Science of tooth movement

1. BIOLOGY OF TOOTH
MOVEMENT
PRESENTED BY
RANJEET SINGH

2. CONTENTS
 Introduction
 History
 Events occurring in OTM
 Periodontal structure
 Phases of tooth
movement
 Theories of tooth
movement
 Biologic control of tooth
movement
 Effects of force
magnitude
 Effects of force
distribution & types of
tooth movement
 Effects of force
distribution & force decay
 Iatrogenic effects of
orthodontic treatment.

3. INTRODUCTION
 An Orthodontic appliance transfers
mechanical stresses through the tooth to the
periodontium where they are translated into
physical, chemical, and electrical signals to
cells that activate tissue remodeling which
allows tooth movement.
 The orthodontist is able to control the quantity
and quality of the force system applied to the
tooth, but the speed and the way in which the
tooth moves is ultimately determined by the
biological response.

4.  To interpret the biological responses to
activation of any orthodontic appliance, each
interface in the process must be thoroughly
understood.
 Hence, I will be discussing some of the biologic
aspects of biomechanics that may lead to the
application of molecular and cell biology
currently so important in medical science as well
as to the field of orthodontics.

5. HERITAGE
 18th Century  Hunter provided the first
explanation for orthodontic tooth movement.
 1815  Delabbare remarked that pain and
swelling of paradental tissues occur following the
application of orthodontic forces to teeth. In
contemporary terms, Delabbare introduced the
notion that inflammation is an integral part of
orthodontic tooth movement.

6.  1888  Farrar hypothesized that tooth
movement is due, to bending of alveolar bone
by applied forces.
 1892  Wolff supported Farrar in that he said
internal architecture of bone is dictated by the
mechanical forces that act upon it.

7.  1904 to 1905  Sandstedt reported on the
histomorphology of tissues surrounding orthodontically
treated teeth. Landmark experiment, which was
performed on a dog, concluded that force induced tissue
changes that are limited to the PDL and its alveolar bone
margin. At the end of 3 weeks of treatment, Sandstedt
observed no bone growth in the stretched PDL, and
bone resorption in the area of PDL compression.
 Cell death occurred in the compressed PDL when the
applied force was excessive, and the alveolar bone
resorbed as a result of osteoclastic activity in adjacent
marrow spaces (Undermining resorption).

8.  Six years later, Oppenheim in contrast to
Sandstedt reported after conducting an experiment on
a juvenile baboon that no demarcation was seen
between the old and new bone, but rather a trabecular
structure that strongly suggested a complete
transformation of the entire alveolar bone.
 Schwartz (1932) defined orthodontic forces as being
“not greater than the pressure in the blood capillaries (20
to 26 g/cm2 of root surface).

9.  Reitan (1950) explored in detail the
morphological changes in the stressed
PDL. He used human material
extensively along with animals and
concluded that PDL cells in sites of
tension proliferate, and that newly
formed osteoid in these areas resorb
slowly when subjected to pressure.

10.  Storey (1952) realized that the rate of
orthodontic tooth movement in humans varies
and is unpredictable and suggested that it
depends upon the magnitude of the applied
force.
 He conducted a series of experiments in
rodents and concluded that the process of tooth
translation through bone consist of 3 different
phenomenon.
 Bioelastic, 2) Bioplastic, 3) Biodisruptive.

11.  The PDL and alveolar bone, due to their fluid-
fiber composition, can be deformed elastically by
external forces, which also evoke cellular
activities. When the tissue elastic limit is
reached, it starts to deform plastically, with
adaptive proliferation and remodeling reactions.
 Prolonged forces that exceed the bioplastic limit
result in biodisruptive deformation, with
ischaemia, cell death, inflammation and repair.

12.  Thus Reitan and Storey’s investigations
demonstrated the complexity of the tissue
reaction during tooth movement. It was no
longer perceived as a simple phenomenon of
applied force causing the tooth to move within
the PDL, leading to tension and compression,
and subsequent bone formation and resorption,
but rather as a dynamic set of events that
involved profound alterations in cellular functions
and changes in matrix composition.

13. “how” does the PDL and Alveolar
bone responds to applied
forces ?????.

14. CASCADE OF EVENTS THAT FOLLOW AFTER
APPLICATION OF ORTHODONTIC FORCE
Orthodontic force
On a tooth
(events at the
Microscopic level)
Alteration in blood flow
Reduced oxygen level
At compressed area
Increase oxygen level
At tension area
Release of piezoelectric
signals due to bone
Bending crystal
deformation
Release of
Neurotransmitters such as
Substance P,vasointesstinal
Polypeptide VIP,
calcitonin gene related
peptide

15.  Cells of the PDL ( FIBROBLASTS &
OSTEOBLASTS) possess receptors for these
substances & are highly interactive.
 These interactions lead to transient increase in
the intracellular levels of 2nd
messengers such
as CAMP( cyclic adenosine monophosphate)
,CGMP(cyclic guanosine monophosphate),
IP3(inositol phospatase), calcium etc.
 In the nucleus of each cell each different 2nd
messengers account for differential
patterning ,protein synthesis & gene
expression.

17. ROLE OF PROSTAGLANDINS IN
MEDIATING OTM
 Prostaglandins are synthesized from
fatty acids by PG synthetase found in
the mammalian tissue.
 Its most abundant precursor is
arachidonic acid which is present in the
membrane phospholipids of cells.
 Arachidonic acid can be released by
either by phospholipidases activated by
direct cellular damage or by non
destructive perturbation of the
membrane be it physical ,chemical or
hormonal.

18. PROSTAGLANDINS
Cause an
increase
in the
CAMP
,Ca 2+
Cause an
increase
in the
CAMP
,Ca 2+
Activates osteoclastic activity
Stimulate osteoblastic cell
Differentiation & new bone
formation

19. CYTOKINES & GROWTH FACTORS IN OTM
 The early phase of OTM involves an acute inflammatory
response characterized by periodontal vasodilatation &
migration of leucocytes out of the PDL capillaries.
 Inflammatory mediators such as PG’s & interleukin 1
interact with bone cells.
 Cytokines are released by leukocytes may interact
directly with bone cells or indirectly via neighboring cells
such as monocyte macrophages , lymphocytes or
fibroblasts.
 Cytokines can either induce bone remodeling , bone
resorption & new bone formation.

20. CYTOKINES
Tumor necrosis
Factor (TNF)
Granulocyte ma
cophage colony
Stimulating factor
(GMCSF)
(M-CSF)
Interleukin 1B
IL-6
cytokines
Stimulate bone resorption &
Induce osteoclast formation
Osteoblasts
regulate the
activity of
osteoclasts &
their release
through
cytokines

21.  Growth factors are also released during
inflammation and repair by the cells of PDL &
bone.
 They are released & activated during bone
resorption.
 The factors include fibroblast growth factor (B
fgf ),( a FGF ) , Insulin like growth factor ( IGF
-1 , IGF – 11 ) ,Transforming growth factor b
(TGF), platelet growth factor , bone
morphogenic proteins (BMP)

22.  IGF I & IGF – II
 FGF
 BMP
 Increase type I collagen
& matrix synthesis by
osteoblasts.
 Increase replication of
osteoblasts.
 Encourage mesenchymal
progenitors to
differentiate into both
osteoblasts &
chondrocytes.

23. DETECTION OF MECHANICAL STRAIN
BY BONE CELLS
 Cells responsible for sensing mechanical
strains in the bone are osteoblasts &
osteocytes.
 Three theories are suggested:
 Strain release potentials
 Activation of ion channels
 Extracellular matrix & cytoskeleton
reorganization.

24. Strain release potentials
 Application of small bending forces to
bones is known to produce flow of
interstitial fluid through the canalicular
network generating steaming potentials.
 These forces are first detected by
osteocytes which are mechanosensors
of the bone. these in turn activate
osteoblasts or osteoclasts to produce
bone remodeling.

25. Activation of ion channels
 Ion channels are tunnel shaped proteins
that cross the width of cell membrane.
 They serve as conductive pathway for
ions that cross the membrane as well as
membranes surrounding intracellular
organelles.
 They can be divided into three groups
depending upon the stimulus needed to
activate them.

26.  Voltage gated: have channel proteins that undergo
conformational changes in response to changes in the
transmembrane potential.
 Ligand gated: respond to specific ligands that may attach
to the cell membrane near channel opening.
 Mechanosensitive : these respond to mechanical stimuli
& allow the passage of cations namely calcium &
potassium. Orthodontic force affects the
mechanosensitive ion channels of osteoblastic cells
thereby producing a large increase in intracellular
calcium.

27. Extracellular matrix & cytoskeleton
Reorganization
 The macromolecules which make up the
ECM include collagen & glycose
aminoglycans which are secreted by the
fibroblasts of the PDL & osteoblasts of
bone.
 The non collagenous matrix consists of
proteoglycans & various glycoproteins.
 The matrix metalloproteins (MMPS)
represent major class of enzymes
resposible for ECM metabolism.

28.  Cytoskeleton represents a framework
attaching cell to cell or cell to extra
cellular matrix, thereby presenting a
possibility of transducing mechanical
forces acting on cells or on their adjacent
matrices.

29. PRINCIPLE
 PROLONGED PRESSURE
TOOTH MOVEMENT
Bone around
the tooth
remodels.
Added &
removed
selectively
Bone around
the tooth
remodels.
Added &
removed
selectively
Since bone response is primarily mediated
by the periodontal ligament ,tooth
movement is primarily a PERIODONTAL
LIGAMENT PHENOMENON.

30. TYPES OF TOOTH MOVEMENTS
 Physiologic : tipping of the tooth in its
socket during functioning.
 Changes that occur in the tooth position
during & after eruption.
 Normal & routine in nature & the tooth is
designed to undertake it.

31.  Migration: changes observed in tooth
position as a result of periodontal
breakdown or loss of tooth contact .
 Orthodontic : due to pressure
application on the tooth which results in
the remodeling of the surrounding bone
leading to tooth movement.

32. PERIODONTAL LIGAMENT STRUCTURE
& FUNCTION
 Each tooth is attached to
& separated from the
adjacent alveolar bone by
a heavy collagenous
supporting structure, the
periodontal ligament.
 Pdl occupies a space of
width 0.5mm around all
parts of the root.

33. Cells and Fluids of the PDL:
 PDL is a soft tissue
envelope separating the tooth
from the alveolar bone.
 it is comprised of cells and
extracellular matrix, which
consists of collagen and ground
substance.
 It contains an intricate network
of blood vessels and nerve
endings, and is very cellular.
The majority of PDL cells are
fibroblasts.

34.  Osteoblasts, either active or in the form of lining
cells, occupy the alveolar bone surface
bordering the PDL, while cementoblasts cover
the dental root surface that interfaces with the
PDL.

35. BMP
TGF
Mesenchymal
Pluripotent
progenitor
cells
OSTEOBLASTS
Secrete extracellular organic matrix
including osteocalcin,osteonectin,
type 1 collagen,alkaline
posphatase,proteoglycans & growth
factors.
respond to orthodontic force with the help of
integrin which is a membrane protein.these help to
translate the mechanical strain into a signal which
stimulates a gene to make the cell develop ligands
which allow intracellular communication.

36.  Osteocytes : proprioceptive &
responsive cells of the bone.
 Intermittent force increases the levels of
glucose 6 phosphate dehyrogenase ,
insulin like growth factor 1 within 6 hours
of mechanical loading.
 Monocyte haemopoietic cells
differentiate into osteoclasts which
cause bone resorption.

37.  Osteoblasts itself regulate the
differentiation of osteoclast through
osteoblast membrane bond RANK
(receptor activator nuclear factor ligand)
interacts
MONOCYTE
OSTEOCLASTS
XOsteoprotegerin

38.  Clusters of epithelial cells, the rests of
Malassez, are spread in the PDL in the
vicinity of the root surface, while
capillaries are usually more numerous in
the center of the ligament and in the
zone closer to the alveolar bone. Cells
migrating out of these capillaries, such
as lymphocytes, macrophages and mast
cells, can be observed throughout the
PDL.

39.  The PDL contains an elaborate network of neural
filaments that arise from the trigeminal nerve.
Myelinated and unmyelinated fibers are found in the
PDL, some terminating as “free” nerve endings, mostly in
the inner part of the PDL, while others terminate as
knob-like enlargements or as coiled nerve endings.
 Unmyelinated fibers usually follow PDL blood
vessels and may have a vasomotor action. In this
capacity, PDL nerve fibers may release, when stressed
mechanically, vasoactive peptides that regulate
movement of leukocytes out of capillaries, thereby
regulate local inflammatory response.

40.  In addition to providing the PDL with a variety of
leukocytes, the vascular system also contributes
to its fluid composition.
 Bien (1966), thoroughly analysed the dynamics
of PDL fluid in relation to tooth movement, and
identified 3 sources of fluid in the PDL,
cellular, vascular and interstitial. The latter is
localized in the ground substance and acts as a
thioxotropic gel, which is jelly-like when not in
motion and flows quite easily under pressure.

41.  When subjected to a steady force, this fluid flows
within the PDL out of areas of compression and
into areas of tension. This fluid flow, which
starts as soon as the force is applied to a tooth
and is maintained over extended periods of time,
is apparently a crucial step in the
physiochemical behavior of the PDL.

42.  The fluid motion & rearrangement signifies the
onset of distortion of PDL cells and fibers. This
distortion of PDL, which is seen, microscopically
as widening in areas of tension and narrowing in
sites of compression, may result in the release
of vasoactive neuropeptides, appearance of
stress-generated potentials, and alterations of
cellular shape.

43. RESPONSE TO NORMAL FUNCTION
 Masticatory function teeth & pdl are
subjected to intermittent heavy forces.
 Tooth contact lasts for 1 sec or less
 Forces range from 1 – 2 kg when soft
substances are chewed & can be up to 50kg’s
against a more resistant object.
 Quick displacement of the tooth is prevented by
the incompressible tissue fluid.
 The force is trasmitted to the bone & the bone
bends.

44.  bone bending.
Skeletal regeneration & repair
Piezo electric
currents ,that appear to
be important stmulus

45. Orthodontic force
Movement of PDL fluid
Gradual distortion of
PDL matrix &cells
Piezoelectric effect
Capillary
vasodilatation
Migration of
leukocytes into
the extravascular
space
Alteration of cellular shape
Cytoskeleton configuration
& ion channel permeability
Generation of
streaming potential
That affect PDL &
alveolar bone cells.
Bending of alveolar
bone
Neuropeptide release from
PDL afferent nerve endings
Synthesis & release of
Growth factors, cytokines & PGs

46.  Very little fluid within the pdl is squeezed out
during first second of pressure application.
 If the pressure is maintained , the fluid is rapidly
expressed , the tooth is displaced within the pdl
space & the ligament is compressed against the
adjacent bone, causing pain.
 Pain is felt after 3 – 5 secs of heavy force
application.

47. Physiologic response to heavy
pressure against a tooth.
 < 1 sec
 1 – 2 sec
 3 – 5 sec
 PDL fluid incompressible ,
alveolar bone bends,
piezo electric signals
generated.
 PDL fluid expressed ,
tooth movement within
PDL space
 PDL fluid squeezed out,
tissues compressed
immediate pain if
pressure is heavy

48.  PDL is beautifully adapted to resist forces of
short duration.
 It quickly looses its adaptive capability as the
tissue fluids are squeezed out of its confined
area.
 Prolonged force ,even of low magnitude ,
produces a different physiologic response i.e.
remodeling of the adjacent bone.
 Orthodontic tooth movement is made
possible by the application of prolonged
forces.

49. ROLE OF PERIOONTAL LIGAMENT IN THE
ERUPTION & STABILIZATION OF TEETH
 Forces generated within the PDL itself can
produce tooth movement. The eruption
mechanism in the PDL is dependent upon the
metabolic events occurring within the PDL. e.g..
Formation of crosslinkages & maturational
shortening of the collagen fibers.
 It provides stabilization of teeth against
prolonged forces of light magnitude by
generating a force to maintain the equilibrium
situation of the teeth.

50.  Orthodontic forces below the stabilization level
are ineffective.
 Active stabilization can overcome 5 to 10gm/cm
sq of unbalanced soft tissue resting pressure.

51. Initial effects of orthodontic forces on Para
dental tissue:
 Orthodontic force results
in the pouring of cells
from the nervous and
immune systems, into the
stressed PDL.
 In addition the products
of the endocrine system
are also routinely
delivered into the PDL
through circulation.

52.  Thus, on the biochemical
level, mechanical forces
can result in the
simultaneous exposure of
PDL cells to signals from
the nervous, immune
and endocrine systems,
leading to intricate and
fascinating interactions
and cellular responses.

53. TISSUE RESPONSES IN PERIODONTIUM:
 Application of a continuous force on the crown of the
tooth leads to tooth movement within the alveolar i.e.
marked initially by narrowing of the PDL membrane,
particularly in the marginal area. After a certain period
osteoclasts differentiate along the alveolar bone wall
after 30 to 40 hours.
 Phases of tooth movement: primary & secondary
 Tooth movement generally occurs in the secondary
phase when the hyalinized tissue has disappeared after
undermining resorption.

54. HYALINIZATION
 Initial force application
Impedes vascular circulation
& cell differentiation
Cell degradation
& glass like appearance of the tissue
Compression of the
membrane
Hyalinized tissue
Disintegration of
the vessels walls
& degradation of
the bld. elements

55.  It represents a sterile necrotic area, generally
limited to 1 or 2 mm in diameter. The process
displays 3 main stages;
 Degeneration
 Elimination of the destroyed tissue
 Establishment of a new tooth attachment
 unavoidable

56.  Degeneration starts where the pressure is
highest and the narrowing of the membrane is
most pronounced. It may be limited to parts of
the membrane or extend from the root surface to
the alveolar bone.
 It is generally due to lack of blood supply.

57.  In hyalinized zones the cells cannot
differentiate into osteoclasts and no bone
resorption can take place from the PDL
membrane.
 Tooth movement stops until the adjacent
alveolar bone has been resorbed, the hyalinized
structures removed, and the area repopulated
by cells.
 A limited hyalinized area occurring during the
application of light forces may be expected to
persist from 2 to 4 weeks in a young patient.
When high density is present, the duration is
longer.

58.  The peripheral areas of the hyalinized
compressed tissues are eliminated by an
invasion of cells and blood vessels from the
adjacent undamaged PDL. The hyalinized
materials are ingested by the phagocytic activity
of macrophages and are completely removed.

59.  The adjacent alveolar bone is removed
by indirect resorption after a delay of
several days by cells that have
differentiated into osteoclasts on the
surface of adjacent marrow spaces.
 This process is known as undermining
resorption since the attack is from the
underside of the lamina dura rather than
perioontal ligament proper.

60.  When the orthodontic force applied to human
teeth are kept within the optimal range used in
orthodontic practice, the osteocytes of the
alveolar bone adjacent to the hyalinized PDL
reveal no signs of degeneration or cell death
with necrosis of the bone.
 Osteoclasts are formed directly along the bone
surface in areas corresponding to compressed
periodontal ligament. This is called as direct
frontal resorption.

61. SECONDARY PERIOD OF TOOTH MOVEMENT:
 the PDL is considerably widened. The osteoclasts attack
the bone surface over a much wider area. As long as
the force is kept within certain limits or gentle
reactivation of the force is undertaken, further bone
resorption is predominantly direct.
 The main feature is the deposition of new bone on the
alveolar surface from which the tooth is moving away;
however, degenerative changes, with reduction in
number of cells may be observed.
 Cell proliferation is usually seen after 30 to 40 hours in
young human beings. Shortly after cell proliferation has
started, osteoid tissue is deposited on the tension side.

62.  The original PDL fibers become embedded in
the new layers of osteoid, which mineralizes in
the deeper parts. New bone is deposited until
the width of the membrane has returned to
normal limit and simultaneously the fibrous
system is remodeled.

63. PHASES OF TOOTH MOVEMENT
 INITIAL PHASE: follows immediately after the
application of a force on a tooth.
 Sudden displacement of the tooth within the
socket.
 It is due to bending of bone.
 LAG PHASE: Characterized by very little tooth
movement.
 It is longer if heavy forces are applied due to
rearward resorption & shorter when light forces
are applied since very little area of hyalinization
is seen & resorption is Frontal.
 POST LAG PHASE: REMOVAL OF
HYALINIZED TISSUE.

64. PERIODONTAL LIGAMENT & BONE RESPONSE TO
SUSTAINED ORTHODONTIC FORCE
 ORTHODONTIC FORCE
Heavy force Lighter force
Pain,
necrosis of
cellular elements
Undermining
resorption
Remodeling of the
tooth by frontal resorption
Objective of orthodontic
tooth movement

65. Linear Rate of Resorption:
 The limiting factor in the rate of tooth
movement is bone resorption. The
access of osteoclasts to the bone that is
in the path of tooth movement is limited
by the compression and necrosis of the
PDL. Undermining resorption is
necessary if the vascularity of the PDL is
compromised in the area of maximal
compression.

66.  The linear rate of resorption for humans is probably ~20
µm/day.
 theoretical limit for the rate of progressive tooth
movement through cortical bone of ~0.6 mm/month.
 In mandibular molars it is ~0.34 mm/month. This lack of
tooth movement efficiency probably reflects the
necessity to resorb more cortical bone in the mandible
and the tendency for a compressed PDL to limit vascular
access of osteoclasts to the PDL/bone interface. The
problem is accentuated when an excessive activation
during active treatment results in an area of PDL
necrosis, which requires undermining resorption to
remove bone in the path of tooth movement.

67.  Maxillary molars move twice as fast as
compared to mandibular molars in the
same patient. This is probably because
of the increased surface area of resisting
bone in the maxilla, which is primarily of
trabecular nature.

68.  An adequate PDL blood supply is
essential for tooth movement since.
 Nutritional demands of the adapting
tissues are relatively high.
 Osteoblasts are derived from
perivascular pericytes
 Preosteoclasts circulate in the blood and
pass through the blood vessel wall to
enter the tissue and form osteoclasts.

69.  The complexity of histological response
to tooth movement suggests that, 2
avenues are involved in enhancing
modeling.
 Vascularly mediated recruitment of
preosteoclasts.
 Mechanical activation of existing
osteoclasts in and around PDL.

70. Genetic Control Mechanism:

Atleast 26 genes are involved including the tyrosine
kinase (Src) gene.
Core binding factor A (cbfa) ,transforming growth factor
(TGF) :These promote osteoblast precursor proliferation,
markers of bone formation.
There is evidence that M-CSF, C-Fos,, and
RANK-Kappa B are required for osteoclast
differentiation, whereas C-Src and MitF (Microphthalmia
transcription factor) are required for osteoclast activity
after the cells have formed.
Osteoclast differentiation and activation is controlled by
a group of gene related to TNF (tumour necrosing factor)
and its receptor (TNFR).

71. Endocrine Control:
 GH, increases anabolic bone
modeling both by direct interaction with
GH receptor on osteoblasts and via
locally produced IGF-1 (Autocrine /
Paracrine function).
 Bone morphogenetic proteins (BMPs)
encourage mesenchymal progenitors
to differentiate into osteoblasts &
chonrocytes.

72. Biologic control of tooth movement
 Theories of tooth movement
 BONE BENDING/PIEZOELECTRIC/BIOELECTRIC THEORY:
 Piezoelectricity is a phenomenon observed in many crystalline
structures. The deformation of the crystal structure produces a flow
of electric current as electrons are displaced from one part of the
crystal lattice to another.
 These electric signals are produced when alveolar bone flexes and
bends.
 Piezoelectric signals have 2 important characteristics:
 A quick decay rate : when a force is applied a piezoelectric signal
is created which quickly dies away even though the force is
maintained.

73.  The production of an equivalent signal, opposite
in direction ,when the force is released.
 Both these characters are explained by the
migration of electrons from one location to
another within the crystal lattice under the
application of pressure leading to production of
electric charge.
 As long as the force is maintained the crystal
structure is stable & no further electrical events
are observed.
 When the force is released ,the crystal returns
to its original shape and a reverse flow of
electrons happens.

74.  Apart from bone other structures which
have piezoelectric properties are:
 Collagen
 Hydroxyapatite
 Collage hydroxyapatite interface
 The mucopolysaccharide fraction of the
ground substance.

75.  Application of force
results in the bending
of of adjacent bone.
 Areas of concavity
are associated with
negative charge &
cause bone
deposition.
 Areas of convexity
are associated with
positive charge &
cause bone
resorption.

76.  Ions in the fluids that bathe living bone interact
with the complex electric field generated when
the bone bends, causing temp. changes as well
as electric currents.
 Both convection & conduction currents can be
detected in the extracellular fluids.
 The small voltages that can be observed are
called the “streaming potentials.”

77.  A 2nd
type of endogenous electric signal called the
“bioelectric potential” can be observed in bone that is
not being stressed.
 The role of this bioelectric potential is not known but
experiments have indicated that one can modify cellular
activity by adding exogenous electric signals.
 Electromagnetic fields can also affect cell membrane
potentials & permeability & thereby trigger changes in
the cellular activity. These can also modify bone
remodeling on which the tooth movement depends.

78. PRESSURE TENSION THEORY
 Proposed by Schwartz in 1932
 Simplest & most widely accepted.
 Relies on chemical stimulation for cellular
differentiation.
 Chemical messengers are important for bone
remodeling & tooth movement.
 Pressure Alteration in blood flow within
the PDL
Movement of the tooth
within the PDL space

79.  Blood flow is decreased
where the PDL is
compressed & is usually
compressed or
maintained where the
PDL is under tension.
 Alteration in the blood
flow causes changes in
the chemical
environment.
 .e.g. oxygen level
decreases in
compressed areas &
increases in the areas of
tension.
 These changes stimulate
the release of biologically
active agents that would
stimulate cellular
differentiation.

80.  Alteration in blood flow
Release of chemical messengers
Activation of cells
Due to
pressure
within the
PDL
Due to
pressure
within the
PDL

81. BLOOD FLOW THEORY /FLUID DYNAMIC
THEORY
 Given by BIEN in 1966.
 Tooth movement occurs as a result of alterations
in fluid dynamics in the periodontal ligament.
 When a force of short duration is applied on to a
tooth , the fluid in the periodontal ligament space
escapes through tiny vascular channels.
 When the force is removed, the fluid is
replenished by diffusion from capillary walls &
recirculation of the interstitial fluid.

82.  Force of greater magnitude & duration causes
the interstitial fluid in the PDL space to get
squeezed out & move towards the apex &
cervical margins.
 This causes slowing of tooth movement & is
called the “ squeeze film effect”
Compression of
PDL on pressure
side
Compression
of the bld
vessels
Formation of aneurysm
Escape of bld gases
into the interstitial
fluid
Creating favourable
environment for
resorption
Force

83. Clinical application of the knowledge of
histological aspects of orthodontic
tooth movement.
 Prostaglandins(1-3ug)
 Vit D:
 Increase tooth movement
when administered
systemically or injected.
 Disadv: associated with
root resorption when the
dosage increases.
 But oral administration of
calcium combats the
tendency of root
resorption.
Enhances tooth movement. The
Number of osteoblasts on the tension
side are greater than PG aministration

84.  Steroid therapy
 PTH
 L –arginine ( nitric oxide
precursor)
 osteocalcin
 Suppresses OTM
 Increases clastic
activity.but it can be upto
48 hrs before 1st
osteoclasts appear.
 Increases bone
remodeling & orthodontic
tooth movement.
 Increases OTM since it
enhances
osteoclastogenesis on
the pressure side.

85. BIBLIOGRAPHY
 Contemporary orthodontics 4th
edition :
proffit
 Advances in the biology of tooth
movement : A review : jios 2006
 Graber Venersdall

86. To be
continued…