PHOSPHOPROTEINS : In phosphoprotein phosphate group is attached to serine. It act as a seed in dentin for mineralization. MATRIX VESICLE MECHANISM:

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This theory states that the initial mineralization of connective tissue involves a cellular activity. Matrix vesicle of cellular origin contain crystals. Cluster of crystal grows & coalesce until whole matrix is mineralized. Matrix Vesicle Theory: According to this theory, due to the presence of vesicles containing apatite crystals near each cartilage cell which aggregate and form a matrix which is mineralized. Matrix Vesicle : They are oval or round bodies surrounded by a membrane. consisting of

metalloproteinase, pyrophosphatase, Ca ATP ase, Alkaline PO4 ase which are able to bind to Ca & inorganic phosphate, forming calcium phosphate.They lie in intercellular matrix & in contact with collagen fibers.They represent early locus of calcification in cartilage , bone, mantle dentin & many calcifying extraskeletal tissue. There are 2 types of vesicles: Type I Vesicles: These are substances extruded from the cartilage cells. Cause breakdown of proteoglycans and GAG. Type II Vesicles: These are detached pieces of cartilage cells, are bounded by trilamellar membrane. Promote mineralization by a blend of booster and seeding mechanisms. After osteoblasts have produced a complete and maturated ECM, hydroxyapatite mineral is deposited in the ECM. Bone mineralization is a complicated process controlled by many factors including calcium and phosphate concentrations, enzyme activity, and the composition of the ECM. Initiation of mineralization requires the precipitation and attachment of hydroxyapatite crystals to the ECM. One possible mechanism of hydroxyapatite crystal formation is via extracellular matrix vesicles(MVs). It has been demonstrated that osteoblasts produce MVs by polarized budding and pinching-off vesicles from specfic regions of their outer plasma membranes. After MVs are released into the ECM they initiate formation of the first mineral crystals.

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 The osteoblast differentiation marker alkaline phosphatase is suggested to play a role in the mineralization process, where it hydrolyses organic phosphate substrates to release free inorganic phosphate. This enzyme is highly expressed in MVs together with several phosphate and calcium transporters. These transporters increase local calcium andphosphate concentrations and thereby initiate hydroxyapatite crystal formation. Although there is evidence for these MVs it might well be that mineralization in bone is initiated via other additional mechanisms as well.

BONE HISTOLOGY: All bone have dense outer sheet of compact bone. Centrally it contains medullary cavity. In living bone, cavity is filled with red or yellow bone marrow that is interrupted particularly at the extremeties of long bone by trabeculae. Trabeculae, cancellous or spong bones are termed used to describe this network. These two type of bone behave differently and have different metabolic response. Histologic they consists of microscopic layer or lamellae. Three layer are presents: 1) Circumferential lamellae: Enclose the entire adult bone, & form the outer & inner perimeters. 2) Concentric lamellae: It makes up the bulk of compact bone & form the basic metabolic unit of bone, the osteon ( Also k/a haversion system ). Osteon is oriented parallel to the long axis of bone. In the centre is haversion canal , which is covered by single layer of bone cells. Haversion canals are interconnected by Volkmann canals , that contains blood vessels & they are present throught the compact bone. 3) Interstitial lamellae: They are interspersed between adjacent concentric lamella & fill the space. they are fragements of concentric lamella created during remodeling.

Periosteum is the connective tissue that surrounds the compact bone. It consists of two layers.

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1) Outer fibrous layer: 2) Inner bone cell layer: It is lined by endosteum However the layer are not demarcated & consists of loose connective tissue. Periosteol surface of bone is more active in bone formation than endosteol one.

HEMOPOIETIC TISSUES IN BONE: It consists of : 1) Red Marrow: It is present in young bone and present in infants. It contains stem cells of both fibroblasts mesenchymal cells type & blood cell lineage. 2) Yellow Marrow: It is present in old bone. i.e, is in adults. It is seen in epiphysis of long bone & consist of increased fat cells.

Yellow marrow changes to red one, if the person is anemic and needs increased red blood cell production.

BONE CELLS: Different cells are responsible for formation, resorption & maintenance of osteo architecture:

1) OSTEOPROGENITOR CELL: Stem cells of mesenchymal origin. They can proliferate & convert themselves into osteoblast whenever there is need for bone formation.They are small, pale staining, spindle shaped cells that are present on all non resorbing surfaces of living bone. It is a constituents of 2 membrane i.e. 1. As the deepest layer of periosteum 2. Lining the endosteum that lines the internal surface of all cavities with in the bone. Osteogenic cells constitute a population of bipotential stem cells that can give rise to bone/ cartilage. Bone in the region of well vascularity. Cartilage in non vascular or less vascular areas. 2) OSTEOBLASTS: Osteoblasts are mononucleated cells that synthesize collagenous and non collagenous bone matrix proteins; some of these constituents first accumulate as an uncalcified matrix called osteoid that comprises mainly collagen that act as a scaffold for the deposition of

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the apatite crystals of bone. Osteoblasts arise from pluripotent stem cells, which are of mesenchymal origin.

Preosteoblasts or osteoblasts exhibits high levels of alkaline phosphatase on the outer surface on their plasma membrane. Functionally, the enzyme believed to cleave organically bound phosphate. The liberated phosphate likely contributes to the initiation and progressive growth of bone mineral crystals. These cells contain an extensive Golgi complex surrounded by abundant rough endoplasmic reticulum (rER) profiles.

Osteoblasts are cuboidal cells or slightly flattened cells that are primarily responsible for the production of the organic matrix of bone. The major constituents of this matrix are type I and type V collagen and small amounts of proteoglycans and several non collagenous proteins. Collagen fibers synthesize in Golgi complex and packed in secretory vesicles. And these granules secreted along the surface of the cell apposed to forming bone. These molecules assemble extracellularly and form osteoid layer.

Noncollagenous proteins granules also secreted along the surface of the cell apposed to forming bone. The role of noncollagenous proteins to regulate mineral deposition. In addition to structural proteins, osteoblasts secrete a variety of cytokines that help regulate cell metabolism. A key factor in the rate of bone cell development is the elaboration of a number of growth factors by osteoblasts, their precursors or both.

Osteoblasts secrete several members of the bone morphogenetic proteins (BMP) superfamily, including BMP-2, BMP-7, and transforming growth factor-B, in addition insulin like growth factors, platelet derived growth factors and fibroblastic growth factors. The combination of IGF-1, TGF-B, and PDGF increase the rapidity of bone formation and bone repair. And will likely be important in future dental therapy. The hormones most important in bone metabolism are parathyroid hormone (PTH), 1,25dihydroxyvitamin D, calcitonin, estrogens, and the glucocorticoids. The action of PTH and vitamin D are biphasic, enhancing bone resorption at high concentration but supporting bone formation at lower concentration.

Calcitonin and estrogen inhibit resorption, whereas the glucocorticoids inhibit resorption and formation. Osteoblasts form a cell layer over the forming bone surface and have been
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proposed to act as a barrier that controls the ion flux into and out of bone. When the bone is no longer forming, osteoblasts flatten substantially extending along the bone surface. These cells, termed bone lining cells. Bone lining cells cover most surfaces in adult skeleton. 3) OSTEOCYTES: As osteoblasts form bone, some become entrapped within matrix they secrete, whether mineralized or non mineralized; these cells then called osteocytes. The number of osteoblasts that become osteocytes varies depending on the rapidity of bone formation; the more rapid the formation, the more osteocytes are present per unit volume. After their formation osteocytes become reduced in size. The space in the matrix occupied by an osteocyte called the osteocytic lacuna. Narrow extensions of these lacunae form enclosed channels, or canaliculi, that house radiating osteocytic processes. Through these channels osteocytes maintain contact with adjacent osteocytes and with the osteoblasts or lining cells on the bone surfaces. This places osteocytes in an ideal position to sense the biochemical and mechanical environment and to respond themselves or to transduce signals that affect the response of the other cells involved in bone remodeling to maintain bone integrity and vitality, particularly for the repair of microcracks. Failure of any part of this interconnecting system results in hypermineralization and death of bone. This nonvital bone then may be resorbed and replaced during the process of bone turnover. 4) OSTEOCLASTS: Osteoclasts are multinucleated cells. These are much larger cells in compare to other bone cells. They often are seen in clusters.The osteoclasts is characterized cytochemically by possessing tartrate- resistant acid phosphatase with in its cytoplasmic vesicles. Which distinguish it from Giant cells.Typically osteoclasts are found against the bone surface occupying hollowed-out depressions called Howships lacunae that they have created. Under the electron microscope, multinucleated osteoclasts exhibit a unique set of morphologic characteristics. Adjacent to the tissue surface, the multinucleated osteoclast cell membrane is thrown into deep folds that form a ruffle border. At the periphery of this border the plasma membrane apposed closely to bone surface, and the adjacent cytoplasm, devoid of cell organelles, is enriched in actin, vinculin, and taline, fibrillar contractile proteins. This clear or sealing
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zone not only attaches the cells to the mineralized surface but also isolates a microenvironment between them and the bone surface. SCANNING ELECTRON MICROSCOPIC APPEARANCE

A. ALVEOLAR SURFACE ON WHICH BONE FORMATION IS OCCURING Presence of numerous small calcified nodules within & around collagen fibers. Sharpeys fibers appear as small , dark circular areas & larger ovoid areas represent lacunae occupied by osteocytes. Orientation of collagen is parallel to bone surface. B. ALVEOLAR BONE SURFACE ON WHICH BONE RESORPTION IS OCCURING How ship's resorption lacunae are seen. No Sharpey's fibers are present. Also exhibit snail- track resorption lacunae C. ALVEOLAR BONE SURFACE WHER NEITHER BONE DEPOSITION NOR RESORPTION IS OCCURING Surface is known as resting surface. Characterized by projections marking the sites of extrinsic mineralized Sharpey's fibers separated by smooth areas containing intrinsic mineralized collagen fibers. HISTOLOGICALLY TWO TYPES OF BONE ARE PRESENT: 1) MATURE BONE A) Compact bone B) Cancellous bone 2) IMMATURE BONE

DIFFERENCE BETWEEN MATURE AND IMMATURE BONE: MATURE BONE Adult bone Lamellar bone Contains less cells Small lacunae Cells direction same as lamella Arrangement of Fibres parallel
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IMMATURE BONE Fetal bone Non lamellar More cells Large lacunae Randomly arranged cells Random arrangement

 Less ground substance Stains eosin Prolonged sec mineralisation Less rapid

More ground substance Hematoxylin Heavily mineralised Forms rapidly

CANCELLOUS BONE:

Bony plates which forms the meshwork of cancellous bone c/a trabeculae. Each trabeculae made up of number of lamellae b/w which there are lacunae containing the processes of osteocytes. Canaliculi , containing the processes of osteocytes radiating from lacunae. Cancellous bone has large soft tissue spaces which are initially filled with vascular loose connective tissue but later with myeloid tissue. Trabeculae are arranged in haphazard manner. Trabeculae of spongy bone follow the lines of stress & can realign if the direction of the stress changes. COMPACT BONE:

Made up of lamellae & is pervaded by lacunae (containing osteocyte ) & by canaliculi. Lamellae are arranged in the form of concentric rings which surround a narrow Haversian canal, which is present at center of each ring. canal is lined by osteogenic cells and encloses blood vessels and nerve. This multilayered arrangement forms osteon or

haversion system. Osteons, they represent the basic structural unit of compact bone. Osteon is generally 3 5mm long, have an average diameter 0.3mm & made up of approximately 6 lamellae. In b/w adjoining osteons there are angular intervals occupied by interstitial lamellae. Haversian canal also communicate with the marrow cavity & with the external surface of bone through channels c/a Volkmann canal. STRUCTURE OF THE ALVEOLAR PROCESSES:

The alveolar process may be define as that part of the maxilla and the mandible that forms and supports the sockets of the teeth. No distinct boundaries exist between the body of the maxilla & the mandible and their respective alveolar processes.

Alveolar process is divided in to two: 1) Alveolar bone proper

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2) Supporting alveolar bone

ALVEOLAR BONE PROPER : Thin lamellae of bone that surrounds the root of the tooth & gives attachment to principal fibers of PDL. Compact bone lining the socket has been given several names 1. Cribriform plate it is called cribriform plate because of the sieve like appearance produced by numerous vascular channels. 2. Bundle bone it is called bundle bone because because bundles of sharpeys fibers pass into it from PDL. 3. Lamina dura it is called lamina dura because in radiograph it appears as dense white line. Its radiopaque appearance relates to the quantity of bone & not due to any greater degree of mineralization than adjacent bone. SUPPORTING ALVEOLAR BONE : It surrounds Alveolar bone proper & gives attachment to socket. It is divided into two parts: (a) Cortical plates : it is made up of compact bone . Has inner & outer cortical plate. (b) Spongy bone : it fills the area b/w inner & outer cortical plate.

Individual sockets are separated by plates of bone c/a Interdental septa. Roots of multi rooted teeth are divided by Interradicular septa. Thickness of external alveolar plate is 1.5- 3mm. Its thick over posterior than anterior teeth. Thickness depends upon tooth position & inclination.

The cortical plate consists of surface layers of fine fibered lamellar bone supported by compact Haversian system. It is thinner in maxilla and thickest on the buccal aspect of mandibular premolar and molars. The trabecular bone occupy the central part. Yellow marrow, rich in adipose cells, generally fills the intertrabecular spaces. Trabecular bone is absent in the region of anterior teeth and in this case, the cortical plate and alveolar bone are fused together. The important part of this complex, in terms of tooth support, is the BUNDLE BONE.

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FUNCTION OF ALVEOLAR BONE : Anchor the teeth with help of sharpeys fiber Protect the developing tooth bud Absorb and distribute the occlusal forces Supply blood to the periodontal ligament Organizes and control the eruption of tooth Helps in movement of tooth for proper occlusion -

BONE REMODELING:

Bone modeling refers to the process by which over all size and shape of bone is established. It extends from embryonic to pre adult group. Bone formation occurs at much greater rate than bone resorption.In diseased person bone resorption increases. Formation of bone occurs on periosteal surface and is destroyed on endosteal surface.

BONE REMODELLING is defined as replacement of old bone by new. During growth of a child, deposition is more than resorption which increases the bone mass. In adult phase rate of deposition is equal to resorption. In old age, resorption is more so bone mass is decreased. In diseased phase resorption is more than deposition.

STEPS IN REMODELLING OF BONE: 1) ACTIVATION STAGE 2) RESORPTION STAGE 3) REVERSAL STAGE 4) FORMATION STAGE 5) RESTING STAGE

OSTEOCLAST ACTIVATION & BONE RESORPTION: Osteoblast play a major role by exposing the minerals to the osteoclast & releasing a soluable factor that activates the cells. Ruffled border appears in region next to the bone surface , finger like projection of the cytoplasm creates the surface suited for extensive exchange bteween cell and bone.
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Attachment of osteoclast to the sealing zone is due presence of alpha v beta 3 which is expressed by resorbing osteoclasts. Initial phase involve dissolution of minerals phase by Hcl. The protons for the acid arise from the activity of cytoplasmic anhydrase II, which is synthesized in the osteoclast. The protons are than released across the ruffled border into the resorption zone by an ATP consuming proton pump. This leads to fall in pH to 2.5 to 3 in the osteoclast resorption space.

Now this enzymes are synthesized in RER , transported to golgi complexes and moved to the ruffled border in the transport vesicles, and the contents are released into sealed compartments, creating extracellular lysosomes.

Cathepsin degrade major amount of type 1 collegen & other non collagenous proteins, which have been already demineralized by the acidic environment. Once liberated from bone the free organic & non organic particles of bone matrix are taken in or endocytosed from the resorption lacunae, across the ruffled border, into the osteoclast.

These are than packed into membrane bound vesicles within cytoplasm of osteoclasts. These content pass across the cell and fuse with FSD A SPECIALIZED region of the basal membrane. Than these vesicles are released into the extracellular space through the process of exocytosis.

REVERSAL STAGE :

As osteoclast move through compact bone, they create resorptive channel. The leading edge of resorption is termed as CUTTING ZONE. There is migration of preosteoblasts onto the roughened surface of the bone channel. Preosteoblasts is converted to osteoblasts. Osteoblasts deposits onto the resorbed bone thin layer of non- collagenous matrix protein. This layer is called as REVERSAL LINE. FORMATION STAGE:

Reversal line is composed of atleast bone sialoprotein and osteopontin and acts as cohesive, mineralized layer between old bone & new bone.New bone is formed on the top of the cement line by the same osteoblasts. Osteoblasts gets embedded in bone matrix and becomes osteocytes. Once the formation is complete haversian canal contains a blood vessel and a layer of inactive osteoblasts, the lining cells that communicate by means of cell processes with the embedded osteocytes.

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FACTORS THAT INHIBIT BONE RESORPTION: AGENT FUNCTION \ USE Acts directly on osteoclasts Inhibits eicosanoid synthesis Inhibits osteoclastic resorption Inhibits PG synthesis Inhibits both proliferation and differentiation of osteoclast progenitors Inhibits osteoclast formation and differentiation Binds to IL receptors. Also effective against TNF

Calcitonin Glucocorticoids Biphosphonates Indomethacin Interferon TGF IL 1 receptor antagonist

AGEING AND BONE TISSUE:

Aging has two principal effects on bone tissue. The first is the loss of calcium and minerals from bone matrix. This usually begins after the age of 30 yrs in females and accelerates greatly around the age of 40-45 yrs as levels of estrogen decrease.This causes a reduced ability to produce the organic matrix, mainly collagen. This causes the bones to become brittle and susceptible to fracture.

AT BIRTHThe mandibular canal is of a larger size running close to the lower border. The mental foramen opens near the socket of the first deciduous molar tooth. The angle is obtuse at about 175 degrees, and the condyloid process is nearly in line with the body. The coronoid process is larger and is above the level of the condyle.

AFTER BIRTH ( IN CHILDHOOD)The body increases in length, specially behind the mental foramen to accommodate the three additional teeth.The depth of the body increases owing to increased growth of the alveolar part, to afford room for the roots.The chief part of the body lies above the oblique line. The mandibular canal is situated just above the mylohyoid line. The mental
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foramen returns to its adult position, and the angle is less obtuse to about 140 degrees in the 4th year of life. DURING ADULTHOODThe mental foramen opens mid-way between the upper and lower borders.The mandibular canal runs more nearly parallel to the mylohyoid line. The ramus is almost vertical in direction with the angle about 110 120 degrees. The condyle is placed above the coronoid process and also there is deepening of the Sigmoid notch. IN OLD AGEIn old age, the volume of bone reduces greatly due to the loss of teeth and consequent resorption of the alveolar processes. As a result the chief portion of the bone is found below the oblique line. The mandibular canal with the mental foramen opening from it is closer to the alveolar border. The ramus is oblique in direction and the condyle is more or less bent backwards. CLINICAL CONSIDERATION: Many osseous grafting materials are currently avaliabe for successful treatment of bony defects. Bone grafting to stimulate bone deposition has been used in periodontal surgery since 1970s. it involves a surgical procedure to place bone or bone substitute material into a bone defect with a objective of producing new bone and possibly the regeneration of periodontal ligament and cementum. AUTOGRAFTS: It utilizes the patients bone, which can be obtained from intra oral or extra oral sites. They are the best material for bone grafting, are very well accepted by the body and may produce the fastest rate of bone growth. How ever there is risk of additional discomfort and a secondary procedure. With autografts the patient is assured of protection from diseases transmission and/or immune reaction. Any bone that is not a major bone can be used during an autograft procedure. Commonly, bone fragments taken from the chin, ribs, skull, or iliac crest are used. Small portions of an autograft bone are taken from a patient's body through surgery, though the remainder of the autograft bone is left untouched, and this section of the bone heals fairly quickly. ALLOGRAFTS: They are obtained from other human source, typically highly processed bone powder from human cadavers. The age and health of the donor can affect the rate of
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bone regeneration. There is risk of diseases transmission and rejection of graft. The allograft are freeze dried at ultra low temperature and dried under high vaccum. Allograft induce bone growth and provide an environment that increases the body regenerative process. There are three types of bone allograft available:[5] 1. Fresh or fresh-frozen bone 2. Freeze-dried bone allograft (FDBA) 3. Demineralized freeze-dried bone allograft (DFDBA)

XENOGRAFT: They are obtained from animal sources, usually cow and/or pig. They include processed animal bone or growth protein. Again, the risk of diseases transmission and /or rejection is reduced by processing. Xenotransplants could save thousands of patients waiting for donated organs. The animal organ, probably from a pig or baboon could be genetically altered with human genes to trick a patients immune system into accepting it as a part of its own body. They have re-emerged because of the lack of organs available and the constant battle to keep immune systems from rejecting allotransplants. Xenotransplants are thus potentially a more effective alternative. SYNTHETIC BONE GRAFT: Synthetic material carry no risk of diseases transmission or immune system rejection. They help create an environment that facilitate the body regenerative process. Eg: are natural and synthetic hydroxyl appetites, ceramics, calcium carbonate, silicon containing glasses, and synthetic polymers. BONE LESIONS: A. Genetic and Developmental Cherubism Achondroplasia Osteogenic imperfecta Marfans syndrome Cleidocranial dysplasia Osteopetrosis
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B. Infections Osteomyelitis Alveolar osteitis C. Nutritional / Metabolic Rickets scurvy D. Hormonal Imbalance Pituitary dwarfism Gigantism Acromegaly Primary hyperparathyroidism Secondary hyperparathyroidism E. Aging Osteopenia Osteoporosis F. Others Pagets disease of bone Osteoradionecrosis Aneurysmal bone cyst Traumatic bone cyst Massive osteolysis

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CONCLUSION

Since the bone tissue is such a dynamic and ever changing tissue and that it closely relates to various other organ systems of the body, including the maxillo-facial region, it is imperative that we try and maintain it in its prime condition for as long as possible.

A healthy bone tissue greatly enhances the quality of life.

REFRENCES: Orbans,oral histology and embryology,12th edition. Tencates oral histology,7th edition Berkovitz , atlas of oral anatomy ,histology and embryology third edition Hams histology ninth edition Text book oral and dental histology withembryology Current concepts of bone mineralization: hidehiro ozawa. Journal of oral bioscience 2008. Minireview: Transcriptional Regulation in Development of Bone: Tatsuya Kobayashi and Henry Kronenberg journal of endocrinology: 2006 Internet source,

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