GOOD MORNING

PHYSIOLOGY OF

BONE

By- Dr. Dwij Kothari

1st year MDS

CONTENTS

Introduction

Definition

Functions of bone

Classification of bone

Types of bone

Structure of bone

Macroscopic

Microscopic

Bone ossification

Types of bone cells

Growth and development

Bone physiology

Calcium metabolism

Composition of bone

Bone remodeling

Effect of other hormones on bone

Prosthodontic considerations

Conclusion

References

INTRODUCTION

Bone is a highly vascular connective tissue.

They are rigid organs that support and protect the

various organs of body; produce red and white blood

cells and store minerals.

Bones come in a variety of shapes and have a

complex internal and external structure, are light

weight yet strong and hard, and serve multiple

functions.

Types of tissue found in bones are mineralized

osseous tissue, marrow, endosteum, periosteum,

nerves, blood vessels and cartilage.

At birth there are over 270 bones in an infant

human’s body. But many of these fuse together as the

child grows, leaving a total of 206 separate bones in

an adult.

DEFINITION Bone – is the hard portion of the connective tissue

which constitutes the majority of the skeleton;

It consists of an inorganic or mineral component and

an organic component (the matrix and cells);

The matrix is composed of collagenous fibers and is

impregnated with minerals, chiefly calcium phosphate

(approx 80%) and calcium carbonate (approx 10%),

thus imparting the quality of rigidity.

(GPT 8)

FUNCTIONS OF BONE

Bones provide the framework and protectthe soft tissues and vital organs of the body.

Acts as reservoir of minerals.

Is the site of productionof blood cells.

Helps in nerve muscle conduction.

Classification of bone

1) According to position

Axial skeleton

Appendicular skeleton

2) According to shape

Long bones

Short bones

Flat bones

Irregular bones

Pneumatic bones

Sesamoid bones

3) According to development

Membrane(dermal) bones

Cartilaginous bones

Membrano-cartilaginous

bones

4) Structural classificationCompact bones

Cancellous spongy or

trabecular bones

CLASSIFICATION OF BONES:

- According to Position :

Appendicular skeleton –bones forming

appendeges of body.

e.g Bones of the limbs, shoulder, and hip

Axial skeleton – bone forming axis of body.

e.g Skull, rib, sternum and vertebrae.

According to Shape :

1) LONG BONES-

• Longer than they are wide (e.g

Humerus)

• Consist of a long shaft with two

expanded ends - epiphyses

• Primarily compact bone but may

have a large amount of spongy

bone at the ends or extremities

• Typical , Miniature and Modified

long bones.

2) SHORT BONES-

• Shape – cuboidal ,trapezoid or

scaloped

• Carpal & tarsal bones

3) FLAT BONES-

• Thin, flattened and a bit curved

(e.g. sternum , scapula , & vault

of skull)

4) IRREGULAR BONES-

• Vertebra, hip bones, bones in the

base of the skull

5) PNEUMATIC BONES-

•Irregular bones contain large air

spaces lined by epithelium

•Maxilla, sphenoid, ethmoid

6) SESAMOID BONES-

•Bony nodules embedded in tendons

or joint capsules.

•Patella, fabella etc.

According to development of bone :

Membranous ( ectodermal) bone

Ossify in membrane – derived from intra membranous

ossification

Bones of vault of skull and facial bones

Cartilaginous ( endochondral ) bone

Endochondral ossification

Vertebral colums , thoracic cage bones of limbs

Membrano-cartilaginous bones

Clavicle, mandible, sphenoid, occipito temporal

Compact Bone

Solid bone,

Dense in texture but porous

Except for those

accommodating cells,

processes and blood vessels

Arms and legs

Adaptation to bending and

twisting forces

Spongy bone

Open in texture ,

meshwork of trabeculae

Usually interior of bone

Many spaces between

spicules (or trabeculae) of

bone

Marrow found within the

spaces

Spine, ribs, jaw, wrist

Adaptation of

compressive forces

According to structure of bone :

Compact bone morphology

Lacuna

Osteocyte home

Haversian canal

Central canal for blood

vessels, etc

Canaliculi

Osteocyte processes

Lamellae

Concentric circles

representing

appositional bone

deposition

Spongy (trabecular) bone

Consists of thin plates

between whom spaces are

present

Radiographically,

•TYPE 1 : Regular and horizontal

trabeculae.

• TYPE 2 : Irregularly arranged

numerous delicate trabeculae.

At microscopic level, there are 4 types of bone.

* Woven bone

* Lamellar bone

* Composite bone

* Bundle bone

( Contemporary implant dentistry , MISCH, 3rd

edition)

Woven bone

Relatively weak, disorganized, and poorly

mineralized.

Serves a crucial role in wound healing by

(1) Rapidly filling osseous defects,

(2) Providing initial continuity for fractures and

osteotomy segments,

(3) Strengthening a bone weakened by surgery or

trauma.

Lamellar bone

Strong, highly organized, well- mineralized tissue.

Makes up more than 99% of the adult human

skeleton.

Provides good strength.

The full strength lamellar bone that supports an

endosseous implant is not achieved until about 1 year

postoperatively. Contemporary implant dentistry, MISCH, 3rd edi.

Composite bone

Osseous tissue formed by the deposition of lamellar

bone within a woven bone lattice, a process called CANCELLOUS COMPACTION.

Quickest means of producing relatively strong bone.

When the bone is formed in the fine compaction

configuration, the resulting composite of woven and

lamellar bone form structures known as primary

osteons.

Bundle bone

It is a functional adaptation of lamellar structure to allow attachment of tendons and ligaments.

Perpendicular straitions, called Sharpey’s fibers, are the major distinguishing characteristics of bundle bone.

Distinct layers of bundle bone usually are seen adjacent to the PDL along physiologic bone- forming surfaces.

ANATOMY: STRUCTURE OF BONE

Diaphysis

Epiphysis

Metaphysis

Articular cartilage

Periosteum

Endosteum

Medullary or marrow

cavity

A typical long bone consist of following

(The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th edition)

Structure of Short, Irregular, and Flat Bones

Thin plates of periosteum-covered compact bone on the outside

with endosteum-covered spongy bone (diploë) on the inside

Have no diaphysis or epiphyses

Contain bone marrow between the trabeculae

Two fundamental factors which lead to strength of bone are

intimate combination of mineral salts and fibrous tissue and

the units of concentric microscopic tubular lamellae.

The bone substance forms trabeculae running in directions

suited to their functions.

The trabeculae are strongly developed in regions subjected to

compression or tensile stresses.

Microscopic structure of bone

Bone is composed of basic units called lamellae.

Lamellae are thin plates of bone.

Each lamellae has,

- gelatinous matrix

- ground substance of collagen fibres

- calcium salts deposited in matrix

Lamellae are placed one above

another with small spaces between

them. They are called lacunae.

Lacunae contains osteocytes.

Lamellae arranged as -concentric

plates around a small central canal.

• Called a haversian system or

osteon.

Volkman’s canals interconnecting

channels containing blood vessels &

the adjacent haversian canals

Lamellae are 3 types based on their placement.

a) circumferential lamellae – these enclose entire adult

bone, forming its outer perimeter.

b) concentric lamellae – these make up the bulk of

compact bone.

c) interstitial lamellae – are interspersed between

concentric lamellae and filling spaces between them.

PHYSIOLOGY OF BONE FORMATION:OSSIFICATION

• The process by which bone forms is called OSSIFICATION.

• The skeleton of a human embryo is composed of fibrous

connective tissue membrane formed by embryonic connective

tissue (mesenchyme) and hyaline cartilage that are loosely shaped

like bones.

• They provide supporting structure for ossification.

• Ossification begins around the 6th or 7th week of embryonic

life and continues throughout adulthood.

BONE OSSIFICATION

Involves both production of organic bone matrix and

calcification

This is NOT bone GROWTH!!!

Two types of ossification:

Intramembranous

Endochondral

Bone formation follows one of 2 patterns;

1. Intramembranous ossification- refers to the formation of bone

directly on or within the fibrous connective tissue membranes.

2. Endochondral ossification- refers to the formation of bone in

hyaline cartilage

•Maxilla forms by intramembranous ossification.

•Mandible forms partly by intramembranous and partly by

endochondral ossification.

•Greater part of body, ramus, condylar and coronoid process are

intramembranous in origin.

•Only the tip of condylar and coronoid process are of

endochondral origin.

INTRAMEMBRANOUS OSSIFICATION

1) At the site where bone will develop, mesenchymal cells become

vascularized, cluster and differentiate –

• First into osteoprogenitor cells and then into osteoblasts.

• The site of such a cluster is called a centre of ossification.

• Osteoblasts secrete the organic matrix of bone and gets

surrounded to become osteocytes.

• Later calcium & other minerals are deposited and tissue

calcifies.

2) As the bone matrix forms, it develops into trabeculae. As

trabeculae develop in various ossification centres, they fuse

with one another to create the open latticework appearance of

spongy bone. Connective tissue in trabecular spaces

differentiates into red bone marrow.

3) On the outside of bone, vascularized mesenchyme develops

into periosteum. Eventually, Some of the spongy bone is

replaced by the cortical bone. This will remodeled to reach its

adult size & shape.

ENDOCHONDRAL OSSIFICATION

1) Development of the cartilage model.

• Mesenchymal cells differentiate into

chondroblasts which form the

hyaline cartilage model

• A membrane called perichondrium

develops around the cartilage

2) Growth of the cartilage model

•Cartilage model grows by interstitial & appositional growth

•Chondrocytes in mid-region calcify the matrix

•Vacated lacunae forms small cavities

•Osteoblasts in perichondrium produce periosteal bone collar( once

perichondrium starts to form bone, it is known as periosteum)

3) Development of primary ossification center

•Near the middle of the model, capillaries of the periosteum grow into

the disintegrating calcified cartilage.

•These vessels and the osteoblasts, osteoclasts & red marrow cells, are

known as the periosteal bud.

•With the development of periosteal bud, primary ossification center

and medullary cavity forms.

4) Development of the diaphysis and epiphysis

•The diaphysis, which was once a solid mass of hyaline cartilage, is

replaced by compact bone.

•When blood vessels( epiphyseal arteries) enter the epiphysis,

secondary ossification centers develop. ( usually around the time of

birth)

Stages in formation of bony lamellae

After secondary ossifying center develops –

Osteogenic cells become osteoblasts

Lies along the surfaces of bars or plates of bone

Osteoblasts lay down a layer of ossein fibrils – osteoid.

Lamellus of bone formed

Osteoblasts now lay down another layer of osteoid over

first lamellus.

Types of bone cells*Osteoprogenitor – resting cell that can transform into

an osteoblast and secrete bone matrix

*OSTEOBLASTS – Produces new bone, derived from

bone marrow cells

*OSTEOCYTES – not clear, osteoblasts when they lose

their activity become osteocytes

*OSTEOCLASTS – lyse or eat away bone, derived from

precursors of monocyte in the bone marrow

Osteoprogenitar cells

* Appearance

pale staining,

small, spindle shaped

* Location

present on all non-

resorbing surface

* Function

give rise to osteoblasts in

vascularized regions

chondroblasts in avascular

regions

Osteoblasts

* Appearance

Large nondividing cells,

eccentric nucleus, basophilic

cytoplasm, negative Golgi

image, cytoplasmic processes.

* Function

Synthesize and secrete organic

constituents of bone matrix

(osteoid)

aid in calcification.

Osteocyte

Appearance

* smaller and less

basophilic than

osteoblast,

* have interconnecting

processes

Function

* forms bone matrix in

repair conditions.

* release calcium ions from

bone matrix when calcium

demands increase

Osteoclast

Appearance

multinucleated,

non-dividing cells,

very acidophilic.

Have a ruffled border

and clear zone

Origin

From blood monocytes/

macrophages

Function

move around on bone surfaces,

resorb bone matrix

Focal decalcification and extra cellular digestion by acid hydrolases and uptake of digested material

Periosteum

A thin connective tissue

layer surrounding bone

Contains the cells that

are the source of bone

Osteoprogenitor cells

Must be preserved

during surgery

Growth and development

GROWTH – An increase in size (TODD)

DEVELOPMENT – is progress towards maturity (TODD)

GROWTH SPURTS – sudden increase in growth.

a) Just before birth

b) 1 year after birth

c) Mixed dentition growth spurt – boys (8-9 years) girls (7-9 years)

d) Pre pubertal growth spurt – boys (14-16 years) girls (11-13 years)

Mechanism of bone growth

The changes that bone deposition and resorption can produce are,

a) Change in size

b) Change in shape

c) Change in proportion

d) Change in relationship of the bone with adjacent structures.

A combination of bone deposition and resorption resulting in a growth movement towards the depositing surface is “cortical drift”

Displacement –

movement of the

whole bone as a unit.

a) Primary displacement

b) Secondary

displacement

Theories of bone growth

GENETIC THEORY – growth is controlled by genetic

influence.

SUTURAL GROWTH THEORY (SICHER) – cranio facial

growth occurs at the suture

CARTILAGINOUS THEORY( JAMES SCOTT) – intrinsic

growth controlling factors are present in cartilage and

periosteum with sutures being only secondary.

THE FUNCTIONAL GROWTH MATRIX CONCEPT

(MELVIN MOSS) – claims that the origin, form, position,

growth and maintenance of all skeletal tissues and organs are

always secondary, compensatory and necesssary responces to

chronologically and morphologically prior events / processes

that occur in specifically related non skeletal tissues, organs /

functioning spaces.

VAN LIMBORG’S THEORY (1970) – suggested the

following 5 factors that he believed controlled growth.

a) Intrinsic genetic factor

b) Local epigenetic factors

c) General epigenetic factors

d) Local environmental factors

e) General environmental factors

ENLOW’S EXPANDING ‘V’

PRINCIPLE – the growth

movements and

enlargements of these bones

occurs towards the wide end

of ‘v’ as a result of

differential deposition and

selective resorption of bone.

Growth factor that regulate bone

remodelling

1. Insulin – like growth factors (IGF) I & II

2. Transforming growth factor –b (TGF – b) superfamily,

including the bone morphogenetic proteins (BMPs)

3. Fibroblast growth factors (FGF)

4. Selected cytokines of the interleukin (IL), tumour necrosis

factor (TNF), & colony – stimulating factor (CSF) families

Functions of growth hormone

It has effects:

1) On growth of skeleton, skeletal muscle

and viscera.

2) On metabolism of a) carbohydrate b)

protein c) fat d) electrolytes.

3) On milk production - lactogenic effect.

4) On erythropoisis.

Bone physiology

- CALCIUM METABOLISM

- BONE REMODELLING

Calcium metabolism

Daily intake - 1000mg

Intestinal absorption – 350

Secretion in gastrointestinal juices – 250

Net absorption over secretion – 100

Loss in feces – 900

Excretion in the urine – 100

* Sources of calcium:

Milk and milk products, egg, vegetables (phytic acid)

BONE’S ROLE IN CALCIUM METABOLISM

Decrease in ca2+level

Receptors

Parathyroid gland cells detect lowered ca2+ conc

Control center

PTH gene

turned on

INPUTcAMP

OUTPUT release of PTH

Effector

Osteoclast increase bone resorption

Kidney release ca2+ in blood, excrete phosphate in urine, and produce calcitriol

Response

Increase in blood ca2+ level

Return to homoestasis when response brings ca++ back to normal

Some stimulus disrupts homeostasis by causing

Calcium in the plasma and interstitial fluid

Average Plasma calcium concentration – 9.4mg/dl

Equivalent to 2.4 mmol of calcium per liter

Calcium in the plasma – 3 forms

1. 40% combined with plasma proteins - nondiffusible through

capillary membrane

2. 10% diffusible through capillary membrane but non ionized

3. 50% diffusible and ionized

Clinical manifestations

HYPOCALCEMIA

1) Concentration of serum calcium is low but calcium is normal, so no tetany results.

2) calcium is low, so tetany results.

Cause – PTH deficiency, vit-D deficiency, etc.

HYPERCALCEMIC STATES

When blood level of calcium rises above 12mg/dl

1) Drowsiness

2) Decreases the QT interval of heart – causes constipation.

3) Calcium deposits in soft tissues

TETANY

- Due to hyperirritability of motor nerve fibres supplying the skeletal muscle.

- Painful tetanic contraction of the muscles resulting in spasm.

- Trousseau’s sign

COMPOSITION OF BONE

Bone

Inorganic 65% Organic 35%

(Primarily calcium phosphate

which is present in form of

Highly insoluble crystals of Collagen 90-95 % Ground substance 5-10 %

Hydroxyapatite) •Glycoprotein

•Proteoglycan

•Sialoproteins

•Lipids

Bone and its relation to extracellular

calcium and phosphate

Organic matrix of bone

90-95 % is collagen fibres, which gives bone its powerful

tensile strength.

5-10 % is a homogeneous gelatinus medium called ground

substance.

Ground substance is composed of extracellular fluid plus

proteoglycans like chondroitin sulfate and hyaluronic acid

which helps to control the deposition of calcium salts.

Bone salts

Major crystalline salts, hydroxyapatite of bone are principally

composed of calcium and phosphate.

Ca10 (PO4) 6 (OH) 2

Each crystal – 400 Å long, 10-30 Å thick, 100 Å wide

Shape – long , flat plate

The relative Ca/P ratio on a weight basis is 1.3 -2

Magnesium, sodium, potassium and carbonate ions are also

present. They are believed to be conjugated

TENSILE AND COMPRESSIONAL STRENGTH OF BONE

Collagen fibers provide bone with great tensile strength while

Inorganic salts allow bone to withstand compression.

Calcium exchange between bone and

extracellular fluid

Whenever calcium salts are injected intravenously or removed from the circulating body fluids, the concentration returns to normal within 30 minutes to 1 hour due to exchangeable calcium present in bone, about 0.4-1% of the total bone calcium.

It provides a rapid buffering mechanism to keep the calcium ion concentration in equilibrium.

Bone remodelling

Deposition of bone by the Osteoblasts :

o Found on the outer surfaces of bone and in the bone cavities.

o Small amount of osteoblastic activity occurs continually - in all living bones

( on about 4% of all surfaces at any given time in an adult)

Absorption of bone by Osteoclasts:

oLarge phagocytic, multinucleated cells.

oNormally active on < 1% of bone surfaces in an adult

Bone remodelling cycle

Process of bone remodelling

Value of continual bone remodelling

Adjusts its strength in proportion to the degree of bone stress,

bone thickens when subjected to heavy loads.

Shape of the bone can be arranged for proper support of

mechanical forces

New organic matrix is needed as the old organic matrix

degenerates, thus normal toughness of bone is maintained.

Repair of a fracture activates all the periosteal and intraosseous

osteoblasts and also new osteoblasts are formed from

osteoprogenitor cells.

Within a short period of time osteoblastic tissue and new

organic bone matrix followed by deposition of calcium salts

develop between the two broken ends of the bone.

This is called a callus.

Bone remodelling and repair

HEALING OF EXTRACTION SOCKET

The removal of a tooth initiates the sequence of

inflammation, epithelization, fibroplasia & remodeling.

Socket heals by secondary intention & it takes

minimum of 6 months for healing of a socket to the degree to

which it becomes difficult to distinguish from the surrounding

bone when viewed radiographically

When a tooth is removed, the remaining empty

socket consists of cortical bone (radiographic lamina dura) &

a rim of oral epithelium left at the coronal portion.

In 30 minutes, the socket fills with blood, which coagulates &

seals the socket from the oral environment.

During the 1st week, inflammatory stage takes place.

All debris, bone fragments & contaminating bacteria will be

removed by leukocytes

Fibroplasia begins with the ingrowth of fibroblasts &

capillaries

Epithelium migrates along the inner surface until they meet

or till the bed of granulation tissue

At the end of 1st week osteoclasts accumulate along the

crestal bone.

During the 2nd week,

Large amount of granulation tissue fills the socket.

Osteoid deposition has begun along the alveolar bone lining

the socket

(In smaller sockets the epithelium may have become fully

intact by this point.)

During 3rd & 4th week,

The process started in 2nd week will continue & healing with

epithelization of most sockets complete at this time.

The cortical bone continues to resorb from crest & walls of the

socket & new trabecular bone is laid down across the socket.

During 4th – 6th month,

It is not until 4 – 6 months after extraction, the cortical bone

lining a socket is fully resorbed, which is radiographically evident

when there is loss of distinct lamina dura.

The epithelium moves towards the crest & eventually becomes

level with the adjacent crestal gingiva.

At Ist year, the only remnants visible after 1 year is the rim of

poorly vascularized fibrous tissue (scar) that remains on the

edentulous ridge.

During 2nd month,

Histologically the socket is filled with immature bone by

the end of second month and there is some quantitative loss when

healing is uneventful. This loss in quantity during normal healing

after extractions is one of the reasons of waiting period of 6 weeks

to 2 months is often advocated prior to the placement of the

dentures

Effects of other hormones on bone

Parathyroid hormone

4 parathyroid glands located

immediately behind the

thyroid gland – one behind

each of the upper & each of

the lower poles of the

thyroid.

Each gland is 6mm long,

3mm wide, & 2mm thick.

Contains mainly chief cells & moderate no. of oxyphilcells.

Chief cells secrete PTH & oxyphil cells are believed to be modified or depleted chief cells that no longer secrete hormone.

PTH is first synthesized on the ribosomes in the form of a preprohormone, a polypeptide chain of 110 amino acids.

Effect on bone

PTH accelerates removal of calcium from bone by 2 processes.

Its initial effect is to stimulate osteolysis.

A 2nd more slowly developing effect of constant exposure to

PTH is to stimulate the osteoclasts to resorb completely

mineralized mature bone.

PTH also has anabolic actions on bone.

Effects of glucocorticoids on bone

metabolism Bone formation

Most important

Bone resorption Probably only during 1st 6 – 12 months of Rx

OC production & postponed apoptosis

Long term, bone turnover

Intestinal absorption of calcium

Urinary phosphate & calcium loss Direct effect on kidney

Secondary Hyperparathyroidism

Bone loss

Early but temporary

Thyroid gland

Regulates metabolism and blood calcium levels.

On skeletal system. Thyroxineis required for the growth and maturation of epiphysealcartilage so that in the absence of this hormone, linear skeletal growth does not occur.

Excess thyroxine causes osteoporosis because of calcium drainage from the bone.

Calcitonin

A peptide hormone secreted by thyroid gland.

Tends to decrease plasma calcium concentration &, in general,

has effects opposite to those of PTH.

Synthesis & secretion of calcitonin occur in the parafollicular

cells, or C cells, lying in the interstitial fluid of the thyroid

gland.

Calcitonin actions

The major effects of calcitonin administration is a rapid fall in the plasma calcium concentration, caused by inhibition of bone resorption.

Calcitonin is a physiologic antagonist to PTH with respect to calcium. However, with respect to phosphate, it has the same net effect as PTH ; that is, it decreases the plasma phosphate level.

Bone disease in hyperparathyroidism

In mild hyperparathyroidism bone can be deposited rapidly

enough

In severe hyperparathyroidism the bone may be eaten away

almost entirely

Radiograph shows extensive decalcification and large punched

out cystic areas of the bone that are filled with osteoclasts in

the form of so called giant cell osteoclast tumors

Multiple fractures of the weakened bones from slight trauma

The cystic bone disease of hyperparathyroidism is called

osteitis fibrosa cystica

Large quantities of plasma alkaline phosphatase – due to

osteoblastic activity

Vitamin D

Source :-

1. Produced in the skin by ultraviolet radiation (D³)

2. Ingested in the diet (D² & D³)

Not a classic hormone

Minimum daily requirement is approximately 2.5μg, & the recommended daily intake is 10μg (400 units)

Most important diet sources are fish, plants, grains and milk.

Rickets

- In prolonged case , the compensatory increase in PTH secretion causes extreme osteoclasticabsorption of the bone

- Bone becomes weaker and imposes marked physical stress on the bone resulting in rapid osteoblastic activity

- These laid down large quantities of osteoid which does not become calcified

Osteomalacia

Deficiencies of vitamin D

and calcium occur as a

result of steatorrhea

Poor absorption of calcium

and phosphate

This almost never proceeds

to the stage of tetany but

often is a cause of severe

bone disability

Prosthodontic considerations

DEFINITION

Alveolar bone – “ The bony portion of the mandible or maxillae in which the roots of the teeth are held by fibres of the periodontal ligament ”.(GPT- 8)

Residual ridge resorption – A term used for the diminishing

quantity and quality of the residual ridge after teeth are

removed. (GPT – 8)

BONE SUBSTITUTES

I) Bone graft materials

AUTOGENOUS BONE GRAFTS

a) Bone from intra-oral sites: osseous coagulum, bone blend,

intra-oral cancellous bone marrow transplants,bone swaging.

b) Bone from extra-oral site: iliac autografts

ALLOGRAFTS

a) Undecalcified freeze-dried bone allograft (FDBA)

b) Decalcified freeze-dried bone allograft (DFDBA):

bone morphogenic proteins BMP, osteogenin

XENOGRAFTS

Calf bone ,keil bone, anorganic bone

II) Non-bone graft materials

• Sclera

• Cartilage

• Plaster of paris

• Calcium phosphate biomaterials

2 types of calcium phosphate ceramics have been used:

1) hydroxy apatite

2) Tricalcium phosphate

• Bioactive glass

• Coral derived materials

RESIDUAL BONE AND MAXILLOMANDIBULAR

RELATION

•It is generally agreed that residual edentulous alveolar ridges resorb;

however there remains some controversy regarding the effect of

dentures on the process.

•Some authorities discussed the concept of disuse atrophy and

recommended that dentures be constructed and worn to preserve the

alveolar ridge. In contrast, others have emphasized the mechanical

trauma that is associated with the wearing of complete dentures

CHANGE IN FUNCTION:

The reaction of the bone to a change in function is

subjected to the supreme test when the natural teeth are extracted

and replaced with dentures.

WOLFF’s LAW states that a change in form follows a change in

function owing to the alteration of the internal architecture and

external conformation of the bone, in accordance with

mathematical laws.

Intermittent Stimulation Bone Apposition

Constant stimulation (Irritation) Bone Resorption

REACTION TO PRESSURE

•Bone builds in response to tensile stimulation, like the pull of a

ligament or muscle. Once the teeth are removed, dentures cannot

provide such stimulation.

•A denture is potentially capable of exerting steady pressure and also

intermittent heavy pressure that can interrupt the blood supply,

resulting in resorption.

•For this reason the dentures should be removed at least 8 of every 24

hour

•CHANGES IN THE SIZE OF BASAL SEAT:

•Maxillary teeth generally flare downward and outward, so bone

reduction generally is upward and inward.

•Since the outer cortical plate is thinner than the inner cortical plate,

resorption from the outer cortex tends to be greater and more rapid.

•The anterior mandibular teeth generally incline upward and forward

to the occlusal plane, whereas the posterior teeth are inclined slightly

lingually.

•The outer cortex is generally thicker than the lingual cortex. Also,

the width of the mandible is greatest at its inferior border. As a result,

the mandibular residual ridge appears to migrate lingually and

inferiorly in the anterior region and to migrate buccally in the

posterior region.

• Consequently, the mandibular arch appears to become wider

posteriorly as resorption progresses

4 clinical factors related to resorption rate :

I. Anatomic factors comprise size, shape, and density of

ridges, thickness and character of mucosal tissue, the ridge

relationship, and number and depth of sockets. Resorption rate

of residual ridges depend on bone volume and bone density.

II. Metabolic factors - nutritional, hormonal, other metabolic

factors that influence the osteoblasts and osteoclasts activity.

III. Functional factors - consist of frequency, intensity,

duration, and direction of force which translated into biologic

cell activity.

Bone formation or bone resorption may result.

Atwood, DA. Some, clinical factors related to rate of resorption of residual

ridges. J Pros Dent 1962; 12:441-50.

IV. Prosthetic factors - technique, materials, concepts,

principles and practices .

Procedures used in complete denture service to minimize the

loss of alveolar bone include:

Recording the tissues in the impression at their rest position.

Decreasing the number of teeth.

Decreasing the size of food table

Developing an occlusion that eliminates, as much as possible,

horizontal forces and those that produces torque

Extending the denture bases for maximum coverage within

tissue limits.

Eating by placing small masses of food over the posterior

teeth where the supporting bone is best suited to resist force.

Removing the dentures for at least 8 of every 24 hours for

tissue rest.

OSTEOPOROSIS

It is the loss of bone mass & density throughout the body,

including the jaws.

The basic problem is that resorption outpaces bone formation.

The common causes are:

Lack of physical stress on bones.

Malnutrition

Lack of vitamin C

Postmenopausal lack of estrogen secretion

Old age

Cushing syndrome

Riggs & Ganguly (1991) distinguished two distinct syndromes of

involutional osteoporosis.

1. Type1/postmenopausal osteoporosis: in which a loss of

trabecular bone is predominant, resulting in fractures of

vertebrae and wrist.

2. Type2/senile osteoporosis: in which both cortical and cancellous

bone are lost, resulting in hip fractures as well.

B. LAWRENCE RIGGS , CONSTANTINOS D. CONSTANTINOU, LARISA SEREDA, ARUPA GANGULY,

, Mutation in a gene for type I procollagen (COL1A2) in a woman

with postmenopausal osteoporosis, Proc. Natl. Acad. Sci. USA

Vol. 88, pp. 5423-5427, June 1991

Prevention of senile osteoporosis

Men – physical activity, exposed to sun light, adequate amount

of calcium containing foods or medicinal forms of calcium.

Women – estrogen therapy, vitamin D supplements, use of

fluorides, increased calcium intake.

(H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture

syndrome in senile osteoporosis: A nutritional consequence?, journal of bone and

mineral research )

AGING AND BONE TISSUE

There are 2 principal effects of aging on bone tissue.

The first is the loss of calcium and other minerals from bone matrix

(demineralization). This loss usually begins after age 30 in females,

accelerates greatly around age 40 to 45 as levels of estrogen decrease,

and continues until as much as 30% of calcium is lost by age 70. In

males calcium loss does not begin until after age 60.

The second principal effect of aging on the skeletal system is a

decrease in the rate of protein synthesis. The bones become brittle and

susceptible to fractures.

CONCLUSION

Physiological principles govern all aspects of

prosthodontic treatment and long term function. An

understanding of the fundamental physiology, metabolism, and

biomechanics of bone is essential for clinicians placing and

restoring these devices.

With this knowledge of bone physiology, it is possible to

institute procedures in prosthodontics that will assure a prosthesis

which would be more acceptable to the patients.

References

Text book of medical physiology, Arthur.C.Guyton, 9th edition.

Essentials of medical physiology, K.Sembulingam, 3rd edition.

Physiology, Robert.M.Berne, 5th edition.

Orthodontics, current principles and techniques, Thomas.M.Graber, 3rd edition.

Orthodontics, the art and science, S.I.Bhalaji, 5th

edition.

The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th edition.

New atlas of human anatomy, Thomas.O.Mccracken. 2nd edition.

Robbins and cotran basic pathology, kumar, cotran, robbins, 7th edition.

Oral histology (development, structure and function) A.R.Ten cate, 6th edition.

Oral anatomy, histology and embryology, B.K.B.Berkovitz,G.R.Holland, B.J.Moxham 4th edition.

Clinical biochemistry , ALLAN GAW, ROBERT A. COWAN,

DENIS ST.J.O’REILLY, MICHAEL J. STEWART, JAMES SHEPHERD.

Human Embryology, Inderbir Singh, 7th edition.

Contemporary implant dentistry , misch, 3rd edition.

Douglas C. Wendt, The degenerative denture ridge-Care and

treatment,J. Prosthet Dent 1974;32,5:477-492.

Dr. AJAY GUPTA, Dr. BHAWANA TIWARI, Dr. HEMANT GOEL, Dr

HIMANSHU SHEKHAWAT, RESIDUAL RIDGE RESORPTION : A

REVIEW, Indian Journal of Dental Sciences, march 2010 , vol 2 issue 2.

H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P.

Fernandez, Crush fracture syndrome in senile osteoporosis: A

nutritional consequence?, journal of bone and mineral research

David J. Baylink, Jon E. Wergedal, Kenji Yamamoto, and

Eberhard Manzke, Systemic factors in alveolar bone loss, J

Prosthet Dent. 1974;31,5:486-505.

Atwood, DA. Some, clinical factors related to rate of

resorption of residual ridges. J Pros Dent 1962; 12:441-50.

Charles H. Chesnut III, and Patricia J. Kribbs, Osteoporosis:

Some aspects of pathophysiology and therapy, jpd 1982 Jul;

48(1)4-7.

Physiology & anatomy , A Homeostatic approach, John

Clancy , Andrew j Mcvica.

THANK YOU ALL

NEXT SEMINAR IS ON : 3-08-2012

SPEECH MECHANISM

BY- Dr. Baxi Harsh

1st year M.D.S.