alveolar bone

ALVEOLAR BONE

Seminar by,Dr. Smijal GM

MDS 2016

CONTENTS• BONE DEVELOPMENT• INTRODUCTION• DEVELOPMENT OF ALVEOLAR BONE• FUNCTIONS• COMPOSITION OF BONE• CLASSIFICATION OF ALVEOLAR BONE• GROSS MORPHOLOGY• HISTOLOGY• BONE FORMATION• BONE RESORPTION• BONE REMODELLING• BONE LOSS IN VARIOUS CONDITIONS• CONCLUSION

BONE

• Bone is a dynamic structure that is adapting constantly to its environment and they are essential elements for locomotion, antigravity support and life sustaining functions such as mastication

BONE DEVELOPMENT

• The process of bone formation is called osteogenesis .

1. Endochondral bone formation2. Intramembranous bone formation3. Sutural bone formation

ENDOCHONDRAL BONE FORMATION

INTRAMEMBRANOUS BONE FORMATION

SUTURAL BONE GROWTH

• Bone forms along suture margins• Found in skull• Fibrous joints between bones• Allow only limited movement• Helps skull and face to accommodate growing organs

like eyes and brain

INTRODUCTION

The portion of maxilla &

mandible that forms and

supports the tooth sockets

RAPID REMODELING

ATTACHMENT APPARATUS

• TOOTH ERUPTION

• FUNCTIONAL DEMANDS

• ROOT CEMENTUM

• PERIODONTAL MEMBRANE

• ALVEOLAR BONE

FUNCTIONS

To house the roots of teeth,

which is achieved by the insertion

of Sharpey’s fibers into the alveolar bone

proper.

Provides attachment to

the forming periodontal

ligament

Absorb and distribute occlusal

pressures generated during tooth contacts.

Also gives attachment to

muscles

Provides a framework for the marrow

Reservoir of ions, especially Ca

2/3-INORGANIC

MATTER

1/3 ORGANIC MATTER

• Hydroxyapatite crystals• Formed from minerals-

calcium and phosphate along with hydroxyl, carbonate, citrate

• Mg, Na, K ,Fl , – smaller quantity

• 90% Collagen (primarily Type I)• 11-12% Noncollagenous proteins-

• Osteocalcin• Osteonectin• BMP• Sialoprotein• Phosphoproteins• Proteoglycan

COMPOSITION OF BONE

DEVELOPMENT OF ALVEOLAR BONE

• Alveolar process consists of bone which is formed both by cells from the dental follicle (alveolar bone proper) & cells which are independent of tooth development

• Maxilla & mandible develop-- 1st branchial arch or mandibular arch.• The maxilla forms within the maxillary process & mandible forms

within the fused mandibular processes of mandibular arch.• Both jaw bones start as small centres of intramembraneous

ossification around stomodeum

Both maxilla and mandible develop

intramembranously.

8th week in utero.

Alveolar process develops from the

dental follicle during eruption of

tooth

Bell stage-- developing bone becomes closely

related

The size of the alveolus is

dependent upon the size of the

growing tooth germ.

Resorption - inner wall of the alveolus Deposition -outer

wall.

The developing teeth lie in a trough

of bone -Tooth Crypt.

Teeth separated from each other by the development of interdental septa.

With the onset of root formation,

interradicular bone develops in

multirooted teeth.

When a deciduous tooth is shed, its alveolar bone is

resorbed.

Alveolar process gradually

incorporated into maxillary or

mandibular body.

Permanent tooth moves into place,

developing its own alveolar bone from

its own follicle.

CLASSIFICATION OF ALVEOLAR BONE

BASED ON THE FUNCTIONAL ADAPTATION

Alveolar bone proper

Supporting alveolar bone

KEVITTS CLASSIFICATION

Hypocalcemic

Normal

Hypercalcemic

RADIOGRAPHIC APPEARANCE

Type I- Regular interradicular &

interdental trabeculae; horizontal in a ladder like arrangement. Common in

mandible.

Type II- Irregularly arranged, numerous,

delicate interdental and interradicular trabeculae.

Common in maxilla.

HISTOLOGICALLY

MATURE

COMPACT

CANCELLOUS

IMMATURE WOVEN BONE

LINLOW 1970

• CLASS I BONE STRUCTURE: this ideal bone type consists of evenly spaced trabeculae with small cancellated spaces

• CLASS II BONE STRUCTURE: this bone has slightly larger cancellated spaces with less uniformity of the osseous pattern

• CLASS III: BONE STRUCTURE: large marrow filled spaces exists between bone trabeculae

QUALITY 1• HOMOGENOUSCOMPA

CT BONE

QUALITY 2• THICK LAYER OF

COMPACT BONE SURROUNDING A COREOF DENSE TRABECULAR BONE

QUALITY 3• THIN LAYER OF

CORTICAL BONE SURROUNDING DENSE TRABECULAR BONE OF FAVOURABLE STRENGTH

QUALITY 4• THIN LAYER OF

CORTICAL BONE SURROUNDING A CORE OF LOW DENSITY TABECULAR BONE

LEKHOLM AND ZARB IN 1985

MISCH BONE DENSITY CLASSIFICATION

• D1: bone is primarily dense cortical bone• D2: bone has dense to porous cortical bone on the crest and, within the

bone, has coarse trabecular bone• D3: have thinner porous cortical crest and fine trabecular region next to

the implant• D4: bone has almost no crestal cortical bone. The fine trabecular bone

composes almost all of the total volume of the bone next to the implant– D5: a very soft bone, with incomplete mineralization and large intertrabecular

spaces. Often immature bone in developing sinus grafts

MAXILLA/MANDIBLE

ALVEOLAR PROCESS

ALVEOLAR BONEPROPER

BUNDLE BONE

LAMELLAR BONE

INNER & OUTER CORTICAL PLATES TRABECULAR BONE INTERDENTAL SEPTA INTERRADICULAR

SEPTA

BASAL BONE

GROSS MORPHOLOGY

• Outer alveolar plate

• Inner alveolar plate

• Interdental septum

• Interradicular septum

GROSS MORPHOLOGY

CRIBRIFORM PLATE

• Cribriform plate (anatomic term)/ Lamina dura (radiographic term)/ Bundle bone (histologic term)

• Cribriform plate thickness- 0.1 to 0.5mm

• External alveolar plate thickness – 1.5 to

3mm around posterior teeth, highly variable

around anterior teeth

Alveolar process is continuous with basal

bone of maxilla and mandible

Arbitrarily the root apices delineate the

alveolar bone from basal bone

INNER & OUTER CORTICAL PLATES

CORTICAL BONE

Cross-section at midroot level-maxilla Cross-section at coronal third of root- Mandible

Cross-section at apical third of root- Mandible

ALVEOLAR BONE PROPER

• The alveolar bone proper is a thin layer of compact bone.• Continuation of the cortical plate and forms the tooth socket. • It surrounds the roots of the teeth and gives attachment to the

principal fibres of the Periodontal ligament.• Referred to as Cribriform plate -reflects a sieve-like appearance

produced by numerous vascular canals.• Double Fibrilar Orientation

• Called Bundle bone as numerous bundles of Sharpey’s fibres pass into it from the Periodontal ligament.

• It appears as dense white line in radiographs- Lamina dura.• Break in continuity of lamina dura at the proximal aspects of

crest of interdental septum has been considered as the earliest radiographic change in periodontitis.

CANCELLOUS BONE• Spongy bone (anatomic term)/ Trabecular bone (radiographic term)/

Cancellous bone (histologic term)• Presence of trabeculae enclosing irregular marrow spaces lined with a layer of

thin, flattened endosteal cells• Matrix consists of irregularly arranged lamellae separated by incremental and

resorption lines• Type 1: The interdental and interradicular trabeculae are regular and horizontal

in a ladder like arrangement. • Type2: Shows irregularly arranged numerous delicate interdental and

interradicular trabeculae

Cancellous BoneCompact Bone

Shelf like bone

CORTICAL BONE SPONGY BONE

About 85% of bone About 15% of bone

Lesser turnover than spongy Higher turnover

Remodel about 3% of its mass each year remodel about 25% of its mass each year

Mechanical/protective role More metabolic function

INTERDENTAL SEPTUM• Bony partition that separate the adjacent alveoli• Coronally septa is thin and consists of only fused inner cortical plates• Apically septa is thicker and contain intervening cancellous bone

• Mesiodistal angulation of interdental septum is parallel to line drawn between CEJ of approximating teeth (Ritchey et al, 1953)

• If interdental space is narrow, septum may consist of only cribriform plate

• If roots are too close together, an irregular window can appear in the bone between adjacent roots

Diagram of relation between CE junction of adjacent teeth shape of crest of alveolar septa

• The shape of the interdental bone is a function of the tooth form and the embrasure width.

• The more tapered the tooth, the more pyramidal is the bony form. • The wider the embrasure, the more flattened is the interdental bone

mesiodistally and buccolingually

ALVEOLAR CREST• Formed when the inner and outer

cortical plates meet

• The margin is thin & knife edged in

vestibular surfaces of anterior and

rounded/beaded in posterior teeth

• Most prominent border of interdental

septum

INTERRADICULAR SEPTA• The bone between the roots of multirooted teeth .• Both of them contain perforating canals of

Zukerkandl & Hirschfeld [nutrient canals].

BASAL BONE• It is the osseous tissue of the

mandible and the maxilla except the alveolar process.

• Anatomically, there is no distinct boundary that exists between the body of the maxilla / mandible and their alveolar process.

BONE MARROW• Embryo and newborn, • Ribs, sternum, vertebrae, skull,

humerus• Hemopoiesis

Red hematopoietic

marrow

• Adult• Red marrow foci found sometimes

in maxillary tuberosity, symphysis and angle of ramus

• Storage of energy

Yellow fatty marrow

OSSEOUS TOPOGRAPHY:Normally: prominence of the roots with the intervening vertical depressions that taper toward the margin.

On the labial version: the margins of the labial bone is thinned to a knife edge & presents an accentuated arc in the direction of the apex.

On the lingual version: the margins of the labial bone is blunt & rounded & horizontal rather than arcuate.

HISTOLOGY

CELL

SOSTEOGENIC CELLS

OSTEOBLASTS

OSTEOCYTES

BONE LINING CELLS

OSTEOPROGENITOR CELLS

OSTEOCLASTIC CELLS OSTEOCLASTS

MAT

RIX

COM

PON

ENT

INORGANICCALCIUM

HYDROXYL APATITE CRYSTAL

ORGANIC

COLLAGEN MATRIX

NON COLLAGENOUS

PROTEIN

OSTEOCALCIN

OSTEOPONTIN & BONE SIALOPROTEIN

OSTEONECTIN

PROTEOGLYCAN

LYSYL OXIDASE AND TYROSINE RICH ACIDIC MATRIX PROTEINS (TRAMP)

OSTEOBLASTS• During embryonic development, intramembranous bone of the maxilla and mandible

initially forms from osteoblasts arising from condensing mesenchyme in the facial region • The most active secretory cells in bone

• Basophilic, plump cuboidal / slightly elongated cells.• Rich in synthetic & secretory organelles- rough endoplasmic

reticulum, golgi apparatus, secretory granules & microtubules• Also contain other organelles associated with cell metabolism-

mitochondria & endosomal/ lysosomal elements & extensive cytoskeleton

Produce-- • Type I collagen• Noncollagenous bone proteins like Sialoprotein, Osteopontin, Osteonectin• Growth factors –BMP, Transforming growth factor, insulin like growth factor, platelet

derived growth factor, fibroblastic growth factor

Express and release alkaline phosphatase, which has been shown to be closely associated with new bone formation.

Total alkaline phosphatase activity has been recognized as a reliable indicator of osteoblast function

• In addition, it has a controlling influence in activating Osteoclasts. It contains receptors for the parathyroid hormone and regulates the osteoclastic response to this hormone. Periosteum also serves as an important reservoir of osteoblasts

OSTEOBLASTDOPCIOPCSTROMAL STEM CELLS

BMPGROWTH FACTORS

SYSTEMIC & BONE GF

Periodontology 2000/2000

Osteocytes are ‘entrapped’ osteoblasts

within bone

Osteocytes occupy spaces

(lacunae) in bone and are defined as cells surrounded by bone matrix.

Decreased quantity of synthetic and

secretory organelles

Numerous and extensive cell processes that

ramify throughout the bone in

canaliculi and make contact via gap junctions with

processes extending from

other osteocytes or from osteoblasts or bone lining cells at the surface of the

bone

OSTEOCYTES

BONE LINING CELLSWhen bone surfaces are neither in the formative nor resorptive phase, the surface is completely lined by a layer of flattened cells termed Bone lining cells.

Regarded as Postproliferative osteoblasts.

Retain gap junctions with osteocytes

Functions to control mineral homeostasis & endure bone vitality.

OSTEOPROGENITOR CELLS

• The stem cell population that give rise to osteoblasts are termed Osteoprogenitor cells.

• They are fibroblast-like cells, with an elongated nucleus and a few organelles.

• Their life cycle may involve upto about eight cell divisions before reaching the osteoblast stage.

• They reside in the layer of cells beneath the osteoblast layer, in the periosteal region, in the periodontal ligament or in the marrow spaces.

OSTEOCLAST• Originate from hematopoietic tissue• Fusion of mononuclear cells (blood derived

monocytes) to form a multinucleated cell• Very large, 5-50 nuclei• Active on less than 1% of bone surface• Mobile and capable of migrating• Lie in Howships lacunae• Acidophilic cytoplasm• Active osteoclasts- ruffled border facing

bone (hydrolytic enzymes are secreted)• Increases surface area

At the periphery of the ruffled border, the plasma membrane is smooth and closely apposed to the bone surface.

The adjacent cytoplasm, devoid of cell organelles,enriched in actin,vinculin,and talin,proteins associated with integrin mediated cell adhesion. This region is called the Clear (Sealing) zone.

This zone, thus creates an isolated micro environment in which resorption can take place.

• Several osteoclasts excavating a large area of bone which is the leading edge of resorption is termed as the Cutting cone.

• Released cytokines [ Bone Morphogenic Proteins & Insulin like Growth Factor] stimulate stem cells to differentiate into osteoblasts.

• These osteoblasts secrete osteoid known as Filling cone.

Pluripotential mononuclear precursor)

Stimulated to proliferate and differentiate-monocyte-

macrophage colony-stimulating factor.

M-CSF is required for both proliferation and differentiation of

osteoclasts.

RANKL required for differentiation into mature osteoclasts and for

osteoclast activity.

Interaction between RANK and RANKL induces osteoclast

differentiation and activity.

Osteoclast differentiation and activation is inhibited by osteoprotegerin (OPG),

RANKL expressed on plasma membrane of stromal and osteoblastic cells bind to RANK expressed on osteoclastic progenitors to induce a signaling cascade leading to differentiation and fusion of osteoclast precursor cells.

Osteoclast differentiation and activation is inhibited by osteoprotegerin (OPG), which is a member of the TNF receptor family and is secreted by osteoblastic cells

STRUCTURAL LINES IN BONE

Reversal line or cementing line--The site of change from bone resorption to bone deposition is represented by a scalloped outline. -Rich in sialoprotein & osteopontin.

Resting line – Rhythmic deposition of bone with periods of relative quiescence seen as parallel vertical lines.

MATRIX COMPONENTS• The bone matrix is formed of collagen fibers in which plate like

crystals of carbonated hydroxyapatite (Ca10[PO4]6[OH]2) are deposited.

• Other proteins- proteoglycans, acidic glycosylated and non-glycosylated proteins, regulate the formation of collagen fibrils and mineral crystals or provide continuity between the matrix components and between the matrix and cellular components

• Small amounts of carbohydrate and lipid1/3rd of matrix• Inorgnanic components 2/3rd of matrix- calcium and phosphate in

the form of poorly crystalline, carbonated apatite (dahlite)

COLLAGEN

• Collagen comprises the major (80–90%) organic component in mineralized bone tissues.

• Type I collagen (>95%) is the principal collagen in mineralized bone, together with Type V (<5%) collagen.

• In addition, both type III and XII collagens are also present.• Sharpey’s fibres contain type III collagen with type I collagen. • The expression of type XII collagen in alveolar bone is related to mechanical

strain.• Type I,V & XII are expressed by osteoblasts• Type III & some type XII collagen appear to be produced by fibroblasts

during formation of periodontal ligament

NONCOLLAGENOUS PROTEINS

• Comprise the remaining 10% of the total organic content of the bone matrix.

OSTEOCALCIN

• First non collagenous protein to be recognized.• Found in bone matrix and specifically localizes to developing bone • It is also called bone gla protein as it contains the amino acid γ-

carboxy glutamic acid.• It is regulated by Vitamin D3 and Parathyroid hormone.• The carboxy terminal segment of osteocalcin acts as a

chemoattractant to osteoclast precursors, suggesting a role in bone resorption.

• It is also believed to be involved in bone calcification as it is a calcium binding protein.

OSTEOPONTIN AND BONE SIALOPROTEIN• They were previously termed as Bone sialoproteins I and II.• Bone sialoprotein is thought to function in the initiation of mineral crystal

formation in vivo.• Osteopontin is a potent inhibitor of hydroxyapatite crystal growth.• Osteopontin transcription is strongly upregulated by Vitamin D3 whereas Bone

sialoprotein transcription is suppressed by Vitamin D3.• It could play a role in the regulation of cell adhesion and proliferation, and in the

modulation of cytokine activity

SPARC (secreted proteins & acidic rich in cysteins) / Osteonectin / BM-40

• It is predominantly bound to hydroxyapatite crystals.• SPARC, which has also been characterized in basement

membranes as BM40, is a secreted calcium-binding glycoprotein that interacts with a range of extracellular matrix molecules.

PROTEOGLYCANS

• Chondroitin sulfate proteoglycan.• Two small proteoglycans, Biglycan (chondroitin sulfate

proteoglycan I) and Decorin (chondroitin sulfate proteoglycan II).

• These regulate collagen synthesis.

• Byglycan• Byglycan is more prominent in developing bone and has

mineralised to pericellular areas • Its precise function is not known,but it can bind TGF-β and

extracellular matrix macromolecules including collagen and thereby regulate fibrillogenesis

• Decorin• Binds mainly with in the gap region of collagen fibrils and

assuggested by its name,decorates fibril surface • The primary calcification in bones as reported to follow

removal of decorin and the fusion of collagen fibrils

LYSYL OXIDASE AND TYROSINE RICH ACIDIC MATRIX PROTEINS (TRAMP)

• Lysyl oxidase is a critical enzyme for collagen crosslinking.• TRAMP, also known as dermatopontin, binds to Decorin.

DEVELOPMENT OF BONE CELLS

VASCULAR SUPPLY

Derived from inferior and superior alveolar arteries of maxilla and mandible, venous drainage accompanies the arterial supply

NERVE SUPPLY

Branches from anterior, middle and posterior superior alveolar nerves for maxilla and branches from inferior alveolar nerve for mandible

BONE FORMATION

• Formation of bone, which appears to be linked with bone resorption to maintain bone mass, involves the proliferation and differentiation of stromal stem cells along an osteogenic pathway that leads to the formation of osteoblasts

• Osteoblasts synthesize the collagenous precursors of bone matrix and also regulate its mineralization

Osteoblasts synthesize and lay down precursors of type I collagen.

Osteoblasts also produce osteocalcin and the proteoglycans of ground substance and are rich in alkaline phosphatase, an organic phosphate-splitting enzyme.

The collagen (type I) formed by osteoblasts is deposited in parallel or concentric layers to produce mature (lamellar) bone.

When bone is rapidly formed, as in the fetus or in certain conditions (eg. Fracture callus), the collagen is not deposited in a parallel array but in a basket-like weave and is called woven, immature, or primitive bone.

The main mineral component of bone is an imperfectly crystalline hydroxyapatite [Ca10(PO4)6(OH)2] The mineral crystals, are deposited along, and in close relation to, the bone collagen fibrils.

Calcium and phosphorus are derived from the blood plasma and from nutritional sources

The extracellular matrix of bone is mineralized soon after its deposition

Very thin layer of unmineralized matrix is seen on the bone surface, and this is called the osteoid layer or osteoid seam.

As the process of bone formation progresses, the osteoblasts come to lie in tiny spaces (lacunae) within the surrounding mineralized matrix and are then called osteocytes.

REGULATORS OF BONE FORMATION

• The overall integrity of bone is controlled by hormones, proteins secreted by hematopoietic bone marrow cells and bone cells.

HORMONES• Parathormone• Vitamin D3 • Glucocorticoids • Thyroid Hormone• Growth Hormone • Insulin

LOCAL REGULATORS

• Platelet derived growth factor

• Insulin growth factors

• Transforming growth factor-β

• Bone morphogenetic protein

• Fibroblast growth factor

• PTH affects bone cell function, may alter bone remodeling, and cause bone loss.

• PTH acts on both bone-resorbing cells (osteoclasts) and bone-forming cells (osteoblasts)..

PARATHORMONE

• When administered continuously, it increases osteoclastic bone resorption and suppresses bone formation.

• When administered in low dose intermittently, it stimulate bone formation, a response that has been called the anabolic effect of PTH

VITAMIN D3

• Osteoclast number and activity.• Ruffled border size• Clear-zone volume.

• Mature osteoclasts do not have receptors.

• Effect on osteoclastic bone resorption is to stimulate the fusion of differentiated osteoclast progenitors to form mature cells.

• Influences and modulates cytokine production by immune cells.

• Stimulates osteoclastic bone resorption in vitro and in vivo.

• Very slow onset of action, with a shallow dose-response curve.

ESTROGENS The increase in bone resorption

• The direct effect is mediated by specific receptors found in osteoblast and osteoclast lineages. .

• Indirect effects of estrogen result from enhancing the expression of growth factors like insulin like growth factor (IGF-1) and transforming growth factor-(TGF).

BONE RESORPTION BONE FORMATION BONE LOSS

INITIAL INCREASE IN BONE TURNOVER

ESTROGEN WITHDRAWAL

CALCITONININHIBIT OSTEOCLASTIC BONE RESORPTION

EFFECTS SHORT LIVED

DECREASED SENSITIVITY AFTER PROLONGED EXPOSURE

DECREASE IN RECEPTOR

SECOND POPULATION OF OSTEOCLAST NO RESPONSIVE TO

CALCITONIN EMERGES

PLATELET DERIVED GROWTH FACTOR

INCREASE BONE COLLAGEN SYNTHESIS & RATE OF BONE MATRIX APPOSITION

PRODUCED BY OSTEOBLASTS MAINLY DERIVED FROM SERUM & PLATELETS

STIMULATES DNA SYNTHESIS AND CELL REPLICATION IN OSTEOBLASTS

INSULIN GROWTH FACTORS• Increases • Preosteoblastic cell replication • Osteoblastic collagen synthesis• Bone matrix apposition

Decrease degradation of collagen

Synthesised by bone cells and is present in substantial concentrations in the bone

TRANSFORMING GROWTH FACTOR Β

• Synthesised by osteoblasts in an active form

Stimulate • preosteoblastic cell replication • Osteoblastic collagen synthesis• Bone matrix apposition • Alkaline phosphatase activity

BONE MORPHOGENETIC PROTEINS

• Belonging to TGF- β family ,possessing osteoinductive qualities

Induces • Chondrocyte differentiation• Matrix mineralization • Osteoblasts precursor cells into more mature

osteoblasts• Collagen production by mature osteoblasts

FIBROBLASTS GROWTH FACTOR

• Exerts its effects on bone formation ,primarily through increased proliferation of osteoprogenitor cells

• Promotion of osteogenic differentiation

BONE RESORPTIONIt is the process of removal of mineral and organic components of extracellular matrix of bone by osteolytic cells called osteoclasts.SEQUENCE OF EVENTS OF BONE RESORPTION

• First phase - Formation of osteoclast progenitors in the hematopoietic tissues.

• Second phase - Activation of osteoclasts at the surface of mineralized bone.

• Third phase - Activated osteoclasts resorbing the bone.

FORMATION OF OSTEOCLASTS

Ten cate –sequence of events

• Attachment of osteoclast to the mineralized surface of bone.• Creation of sealed acidic enviroment through action of the

proton pump,which demineralize the bone and expose the organic matrix

• Degradation of the exposed organic matrix to its constituent amino acids by the action of released enzymes ,such as acid phosphatase and cathepsin.

• Sequestring of mineral ions and amino acids with in the osteoclast.

ALTERATIONS IN THE OSTEOCLAST

• Development of a ruffled border

• Sealing zone at the plasma membrane.

RESORPTION ACTIVITY

PROCESS OF RESORPTION

Initiated by active secretion of protons through a

vacuolar type atpase(v-atpase) and passive transport of chloride

through a chloride channel

Hydrochloric acid leads to dissolution of the inorganic

matrix of the bones

The enzyme CAII catalyzes conversion of CO2 and H2O into H2CO3, which ionizes

into H+ and HCO3 - , thereby providing the

protons for the v-atpase

Basolateral exchange of HCO3 - ions for cl- by anion

exchanger 2 provides cl- ions required for the intense acidification

occurring in the resorption lacuna

Proteolysis of the type I collagen matrix in bones is

mainly mediated by the cysteine proteinase,

cathepsin K.

The neutral MMPs also appear to play a minor role

during organic matrix degradation

The resorbed material is removed from the

resorption pit by uptake and transcytosis through the

osteoclast

After completing resorption, osteoclasts either undergo

apoptosis or perform a further round of resorption

Cathepsin-K

• It is a collagenolytic enzyme. • Degrades major amount of Type I

Collagen and other noncollagenous proteins.

Matrix metalloproteinase(MMPs)

• MMP-9 (Collagenase B) - osteoclast migration.

• MMP-13- osteoclast differentiation.

ENZYMES OF OSTEOCLAST

ROLE OF TRAP IN BONE RESORPTION

• Tartarate resistant acid phosphatase (TRAP) is synthesized as a latent inactive proenzyme.

• This active enzyme plays a role in bone resorption inside and outside the osteoclast cell.

• In osteoclasts, TRAP is localized within the ruffled border area, the lysosomes, the Golgi cisternae and vesicles

INTRACELLULAR ROLE OF TRAP

• Intracellularly TRAP has been localised in the vesicles of osteoclasts.

• It is released into the extracellular environment as an active enzyme by exocytosis.

EXTRACELLULAR FATE OF TRAP

• Metabolised by the liver and/or removed in the urine.• The concentration of TRAP in serum can be assessed by

immunoassay. • Has a quantitative and dynamic relation to the amount of

resorption taking place on a day to day basis.

MEDIATORS OF BONE RESORPTION

BONE REMODELING• The process by which overall shape and size of bones is

established is referred to as bone remodelling or turnover.• It occurs in discrete, focal areas involving groups of cells called

bone remodelling or basic multicellular units.

During this phase bone is formed along the periosteal surface and destroyed along the endosteal surface

The status of bone represents the net result of a balance between the two processes.

‘Coupling’ of bone resorption and formation

BONE MULTICELLULAR UNIT• Bone remodelling are characterized by the presence of a BMU

(bone multicellular units) .

OsteoclastsOsteoblasts

Blood vessels & Pericytes

• The main functions of remodeling are-To prevent the accumulation of damaged and fatigued bone by

regenerating new bone.To allow bone to respond to changes in mechanical forces.To facilitate mineral homeostasis.

Regulation of bone remodeling is a complex process involving hormones and local factors acting in a autocrine and paracrine

manner on the generation and activity of differentiated bone cells – Sodek et al 2000

Decrease in blood Ca

Detected by receptors on chief cells

of parathyroid gland

Release of PTH

Stimulate osteoblaststo release IL-1 and IL-6

Stimulates monocytesto migrate to area

Monocytes coalesces to form multinucleated

osteoclasts in presence of LIF-

Bone resorption

Release of Ca ions from hydroxyapetite crystals

Normal blood calcium levels

PTH secretion stopped by feedback mechanism

Leukemia inhibiting factor released by osteoblasts

Bone resorption

Organic matrix resorbed with hydroxyapetite

Collagen breakdown

Release of organic substrate which are covalently

bound to collagen

Stimulates differentiation of

osteoblasts

Bone deposition

SEQUENCE OF EVENTS IN BONE REMODELLING

• the osteoclasts excavate the layer of bundle bone and then resorb the supporting bone.

• They remove all the mineralized material, so that the periodontal ligament fiber bundles become detached at their point of insertion in bone.

• The periodontal ligament anchorage is locally lost

• Mononucleated phagocyte-like cells come in contact with the bone surface; these cells may complete resorption and deepen the lacunae

• After sometime, resorption ceases and osteoclasts are replaced by osteoblasts

• Osteoblasts deposit on to the resorbed bone surface a thin coating of non-collagenous matrix proteins.

• The osteoblasts get entrapped =osteocytes.

• Fragments of lamellae from old bone haversian systems=interstitial lamellae.

The leading edge of resorption – Cutting cone

Released cytokines [ BMP & IGF] stimulate

stem cells to differentiate into

osteoblasts.

osteoblasts secrete osteoid -

Filling cone

FACTORS INFLUENCING REMODELLING

• Functional requirements

• Age related changes in bone cells

Local influence

s

• Hormones (PTH, vit D, calcitonin)

Systemic influence

s

REGULATION OF BONE REMODELLING

REGULATORY LOCAL FACTORS IN BONE REMODELLING

REGULATION OF BONE REMODELING

• Mechanical

• Local

• Systemic

MECHANICAL CONTROL

Mechanical stimulation of bone tissue accelerates periosteal bone formation in regions of high stress and effectively strengthens bones.

Mediators of bone remodellingBONE RESORBERS :• Parathyroid Hormone• Vitamin D3 • Cytokines• IL -1• IL-6• TNF α and β • Colony stimulating factors• Prostaglandins and other

arachidonic acid metabolites • RANKL/ OPG-L / TRANCE • Bacterial products

BONE PROTECTORS :• Calcitonin • Bisphosphonates• Statins• Osteoprotegerin• Interferon gamma • Glucocorticoids• Indomethacin/Aspirin• IL-1 receptor antagonist• Estrogen• Leptin

FACTORS PROMOTING BONE RESORPTION

• Parathyroid Hormone – 84 amino acid single chain

– Physiological concentration = bone formation, increase calcium reabsorption

from kidneys

– Increased concentration = bone resorption

– Affect osteoclasts through receptors on preosteoblasts, osteoblasts and lining

cells

• PTH related peptide - produced by malignant tumors

– structure and action similar to PTH ,activate RANKL which lead to resorption

• Vitamin D3 – steroid like compound

–Affect on bone resorption = differentiation of committed

progenitor cells to mature cells

• Cytokines – short range soluble mediators

• IL -1 – powerful and potent bone resorbing cytokine

–Both IL1- α and IL – β are equally potent

– Effect by direct action on OC lineage .. Stimulate resorption

–Or stimulating production and release of PGE2

• IL-6 – responsible for formation of cells with osteoclastic phenotype=stimulate resorption

• TNF α and β - multifactorial cytokines produced by lymphocytes– Stimulate osteoclastic resorption–Partly action mediated by PGE2– Inhibit differentiation and function of osteoblast–Produced by some tumors – paraneoplastic syndrome

• Colony stimulating factors – – Stimulate differentiation of osteoclast precursors into mature cells.

• Prostaglandins and other arachidonic acid metabolites – –Prostaglandins are slow acting but powerful mediators–Produced by osteoblasts– Increased doses – inhibitory … Decreased doses – stimulate bone

formation–Other derivates like leukotrienes are capable of resorption

• RANKL/ OPG-L / TRANCE - –Cell protein present on osteoblastic / stromal cells

• Bacterial products – stimulate resorption–May act as foreign antigens

FACTORS THAT INHIBIT BONE RESORPTION

• Calcitonin – synthesized by C- cells of thyroids

– Inhibits osteoclastic bone resorption

–Acts directly on osteoclasts =cause an increase cAMP and

contraction of osteoclast membrane

–Dissolution of osteoclast into mononuclear cells

– Its action is short lived (Wener et al)

•May be due to down regulation of receptors

• Or emergence of osteoclast population not sensitive to calcitonin

• Bisphosphonates ––binds to hydroxyapatite making mineralized tissue less accessible– Inhibit osteoclast mediated bone resorption…– Inhibit host enzymes esp. MMP’s–Disadv : thought to cause bone necrosis

• Statins – cholesterol lowering drugs– Stimulate bone formation – Increased expression of BMP-2 ( Mundy et al.)–Positive effect on proliferation and osteoblastic differentiation of

PDL cells

• Osteoprotegerin - – IL-1 and TNF-α regulate their expression– Expressed by Bone marrow stromal cells ,osteoblasts , PDL cells– Increased RANKL/OPG ratio in GCF is associated with PDL disease– (Crotti et al. 2004, Mogi et al 2007)

• Interferon gamma -– Inhibit IL-1 and TNF-α – Inhibits proliferation and differentiation of osteoclast progenitors

• Glucocorticoids –

– inhibit synthesis of eicosanoids

• Indomethacin/Aspirin –

– Inhibit PG synthesis

• IL-1 receptor antagonist –

–Binds to IL-1 receptors

–Produced by monocytes and monocytoid cell lines

• Estrogen –

• Inhibits increase in bone resorption associated with menopause.

• Enhances expression of TGF-β & IGF– 1 in cells with osteoblast

phenotype

• Blocks osteoblasts synthesis of IL-6

• Promotes apoptosis of osteoclasts

• Leptin –

–Mainly secreted by adipocytes and in small amounts by T-cells,

osteoblasts

– Stimulate secretion of IL-1 receptor antagonist

LEPTIN – Indirect central action

• Leptin regulates bone metabolism indirectly in the hypothalamus thereby activating the sympathetic nervous system (SNS)

• Bone loss is accelerated showing that the central effect of leptin seems to be antiosteogenic.

LEPTIN-Direct peripheral action

• Additionally, leptin has a direct anabolic effect within the bone driving the differentiation of bone marrow stem cells into the osteoblastic cell lineage.

• The overall effect of leptin on bone might be bimodal depending on leptin serum concentrations.

AGE CHANGES

• Similar to those occurring in remainder of skeletal system• Osteoporosis with ageing• Decreased vascularity • Reduction in metabolic rate and healing

capacity(implants, extraction sockets, bone grafts)• Bone resorption may be increased or decreased • More irregular periodontal surface

FACTORS DETERMINING BONE MORPHOLOGY

• Normal variation in alveolar bone• Exostoses• Tauma from occlusion• Food impaction• Aggressive periodontitis

NORMAL VARIATION IN ALVEOLAR BONE

• Thickness, width and crestal angulation of interdental septa• Thickness of facial and lingual alveolar plates• Fenestrations and dehiscences• Alignment of teeth• Root and root trunk anatomy• Root position within alveolar process• Proximity with another root surface

LOWER INCISOR WITH THIN LABIAL BONE

UPPER MOLAR WITH THIN FACIAL BONE UPPER MOLARS WITH

THICK FACIAL BONE

FENESTRATION & DEHISCENCE

• Facial > lingual• Anteriors > posteriors• Frequently bilateral• 20% of all teeth affected• Caused due to malposition, root prominence, labial protrusion

and a thin cortical plate• Can complicate procedure and outcome of periodontal surgery

ETIOLOGYExcessive occlusal force • Stahl S et al/ 1963- found attrition present in all the teeth

identified as having fenestration• Edel A/1981- could find no clear relationship between the

presence of occlusal wear and the presence of dehiscences and fenestrations

• Rupprecht RD et al/2001- the affected teeth and the entire dentition of the affected skulls lack attrition

(Schroeder HE /1976)

• Dehiscences were a consequence of teeth malalignment Variation in teeth positioning in the arch (such as buccoversion, linguoversion, supereruption, intrusion) appears to be the major determinant factor

• The more the deviation from the normal bucco-lingual inclination of the tooth, the more the defect

EXOSTOSIS

• These are outgrowths of bone of varied size and shape.• They can occur as small nodules, large nodules, sharp ridges,

spike-like projections or any combination of these.• In rare cases, found to develop after the placement of free

gingival grafts.

BUTTRESSING BONE FORMATION (LIPPING)

• Bone formation sometimes occurs in an attempt to buttress bony trabeculae weakened by resorption.

• When it occurs within the jaw, termed Central buttressing bone formation.

• When it occurs on the external surface, termed Peripheral buttressing bone formation

• The latter may cause bulging of the bone contour, termed as Lipping, which sometimes accompanies the production of osseous craters and angular defects.

• Buttressing bone- adaptive mechanism against occlusal force (thickened cervical portion of alveolar plate)

FOOD IMPACTION• Forceful wedging of food into the periodontium by occlusal

forces• Interdental bone defects often occur where proximal contact is

abnormal or absent.• Pressure and irritation from food impaction contribute to the

inverted bone architecture.• Poor proximal relationship may result from a shift in tooth

position because of extensive bone destruction preceding food impaction.

AGGRESSIVE PERIODONTITIS

• Vertical or angular pattern of alveolar bone destruction is found around the first molars.

• The cause of the localized bone destruction is unknown.

BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE

• Horizontal bone loss• Bone deformities• Vertical or angular defect• Osseous craters• Bulbous bone contour• Reversed architecture• Ledges• Furcation involvement

HORIZONTAL BONE LOSS• Most common pattern of bone loss in periodontal disease.• Bone is reduced in height. • Bone margin remains approximately perpendicular to the

tooth surface.• The interdental septa and facial and lingual plates are

affected, but not necessarily to an equal degree around the same tooth.

BONE DEFORMITIES (OSSEOUS DEFECTS)

• Different types of bone deformities seen in periodontal disease.

• Presence may be suggested on radiographs.• Careful probing and surgical exposure of the areas required

to determine their exact nature.

VERTICAL OR ANGULAR DEFECTS

• Occur in an oblique direction, leaving a hollowed-out trough in the bone along side of the root; the base of the defect is located apical to the surrounding bone.

• Vertical defects occurring interdentally can generally be seen on the radiograph, although thick, bony plates sometimes may obscure them.• Angular defects can also appear on facial and lingual or palatal

surfaces but are not seen on radiographs.

ACTUAL OR APPARENT VERTICAL DEFECT?

• Line drawn across adjacent CEJ’s should parallel crestal lamina dura

• (Ritchey & Orban 1950)

OSSEOUS CRATERS

Concavities in the crest of the interdental bone confined within the facial and the lingual walls.

Reasons for high frequency of interdental crater

Interdental area collects plaque and is difficult to clean. The normal flat or even concave faciolingual shape of the

interdental septum in lower molars may favor formation. Vascular patterns from the gingiva to the center of the crest

may provide a pathway for inflammation

BULBOUS BONE CONTOURS

• Bony enlargements caused by exostoses, adaptation to function or buttressing bone formation.

• Found more frequently in the maxilla than in the mandible.

REVERSED ARCHITECTURE LEDGES

FURCATION INVOLVEMENT• Invasion of the bifurcation and

trifurcation of multirooted teeth by periodontal disease.

• The number of furcation involvements increases with age.

DISTRIBUTION OF BONE DEFECTS IN CHRONIC PERIODONTITIS

• Chronic inflammatory periodontal disease leads to changes in the normal architecture of alveolar process .

• Two theories1 .That the form of the defect is related to the occlusal stress in the

related tooth or teeth (Glickman & Smulow1962)

2 That the form of the defect is related to the original anatomy of the alveolar process (Pritchard 1965)

DEFORMITIES OF ALVEOLAR PROCESS

Trench• Term is applied when bone loss affects two or three

confluent surfaces of the same tooth

MOAT/CIRCUMFERENTIAL DEFECT

• Valley like depression seen between root and external bone when bone loss is more than 5-6mm

• Deformity involves all four surfaces of tooth it is described as a moat

RAMP(FL/FP,Linguo Palatal,interproximal )• Describes deformity that results when both alveolar bone and its

supporting bone are lost to the same degree in such a manner that the margins of the deformity are at different levels.

• 2)cratered ramp and 3)ramp into trench

REVERSE ARCHITECTURE• These defects are produced by • Loss of interdental bone, including the facial and/or lingual plates, without concomitant loss of radicular bone, thereby reversing the normal architecture.• More common in the maxilla.

A-POSITIVE ARCHITECTURE

B-FLAT ARCHITECTURE

C-REVERSE ARCHITECTURE

PLANE • This term is applied when both alveolar bone and supporting bone

is lost to the same degree such that the margins of the deformity are at the same level.

• It can be considered horizontal bone loss about one tooth or portion of a tooth.

MARGINAL GUTTER

• A shallow linear defect between marginal bone of the radicular cortical plate or interdental crest, extending the length of one or more root surfaces.

BONE LOSS IN VARIOUS CONDITIONS1. Bone destruction caused by extension of gingival

inflammation. 2. Bone destruction caused by trauma from occlusion.3. Bone destruction caused by systemic disorders-

EXTENSION OF GINGIVAL INFLAMMATION

PATHWAY OF INFLAMMATION

INTERPROXIMALLY FACIALLY & LINGUALLY

1. Interproximally from gingiva into bone:

2. from the bone into the periodontal ligament

3. gingiva to periodontal ligament

1. from gingiva along the outer periosteum

2. from periosteum to the bone

3. from gingiva into periodontal ligament

Inflammation destroys the gingival and transseptal fibers,

There is continuous tendency to recreate transseptal fibers across the crest of interdental septum as a result, transseptal fibers are present, even in case of extreme periodontal bone loss

Spreads into the marrow spaces and replaces the marrow with a leukocytic and fluid exudate, new blood vessels and proliferating fibroblasts

Multinuclear osteoclasts & mononuclear phagocytes increase in number, and bone appear lined with Howship lacunae

In marrow spaces resorption proceeds from within, causing thinning of surrounding bony trabeculae and enlargement of marrow spaces, followed by destruction of bone and reduction in bone height

TRAUMA FROM OCCLUSION

• Can occur in the absence or presence of inflammation• In absence of inflammation: • Increased compression & tension of PDL• Increased osteoclasis of alveolar bone to necrosis of PDL and

bone and the resorption of bone and tooth structure• Reversible- can be repaired if offending forces are removed• Persistent TFO results in funnel shaped widening of crestal

portion of the PDL with resorption of adjacent bone

• With inflammation• Aggravates bone destruction caused by inflammation and

results in bizarre bone patterns

BONE DESTRUCTION CAUSED BY SYSTEMIC DISRODERS

• Local & systemic factors regulate the physiologic equilibrium of bone

• When a generalized tendency toward bone resorption exists, bone loss initiated by local inflammatory processes may be magnified

• Endocrine disorders: –Hyperparathyroidism–Hypoparathyroidism–Hyperpitutarism–Hyperthyroidism–Hypothyroidism–Diabetes mellitus–Cushings syndrome

• Metabolic disorders – Osteoporosis– Rickets and osteomalacia– Osteopetrosis– Hypophosphatasia– Hypophosphatemia– Renal osteodystrophy

• Other systemic diseases– Progressive systemic sclerosis– Sickle cell anaemia– Thalassemia– leukemia

ENDOCRINE DISRODERS

Hyperparathyroidism• It is an endocrine abnormality in which there is an excess of PTH• Osteitis fibrosa generalisata(cystica): refers to pattern of generalised

rarefaction of bone.• Bones appear quite radiolucent with thin cortices and hazy indistinct

trabeculae. • Thinning of the cortical boundaries • Density of the jaws is decreased • The teeth stand out in contrast to the radiolucent jaws • Normal trabecular pattern to ground glass appearance • Trabeculae are numerous small randomly oriented • Loss of lamina dura

Hypoparathyroidism

• Uncommon condition may be due to damage of the removal of the parathyroid gland during thyroid surgery

• Calcification of basal ganglion• Dental enamel hypoplasia• External root resorption• Delayed eruption• Root dilacerations

Hyperpitutarism

• Results from hyperfunction of the anterior lobe of the pituitary increases the production of the growth hormone

• Enlargement of the mandible• Increase in the length of the dental arches• Thickness and height of the alveolar process may increase• Hypercementosis-may be result of functional and structural

demands of teeth instead of the secondarily hormonal affect

Hypopitutarism

• Reduced secretion of the pituitary hormones • Third molar buds may be completely absent • Mandible is small

Hyperthyroidism

• Synonyms: Graves disease, Thyrotoxicosis• Excessive production of thyroid hormone• Generalized decrease in bone density.• Early eruption and premature loss of primary teeth

HYPOTHYROIDISM

• Synonyms; myxedema, cretinism• In sufficient secretion of thyroxin• Delayed eruption • Short roots • Thinning of lamina dura• Maxilla and mandible are small• External root resorption

Diabetes mellitus

• Bone size and bone mass are reduced• Contribution of advanced glycation end-products (AGEs) to

decreased extracellular matrix production and inhibition of osteoblast differentiation

Cushing's syndrome

• Due to excess secretion of glucocorticoids• Generalized osteoporosis• Granular bone pattern• Partial loss of lamina dura

METABOLIC DISORDERS

Osteoporosis

• Generalized decrease of bone mass• Imbalance between bone formation and resorption• Decrease in bone formation result in changes in trabecular

architecture ,volume of trabecular bone, size and thickness of individual trabeculae.

• Trabeculae are thin and indistinct.(Diffuse granularity)• Thinning of cortical boundaries• Lamina dura is thinned

Rickets and osteomalacia • Inadequate serum calcium and phosphorus levels . • Result from defect in normal activity of metabolites of vitamin d .• Accumulation of osteoid in place of mineralized bone. • Rickets – Cortical walls may be thinned,– Cancellous bone trabeculae becomes reduced in density, number, thickness. – Lamina dura may be thinned

• Osteomalacia– Generalized rarefaction of jaws– Cortical thinning– Homogenous granular appearance.– Lamina dura is thinned or lost

Hypophosphatasia

• Due to defective production or function of alkaline phosphatase.

• Jaws: generalized radiolucency of maxilla and mandible.• Lamina dura is thin• Both primary and permanent tooth have thin enamel, large

pulp chambers.• Tooth is hypoplastic.

Renal osteodystrophy

• Renal rickets bone changes result from chronic renal failure• General: generalized decreased bone density and thinning of

cortical boundaries• Jaws: decrease in no of trabeculae, pattern is granular • Hypoplasia of tooth• Loss of lamina dura

Hypophosphatemia

• Synonym -vitamin d resistant rickets.• Group of inherited conditions that produce renal tubular

disorders resulting in excessive loss of phosphorus• Osteoporotic jaws, granular trabecular pattern• Thinning of cortical boundaries.• Thin enamel caps , large pulp chambers.• Lamina dura become sparse.• Premature loss of tooth

Osteopetrosis• Synonyms: albers –schonberg and marble bone disease• Disorder of bone results from a defect in the differentiation and

function of osteoclasts• Increased density bilaterally symmetrical • Internal aspect of bone is radio-opaque.• Entire bone is enlarged. • Increased radio-opacity of jaws . • Delayed eruption, loose tooth, malformed roots, missing tooth, poorly

calcified, more prone to caries. • Lamina dura is thicker than normal

Progressive systemic sclerosis • Synonym: scleroderma• It is a generalized connective tissue disease that causes

excessive collagen deposition resulting in hardening(sclerosis) of the skin and other tissues

• Mandibular erosions in area of muscle attachments.• Widening of PDL space at expense of surrounding alveolar

bone• Resorption is bilateral and symmetric.• Lamina dura remains normal

Sickle cell anaemia

• Sickle cell anemia is an autosomal recessive, chronic, hemolytic blood disorder.

• Thinning of trabeculae, and reduced in number • Remaining trebeculae appear coarsened and sharply defined• Prominent horizontal trabeculae between the teeth have stepladder

pattern. • Lamina dura is normal • May be sclerotic areas in bone that represents healed infracts.• Thinning of inferior border of manndible.

Thalassemia

• Cooleys anaemia, erythroblastic anaemia• It is a hereditary disorder that results in a defect in hemoglobin

synthesis• The jaws appear radiolucent, with thinning of the cortical

borders and enlargement of the marrow spaces.• The trabeculae are large and coarse • The lamina dura is thin, and the roots of the teeth may be

short.

Leukemia

• Malignancy of the hematopoeitic tissue involving one of the leukocytic cell types

• The formation of tooth crowns may be incomplete or delayed • The cortices of the tooth crypts may be partially or completely

destroyed • Loss of lamina dura.• Trabecular architecture of the jaw bone is almost destroyed

CONCLUSION

• The alveolar processes develop and undergo remodeling with the tooth formation and eruption- Tooth dependent bony structure.

• Although its constantly changing its internal organization, it retains the same form from childhood through adult life.

• The coupling of bone resorption with bone formation constitutes one of the fundamental principles by which bone is remodeled throughout its life.

REFERENCE

• Clinical periodontology & implant dentistry 5th edition – jan lindhe• JAROSODEK&MARCD. MCKEE-Molecular & cellular biology of alveolar

bone, periodontology 2000, vol 24 ,99-126• K. Henriksen, J. Bollerslev, V. Everts, and M. A. Karsdal-Osteoclast

Activity and Subtypes as a Function of Physiology and Pathology—Implications for Future Treatments of Osteoporosis, 2011 Endocrine reviews, 31-63

• Contemporary Implant Dentistry, Carl E. Misch• Carranza’s Clinical Periodontology, Newman, Takei, Klokkevold, Carranza