Alveolar Bone 3c3b5l

ALVEOLAR BONE

Bone – one of the hardest tissue. Both elastic & tough

a. b. c. d. e.

Functions: Provides shape & Provides site of attachment of muscles & tendons Protects vital organs Storage site for minerals Marrow – development & storage of blood cells

CLASSIFICATION: 1. Based on shape LONG: have shaft composed of compact bone with central medullary cavity containing marrow tissue. Ends are called epiphysis Eg: humerus, radius, ulna, femur, tibia, fibula, fingers & toes SHORT: cube shaped with equal length & width. Spongy bone covered with thin layer of compact bone. Marrow space is present but no marrow tissue Eg: carpals & tarsals FLAT: thin, flat, curved. No marrow cavity Eg: sternum, ribs, scapula, clavicle, skull – roof, parietal, frontal, temporal & occipital IRREGULAR: various shapes – notched or ridges. Mainly composed of spongy bone with marrow but no marrow cavity Eg: vertebrae, ethmoid, sphenoid, pelvic bones, heel bone, mandible SESAMOID BONES: develop in tendons – patella (knee cap)

2. Based on development – ENDOCHONDRAL: formed by replacement of hyaline cartilage Eg: bones of trunk & extremities INTRAMEMBRANOUS: replacement of CT with bony tissue Eg: cranial & facial bones, mandible, clavicles 3. Based on microscopic structure – WOVEN/IMMATURE: irregularly oriented collagen fibers Seen in alveolar bone & during healing of fracture Bone formation is rapid- incorporates osteocytes MATURE: Compact / lamellar bone: tightly packed osteons. Arrange in layers Cancellous / spongy bone: honey comb appearance – large marrow cavity with plates of trabecular bone

composition

MINERAL COMPONENT: 

Made of hydroxyapatite crystals – carbonate and calcium phosphate content is less than normal hydroxyapatite crystals



Arranges as plates or leaf like structures



Closely packed with long axis parallel to collagen fibers



Gaps between are filled with water and organic molecules



Contain Ca, P, OH, CO3, Mg, Zn, Na, Pb, K, etc

ORGANIC MATRIX: also called as osteoid Contain both collagenous and noncollagenous proteins

Collagen: •

Collagen – I: Major component in bone. Along with collagen – V forms basic structure in CT

•

Elasticity of collagen provides resilience to bone preventing fracture

•

Alveolar Bone – collagen – I, V, III, XII Sharpey’s fibers: type – III & V type – XII: present in bone. Expressed only in mechanical strain type – III & XII: in PDL (fibroblasts) type – I, V, XII: by osteoblasts

Collagen imparts pink/red color in H&E stain In wove bone: arranged as interwoven with more interfibrillar space In mature bone: fibers are arranged as sheets. Fibers are arranged perpendicular to each other. Little interfibrillar space

• Non collagenous proteins: 10% of organic matrix Endogenous – produced by osteoblasts Exogenous – albumin – derived from blood – incorporated into matrix during osteosynthesis

OSTEOCALCIN:      

First to be identified Also called as bone gla protein Contains carboxy glutamic acid Regulated by Vit – D and PTH Bone resorption – as carboxy terminal chemoattractants to osteoclast precursors Bone deposition: Ca binding protein

acts

as

OSTEOPONTIN & SIALOPROTEIN:   

Termed as bone sialoprotein – I & II Glutamic acid – more in sialoprotein Aspartate – more in osteopontin

BSP – restricted to mineralized tissue Functions to in initiation of mineral crystal formation Suppressed by Vit - D 

OSTEOPONTIN – inhibitor of crystal growth More at cell matrix interface – mediates attachment of bone cells Upregulated by Vit - D 

OSTEONECTIN: •

Binds to hydroxyapatite crystals

•

Calcium binding glycoprotein

•

Interacts with extracellular matrix

•

Regulates cell adhesion and proliferation

•

Also modulates cytokine activity

PROTEOGLYCANS: •

Chondroitin sulfate glycoprotein – non mineralized bone

•

Biglycan & decorin – EDTA bone extracts. Decreases with bone maturation Biglycan – more in developing bone & mineralized adj to pericellular areas. Binds to TGF – beta- regulates fibrillogenesis Decorin – found in gap btwn fibers. Calcification occurs by fusion of collagen fibrils & removal of decorin •

Chondrotin sulfate proteoglycan crystals

seen in mineral

LYSYL OXIDASE & TRAMP: •

Components of demineralized dentin and bone

•

Lysyl oxidase – needed for collagen cross linking

•

TRAMP – also called dermatopontin. Binds decorin and TGF – beta

MATRIX GLA PROTEINS & α2HS GLYCOPROTEINS:  not secreted by osteoblasts  Matrix GLA protein – mineral binding protein Mineralized by vascular smooth muscle cells and chondrocytes  α2HS – produced by liver Compromises inhibition of apatite formation

•

Other are:

proteins

secreted

Proteases Protease inhibitors

IGF – I, PDGF and TGF- β increases rapidity of bone

Cytokines BMP: BMP – 2, BMP – 7, TGF –β IGF- I and II PDGF FGF

formation and bone repair

BONE HISTOLOGY: • •

Dense outer sheet – compact bone Central – medullary cavity. Show network of bone trabeculae

• •

Outer layer – periosteum. Outer – fibrous, inner – bone cells Inner layer – endosteum

•

Periosteal & endosteal suurfaces: lamellae are arranged in parallel to bone surface – circumferential lamellae

•

Deep to circumferential lamellae – lamellae are arranged in small concentric layers around vascular core – osteon (concentric lamellae)

•

Interstitial lamellae: remnants of osteons left behind during remodelling

.

BONE HISTOLOGY: Reversal line – marks limit of bone erosion and bone formation More irregular in outline Resting line – denotes rest period during bone formation Regular appearance

•

OSTEOBLASTS:

•

Mononucleated cell derived from osteoprogenitor mesenchymal cells

•

Formed from bone marrow, CT

•

Periosteum – acts as reservoir – child growth, fractures, osteo tumors

MORPHOLOGY:  Basophilic, plump cuboidal or elongated cells 

Produce osteoid composed of collagen – I and non collagenous proteins



Abundant protein synthesizing organelles – basophilia is due to RER



Nucleus is eccentrically placed – far from osteoid



Canaliculi – due to deposition of org matrix around cell bodies and cytoplasmic processes



Canaliculi – connect with each other and other osteocytes – gap & adherens junctions. Aids in intercellular adhesion & cell – cell communication



Contain prominent bundles of actin , myosin & cytoskeletal proteins – maintaining cell shape, motility and attachment

FORMATION:  Undifferentiated pluripotent stromal stem cells inducible osteoprogenitor cells determined osteoprogenitor cells osteoblasts

FUNCTIONS:  Formation of new bone  Regulate bone remodelling & mineral metabolism  Mineralization of osteoid  Secrete collagen – I, V, osteonectin, osteopontegrin , proteoglycans etc

osteopontin,

 Show high levels of AlkP on outer surface – differentiates preosteoblasts from fibroblasts  Resorbing factors – PTH, Vit – D, IL – 1, TNF. Osteoblasts contain receptors for these – transfers to osteoclast

 Overall function is regulated by harmones, proteins of hematopoietic marrow and bone cells

 PTH: regulates serum calcium levels by bone resorption – indirectly by osteoblasts initiation (osteoclasts are devoid of PTH receptors). Also by TGF – β and IGF – I  Vitamin – D: increases serum Ca levels by 1. Ca absorption from intestine 2. promote bone resorption – stimulates osteopontin & osteocalcin secretion by osteoblasts – suppresses collagen formation  Growth harmone: required for deposition. Mediated via receptors on osteoblast surface  Insulin: directly stimulates osteoblasts - aid in deposition  BMP: induce new bone formation – aid in migration, aggregation, proliferation of mesenchymal cells & aid in osteogenic differentiation. No effect on matrix formation TGF- β and IGF’s have same effects

 FGF: increase cell proliferation & osteogenic differentiation  Glucocorticoids: aid in differentiation & matrix formation  PDGF: promotes osteogenesis BONE LINING CELLS:  On completing osteoblastic function 1. entrapped in bone – osteocytes 2. remain on surface – lining cells – flattened, non bone forming  Very few organelles. Retain gap junctions with osteocytes for vitality  50-60% of osteoblasts: undergo apoptosis due to TNF and glucocorticoid & estrogen withdrawl

OSTEOCYTES: o

Number of osteoblasts becoming osteocytes depend on rapidity of bone formation – woven & repair bone (more) than mature bone

o

Osteocyte reduced in size – space around is called lacunae

o

Lacuna – ovoid / flattened. Extensions are called canaliculi which contain osteocytic processes

o

Canaliculi don’t extend beyond an osteon. No communication with adjacent osteon. Maintain with osteoblasts and lining cells. Aid in maintaining bone integrity and bone vitality – failure causes death of bone

o

Canaliculi – penetrate matrix for diffusion of gases, nutrients and waste

•

Have ellipsoidal cell body – parallel to adj lamellae

•

Oval nucleus with narrow rim of basophilic cytoplasm

•

Very few organelles with few matrix protein synthesis

• Old cells – retract the canaliculi Dead cells – lacunae & canaliculi are filled with debris

OSTEOCLASTS: o

Involved in bone resorption

MORPHOLOGY:  Lie in resorption bays - howship’s lacunae  Large multinucleated cell – 15 to 20 nuclei. More nucleus more resorption  Variable shape due to motility  Cytoplasm – acid phosphatase granules and vesiscles  Extensive mitochondria throughout except at ruffled end  RER is less and golgi is abundant along with microtubules  Cathepsin containing granules are close to ruffled end – involved in resorption

FORMATION: •

Hematopoietic cell multinucleated giant cells osteoclast differentiation via cell – cell interactions with osteoblasts

REGULATORS: •

RANK & RANKL are receptor and ligands present on osteoclasts – differentiation into mature osteoclasts and osteoclastic activity

•

M- CSF: for both proliferation & differentiation of osteoclasts

•

Osteoprotegerin: RANKL antagonist. Inhibits osteoclast formation & bone formation. Produced by active osteoblasts

•

Estrogen: inhibits bone resorption – decreases life span of osteoclast by promoting apoptosis

•

Vit – D & PTH: stimulate bone resorption.

•

Calcitonin: inhibits resorption – 1. by inhibiting proliferation & differentiation osteoclastic precursors. 2. reduces ruffled border dimension 3. aid in dissociation from bone surface

of

•

bisphosphonates: inhibits resorption osteoblasts. Used in treating bone disorders

•

PGE2: potent stimulators for resorption. Can also induce bone formation

–

induces

BONE FORMATION: INTRAMEMBRANOUS: 

Direct formation of bone within condensed primitive tissue



Occurs in following steps:

1. Formation of matrix in fibrous membrane 2. Formation of woven bone 3. Appositional growth & formation of compact bone 4. Formation of osteon

FORMATION OF MATRIX: •

Initial site where bone develops – CT is loosely arranged (pale stellate cells with cytoplasmic processes) Development of center of osteogenesis – associated with capillaries growing into mesenchyme Cells proliferate & condense into compact nodules Cells in center differentiate in to osteoblasts – round & basophilic Form org matrix which later calcifies Develop as small irregular shaped spicules

FORMATION OF WOVEN BONE: •

Spicules grow in size – long anastomosing structures – trabeculae. Stain bright pink on H & E. Covered by large osteoblasts which are intensely basophilic Trabeculae extend in radial pattern enclosing the bv Forms the immature / woven bone

External to woven bone – condensation of mesenchyme – periosteum Mesenchymal cells disappear – but leave a layer of flat cells on trabeculae – osteogenic cells Osteogenic cells – form bone in vascular areas & cartilage in avsacular areas

APPOSITIONAL GROWTH & FORMATION OF COMPACT BONE: •

Osteoblasts deposit new layers of matrix on preexisting bone – appositional growth as osteoblasts have their own canaliculi – osteocytes of each layer are linked to bone surface above and to osteocytes below as trabeculae increase in width – new capillaries are inserted to provide nutrition to deeper osteocytes gradual remodeling of trabeculae occurs – maintain shape and size continued apposition and remodeling can result convert cancellous bone to compact bone vascularity in cancellous bone differentiates in to red bone marrow

FORMATION OF OSTEON: as cancellous bone converts into compact bone – narrow canals are formed lined by osteogenic cells canals enclose the vascularity existing in the cancellous bone Lamellae of bone is added by apposition to walls of the spaces – osteons / haversian systems called primitive osteons – short compared to those seen in long bones

WOVEN / IMMATURE BONE

MATURE / LAMELLAR BONE

Intertwined collagen fibers oriented in various directions

Orderly arranged fibers. Collagen fibrils of one lamellae are perpendicular to adj lamellae

Large interfibrillar space – filled with minerals and org matrix

Interfibrillar space is less

Matrix appears blue – indicating high proteoglycan content

More uniform acidophilic staining

Rate of deposition & mineralization are rapid – more osteocytes

Rate of deposition & mineralization are slow – less osteocytes

Rich in BAG – 75 and BSP

Rich in osteocalcin

Low mineral density and high water content

high mineral density and low water content

Can be entirely removed by osteoclasts at a time

Only a part of it can be removed

Matrix vesicels – initiate mineralization

Collagen – initiate mineralization

BONE FORMATION: ENDOCHONDRAL: 

Replacement of cartilage by bone



Occurs in following steps:

1. Formation of cartilage 2. Formation of bone collar 3. Formation of periosteal bud 4. Formation of medullary cavity 5. Formation of secondary ossification center

FORMATION OF CARTILAGE: •

Mesenchymal cells condense & differentiate chondroblasts – form cartilage (hyaline)

into

perichondrium: outer – fibrous & inner – chondrogenic no osteoblasts are produced in chondrogenic layer – becoz of avascular environment growth is by both interstitial & appositional growth length increases by interstitial growth & width by appositional growth

FORMATION OF CARTILAGE: Cells organize into 3 zones: 1. Zone of proliferation: cells are small & flat. Act as new source of cells 2. Zone of hypertrophy & maturation: broadest zone. Chondrocytes are hypertrophic. Secrete type – II collagen and proteoglycans 3. Zone of provisional mineralization: begins by matrix vesicles. Vesicles bud off forming independent units FORMATION OF BONE COLLAR: •.

Capillaries grow into perichondrium – inner cells differentiate into osteoblasts forms a thin collar of bone matrix around mid region of cartilage chondroclasts resorb most of the mineralized cartilage matrix bone collar holds the shaft together more space is created for vascular in growth

FORMATION OF PERIOSTEAL BUD:  Periosteal capillaries are accompanied by osteogenic cells – invade the calcified cartilage – PERIOSTEAL BUD  Initiate ossification center  Osteogenic cells are transformed into osteoblasts – bone matrix formation  Formation of cancellous bone & bits of calcified cartilage – mixed spicule  Network of mixed spicule – primary spongiosa

FORMATION OF MARROW CAVITY: •

ossification center enlarges – osteoclasts destroy the bone – create space in the shaft (medullary cavity)

•

Hematopoietic stem cells enter cavity – marrow tissue

•

2 ends are composed of cartilage (epiphysis) while middle region is bony - diaphysis

FORMATION OF SECONDARY OSSIFICATION CENTER: •

Before or after birth – secondary ossification center

•

Periosteal buds carry bv & mesenchymal cells – retain the cancellous bone unlike primary ossifcation

•

Ossification spreads from secondary center

•

Finally cartilage remains only in 2 sites: articular cartilage & epiphyseal cartilage

• • •

Aids in increasing the length. Long bones have 2 centers and short bones have 1 center Union of 2 ossification centers – epiphyseal line

•

MMP – 9, ossification

osteoclasts

&

VEGF

–

regulate

endochondral

CALCIFICATION: process of deposition of insoluble calcium salts THEORIES OF MINERALIZATION: 1. NUCLEATION THEORY: . Proposed by Neumann & Neumann . Collagen acts as nucleus – aggregates Ca & P ions – hydroxyapatite crystals grow in size spontaneously . Various nucleation sites include: a. Ground substance – sulfated GAG’s and proteoglycans b.

Collagen – dimensions of pores in between fibrils are imp for ingress of ions, formation of ion clusters & aggregation of ion clusters – aid in crystal growth. Along with collagen phosphoproteins induce crystal formation, control the size shape and orientation of crystals

c.

Mitochondria – storage sites for Ca & P. releases ions extracellularly

2. MATRIX VESICLE THEORY: •

Small membrane bound structures. Lie free in the matrix

•

Rounded outgrowths from the chondrocytes and odontoblasts

•

Rich in phospholipids – affinity for Ca

•

Vesicles accumulate Ca & surface act as nucleation site for crystal formation

cell

memb

of

osteoblasts,

3. ALKALINE PHOSPHATASE THEORY: •

hydrolyses phosphate containing substrates and increases the local inorganic phosphate concentration.

•

resides in matrix vesicles budding from chondrocytes, osteoblasts and odontoblasts

•

used as a marker of active tissue mineralization

cell

membranes

of



INHIBITORS OF CALCIFICATION:

 Pyrophosphate  diphosphonates  adenosine triphosphate delay or prevent the transformation calcium phosphate to hydroxyapatite

of

amorphous

 Citrate  magnesium 

proteins like albumin.

 Components of the bone matrix may act locally and inhibit mineralization - proteoglycans

 BONE RESORPTION: • removal of mineral and organic components of extracellular matrix of bone under the action of osteolytic cells  Sequence of events: • first phase - the formation of osteoclast progenitors in the hematopoietic tissues, followed by their vascular dissemination and the generation of resting preosteoclasts and osteoclasts in the bone itself • second phase - consists of activation of osteoclasts at the surface of mineralized bone Alterations in the osteoclast: • Immediately before the resorption event, the osteoclasts undergo changes by assuming a polarity of structure and function - development of a ruffled border and a sealing zone at the plasma membrane • changes occur only in the region of the cell that is next to the bone surface.

•

At the periphery of the ruffled border the adjacent cytoplasm is devoid of cell organelles contains contractile actin microfilaments - clear (sealing) zone.

•

This zone serves to attach the cell very closely to the surface of bone and creates an isolated microenvironment - resorption can take place without diffusion of the hydrolytic enzymes

•

sealing zone to attach themselves to the bone surface

•

Removal of hydroxyapatite:

•

Initial phase involves the dissolution of the mineral phase by the action of hydrochloric acid (HCl).

•

The protons for the acid arise from the activity of cytoplasmic carbonic anhydrase II, synthesized in the osteoclast.

•

protons are then released across the ruffled border into the resorption zone by an ATP consuming proton pump.

•

fall in pH to 2.5–3.0 in the osteoclast resorption space.

•

Degradation of organic matrix:

•

Proteolytic enzymes are synthesized by osteoclasts cathepsin-K and MMP-9 (matrix metalloproteinase)

•

enzymes are synthesized in rough endoplasmic reticulum, transported to Golgi complexes and moved to the ruffled border in transport vesicles

•

contents are released into sealed compartment, creating extracellular lysosomes

•

a visible depression or Howship’s lacunae is excavated into the bone.

•

Removal of degradation products from lacunae:

•

Once liberated from bone, the free organic and nonorganic particles of bone matrix are taken in or endocytosed from the resorption lacunae, across the ruffled border, into the osteoclast.

•

These are then packed in membrane bound vesicles within cytoplasm of osteoclast.

•

These vesicles and their contents across the cell

•

Then the vesicles are released by exocytosis

•

Following resorption, osteoclasts undergo apoptosis, which provides a mechanism for limiting resorptive activity.

•

Factors like TGF-β and estrogen promote apoptosis.

•

PTH and IL-1 act as suppressors prolonging osteoclast activity.

• BONE RESORPTION: • 1. 2. 3.

STAGES: Activation stage Resorption stage Reversal stage

Mediators of bone remodeling:

B. Local factors: • • • • • • •

A. Harmonal: •. Parathyroid hormone (PTH) •. Calcitonin •. Vitamin D metabolites • •. Estrogen receptors •. Growth hormones •. Glucocorticoids

IL – 1 TNF – α Prostaglandins IGF – I & II BMP’s PDGF, FGF, EGF Bacterial products – lipopolysaccharides, capsule, lipotechoic acid, peptidoglycans Mechanical factors

•

MARKERS OF BONE TURNOVER:

A. SERUM MARKERS: •. alkaline phosphatase (total) •. alkaline phosphatase (skeletal isoenzymes) •. osteocalcin •. procollagen I extension peptide B. •. •. •.

URINARY MARKERS: urine calcium – urinary hydroxy proline – collagen crosslink fragments (first to be hydrolysed) •. – urine N-telopeptide (N

• • •

– urine C-telopeptide (C terminus of collagen fibrils) – urine total pyridinoline – urine free deoxypyridinoline

Pathologies caused by improper control of remodeling are: • • • • • • •

Osteoporosis Osteopetrosis malignant bone tumors inflammatory t diseases hyperparathyroidism Paget’s disease hyperthyroidism.

ALVEOLAR BONE: •

alveolar process - defined as that part of the maxilla and the mandible that forms and s the sockets of the teeth

Functions of alveolar bone: • Houses the roots of teeth. • Anchors the roots of teeth to the alveoli - by the insertion of Sharpey’s fibers into the alveolar bone proper. • Helps to move the teeth for better occlusion. • Helps to absorb and distribute occlusal forces generated during tooth . • Supplies vessels to periodontal ligament. • Houses and protects developing permanent teeth, while ing primary teeth. • Organizes eruption of primary and permanent teeth.

•

major changes in the alveolar process begin to occur with development of roots and tooth eruption.

•

As roots develop, the alveolar process increases in height.

•

the cells in the dental follicle start to differentiate into periodontal ligament and cementum.

•

simultaneously some cells in the dental follicle differentiate into osteoblasts and form alveolar bone proper

•

During growth, part of the alveolar process is gradually incorporated into the maxillary or mandibular body while it grows at a fairly rapid rate at its free borders

•

The alveolar process forms with the development and the eruption of teeth, and gradually diminishes in height after the loss of teeth

Structure of alveolar bone Anatomically, no distinct line exists between the body of the jaws and their respective alveolar processes. Occasionally, the alveolar process is fused with underlying bone

ALVEOLAR BONE ALVEOLAR BONE ING ALVEOLAR PROPER BONE LAMELLATED BONE

CORTICAL PLATE

BUNDLE BONE

SPONGY BONE

ALVEOLAR BONE PROPER: surrounds attachment to principal fibers

the

tooth

and

gives

Lamellated bone: • The lamellar bone contains osteons each of which has a blood vessel in a haversian canal. •

Blood vessel is surrounded by concentric lamellae to form osteon.

•

Some lamellae of the lamellated bone are arranged roughly parallel to the surface of the adjacent marrow spaces, whereas others form haversian systems

Bundle bone: • Bone in which the principal fibers of the PDL are anchored. •

Term ‘bundle’ was chosen because, the bundles of the principal fibers continue into the bone as Sharpey’s fibers

•

The bundle bone is characterized by the scarcity of the fibrils in the intercellular substance

•

These fibrils are arranged at right angles to Sharpey’s fibers.

•

The bundle bone contains fewer fibrils than does lamellated bone, and therefore it appears dark in H&E sections

•

fibers are mineralized at the periphery and have a larger diameter.

•

These fibers are less numerous than bundles in the cementum on the opposite side of the PDL

•

collagen adjacent to bone is always less mature than that adjacent to cementum

•

Radiographically, it is also referred to as the lamina dura, because of increased radiopacity - due to the presence of thick bone without trabeculations (X-rays must penetrate

•

alveolar bone proper – lining the inner wall of the socket is perforated by many openings that carry branches of the interalveolar nerves and blood vessels into the periodontal ligament - cribriform plate

•

Bone between the teeth is called interdental septum and is composed entirely of cribriform plate.

•

The interdental and interradicular septa contain the perforating canals - Zuckerkandl and Hirschfeld (nutrient canals) which contain interdental and inter radicular arteries, veins, lymph vessels and nerves

ing alveolar bone consists of two parts: • (a) Cortical plates • (b) Spongy bone Cortical plates: • Cortical plates consist of compact bone and form outer and inner plates of the alveolar processes. •

These are continuous with the compact layers of the jaw bodies. much thinner - maxilla, thick - mandible.

•

thickest in the premolar and molar region of the lower jaw, especially on the buccal side

•

In the maxilla, the outer cortical plate is perforated by many small openings through which blood and lymph vessels

•

In anterior region of both jaws, the ing bone usually is very thin.

•

No spongy bone is present in that region, and the cortical plate is fused with the alveolar bone proper

•

Bone underlying the gingiva is the cortical plate.

•

Both cribriform plate compact bone separated by spongy bone.

• •

and

cortical

plate

Histologically, the cortical plates consist longitudinal lamellae and haversian systems

are

of

Spongy bone: •

Spongy bone fills the area between the cortical plates and the alveolar bone proper

•

These are surrounded by marrow that is rich in adipocytes and pluripotent mesenchymal cells

•

trabeculae contain osteocytes in the osteoblasts or osteoclasts on the surface.

•

These trabeculae of the spongy bone bears the functional forces to which alveolar bone proper is exposed.

•

The cancellous component in maxilla is more than in mandible

interior

and

•

Spongiosa is classified into two main types:

Type I: • the interdental and interradicular trabeculae are regular and horizontal in a ladder like arrangement Type II: • shows irregularly arranged, numerous, delicate interdental and interradicular trabeculae. •

Both types show a variation in thickness of trabeculae and size of marrow spaces.

•

The architecture of type I is seen most often in the mandible and fits in to trajectory pattern of spongy bone.

•

Type II, although functionally satisfactory, lacks a distinct trajectory pattern, which seems to be compensated for by the greater number of trabeculae in any given area. This is more common in the maxilla.

ALVEOLAR CREST: •

shape of the outlines of the crest of alveolar septa on radiograph is dependent on the position of the adjacent teeth.

•

In a healthy mouth the distance between the CEJ and the free border of the alveolar bone proper is constant.

•

If the neighboring teeth are inclined, the alveolar crest is oblique.

•

the inclination is most pronounced in the premolar and molar regions, with the teeth being tipped mesially

•

Cortical bone and alveolar bone meet at the alveolar crest usually 1.5 to 2 mm below the level of CEJ on the tooth it surrounds.

INTERNAL RECONSTRUCTION OF ALVEOLAR BONE: •

During mesial drift of tooth, bone is apposed on the distal and resorbed on the mesial alveolar wall

•

The distal wall is made up almost entirely of bundle bone.

•

However, the osteoclasts in the adjacent marrow spaces remove part of the bundle bone, when it reaches a certain thickness.

•

In its place, lamellated bone is deposited

•

On the mesial alveolar wall of a drifting tooth, the sign of active resorption is the presence of Howship’s lacunae containing osteoclasts

•

periods of resorption alternate with periods of rest and repair

•

Bundle bone is always present in some areas on resorbing side but forms merely a thin layer

•

Islands of bundle bone are separated from the lamellated bone by reversal lines that turn their convexities towards the lamellated bone

•

During these changes, compact bone may be replaced by spongy bone or spongy bone may change into compact bone

•

Alterations in the structure of the alveolar bone are of importance during physiologic eruptive movements of the teeth which are directed mesioocclusally

AGE CHANGES: •

Alveolar sockets appear jagged and uneven.

•

marrow spaces have fatty infiltration

•

The alveolar process in edentulous jaws decreases in size.

•

Loss of maxillary bone is accompanied by increase in size of the maxillary sinus.

•

Internal trabecular arrangement is more open, which indicates bone loss.

•

The distance between the crest of the alveolar bone and CEJ increases with age—approximately by 2.81 mm

CLINICAL CONSIDERATIONS: •

Bone when covered by a vascularized connective tissue exceedingly sensitive to pressure, whereas tension acts generally as a stimulus to the production of new bone. this biologic plasticity that enables the orthodontist to move teeth without disrupting their relations to the alveolar bone.

•

The labial aspect of the alveolar crest is the principal site of resorption, which reduces first in width and later in height

•

pattern of resorption is different in the maxilla and mandible. downward and outward - mandible upwards and inwards - maxilla

•

Nontraumatic loss of anterior maxillary teeth is followed by a progressive loss of bone mainly from the labial side

•

In deciduous dentition, loss of a retained second deciduous molar with no succedaneous permanent tooth to replace it, is also associated with bone loss.

•

The cause for resorption of alveolar bone after tooth loss has been assumed to be due to disuse atrophy, decreased blood supply and localized inflammation

•

Alveolar ridge defects and deformities can also be the result of congenital defects, trauma, periodontal disease or surgical ablation, as in the case of tumor surgery.

•

Lamina dura is an important diagnostic landmark in determining health of the periapical tissues.

•

Loss of density usually means infections, inflammation and resorption of bone socket