Bone physiology

www.indiandentalacademy.comwww.indiandentalacademy.com

CONTENTSCONTENTS
 INTRODUCTIONINTRODUCTION
 FUNCTIONSFUNCTIONS
 CLASSIFICATIONCLASSIFICATION
 BONE MORPHOLOGYBONE MORPHOLOGY
 HISTOLOGYHISTOLOGY
 BONE MODELINGBONE MODELING
 REMODELINGREMODELING
 BONE REACTION TO STRESSBONE REACTION TO STRESS
 BONE METABOLISM AND ITS ABERRATIONSBONE METABOLISM AND ITS ABERRATIONS
 EFFCT OF HORMONES AND DRUGS ON BONEEFFCT OF HORMONES AND DRUGS ON BONE
METABOLISMMETABOLISM
 CLNICAL CONSIDERATIONCLNICAL CONSIDERATION

Bones are the units ofBones are the units of
the skeletal system.the skeletal system.

Bone FunctionBone Function
 1)1) supportsupport
 2)2) protectionprotection
 3)3) movementmovement
 4)4) mineral storagemineral storage
 5)5) blood cell formation (hematopoiesis)blood cell formation (hematopoiesis)

1.Shape of bone1.Shape of bone
 LongLong
 ShortShort
 FlatFlat
 IrregularIrregular
 PneumaticPneumatic
 SessamoidSessamoid
Classification of bone tissuesClassification of bone tissues

2.Macroscopic appearance2.Macroscopic appearance
 Cancellous boneCancellous bone
 Compact boneCompact bone
3.Type of ossification3.Type of ossification
 Endochondral boneEndochondral bone
 Intramembranous boneIntramembranous bone

 4.Organisation of collagen fibres4.Organisation of collagen fibres
1.Woven bone1.Woven bone
 Irregular collagen network.Irregular collagen network.
2.Lamellar bone2.Lamellar bone

Bone morphologyBone morphology

PeriosteumPeriosteum
 Membrane covering the outer surface ofMembrane covering the outer surface of
bone except the articular cartilage.bone except the articular cartilage.
 2 layers2 layers
 Outer fibrous layerOuter fibrous layer
 Inner cellular layerInner cellular layer
 In young bones inner layer containsIn young bones inner layer contains
numerous osteoblast, hence c/anumerous osteoblast, hence c/a
osteogenic layer.osteogenic layer.

 In adults osteoprogenitor cells areIn adults osteoprogenitor cells are
abundant, can form osteoblast when needabundant, can form osteoblast when need
arises.arises.
 Richly supplied with blood vessels.Richly supplied with blood vessels.

Functions of periosteumFunctions of periosteum
 The periosteum provides a mediumThe periosteum provides a medium
through which muscles, tendons,andthrough which muscles, tendons,and
ligaments are attached to bone. Whereligaments are attached to bone. Where
very firm attachment of a tendon to bonevery firm attachment of a tendon to bone
is necessary, the fibre of the tendonis necessary, the fibre of the tendon
continue into outer layers of bone as thecontinue into outer layers of bone as the
perforatingperforating fibres of Sharpeyfibres of Sharpey..
 Nutritive function.Nutritive function.

 Osteogenic role during growth and repair duringOsteogenic role during growth and repair during
later life.later life.
 The fibrous layer of periosteum is sometimesThe fibrous layer of periosteum is sometimes
described asdescribed as limiting membranelimiting membrane that preventsthat prevents
tissue from “tissue from “spilling outspilling out” into neighbouring” into neighbouring
tissues. This is based on observation that iftissues. This is based on observation that if
periosteum is torn osteogenic cells may extendperiosteum is torn osteogenic cells may extend
into surrounding tissues forming exostoses.into surrounding tissues forming exostoses.
(hypothetical)(hypothetical)

Histology of boneHistology of bone
 Bone is blend of cells embedded in a stiffBone is blend of cells embedded in a stiff
calcified intercellular matrix.calcified intercellular matrix.
bone
Inorganic (67%) Organic(33%)
hydroxyapatite Collagen type I (25% ) non collagenous protein (5%)
Osteonectin
Osteocalcin
Sialloprotein
Phosphoprotein
Bone specific protein

Bone cellsBone cells
 1.osteoprogenitor cells1.osteoprogenitor cells
 2.osteoblasts2.osteoblasts
 3.osteoclasts3.osteoclasts
 4.osteocytes4.osteocytes
 5.bone lining cells5.bone lining cells

Osteoprogenitor cellsOsteoprogenitor cells
 Persistant migratory stem cells.Persistant migratory stem cells.
 Can proliferate into osteoblast prior toCan proliferate into osteoblast prior to
bone formation.bone formation.
 Mesenchymal originMesenchymal origin

osteoblastosteoblast

OSTEOCYTEOSTEOCYTE
 Major cell type ofMajor cell type of
mature bone.mature bone.
 Derived fromDerived from
osteoblast which haveosteoblast which have
become imprisonedbecome imprisoned
in matrix.in matrix.
 Average lifespan ofAverage lifespan of
25 years.25 years.

Osteocyte in lacuna.

 Function of osteocytes is not yet clear.Function of osteocytes is not yet clear.
 Have an essential role in maintainence of boneHave an essential role in maintainence of bone
as their death leads to the resorption of the boneas their death leads to the resorption of the bone
matrix by osteoclast activity.matrix by osteoclast activity.
 Small role in matrix turnover.Small role in matrix turnover.
 By means of their communication with the cellsBy means of their communication with the cells
at the bone surface, may act as local sensor ofat the bone surface, may act as local sensor of
the mechanical and chemical state of the bonethe mechanical and chemical state of the bone
and erosion or addition of matrix accordingly.and erosion or addition of matrix accordingly.

osteoclastosteoclast
 Large ,rounded,withLarge ,rounded,with
variable number ofvariable number of
nuclei.nuclei.
 Found where there isFound where there is
active erosion of boneactive erosion of bone
& lie in close contact& lie in close contact
with the bone surfacewith the bone surface
in pits termedin pits termed
resorption bays orresorption bays or
lacunae oflacunae of
HowshipsHowships

 Osteoclast contain numerousOsteoclast contain numerous
mitochondria and vacuoles, rich in acidmitochondria and vacuoles, rich in acid
phosphatase positive lysosomes.phosphatase positive lysosomes.
 The surface of cell at the site of boneThe surface of cell at the site of bone
resorption is highly folded to form a ruffledresorption is highly folded to form a ruffled
membrane.membrane.
 Arise by fusion of mononuclear cells whichArise by fusion of mononuclear cells which
originate in the bone marrow rather thanoriginate in the bone marrow rather than
osteoprogenitor cells.osteoprogenitor cells.

collagencollagen
 Type IType I
 Molecular structure more stronglyMolecular structure more strongly
crosslinked internally,and the gaps withincrosslinked internally,and the gaps within
its fibres is more. These makes it strongerits fibres is more. These makes it stronger
and structurally more inert and the internaland structurally more inert and the internal
gapsgaps (hole regions(hole regions) provides for lodging) provides for lodging
the bone salts.the bone salts.
 64 nm cross striations.64 nm cross striations.

 The collagen contributes much toThe collagen contributes much to
mechanical strength of the tissues.mechanical strength of the tissues.
 Besides contributing to tensile ,Besides contributing to tensile ,
compressive and shearing strength ofcompressive and shearing strength of
bone, the small degree of elasticity shownbone, the small degree of elasticity shown
by collagen imparts a measure ofby collagen imparts a measure of
resilience to the tissue, helping to resistresilience to the tissue, helping to resist
fracture of bone when mechanicallyfracture of bone when mechanically
overloaded.overloaded.

 Collagen fibres are also vital to boneCollagen fibres are also vital to bone
development by providing nucleation sitesdevelopment by providing nucleation sites
within their substructure for mineralwithin their substructure for mineral
deposition and otherwise enhancingdeposition and otherwise enhancing
matrix mineralization.matrix mineralization.

Microscopic organisation ofMicroscopic organisation of
bonebone

LAMELLAR BONELAMELLAR BONE
 Structure of bone in adult is made up ofStructure of bone in adult is made up of
layers orlayers or lamellae.lamellae. This kind of bone isThis kind of bone is
called as lamellar bone.called as lamellar bone.
 Each lamellous is a thin plate of boneEach lamellous is a thin plate of bone
consisting of highly oriented collagenconsisting of highly oriented collagen
fibres and crystals of bone salts i.e.fibres and crystals of bone salts i.e.
hydroxyapatite deposited in gelatinoushydroxyapatite deposited in gelatinous
ground substance.ground substance.

 Between adjoiningBetween adjoining
lamellae small flattenedlamellae small flattened
spaces orspaces or lacunaelacunae areare
present.present.
 Each lacunae containsEach lacunae contains
oneone osteocyteosteocyte
 Spreading out from eachSpreading out from each
lacuna there are finelacuna there are fine
canals orcanals or canaliculicanaliculi thatthat
communicate with thosecommunicate with those
from other lacunae.from other lacunae.
 The canaliculi areThe canaliculi are
occupied by delicateoccupied by delicate
cytoplasmic processes ofcytoplasmic processes of
osteocytes.osteocytes.

WOVEN BONEWOVEN BONE
In contrast to mature bone ,woven boneIn contrast to mature bone ,woven bone
does not have a lamellar structure.does not have a lamellar structure.
Collagen fibres are present in bundles thatCollagen fibres are present in bundles that
appear to run randomly in differentappear to run randomly in different
direction.direction.
All newly formed bone is woven bone.All newly formed bone is woven bone.
It is relatively weak ,disorganised and poorlyIt is relatively weak ,disorganised and poorly
mineralised.mineralised.

 It serves crucial role in wound healing byIt serves crucial role in wound healing by
 1.rapidly filling the osseous defect1.rapidly filling the osseous defect
 2.providing initial continuity for fractures2.providing initial continuity for fractures
and osteotomy segments.and osteotomy segments.
 3.strenghtening a bone weakened by3.strenghtening a bone weakened by
surgery or trauma.surgery or trauma.

 The first bone formed in response toThe first bone formed in response to
orthodontic loading usually is the wovenorthodontic loading usually is the woven
bone.bone.
 The functional limitation of woven boneThe functional limitation of woven bone
are an important aspect both ofare an important aspect both of
orthodontic retention and of the healingorthodontic retention and of the healing
period following orthognathic surgery.period following orthognathic surgery.

COMPACT BONECOMPACT BONE
 Dense texture like ivory.Dense texture like ivory.
 Made up of lamellae.Made up of lamellae.
 Most of the lamellae areMost of the lamellae are
arranged in form ofarranged in form of
concentric ring thatconcentric ring that
surrounds a narrowsurrounds a narrow
Haversian canalHaversian canal presentpresent
at the centre of each ring.at the centre of each ring.
 Haversian canal isHaversian canal is
occupied by bloodoccupied by blood
vessels ,nerve fibres, andvessels ,nerve fibres, and
some cells.some cells.

 One haversian canalOne haversian canal
and the lamellaeand the lamellae
around it constitutesaround it constitutes
the basic unit ofthe basic unit of
bone ,bone , thethe haversianhaversian
system or osteonssystem or osteons..
 Compact boneCompact bone
consist of severalconsist of several
such osteons.such osteons.

 Lamella surrounding theLamella surrounding the
haversian canal ishaversian canal is
concentric lamellaconcentric lamella..
 Between adjoiningBetween adjoining
osteons there areosteons there are
angular intervalsangular intervals
occupied byoccupied by interstitialinterstitial
lamellalamella..
 Near the surface of theNear the surface of the
compact bone the lamellacompact bone the lamella
are arranged parallel toare arranged parallel to
the surface, these arethe surface, these are
circumferentialcircumferential
lamellaelamellae..

Histological sections of bone illustrating the various kinds of lamellae

 In longitudinal section,In longitudinal section,
haversian canals runhaversian canals run
predominantly along thepredominantly along the
length of the bone. Thelength of the bone. The
canals branch andcanals branch and
anastomose with eachanastomose with each
other. They alsoother. They also
communicate with thecommunicate with the
marrow cavity and withmarrow cavity and with
the external surfacethe external surface
through channels calledthrough channels called
asas Canals of VolkmannCanals of Volkmann..

High power view of part of an osteon in transverse section seen with transmitted
light.

Single osteon viewed with polarization optics to illustrate lamellar structure

 During bone formation the first formed osteon do notDuring bone formation the first formed osteon do not
have clear lamellar structure, are called as primaryhave clear lamellar structure, are called as primary
osteon.osteon.
 Are replaced by secondary osteon.Are replaced by secondary osteon.
 Average number of lamellae in each osteon is six.Average number of lamellae in each osteon is six.
 The place where periphery of one osteon meets theThe place where periphery of one osteon meets the
other is marked by presence of aother is marked by presence of a cement linecement line which haswhich has
little or no collagen, and is strongly basophillic due tolittle or no collagen, and is strongly basophillic due to
high content of glycoproteins and proteoglycans.high content of glycoproteins and proteoglycans.
 This marks the limit of bone erosion prior to theThis marks the limit of bone erosion prior to the
formation of an osteon and is therefore known as aformation of an osteon and is therefore known as a
reversal linereversal line..

 Similar basophilic lines occur in theSimilar basophilic lines occur in the
absence of erosion ,where bony growthabsence of erosion ,where bony growth
has been interrupted then resumed . Suchhas been interrupted then resumed . Such
lines are called aslines are called as resting linesresting lines..

CANCELLOUS BONECANCELLOUS BONE
 Honeycomb patternHoneycomb pattern
due to large cavities.due to large cavities.
 The bony plates orThe bony plates or
rods that form therods that form the
meshwork ofmeshwork of
cancellous bone arecancellous bone are
called as trabeculae.called as trabeculae.
 Trabeculae enclosesTrabeculae encloses
wide spaces whichwide spaces which
are filled in by boneare filled in by bone
marrow.marrow.

HISTOGENESISHISTOGENESIS

ENDOCHONDRALENDOCHONDRAL
OSSIFICATTIONOSSIFICATTION

 A. At sites of bone formation,A. At sites of bone formation,
mesenchymal cells becomemesenchymal cells become
closely packed to formclosely packed to form
mesenchymal condensation.mesenchymal condensation.
 B.Some mesenchymal cellsB.Some mesenchymal cells
become chondroblast and laybecome chondroblast and lay
down hyaline cartilage.down hyaline cartilage.
Mesenchymal cells on surfaceMesenchymal cells on surface
of the cartilage formsof the cartilage forms
perichondrium, that containsperichondrium, that contains
osteoprogenitor cells.osteoprogenitor cells.

 Cartilage cells enlargeCartilage cells enlarge
(beginning from(beginning from
ossification centre)ossification centre)
 Surrounding cartilageSurrounding cartilage
matrix calcifies under thematrix calcifies under the
influence of alkalineinfluence of alkaline
phosphotase secreted byphosphotase secreted by
cartilage cells.cartilage cells.
 Cartilage cells die leavingCartilage cells die leaving
behind empty spaces thebehind empty spaces the
primary areolaeprimary areolae

 Blood vessels invade fromBlood vessels invade from
perichondriumperichondrium
 Perivascular cellsPerivascular cells
(OSTEOBLAST) and(OSTEOBLAST) and
OSTEOCLAST come alongOSTEOCLAST come along
with blood vessels. This masswith blood vessels. This mass
of vessel and cells is c/aof vessel and cells is c/a
periosteal bud.periosteal bud.
 Osteoclast erode the primaryOsteoclast erode the primary
areolae (secondary areolae)areolae (secondary areolae)
 Osteoblast form new boneOsteoblast form new bone
 over secondary areolae.over secondary areolae.
 Woven bone formed.Woven bone formed.

 Hyaline cartilage
 Zone of cell multiplication
 Zone of cell hypertrophy
 Matrix calcification
 Chondrlysis and
ossification

INTRAMEMBRANOUS BONEINTRAMEMBRANOUS BONE
FORMATIONFORMATION

Osteoblast
Osteoid
Mineralized bone

Bone Processes During theBone Processes During the
LifespanLifespan
 1)1) growthgrowth
 2)2) modelingmodeling
 3)3) remodelingremodeling
 4)4) repairrepair

GrowthGrowth

Modeling and RemodelingModeling and Remodeling
 Both trabecular and cortical bone grow,Both trabecular and cortical bone grow,
adapt, and turnover by means of twoadapt, and turnover by means of two
fundamentally distinct mechanism ;fundamentally distinct mechanism ;
 ModelingModeling
 RemodelingRemodeling

 In bone modeling, independent sites ofIn bone modeling, independent sites of
resorption and formation change the formresorption and formation change the form
of a bone.of a bone.
 In bone remodeling a specific, coupledIn bone remodeling a specific, coupled
sequence of resorption and formationsequence of resorption and formation
occurs to replace previously existing bone.occurs to replace previously existing bone.
The mechanism for internal remodelling ofThe mechanism for internal remodelling of
dense compact bone involves axiallydense compact bone involves axially
oriented cutting and filling cone.oriented cutting and filling cone.

A schematic cross
section of cortical
bone shows surface
modelling (M), which
is the process of
uncoupled resorption
and formation.
Remodelling(R) is the
turn over of existing
bone.

RemodelingRemodeling
 A. Orthodontic boneA. Orthodontic bone
modeling, site specificmodeling, site specific
resorption andresorption and
formation occursformation occurs
along the PDL andalong the PDL and
periosteal surfaces.periosteal surfaces.
 Remodeling orRemodeling or
turnover occurs alongturnover occurs along
within the alveolarwithin the alveolar
bone along the line ofbone along the line of
force.force.

Bone modeling and its driftsBone modeling and its drifts
(Angle orthodontist 2007)(Angle orthodontist 2007)
Two kinds of driftsTwo kinds of drifts
 Formation driftFormation drift
 Resorption driftResorption drift
 Osteoblasts in formation drifts can formOsteoblasts in formation drifts can form
new bone on large regions of periosteal,new bone on large regions of periosteal,
cortical-endosteal and trabecular surfaces.cortical-endosteal and trabecular surfaces.
 Osteoclasts in resorption drifts can resorbOsteoclasts in resorption drifts can resorb
bone from other similar surfaces.bone from other similar surfaces.

Filling cone and cutting coneFilling cone and cutting cone
Old bone is being removed in segment A by osteoclasts,forming the cutting cone. In
segment B, osteoblasts begin to synthesize the osteoid (filling cone), the osteoid
mineralizes, becoming new bone.

These driftsThese drifts
 Maintains bone shapeMaintains bone shape
 Increase in size of boneIncrease in size of bone
 Can correct deformities from fractureCan correct deformities from fracture
malunions or other problems.malunions or other problems.
 Such drifts also move tooth socketsSuch drifts also move tooth sockets
around in the mandible and maxilla inaround in the mandible and maxilla in
response to orthodontic forces.response to orthodontic forces.

 A. Drift maintainingA. Drift maintaining
shape.shape.
 B. correcting theB. correcting the
deformity in healingdeformity in healing
fracture.fracture.
 C. shows how drift in BC. shows how drift in B
would move the wholewould move the whole
segment to the right insegment to the right in
tissue space.tissue space.

 Lamellar and woven bone can each provide formationLamellar and woven bone can each provide formation
drifts.drifts.
 Larger stimuli are needed to form woven bone thanLarger stimuli are needed to form woven bone than
lamellar bone.lamellar bone.
 Woven bone can appear in;Woven bone can appear in;
 Fracture healingFracture healing
 NeoplasmNeoplasm
 InfectionsInfections
 In the marrow cavity ahead of a tooth subjected toIn the marrow cavity ahead of a tooth subjected to
excessive orthodontic forces.excessive orthodontic forces.
 Adds bone much faster than lamellar drifts.Adds bone much faster than lamellar drifts.
( angle orthodontist 07)( angle orthodontist 07)

 Woven bone evoked by large orthodontic forces.Woven bone evoked by large orthodontic forces.
T-Tooth being forced to left ,this overload madeT-Tooth being forced to left ,this overload made
woven bone on medullary left side of thatwoven bone on medullary left side of that
tooth’s socket.tooth’s socket.
 (angle orthodontist 07)(angle orthodontist 07)

 Basic Multicellular Unit (BMU) is aBasic Multicellular Unit (BMU) is a
wandering team of cells that dissolve anwandering team of cells that dissolve an
area of the bone surface and then fills itarea of the bone surface and then fills it
with new bone in Activation –Resorption –with new bone in Activation –Resorption –
Formation (ARP) sequence.Formation (ARP) sequence.
 Turns over about 0.05 mm3 of preexistingTurns over about 0.05 mm3 of preexisting
bone in about 4 months.bone in about 4 months.
 A BMU’s osteoclastic activity does coupleA BMU’s osteoclastic activity does couple
biologically to its osteblastic activity.biologically to its osteblastic activity.
BONE REMODELING AND BMUBONE REMODELING AND BMU

BMU REMODELING SEQUENCEBMU REMODELING SEQUENCE
1.Origination1.Origination
2. Osteoclast recruitment2. Osteoclast recruitment
3. Resorption3. Resorption
4.Osteoblast recruitment4.Osteoblast recruitment
5.Osteoid formation5.Osteoid formation
6. Mineralization6. Mineralization
7.Mineral maturation7.Mineral maturation
8.Quiescence8.Quiescence

1) The activation connection1) The activation connection
 Continued remodeling for life requiresContinued remodeling for life requires
continually creating new BMU’s to replacecontinually creating new BMU’s to replace
the completed ones.the completed ones.
 BMU creation is primary control of boneBMU creation is primary control of bone
turnover in remodeling.turnover in remodeling.
 (angle orthodontist 07)(angle orthodontist 07)

2. The BMU “ rho fractions”2. The BMU “ rho fractions”
 A BMU can resorb, more bone than itA BMU can resorb, more bone than it
makes, or less, or equal amounts.makes, or less, or equal amounts.
 Let rho equal any such deficit or excess ofLet rho equal any such deficit or excess of
resorption over formation.resorption over formation.
 Can be hence negative ,positive or zeroCan be hence negative ,positive or zero
(angle orthodontist 07)(angle orthodontist 07)
Rho = bone formed - bone resorbed

 3. The envelope connection3. The envelope connection
 Remodelling happens on periosteal,Remodelling happens on periosteal,
haversian, cortical- endosteal andhaversian, cortical- endosteal and
trabecular surfaces or envelopes.trabecular surfaces or envelopes.
(angle orthod 07)(angle orthod 07)

 Bone remodelling occurs faster in childrenBone remodelling occurs faster in children
and spongiosa than adult and compactand spongiosa than adult and compact
bone.bone.
 Increased remodeling tends to removeIncreased remodeling tends to remove
bone next to marrow and make a bonebone next to marrow and make a bone
weaker . Decreased remodeling tends toweaker . Decreased remodeling tends to
conserve bone and its strength.conserve bone and its strength.
(angle orthodontist o7)(angle orthodontist o7)

Regional acceleratory phenomenaRegional acceleratory phenomena
(RAP)(RAP)
 Infection, injury and some tumors can make all normallyInfection, injury and some tumors can make all normally
ongoing local tissue process accelerate.ongoing local tissue process accelerate.
 Usually this RAP hastens healing and improves localUsually this RAP hastens healing and improves local
resistance to infection.resistance to infection.
 It explain the increased modeling and remodeling in theIt explain the increased modeling and remodeling in the
mandible and maxilla following injuries or aftermandible and maxilla following injuries or after
implantation.implantation.
 In tooth extraction and periodontal diseases it canIn tooth extraction and periodontal diseases it can
hasten the ridge resorption, because RAP increaseshasten the ridge resorption, because RAP increases
regional remodeling and hence increased bone loss nextregional remodeling and hence increased bone loss next
to marrow.to marrow.
(angle orthod. 07)(angle orthod. 07)

 Orthodontists can take advantage of theOrthodontists can take advantage of the
intense postoperative modeling andintense postoperative modeling and
remodeling activity to ;remodeling activity to ;
 1) orthopedically position a maxilla with1) orthopedically position a maxilla with
headgear, occlusal biteplates ,or cervicalheadgear, occlusal biteplates ,or cervical
support within a few weeks of after asupport within a few weeks of after a
LeFort I osteotomy.LeFort I osteotomy.
 2)rapidly finish orthodontic alignment of2)rapidly finish orthodontic alignment of
dentition after orthognathic surgery.dentition after orthognathic surgery.

Microdamage and its thresholdMicrodamage and its threshold
 Mechanical fatigue damage normally occurs inMechanical fatigue damage normally occurs in
bone in life.bone in life.
 Remodeling BMU’s usually repair the damageRemodeling BMU’s usually repair the damage
and keep it from accumulating.and keep it from accumulating.
 This is done by removing and replacing theThis is done by removing and replacing the
damaged bone with new bone.damaged bone with new bone.
 Overloading bone can increase theOverloading bone can increase the
microdamage.microdamage.
 This can happen in pathologic fractures and inThis can happen in pathologic fractures and in
bone overloaded by endoprostheses andbone overloaded by endoprostheses and
internal fixation implants.internal fixation implants.

 The largest normally allowed peak boneThe largest normally allowed peak bone
strains lies in 1500 microstrain range.strains lies in 1500 microstrain range.
 In between 2000 -4000 microstrainIn between 2000 -4000 microstrain
increases microdamage.increases microdamage.
 This can loosen dental and orthopaedicThis can loosen dental and orthopaedic
bone implants.bone implants.

 Both modeling and remodeling areBoth modeling and remodeling are
controlled by an interaction of metaboliccontrolled by an interaction of metabolic
and mechanical signals.and mechanical signals.
 These signals do not effect by affectingThese signals do not effect by affecting
only osteoclast or only osteoblast , insteadonly osteoclast or only osteoblast , instead
they affect the whole drift or BMU ,suchthey affect the whole drift or BMU ,such
cells belong to, which then dictate whatcells belong to, which then dictate what
those cells do.those cells do.

Control factors for bone modelingControl factors for bone modeling
1) Mechanical1) Mechanical
 Disuse atrophy - <200microstrainDisuse atrophy - <200microstrain
 Bone maintainence -200 to 2500Bone maintainence -200 to 2500
 Physiologic hypertrophy- 2500 to 4000Physiologic hypertrophy- 2500 to 4000
 Pathologic overload - >4000Pathologic overload - >4000

 2) Endocrine2) Endocrine
 PTHPTH
 Vit. DVit. D
 CalcitoninCalcitonin
 Growth hormoneGrowth hormone
 estrogenestrogen

Factors affecting bone remodelingFactors affecting bone remodeling
 PTH - activation frequencyPTH - activation frequency
 Estrogen - activation frequencyEstrogen - activation frequency

Bone response to stressBone response to stress

 The vertical components of cranium tendThe vertical components of cranium tend
to be loaded in compression (negativeto be loaded in compression (negative
stress).stress).
 The horizontal components are loaded inThe horizontal components are loaded in
tension (positive stress).tension (positive stress).
 Most efficient structures for achievingMost efficient structures for achieving
maximal compressive strength withmaximal compressive strength with
minimal mass in a composite material.minimal mass in a composite material.

2D vectorial analysis of stress in the frontal section of the
human skull.relative to a bilateral bitting force 100
arbitary units , the load is distributed to the vertical
components of the mid face as compressive stress(-
ve).the horizontal structures are loaded in tension (+ve)

 Maxilla transfers stress to entire cranium,Maxilla transfers stress to entire cranium,
whereas mandible must absorb the entire load.whereas mandible must absorb the entire load.
Hence mandible is stronger than maxilla.Hence mandible is stronger than maxilla.
 Maxilla has relatively thin cortices that areMaxilla has relatively thin cortices that are
interconnected by network of trabeculaeinterconnected by network of trabeculae
 maxilla is loaded in compression.maxilla is loaded in compression.
 Mandible has thick cortices and more radiallyMandible has thick cortices and more radially
oriented trabeculae.oriented trabeculae.
 Loaded in bending and torsion.Loaded in bending and torsion.
Differential osteology of maxillaDifferential osteology of maxilla
and mandibleand mandible

 Frontal section of the maxillaFrontal section of the maxilla
and the mandible in the planeand the mandible in the plane
of the first molars.Because itof the first molars.Because it
transmits masticatory load totransmits masticatory load to
the entire cranium the maxillathe entire cranium the maxilla
has thin cortices connected byhas thin cortices connected by
fine trabeculae.the mandible isfine trabeculae.the mandible is
however loaded in bendinghowever loaded in bending
and torsion;it therefore isand torsion;it therefore is
composed of thick corticalcomposed of thick cortical
bone connected by coarsebone connected by coarse
oriented trabeculae.oriented trabeculae.

 1990 Frost : Mechanostat theory-1990 Frost : Mechanostat theory-
Mechanical loading is essential to skeletalMechanical loading is essential to skeletal
health.Control of most bone modelling &health.Control of most bone modelling &
some remodelling process is related tosome remodelling process is related to
strain history.strain history.
 The mechanostat provides a usefulThe mechanostat provides a useful
reference for the hierarchy ofreference for the hierarchy of
biomechanical responses to applied loads.biomechanical responses to applied loads.

 Schematic drawing of the
Mechanostat concept of Frost
as defined by Martin and Burr
Bone formation(F) &
resorption(R) are the
remodelling phenomena that
change the shape or form (or
both) of a bone.The peak
strain history determines
whether atrophy, maintenance,
hypertrophy or fatigue failure
occurs.
 uE= microstrain= percent of
deformation x 1/10000

BONE METABOLISMBONE METABOLISM

CALCIUM METABOLISMCALCIUM METABOLISM
 Bone is the primary calcium reservoir in theBone is the primary calcium reservoir in the
body. Approximately 99% of the calcium isbody. Approximately 99% of the calcium is
stored in the skeleton.stored in the skeleton.
 The continual flux of bone mineral responds to aThe continual flux of bone mineral responds to a
complex interaction of endocrine, biomechanicalcomplex interaction of endocrine, biomechanical
and cell level control factors that maintain theand cell level control factors that maintain the
serum calcium level at about 9 -11 mg%.serum calcium level at about 9 -11 mg%.
 Calcium in bone is mainly in the form of ca-Calcium in bone is mainly in the form of ca-
phosphate and partly as calcium carbonate.phosphate and partly as calcium carbonate.

Calcium balance ;Calcium balance ;
 EqulibriumEqulibrium
 Positive calcium balancePositive calcium balance
 Negative calcium balanceNegative calcium balance

Calcium homeostasisCalcium homeostasis
 Mineral equilibrium is maintained.Mineral equilibrium is maintained.
 When substantial calcium is needed to maintainWhen substantial calcium is needed to maintain
the critical serum calcium level, bone structure isthe critical serum calcium level, bone structure is
sacrificed.sacrificed.
 Supported by three temporally relatedSupported by three temporally related
mechanics ;mechanics ;
 1.immediate regulation in seconds.1.immediate regulation in seconds.
 2.short term regulation in minutes to days.2.short term regulation in minutes to days.
 3. long term regulation over weeks to months.3. long term regulation over weeks to months.

Instantaneous regulationInstantaneous regulation
 Selective transfer of calcium ions in and out of boneSelective transfer of calcium ions in and out of bone
fluid.fluid.
 Bone fluid is separated from ECF by osteoblast or thinBone fluid is separated from ECF by osteoblast or thin
bone lining cells.bone lining cells.
 Decrease in serum ca level stimulates secretion of PTHDecrease in serum ca level stimulates secretion of PTH
which enhances transport of calcium ion from bone fluidwhich enhances transport of calcium ion from bone fluid
into osteocytes and bone lining cells.into osteocytes and bone lining cells.
 Vit.D enhances pumping of calcium ions from bone liningVit.D enhances pumping of calcium ions from bone lining
cells into the extracellular fluid.cells into the extracellular fluid.
 Within physiologic limit it is possible to support caWithin physiologic limit it is possible to support ca
homeostasis without resorbing bone.homeostasis without resorbing bone.

Short term controlShort term control
 Affects the rates of bone resorption andAffects the rates of bone resorption and
formation through action of the threeformation through action of the three
calcific hormones PTH, 1,25 DHCC,andcalcific hormones PTH, 1,25 DHCC,and
calcitonin.calcitonin.
 PTH acting in concert with vit DPTH acting in concert with vit D
accomplishes three taskaccomplishes three task
 1.enhances osteoclast recruitment1.enhances osteoclast recruitment
 2.increases resorption rate2.increases resorption rate
 3.may suppress the osteoblasts.3.may suppress the osteoblasts.

Long term controlLong term control
 Has profound effects on skeleton.Has profound effects on skeleton.
 PTH mediated activation frequencyPTH mediated activation frequency
increases, thus increasing the resorption.increases, thus increasing the resorption.

Hormonal Control of Bone RemodelingHormonal Control of Bone Remodeling
 lowlow blood [Cablood [Ca+2+2
] signals parathyroid] signals parathyroid highhigh blood [Cablood [Ca+2+2
] signals thyroid] signals thyroid

 parathyroid releases PTHparathyroid releases PTH thyroid releases calcitoninthyroid releases calcitonin

 PTHPTH calcitonin stimulatescalcitonin stimulates osteoblastsosteoblasts

 stimulatesstimulates activates Vit. Dactivates Vit. D
 osteoclastsosteoclasts osteoblastsosteoblasts deposit new bonedeposit new bone
 (uses Ca(uses Ca+2+2
))
 osteoclastsosteoclasts degradedegrade ↑↑ CaCa+2+2
absorption inabsorption in
 bone (releases Cabone (releases Ca+2+2
) kidneys & intestines) kidneys & intestines

 blood [Cablood [Ca+2+2
] increases] increases blood [Cablood [Ca+2+2
] decreases] decreases

APPLIED PHYSIOLOGYAPPLIED PHYSIOLOGY

Orthodontics is contraindicated in
patients with active metabolic bone
disease because of excessive
resorption and poor bone
formation.
 However if the metabolic problemsHowever if the metabolic problems
(particularly –ve calcium balance) are(particularly –ve calcium balance) are
resolved with medical treatment,resolved with medical treatment,
these patients can be treatedthese patients can be treated
orthodontically assuming sufficientorthodontically assuming sufficient
skeletal structure remainsskeletal structure remains

OSTEOPOROSISOSTEOPOROSIS

OsteoporosisOsteoporosis::
Generic term for low bone mass.Generic term for low bone mass.
Negative ca balance causes osteoporosis.Negative ca balance causes osteoporosis.
Risk factors:Risk factors:
 Age (after 3rd decade).Age (after 3rd decade).
 Long term glucocorticoid therapy.Long term glucocorticoid therapy.
 Slight stature.Slight stature.
 Menopause.Menopause.
 Excessive smoking,alcohol.Excessive smoking,alcohol.
 Low physical activity.Low physical activity.
 Low calcium,vit. D diet.Low calcium,vit. D diet.
 Kidney failure,liver disease.Kidney failure,liver disease.
Features:Features:
Low bone mass,low radiographic density of jaws, thinLow bone mass,low radiographic density of jaws, thin
cortices, excessive bone resorptioncortices, excessive bone resorptionwww.indiandentalacademy.comwww.indiandentalacademy.com

 WHO has defined osteoporosis on theWHO has defined osteoporosis on the
basis of bone density.basis of bone density.
 If bone densityIf bone density
>833mg/cm sq - normal>833mg/cm sq - normal
648 – 833 mg/ cm sq – osteopenia648 – 833 mg/ cm sq – osteopenia
<648 mg/cm sq - osteoporosis.<648 mg/cm sq - osteoporosis.

 Bone resporption >
bone deposition
 Result: weak, brittle
bones
i, 2001

 TreatmentTreatment::
 - weight-bearing- weight-bearing
exerciseexercise
 - Vit. D & Ca+2- Vit. D & Ca+2
 - bisphosphonates- bisphosphonates
 - calcitonincalcitonin

 Millions of peri and postmenopausal women areMillions of peri and postmenopausal women are
currently taking oral bisphosphonates forcurrently taking oral bisphosphonates for
prevention of osteoporosis.prevention of osteoporosis.
 Orthodontic treatment must come into question.Orthodontic treatment must come into question.
 bone resorption.bone resorption.
 Tooth movement is retarded.Tooth movement is retarded.
 No invasive laser therapy to be used due toNo invasive laser therapy to be used due to
potential risk of bone necrosis.potential risk of bone necrosis.
 Miniscrew anchorage should not be planned.Miniscrew anchorage should not be planned.
(jco 06)(jco 06)

Parathyroid hormone (PTH)Parathyroid hormone (PTH)
 Increases bone resorption by intensifyingIncreases bone resorption by intensifying
osteclast activity.osteclast activity.
 Facilitates conversion of vit D into its finalFacilitates conversion of vit D into its final
active product calcitriol.active product calcitriol.
 Acts on renal tubules to increase calciumActs on renal tubules to increase calcium
reabsorption .reabsorption .
 Net effect is increase in serum calciumNet effect is increase in serum calcium
level.level.

 At cellular levelAt cellular level
 1.osteoblast contain PTH receptors. When1.osteoblast contain PTH receptors. When
PTH binds with its receptors in thePTH binds with its receptors in the
osteoblast, osteoblast secrete interleukins.osteoblast, osteoblast secrete interleukins.
This ILs now intensifies osteoclasticThis ILs now intensifies osteoclastic
activity bone resorptionactivity bone resorption
 Negative feedback;Negative feedback;
 Higher the ca++ level, lower is theHigher the ca++ level, lower is the
production of PTH.production of PTH.

Hyperparathyroidism.Hyperparathyroidism.
 Osteitis fibrosa cysticaOsteitis fibrosa cystica
 Bone pain,pathologic fractures,Bone pain,pathologic fractures,
generalized osteoporosis,giant cellgeneralized osteoporosis,giant cell
tumours of the jaw.tumours of the jaw.
 Histologically:Histologically: The most characteristicThe most characteristic
change in bone is osteoclastic resorption ofchange in bone is osteoclastic resorption of
the trabeculae of the spongiosa & alongthe trabeculae of the spongiosa & along
the blood vessels in the haversian systemthe blood vessels in the haversian system
of the cortex.of the cortex.
 Enhanced rate of orthodontic toothEnhanced rate of orthodontic tooth
movement because of lower bone densitymovement because of lower bone density
and elevated remodeling rate.(JCO 2007)and elevated remodeling rate.(JCO 2007)www.indiandentalacademy.comwww.indiandentalacademy.com

 IN 1988, COLLINS AND SINCLAIRIN 1988, COLLINS AND SINCLAIR
demonstrated that intraligamentous injection of ademonstrated that intraligamentous injection of a
vit D metabolite caused increase in the numbervit D metabolite caused increase in the number
of osteoclast and the amount of tooth movementof osteoclast and the amount of tooth movement
during canine retraction with light forces in cats.during canine retraction with light forces in cats.
 Stimulatory effect on osteoblast can helpStimulatory effect on osteoblast can help
stabilize the orthodontic tooth movement.stabilize the orthodontic tooth movement.
 Could intensify the reestablishment of supportingCould intensify the reestablishment of supporting
tissue, especially alveolar bone, after OTM.tissue, especially alveolar bone, after OTM.
(JCO 2007)(JCO 2007)

Vitamin D deficient ricketsVitamin D deficient rickets
 Any disorder in the vit.D-Any disorder in the vit.D-
Calcium - phosphorusCalcium - phosphorus
axis results inaxis results in
hypomineralized bonehypomineralized bone
matrix.matrix.
 Cessation of calcificationCessation of calcification
of epiphysial growth plateof epiphysial growth plate
cartilage.However thecartilage.However the
cartilage continues tocartilage continues to
grow.Since unmineralizedgrow.Since unmineralized
bone cannot bear weight,bone cannot bear weight,
they bow.they bow.

Adult ricketsAdult rickets
 Seen in postmenopausal women with lowSeen in postmenopausal women with low
calcium intake and little exposure to UVcalcium intake and little exposure to UV
light.light.
Features:Features:
 SofteningSoftening
 distortion,distortion,
 increased tendency towards fracture.increased tendency towards fracture.
 Stress bearing bones have asymmetricStress bearing bones have asymmetric
deformities & long bones have hairlinedeformities & long bones have hairline
fracture.fracture.

Vitamin D resistant ricketsVitamin D resistant rickets
(familial hypophosphatemia, refractory rickets,(familial hypophosphatemia, refractory rickets,
phosphate diabetes)phosphate diabetes)
 Hypophosphatemia & hyperphosphaturiaHypophosphatemia & hyperphosphaturia
associated with decreased renal tubularassociated with decreased renal tubular
reabsorption of inorganic phosphates.reabsorption of inorganic phosphates.
 Familial occurrence,X-linked dominant trait.Familial occurrence,X-linked dominant trait.
 Do not respond to the usual doses of vit. D.Do not respond to the usual doses of vit. D.
 NormocalcaemiaNormocalcaemia with high normal PTH levels.with high normal PTH levels.
 Diminished intestinal calcium & phosphateDiminished intestinal calcium & phosphate
absorption.absorption.
 Decreased growth & short stature.Decreased growth & short stature.
 Normal vit. D metabolism.Normal vit. D metabolism.

Renal rickets(renal osteodystropy)Renal rickets(renal osteodystropy)
Common finding in patients with chronic renalCommon finding in patients with chronic renal
disease.Results from the inability of diseased kidneysdisease.Results from the inability of diseased kidneys
to convert 25-hydroxy cholecalciferol to the activeto convert 25-hydroxy cholecalciferol to the active
form of vit.D.form of vit.D.
A patient with impaired renal function often is a high riskA patient with impaired renal function often is a high risk
for osseus manipulative procedures such asfor osseus manipulative procedures such as
endosseous implants or orthognathic surgery.endosseous implants or orthognathic surgery.
Poor bone quality.Poor bone quality.

““osteomalacia” = “soft bones”osteomalacia” = “soft bones”
 Vit D deficiencyVit D deficiency
 Serum calcium level falls.Serum calcium level falls.
 CauseCause: poor mineralization: poor mineralization
 ResultResult: soft, weak bones: soft, weak bones
 SymptomsSymptoms: pain on weight-bearing: pain on weight-bearing

Vitamin CVitamin C
It has a role in the hydroxylation of proline in collagenIt has a role in the hydroxylation of proline in collagen
synthesis.synthesis.
Vit C furthers the normal development of intercellularVit C furthers the normal development of intercellular
ground substance in bone,dentin & connective tissue.ground substance in bone,dentin & connective tissue.
Effects on bone:Effects on bone:
Osteoblasts fail to form osteoid. Calcified cartilageOsteoblasts fail to form osteoid. Calcified cartilage
(scorbutic lattice) is formed but no bone(scorbutic lattice) is formed but no bone
develops.The calcified cartilage is liable to fracturedevelops.The calcified cartilage is liable to fracture
(trummerfeld zone or zone of complete destruction).(trummerfeld zone or zone of complete destruction).

calcitonincalcitonin
 Secreted by parafollicular or C cells of theSecreted by parafollicular or C cells of the
thyroid.thyroid.
 Effects opposite to parathyroid hormone.Effects opposite to parathyroid hormone.
 Inihibits the osteoclastic activity.Inihibits the osteoclastic activity.
 Promotes calcium deposition in bone.Promotes calcium deposition in bone.
 Lowers serum calcium level.Lowers serum calcium level.

StimulationStimulation InhibitionInhibition
Bone formationBone formation GHGH
CalcitoninCalcitonin
InsulinInsulin
TestosteroneTestosterone
EstrogenEstrogen
CortisolCortisol
MineralizationMineralization CalcitoninCalcitonin
InsulinInsulin
Vit DVit D
CortisolCortisol
Bone resorptionBone resorption ParathormoneParathormone
ThyroxineThyroxine
CortisolCortisol
TestosteroneTestosterone

(jco 2007)(jco 2007)

FLUOROSISFLUOROSIS
 The nature of mineralThe nature of mineral
salts in bone can besalts in bone can be
altered under certainaltered under certain
circumstances. If thecircumstances. If the
content of fluoride ioncontent of fluoride ion
in drinking water isin drinking water is
high ,the fluoridehigh ,the fluoride
content increasescontent increases
rapidly leading torapidly leading to
fluorosis.fluorosis.

Diseases of boneDiseases of bone
Osteogenesis imperfectaOsteogenesis imperfecta
 Brittle boneBrittle bone
 Porosity and fragility of bone.Porosity and fragility of bone.
 Basic defect appears to lie in the organic matrixBasic defect appears to lie in the organic matrix
with failure of fetal collagen to be transformedwith failure of fetal collagen to be transformed
into mature collagen.into mature collagen.
 Thin corticesThin cortices
 Immature spongy boneImmature spongy bone
 Osteoblastic activity retarded.Osteoblastic activity retarded.
 MicrofractureMicrofracture

OsteopetrosisOsteopetrosis
 Failure of osteoclastic bone resorptionFailure of osteoclastic bone resorption
leads to increased bone mass.leads to increased bone mass.
 Results in thickened sclerotic bones withResults in thickened sclerotic bones with
poor mechanical properties.poor mechanical properties.
 Deficient in collagen matrixDeficient in collagen matrix
 Fragile bone.Fragile bone.

Paget’s diseasePaget’s disease
 Characterised by excessive and abnormalCharacterised by excessive and abnormal
remodeling of bone.remodeling of bone.
 Excessive remodeling gives rise to bonesExcessive remodeling gives rise to bones
that are extensively vascularised , weakthat are extensively vascularised , weak
,enlarged and deformed.,enlarged and deformed.
 Intial osteolytic phase by overtly largeIntial osteolytic phase by overtly large
osteoclast .osteoclast .
 Followed by haphazard laying of newFollowed by haphazard laying of new
bone matrix.bone matrix.

 Loss of calcium from boneLoss of calcium from bone

Begins after age 30Begins after age 30

Accelerates at 40-45 yearsAccelerates at 40-45 years

Continues until ~30% of calcium gone by 70Continues until ~30% of calcium gone by 70
yearsyears
 Less calcium loss in malesLess calcium loss in males

Hormonal protectionHormonal protection
Aging and Bone TissueAging and Bone Tissue

 2.2. Decreased rate of protein synthesisDecreased rate of protein synthesis

Decreased ability to produce collagenDecreased ability to produce collagen

Bones become brittleBones become brittle

Reduction in human growth hormoneReduction in human growth hormone

Effect of drugsEffect of drugs

 Bone stress: bone becomes strongerBone stress: bone becomes stronger
with timewith time

Increased deposition of mineral saltsIncreased deposition of mineral salts

Production of collagenProduction of collagen

Increased calcitoninIncreased calcitonin
 Removal of mechanical stressRemoval of mechanical stress

Demineralization of boneDemineralization of bone
Exercise and Bone TissueExercise and Bone Tissue

 Main mechanical stresses:Main mechanical stresses:

Pull of musclesPull of muscles

Pull of gravityPull of gravity
 Immobilized joints and spaceflightImmobilized joints and spaceflight

Similar effectsSimilar effects
 Loss of bone mass: ~ 1% per weekLoss of bone mass: ~ 1% per week

Bone fracture and repairBone fracture and repair

 Process:Process:

Fracture causes blood vessels to breakFracture causes blood vessels to break

Blood clots (fracture hematoma)Blood clots (fracture hematoma)

Hematoma causes cellular responseHematoma causes cellular response
• Swelling and inflammationSwelling and inflammation

Osteoprogenitor cells produce collagen fibersOsteoprogenitor cells produce collagen fibers
• Help connect ends of boneHelp connect ends of bone

 Process:Process:

Vascularized bone sections: increasedVascularized bone sections: increased
osteoblast actionosteoblast action

Osteoblasts produce spongy bone trabeculaeOsteoblasts produce spongy bone trabeculae

Dead portions of bone removed byDead portions of bone removed by
osteoclastsosteoclasts

Compact bone replaces spongy boneCompact bone replaces spongy bone
• Thickening at spot of fractureThickening at spot of fracture

 Distraction osteogenesis is mostDistraction osteogenesis is most
mysterious phenomena of bonemysterious phenomena of bone
physiology.physiology.
 The procedure is based on the law ofThe procedure is based on the law of
tension stress, which states that gradualtension stress, which states that gradual
traction on living tissues creates stresestraction on living tissues creates streses
that can stimulate and maintainthat can stimulate and maintain
regeneration and active growth of theseregeneration and active growth of these
tissues.tissues.

 Distraction osteogenesis begins with theDistraction osteogenesis begins with the
development of a reparative callus similar to thatdevelopment of a reparative callus similar to that
observed during bone repair or fracture healing.observed during bone repair or fracture healing.
 New bone formation is initiated when a tractionNew bone formation is initiated when a traction
force is applied to the bone segments, therebyforce is applied to the bone segments, thereby
interrupting the process of fracture healing andinterrupting the process of fracture healing and
placing callus under tension.placing callus under tension.
 As the callus is stretched ,new bone isAs the callus is stretched ,new bone is
generated parallel to the direction of traction.generated parallel to the direction of traction.
 During this, callus is maintained in center ofDuring this, callus is maintained in center of
distraction gap while routine fracture healingdistraction gap while routine fracture healing
occurs at the periphery of the regenerate.occurs at the periphery of the regenerate.

Clinical considerationsClinical considerations

 During induction of orthodontic toothDuring induction of orthodontic tooth
movement response modeling (frontalmovement response modeling (frontal
resorption) in the PDL and initialresorption) in the PDL and initial
remodeling events (resorption cavities) inremodeling events (resorption cavities) in
cortical bone ahead of the advancing toothcortical bone ahead of the advancing tooth
allows for progressive tooth movement atallows for progressive tooth movement at
a relatively rapid rate.a relatively rapid rate.

 Resorption cavities ahead of moving toothResorption cavities ahead of moving tooth
reduce the density of bone. These intraosseusreduce the density of bone. These intraosseus
cavities are the initial remodeling events thatcavities are the initial remodeling events that
occur during first months of remodeling cycle.occur during first months of remodeling cycle.
 One reason for slow tooth movement in fewOne reason for slow tooth movement in few
patients may be the tendencies for resorptionpatients may be the tendencies for resorption
cavities initiated by orthodontic activation tocavities initiated by orthodontic activation to
complete the remodeling cycle by refilling withcomplete the remodeling cycle by refilling with
new bone if appropriate mechanics are notnew bone if appropriate mechanics are not
maintained.maintained.

Why does cortical bone offer good anchorage?Why does cortical bone offer good anchorage?
 The marrow space contains a large surface area forThe marrow space contains a large surface area for
cellular activity which is indispensable for toothcellular activity which is indispensable for tooth
movement.On the other hand if bone involved in toothmovement.On the other hand if bone involved in tooth
movement is of a compact character the surface areamovement is of a compact character the surface area
where the cellular reaction can take place is greatlywhere the cellular reaction can take place is greatly
reduced.reduced.
 When one is planning orthodontic treatment ,the toothWhen one is planning orthodontic treatment ,the tooth
should remain in spongy bone during movement.On theshould remain in spongy bone during movement.On the
other hand when teeth are pitted against cortical boneother hand when teeth are pitted against cortical bone
they can be used to our advantage to provide morethey can be used to our advantage to provide more
anchorage.anchorage.

Is it easier to move teeth in younger patients ?Is it easier to move teeth in younger patients ?
 The alveolar bone in young persons whoThe alveolar bone in young persons who
comprise the majority of our patients is not verycomprise the majority of our patients is not very
dense. It contains large marrow spaces. Sincedense. It contains large marrow spaces. Since
tooth movement is facilitated by the formation oftooth movement is facilitated by the formation of
resorptive cells,whose number again increasesresorptive cells,whose number again increases
according to the number of marrow spaces.according to the number of marrow spaces.
 Young patients bone is not as dense as elderly.Young patients bone is not as dense as elderly.
 The rate of tooth movement is inversely relatedThe rate of tooth movement is inversely related
to bone density .to bone density .

How soon after extraction can we startHow soon after extraction can we start
treatment ?treatment ?
 Extraction spaces contain tissue undergoingExtraction spaces contain tissue undergoing
reconstruction which is rich in cells & vascularreconstruction which is rich in cells & vascular
supply.Such an area is ideally suitable for toothsupply.Such an area is ideally suitable for tooth
movement & due advantage should be taken ofmovement & due advantage should be taken of
this by commencing treatment as soon asthis by commencing treatment as soon as
possible following extraction. Thereby onepossible following extraction. Thereby one
avoids atrophy & narrowing of the alveolaravoids atrophy & narrowing of the alveolar
process,resulting in bone loss & cortical boneprocess,resulting in bone loss & cortical bone
formation at the extraction site.formation at the extraction site.

Why do teeth move faster in the upperWhy do teeth move faster in the upper
arch?arch?
 Two physiologic factorsTwo physiologic factors
 1. Thin cortices and trabecular bone of1. Thin cortices and trabecular bone of
maxilla offers less resistance.maxilla offers less resistance.
 2.The leading root of mandibular molars2.The leading root of mandibular molars
being translated mesially forms bone thatbeing translated mesially forms bone that
is far more dense than that formed byis far more dense than that formed by
max. molars.max. molars.
 New bone formed in maxilla remodelsNew bone formed in maxilla remodels
rapidly owing to trabecular nature of bone.rapidly owing to trabecular nature of bone.

Why do I have to be careful with casesWhy do I have to be careful with cases
suffering from periodontitis?suffering from periodontitis?
 Moving teeth when progressiveMoving teeth when progressive
periodontal disease is present invitesperiodontal disease is present invites
disaster.disaster.
 Osteoclasts thrive in the diseased tissueOsteoclasts thrive in the diseased tissue
environment.environment.
 On the other hand osteoblastOn the other hand osteoblast
histogenesis is suppressed by inflammatoryhistogenesis is suppressed by inflammatory
disease.disease.
 When teeth are moved in the presence ofWhen teeth are moved in the presence of
active periodontal disease resorption isactive periodontal disease resorption is
normal or even enhanced & bone formationnormal or even enhanced & bone formation
inhibited. This may exacerbate the diseaseinhibited. This may exacerbate the disease
process, resulting in a rapid loss ofprocess, resulting in a rapid loss of
supporting bone.supporting bone.

ConclusionConclusion
 Orthodontics is a bone manipulativeOrthodontics is a bone manipulative
therapy & favourable calcium metabolismtherapy & favourable calcium metabolism
is an important consideration. Because ofis an important consideration. Because of
the interaction of structure & metabolism,the interaction of structure & metabolism,
a thorough understanding of the osseousa thorough understanding of the osseous
structure & function is fundamental tostructure & function is fundamental to
patient selection, risk assessment,patient selection, risk assessment,
treatment planning & retention of desiredtreatment planning & retention of desired
dentofacial relationships.dentofacial relationships.

ReferencesReferences
-- Current principles and techniques –T M. GRABER,Current principles and techniques –T M. GRABER,
ROBERT L. VANARSDALL.ROBERT L. VANARSDALL.
-- Angle orthodontics 94.Angle orthodontics 94.
‘‘ Wolff’s law and bone’s structural adaptations toWolff’s law and bone’s structural adaptations to
mechanical usage’mechanical usage’
-- JCO 2007JCO 2007
‘‘The influence of drugs and systemic factors on OTM.The influence of drugs and systemic factors on OTM.
-- JCO 2006JCO 2006
‘‘Bisphophonates and orthodontic implications.’Bisphophonates and orthodontic implications.’
-- GRAY’S ANATOMYGRAY’S ANATOMY
-- MEDICAL PHYSIOLOGY –CHAUDHARIMEDICAL PHYSIOLOGY –CHAUDHARI
-- ORAL PATHOLOGY –SHAFER’SORAL PATHOLOGY –SHAFER’S
-- Textbook of human histology – INDERBIR SINGHTextbook of human histology – INDERBIR SINGH
-- Craniofacial distraction osteogenesis –MIKHAIL L.Craniofacial distraction osteogenesis –MIKHAIL L.
SAMCHUKAVSAMCHUKAV
-- TENCATETENCATE
-- http://courses.washington.edu/bonephyshttp://courses.washington.edu/bonephyswww.indiandentalacademy.comwww.indiandentalacademy.com

Bone physiology

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Bone physiology

Similar to Bone physiology (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Bone physiology

Editor's Notes