Biology of Tooth Movement-Ortho / Orthodontic Courses by Indian Dental Academy

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BIOLOGY OF TOOTH
Periodontium
Periodontium is a connective tissue organ covered by epithelium , that
attaches the teeth to the bones of the jaws and provides a continually
adapting apparatus for support of teeth during function.
4 connective tissues
Two mineralized
-Cementum
-Alveolar bone
Two fibrous
-Periodontal ligament
-Lamina propria of the gingiva.
Cells
Progenitor cells
Synthetic cells
a) Osteoblasts
b) Fibroblasts
c) Cementoblasts
Resorptive cells
A) Osteoclasts
B) Fibroblasts
C) Cementoclasts

Extra cellular elements
Fibres
-Collagen
-Oxytalan
Ground Substance
-Proteoglycans
-Glycoproteins

Principle Fibres of the Periodontal
Ligament(Collagen Fibres)
1. Alveolar crest group
2. Horizontal group
3. Oblique group
4. Apical group
5. Interradicular group
GINGIVAL FIBRES
1. Circular
2. Alveologingival
3. Dentoperiosteal
4. Dentogingival
5. Transseptal fibres(Accesory fibres)
Alveolar bone

Two parts
1. Alveolar bone proper
2. Supporting alveolar bone
A.- Cortical Plate
B.- Spongy Bone
Alveolar process is formed by intramembranous
ossification.
They can be remodelled owing to the structure.

Active stabilization of teeth against
forces of low magnitude
Response to normal function:
Forces applied on the teeth are-
1-2 kgs when soft
Upto 50 kgs against harder food

Tooth
movement-
Vanarsdall
Peridontally Compromised Teeth
Historical Perspective
1. Celsus
2. Reitan
3. Openheim
4. Norton
5. Burstone
6. Davidovitch

TOOTH MOVEMENT-
Application of orthodontic force
tooth movement on account of
resorption on the pressure side and
deposition on the tension side.
Cascade of
activities-
Tooth
movement
(Norton)
Classification of orthodontic
forces- Schwartz

Four degrees of biologic efficiency.
1
st
Below threshold stimulus.
2
nd
-Most favourable 15-20 gms per square cm.Less than the
blood pressure.
3
rd
-Medium strength.They stop the blood. flow.Tissues are not
crushed.
4
th
Forces are so high that the tissues are crushed. Irrepairable
damage may be caused to the tissues involved.
Theories of orthodontic tooth movement
1) Bioelectric theory -electric signals produced when
alveolar bone flexes and bends. Also called the
piezoelectric theory.

2) Pressure tension theory(Schwartz1932)-related to cellular
changes produced by chemical messengers.

Bien Hydrodynamic damping of tooth movement, J. D. -
1966.

Theories are mutually dependent.
Bioelectric theory
2 unusual characteristics-
1. -quick decay rate
2. -equivalent signal opposite direction
Crystal deformation-electrons migrate due to distortion
of cross linkages between the collagen fibres in the
bones.
Electropositive response (convexity) resorption
Electronegetive (concavity) -deposition
Ions in fluids bathe the bone and cause streaming
potential. Similar but not the same.
No place in natural control of body.

Bioelectric theory
Bioelectric theory
Stress generated signals important-
astronauts.(can also be explained OB
differentiation)
Chewing /orthodontic forces.
Bioelectric signals-active growth, not
exactly known. Exogenous signals
modify tooth movement-lag phase before
tooth movement.
Effect of Pulsed Electromagnetic Field on Tooth
Movement- Stark and Sinclair Ajo - 1987 Feb
Simple non invasive pulsed
electromagnetic (25-Hz) field can cause an
effect on the rate and amount of tooth
movement.
20-experimental,20-control
Guinea pigs

AFTER 10 DAYS
Tooth movement
Osteoclast cell count
Observations-
1. Protein metabolism indicated by creatinine ,craetinine
phosphokinase, uric acid.

2. Na Ca K which are postulated to be the effect of pulsed
electromagnetic stimulation on the cell membrane are not increased.

3. Exciting possibily for future consideration - Ability to initiate and
enhance the bone deposition-use with functional appliances.

Effect of Pulsed Electromagnetic Field on Tooth
Movement- Stark and Sinclair Ajo - 1987 Feb
PRE AND POST EXPERIMENT

CONTROL AND EXPERIMENTAL
GROUP

INCREMENTAL MOVEMENT
Structure of the bone

Pressure -Tension Theory
Relies on chemical signals and not
electrical signals for cellular differentiation
and tooth movement.

Cells causing remodeling of bone
1. OB
2. OC

ORIGIN OF THE CELLS

1) OB-Neural crest cells(OB)- Pre Osteoblasts

a) Contact inhibition.

b) G1,G2 blocked cells.

Differentiation of cells under
mechanical influence
2) OC- Hematogenous in origin
Monocytes have been suggested to be the
predecessors. Progenitors ???
Blocked cells local preosteoclasts &
circulating preosteoclasts.
Cells causing remodeling of bone
mechanical influence-OB & OC
Vit D metabolites
They are known to effect bone formation and
deposition via the differentiation of the comitted
progenitor cells into mature cells.

OSTEOBLASTS
RESORPTIVE FUNCTION
1) OB-Physical barrier-layer of cells on the bone surface.
If these cells are stimulated by PTH they change shape
(round) thus exposing the underlying mineral of the tooth
only affects already differentiated cells.
.

Shape change in cells: mechanism for the
transduction of mechanical forces ( Sandy-
Bdj;1992)
Relationship exists bw cell shape and metabolic
activity.
Flattened cells synthesize more DNA than rounded
cells.
PG and PTH induce change in shape.
Suggested in pressure sites the cells are rounded
and have catabolic effects-tension sites the cells are
flattened and in a synthetic mode.
RESORPTIVE FUNCTION
2) Release certain mediators cytokines-Bring about
osteoclastic resorption.
They are defined as short range soluble
mediators,released from the cells which modulate the
activity of other cells - ( Bone remodeling- Sajeda
Meghji 1992; Bdj ) - lymphokines.

OSTEOBLASTS
Cytokines:Mediators of bone remodeling( -Sandy-
Bdj;1992
-Biology of tooth movement- Norton and Burstone)

Osteoclasts dont work
independently -signal
transmitted to the
osteoclast by an
Osteoblast Cytokine.

RESORPTIVE FUNCTION
3)Osteiod layer covering
the bone is removed by
OB - secrete
collagenase.
P TIMP

Cytokines:Mediators of bone remodeling ( Sandy-
Bdj;1992,-Biology of tooth movement- Norton and Burstone)
TIMP-TISSUE INHIBITOR OF
METTALOPROTEINASES

FORMATIVE-

1)Pressure
2)Production of first messenger( physical/
chemical)

a) Deformation may lead to ca influx
b) Hormones(PTH)
c) Prostaglandins( macrophages )
d) Neurotransmitters(SP)

OSTEOBLASTS
They bind to the cell
surface receptors.

3)Second messengers
a. c AMP
b. c GMP
c. Ca
4)Increased bone activity

OSTEOBLASTS

Trans membrane signaling pathway
PHOSPHOINOITIDASE
INOSITOL
TRIPHOSOHATE
Discovered by VON
EULER 1934
Prostate gland
Yamasaki injection of
exogenous PG increased
osteoclast numbers.

Role of Prostaglandins (Tooth eruption and
orthodontic movement:Sandy-Bdj,1992)
Phospholipids
phopholipase
Arachidonic acids

Prostaglandin's

c AMP

Ca+2

ARACHIDONIC ACID METABOLISM
Leukotrienes and HETE (Leucocytes)
(Hydroxyeicosatetraenoic Acid) , produced
from the same substrate.

Since PGs do not fully account for bone
remodeling associated with tooth movement ,
lipoxygenase products may be involved.
OSTEOCLASTS
Resorptive action
PTH- systemic factor
Cytokines
Mechanical
Ruffled border
Lysosomal enzymes
Osteocytes cytoplasmic processes which help to gauge
the pressure changes and signal the OB.

Osteocytes

Events during bone remodelling
PDL and bone response to sustained
forces on pressure side-

1. Undermining resorption

2. Fontal resorption
Oteoclast differentiation
2 waves
-1
st
wave local cell population.
-2
nd
wave-blood flow.
Optimal force-frontal resoption on pressure
side
Excess force would cause undermining
resorption.
Pattern of bone deposition and resorption
Tooth movement
Tooth movement may be divide into (Graber .Vanarsdall)
- Initial Undermining resorption
- Secondary period-Frontal resorption

Initial phase- 3 main stages
1. Degeneration
2. Elimination of destroyed tissue
3. Establishment of new attachment
1.Degeneration
1. Blood flow
2. Degradation of vessel walls
3. Cellular changes
-Swelling of mitochondria
-Rupture of cytoplasmic membrane leaving only isolated nuclei
between the fibrous elements
The source of cells which differentiate into osteoclasts is
lost. Area is cell free.
Glassy appearing sterile necrotic area caused due to
excessive pressure application -HYALINIZATION

Tooth movement
Tooth movement
2.Elimination of destroyed tissue
Adjacent undamaged areas give rise to the osteoclasts
(multinucleated giant cells) which cause remodeling of
the bone on the peripheral areas.

Invasion of the hyalinized areas by the cellular elements.

Adjacent alveolar bone-undermining resorption
3.Establishment of new attachment
Synthesis of new tissue once the hyalinized tissue is
removed - Fibroblasts.

Macrophages adjacent to
hyalinized areas
Tooth movement
In secondary phase
Osteoclasts differentiate and cause frontal resorption.
Osteoblasts deposit on the tension surface.
On the tension side resorption occurs on the spongiosa
surface of the alveolar bone.
On pressure apposition takes place on the spongiosa
surface.
Remodelling also takes place on the on the periosteal
surface of the bone - helps to maintain the thickness of the
alveoar bone.
Differential Time Course Bw Frontal and
Undermining Resorption
Initial loading leads to some amount of
tooth movement- movement increases with
time-light forces.
Movement takes place in a stepwise
fashion with heavy forces.
Differential Time Course Bw Frontal and
Undermining Resorption
Effects of Tooth Movement and Force
Distribution
Distribution of forces and tooth movement
differ depending upon the type of tooth
movement.
Tipping
-Forces used to
tip the teeth
must be kept low
50gms.
Distribution
Tipping-hyalinization
Caution -alveolar
crest.
Distribution
Bodily tooth movement-uniform loading of
the teeth is seen.
.
Bodily tooth movement

Slight tipping due to the
hyalinized zone formed and
resorption adjacent to it.
Further tipping prevented by
the stretch of the fibres.

Effects of Tooth Movement and
Force Distribution
Rotation
Practically
impossible to bring
about pure rotation
tipping is the
actual mechanism
2 pressure sites and 2 tention sites.usually 1 side shows
frontal and other undermining resorption.After 3-4 weeks
frontal resorption prevails.
Supracrestal fibres-gingival fibres, trans gingival fibres.
Long retention period, supracrestal fibrotomy.
Distribution
TRANSSEPTAL FIBRES

Effects of Tooth Movement and Force Distribution
Intrusion light forces are actually needed for intrusion as the forces
are highly concentrated over a very small area.
If bone compact
as in adults-interrupted
force maybe better.
allows time for cell
proliferation.
Gingival fibres are relaxed
- cause formation of
bony spicules - crestal areas.

Ditribution(Proffit)
1. Tipping 35-60gms
2. Bodily 70-120gms
3. Uprighting 50-100gms
4. Rotation 35-60gms
5. Extrusion 10-20gms
6. Intrusion-10-20gms

Effects of force duration and decay
Duration the second messenger
produced only after 4 hours.
Forces
1. Continuous
2. Interrupted light and heavy
3. Intermittent

Force Duration and Decay
Ideal to have light
continuous forces but
heavier forces can be
allowed if a period of
regeneration and repair
is allowed.
4 week appointment
cycle.
Force Magnitude(Heavy pressure)
Force Magnitude(Light pressure)
AJO-DO 1985 Step Reassessment of force magnitude - Quinn and
Yoshikawa
Modifying the force magnitude as suggested by Storey and Smith
Pressure Versus Response
pressure - movement
Platue
Decline at the
end
Optimum force-
lightest force
producing
maximum
or near maximum movement
Pressure Versus Response
A1-anchor teeth
M1- teeth to be moved

Stationary anchorage
Bodily versus tipping movement- anchor
teeth would move less but if the force is
really high enough to bring posterior teeth
into optimum movement rage they would
move the same amount.
Large forces
Drug Effect on the Response of
Orthodontic Forces
+ve effect
PG
-ve effect
1. Bisphosphanates-act as specific inhibitors of
osteoclast mediated bone resorption.
2. PG inhibitors NSAIDS, indomethacin ,
tricyclic antidepressants,anti arrhythmic
agents,anti malarial drugs, methyl xanthines.
3. Corticosteroids (reduce the inflamation)
Phospholipids
phopholipase Corticosteroids
Arachidonic acids
NSAIDS
Prostaglandins

Drug Effect on the Response of
Orthodontic Forces
The effect of acetaminophen on tooth movement in rabbits -
1997 Angle Orthodontist John J. Roche et al
It is a weak prostaglandin inhibitor - recommended for
use to relieve pain during orthodontic tooth
movement.
14 rabbits were used.
Lower first molar and incisor teeth on one side were
prepared with a perforation hole buccolingually.
Maxilla was excluded from the study-21-day period.
Over the 21 day period, each rabbit was force-fed
1000 mgs of Tylenol (10 ml of solution) per day


On day 21, the rabbits were sacrificed
Impressions of the final interdental distance were obtained
and poured in stone for future examination.

Acetaminophen does not seem to retard orthodontic tooth
movement, related to its lack of anti-inflammatory
properties

Concentrated in the central nervous system
The effect of acetaminophen on tooth movement in
rabbits -1997 Angle Orthodontist John J. Roche,
George J. Cisneros, George Acs.


The effect of acetaminophen on tooth movement in rabbits -
1997 Angle Orthodontist John J. Roche, George . Cisneros,
George Acs.

Role Of Prostaglandins In Orthodontic Tooth
Movement- Dr Anand Patil
1microgram (gm) / injection (inj) of PG-E1 along with lignocaine
as a vehicle was injected on three different days in the vestibular
region distal to the right upper canine in 15 Patients.

The left side was the controlled side with injection of vehicle alone.

Occlusograms of pre and 60 days post canine retraction was obtained
and distal canine movement was calculated by using stable land
marks such as 1st rugae area .

The results showed statistically significant 57% increase in
orthodontic distal canine tooth movement on prostaglandin injected
side as compared with matched controlled left side.
Pre & post
Retraction
Occlusograms
AJO-DO 1983 Jan (62-75): Histochemistry of enzymes
associated with tissue degradation incident to orthodontic
tooth movement - Lilja, Lindskog, and Hamm

A tipping movement had been produced by the
orthodontic forces, and thus two pressure zones-
buccal and lingual.

Acid phosphatase activity Cells randomly
distributed along the bone surface in the alveoli in
non treated cases.

Prostaglandin synthetase - found exclusively in
the bone marrow-not in PDM.


Low force - rapid redistribution to the pressure zones of cells with a
high acid phosphatase activity.

Accompanied by a high enzyme activity in the adjacent osteocytes.

Low forces caused no change in the distribution and activity of LDH at
any time during the treatment.

After 1 day of high force a zone devoid of LDH activity developed in
the buccal pressure zone

No change in the activity of this enzyme was found in the bone marrow
during the treatment



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