Optimal Orthodontic force & Phases of Tooth

Movement
 Optimal Orthodontic Force

Burstone (1962) defined optimal force as the one capable of generating maximal
cellular response from the tooth supporting tissues, including apposition and
resorption of alveolar bone, while maintaining the vitality of these tissues.
 Optimal Orthodontic Force
Schwarz (1932)

The classical definition of optimal force by Schwarz (1932) was

“the force leading to a change in tissue pressure that approximated the
capillary vessels’ blood pressure, thus preventing their occlusion in the
compressed periodontal ligament.”
Forces should not exceed the capillary bed blood pressure
(20-26g/cm2 of root surface).
 Optimal Orthodontic Force
(Daskalogiannakis, 2000)

“The mechanical input that leads to maximum rate of tooth movement with minimal
irreversible
The damage
current concept to the
of optimal root,
force viewsperiodontal
it: ligament and alveolar bone” is
asconsidered to be optimal
an extrinsic mechanical (Daskalogiannakis,
stimulus that evokes a cellular2000).
response, which aims to restore equilibrium by
remodeling of paradental supporting tissues.
 Optimal Orthodontic Force
(Viecilli, 2009 and 2013)

In summary, tooth movement is:

“The resulting event of a sufficiently large change in the bone shape, which is
made viable by mechanical equilibrium, leading to a specific mechanical
distribution of stresses and strains that propitiates an organized
cellular response matching stress patterns.”
(Viecilli, 2009 and 2013).
 Optimal Orthodontic Force

Clinically
• Produces rapid tooth movement
• Causes minimal patient discomfort
• Lag phase of tooth movement is shorter
• Teeth not loosened in the socket
• Reduce Root resorption
• Less demanding on anchorage
 Optimal Orthodontic Force

Small force-area interactions are the stimuli that are “sensed” by cells directly
or indirectly—i.e., the cell can react to stress or strain by initiating a signaling
cascade that affects itself, or other cells.
The cell can also die, being mechanically crushed, or by inhibition of blood
or interstitial fluid flow, directly affecting the metabolism of this cell and
others.
Phases of orthodontic tooth movement
 Phases of orthodontic tooth movement

In 1962, Burstone suggested that, if the

rates of tooth movement were plotted
against time, there would be 3 phases of
tooth movement.
An initial phase,
A lag phase &
A post lag phase

The Initial phase:

Is characterized by rapid TM immediately after the application of force, attributed to
the displacement of the tooth in the PDL space.
 Phases of orthodontic tooth movement

The lag phase:

• Low rates of tooth displacement or no displacement
• This is produced by hyainization of the PDL in compressions areas.
• No further tooth movement occurs until cells complete the removal of all
necrotic tissues.
 Phases of orthodontic tooth movement

The post lag phase:

• The rate of tooth movement gradually or suddenly increases.
 Phases of orthodontic tooth movement

The 1st phase lasts 24 hours to 2 days and represents the initial tooth movement
inside its bony socket.
Phases of orthodontic tooth movement
Phases of orthodontic tooth movement
The relationship between Orthodontic force magnitude & the
rate of tooth movement
The relationship between Orthodontic force magnitude & the rate of tooth
movement during active treatment.

Quinn and
(B)
Yoshikawa
described 4
alternative models
(A)
for this relationship:

* The 1st model (A):

Supposes an on/off switch that is switched on at a certain force level. All forces above
this threshold will lead to the same rate of tooth movement.
* The 2nd model (B):
A force threshold is also indicated. With forces above the threshold, a linear response
relationship is assumed.
 The relationship between Orthodontic force magnitude & the rate of tooth
movement during active treatment.

Quinn and yoshikawa

concluded that the last model (D)
was the best supported by (C) (D)
experimental and clinical data.

* The 3rd model (C):

Forces above a certain threshold are necessary to induce movement. A linear response relationship exists in
a lower force range up to a certain level. Then a plateau is reached, and a further increase of force leads to
a decrease in the rate of TM, until it ceases completely.
* The 4th model (D):
Generally resembles the 3rd, but it lacks the decreasing part.
Theories of orthodontic tooth movement
Bone cell Response to Orthodontic Force

Bone cells respond to Orthodontic Force (OF) by proliferation and increased activity;
however, the mechanisms for conversion of OF into biologic activity are not completely
understood.
The primary stimulus, or first messenger, may alter cell activity through
the plasma membrane.
 Bone cell Response to Orthodontic Force

The intramembranous components that have been shown to mediate effects of the
extracellular stimuli are calcium ions and cell membrane-bound enzymes.
The plasma membrane-associated enzymes, along with Ca++, act to elevate cyclic
nucleotide molecules (CAMP), cyclic guanosine monophosphate (cGMP).
 Bone cell Response to Orthodontic Force

Cyclic nucleotides have been characterized as second messengers; that is, these
molecules convert the membrane effect into a cellular response.
There is evidence that this process is involved in bone cell regulation in response to
orthodontic treatment.
 Mechanisms of Orthodontic Tooth Movement

Orthodontic Force

Forces
transmitted to Forces Forces Forces
periodontal transmitted transmitted to transmitted to
ligament to alveolar nerve endings extracellular
bone matrix
a. Pressure d. Release of
Tension Theory neurotransmitters
c. Formation of micro cracks and
b. Bone Bending fluid flow shear stress theory
& piezoelectric e. Cytoskeleton-
signals theory extracellular matrix
interaction
a. Pressure-Tension Theory:
Sandstedt (1904), Oppenheim (1911) and Schwarz (1932)
a. Pressure-Tension Theory:
Sandstedt (1904), Oppenheim (1911) and Schwarz (1932)
 a. Pressure-Tension Theory:
Sandstedt (1904), Oppenheim (1911) and Schwarz (1932)

The tissue injury generated by OF elicits a classic inflammatory response.

Inflammatory processes are triggered along with the vascular cellular
infiltration of Lymphocytes, monocytes , and macrophages which invade
the inflamed tissue and, contribute to
prostaglandin release and hydrolytic enzyme secretion.

Prostaglandins and collagenase levels

increase at the site of inflamed gingiva and Prostaglandins are generated
periodontal ligaments. from membrane phospholipids
in response to certain localized
irritants or physical stimulators.
 a. Pressure-Tension Theory:
Sandstedt (1904), Oppenheim (1911) and Schwarz (1932)

Local inflammatory responses

stimulate osteoclastic activity.

ges in cAMP levels which are produced by mechanical forces are secondary to an
mmatory process initiated by orthodontic treatment.
ncrease in osteoclast activity is believed to be generated by local elevation of
aglandins and the subsequent increase in cellular cAMP.
 a. Pressure-Tension Theory:
Sandstedt (1904), Oppenheim (1911) and Schwarz (1932)

A second effect of changing cAMP levels is increased

collagenase activity.
Collagenase activity is present in tissues subjected to
orthodontic tooth movement and plays a role in
orthodontically generated bone resorption.

The inflammatory response is characterized by hydrolytic enzyme secretion.

It is probable that increased collagenase activity contributes to increased bone
remodeling.
b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)
Bone Bending
 b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)

The PDL is a continuous hydrostatic system which according to Pascal’s law, any applied
force to this system will be equally distributed to all regions of the PDL.
These forces bend bone, tooth, and the structures of the PDL.
Bone was found to be more elastic than other tissues and to bend far more readily in
response to force application.
b. Bone bending & Peizoelectric signals Theory:
Bassett and Becker (1962), Zengo et al (1973)

resorption
deposition

resorption
deposition
Mechanical stress initiated by
OF or alveolar bone deflection
induces an electrical charge
polarization referred to as a
piezoelectric response.

Bassett and Becker (1962) stated that in response to applied

mechanical forces, there was generation of electric potentials in
the stressed tissues.
 b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)

Baumrind claimed, that strains are induced in bone by deflective forces within
the elastic limit, and bone can reorganizes to accommodate the applied stress.
 b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)

bone resorption

bone formation

According to Wolff’s law which states that:

“Strains are induced in bone by deflective forces within the elastic limit.
“Any mechanical compression stimulates bone formation and
Tension stimulates resorption”.
 b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)

Tension = resorption Tension Compression

Compression = Deposition

“Any mechanical compression stimulates bone formation and

tension stimulates resorption”.
• This theory seems to contradict the orthopedic principle”.
• Epker and Frost (1965) and Zengo et al (1973) clarified that in areas of PDL tension, the
opposing alveolar bone assumed a concave configuration, compressing the bone tissues
which favored bone deposition and vice versa.
 Bone Bending

Osteoblast
During bone bending, areas of concavity assume a activity
Osteoclast
activity
negative charge and areas of convexity assume an Osteoblast
electrical positive charge. activity
It has also been shown that electrically positive areas Osteoclast
promote osteoclastic activity and zones of activity

electronegativity support osteoblastic activity.

The charged matrix may activate membrane
polarization, in turn affecting cAMP.
 Bone Bending

Davidovich & Associates suggest

that the piezoelectric response
propagated by bone bending
incident to OF application may be
functioning as a cellular first
messenger.

Epker and Frost & Zengo and associates documented that changes in the curvature of
bone surfaces, caused by loading, correlate with specific cellular responses.
 Bone
BoneBending
Bending

There is evidence that electrical stimulation elicits prostaglandin synthesis.

Both prostaglandin synthesis and membrane electrical polarization by the piezoelectric
process act on the cell surface cyclic nucleotide pathway,
generating changes in the levels of cAMP.

Changes in cAMP levels have been correlated

with alteration in cell proliferation,
differentiation and activation.
 b. Bone Bending & Peizoelectric signals Theory:
Baumrind (1969)

According to Wolff’s law, the following could be explained:

c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)
 c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)
Osteocytes are
entrapped
osteoblasts within
Numerous and
bone
extensive cell processes
that ramify throughout Osteocyte
Canaliculi
the bone in canlliculi Osteocytes occupy
and make contact via spaces (Lacunae) in
gap junctions with bone and are defined
processes extending as cells surrounded
Lacuna
from other osteocytes by bone matrix
or from osteoblasts or
bone lining cells at the
surface of the bone Decreased quantity of
synthetic and secretory
organelles

Immediately after OF application creating strain in the alveolar bone that may
induce differential osteocyte response.
Osteocytes are mechano-sensory cells capable of detecting mechanical stimuli &
They are regulators of osteoblast & osteoclast function during bone remodeling.
c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)

Numerous and
extensive cell processes
that ramify throughout
osteocyte
the bone in canlliculi canaliculi
and make contact via
gap junctions with
processes extending
lacuna
from other osteocytes
or from osteoblasts or
bone lining cells at the
surface of the bone

The Micro-cracks theory suggests that OF may cause damage to the alveolar bone in the
form of Microcracks causing cellular damage to osteocyte processes
apoptosis & bone resorption.
c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)

Tooth movement occurs due to changes in the fluid dynamics in the PDL.
The periodontal space contains the fluid system, composed of interstitial fluid, cellular
elements and periodontal fibers etc.
Such contents create a unique hydrodynamic condition resembling a hydraulic
mechanism and a shock absorber.
When the force is removed, the fluid is refilled by diffusion from capillary walls and
recirculation of the interstitial fluid.
c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)

Squeeze film Effect

During Orthodontic Tooth Movement

Forces of greater magnitude and direction

The interstitial fluid in the periodontal space is

squeezed out

Moving toward the apex

and cervical margins

Tooth movement
 d. Formation of Micro-cracks and Fluid Flow Shear Stress:

The theory suggests that when OF is converted to strain in bone, the fluid flow is changed.
• On the pressure side, the fluid flow is driven from the high to the low pressure region, leading
to the production of cytokines, apoptosis of osteocytes thus stimulating osteoclastogenesis.
• On the tension side, the increase of pulling force on the bone drives the fluid flow shear
stress on the osteocytes inducing osteocyte activation, osteoblast recruitment & bone
formation.
c. Formation of Micro-cracks and Fluid Flow Shear Stress (Bien)

When the orthodontic force is applied, there is compression of the PDL.

Blood vessels of the PDL get trapped between the principal fibers which results in stenosis.
The vessels above the stenosis then balloons to form an “aneurysm” (bulging of blood vessel)
The formation of these aneurysms and vascular stenosis causes blood gases to escape into the
interstitial fluid.
This creates a favorable local environment for resorption.
d. Release of Neurotransmitters:
d. Release of Neurotransmitters:
 d. Release of Neurotransmitters

Orthodontic force alters the neutral state of

the PDL nerve fibers release of
neuropeptide local neurogenic
inflammation

CGRP (Calcitonin gene related peptide)

• Silent in physiological conditions but contain various neuropeptides as substance P &

(CGRP).
• Syntheized in the perikaryon then stored in peripheral & central nerve terminals.
 d. Release of Neurotransmitters

Orthodontic force alters the neutral

state of the PDL nerve fibers
release of neuropeptides
local neurogenic inflammation

CGRP (Calcitonin gene related peptide)

Since most PDL neurons are wrapped around blood vessels, endothelial cells
are the first to interact with neuropeptide, which in turn bind circulating
leukocytes, facilitating their migration out of the capillaries.
 d. Release of Neurotransmitters

In addition to this peripheral

action, the affected neurons
release neurotransmitters
centrally, causing pain shortly
after appliance activations.

Neuropeptides cause vasodilation and increased vascular permeability, contributing to

increased local blood flow that accompanies inflammation.
Signaling molecules released by these migrating leukocytes interact with various paradental
cells stimulating them to initiate & sustain tissue remodeling.
 e. Cytoskeleton-Extracellular Matrix
Proteoglycan Proteoglycan
molecules complex Collagen fibres

Microfilaments

Intermediate
filament Microtubule
Cytoskeleton
fibronectin integrin Microfilaments Plasma
of cytoskeleton membrane
e. Cytoskeleton-Extracellular Matrix

Cytoskeleton

Integrin

Extracellular Matrix

Cell surface proteins

Fibronectin
Or vitronectin
collagen
 o-Actin
Actin

The cytoskeleton is linked

through the membrane Vinculin

Glycoprotein Integrins to Talin

the extracellular matrix.

Integrins are a family of glycoproteins, which span the cell

membrane from the cytoplasm to the extracellular matrix.
Integrins do not bind directly to microfilament structures,
such as actin, but is dependent on associated proteins for
this function.
Integrin binds to fibronectin in the extracellular matrix
and to talin on the cytoplasmic surface. Actin and vinculin
then bind to this talin-integrin complex.
 Integrins Collagen, fibronectin
Focal adhesions vitronectin

Focal adhesions
Talin

Vinculin

Mechanically induced changes in cell Actin filaments

shape produce a range of effects,

mediated by adhesion molecules
(Integrins) and the cytoskeleton. In this
fashion, mechanical forces can reach
the cell nucleus directly.
BIOLOGIC PATHWAYS OF ORTHODONTIC TOOTH MOVEMENT
 BiOLOGIC PATHWAYS OF ORTHODONTIC TOOTH MOVEMENT

Pathway I represents a biologic response to

orthodontic force.
Pathway II represents the production of a
tissue
inflammatory response generated
by the OF.
 Pathway I
Bone Bending

Osteoblast Osteoclast
activity activity
During bone bending, areas of concavity assume a
negative charge and areas of convexity assume an Osteoblast
activity
electrical positive charge. Osteoclast
It has also been shown that electrically positive areas activity
promote osteoclastic activity and zones of
electronegativity support osteoblastic activity.
The charged matrix may activate membrane
polarization, in turn affecting cAMP.
 Pathway I
Bone Bending Bone Bending

There is evidence that electrical stimulation elicits

prostaglandin synthesis.
Both prostaglandin synthesis and membrane electrical
polarization by the piezoelectric process act on the cell
surface cyclic nucleotide pathway,
generating changes in the levels of cAMP.

Changes in cAMP levels have been correlated

with alteration in cell proliferation,
differentiation and activation.
 Pathway II
Tissue Injury

The tissue injury generated by OF elicits a classic inflammatory response (II, C).
Inflammatory processes are triggered along with vascular and cellular infiltration (II, E)
Lymphocytes, monocytes , and macrophages invade the inflamed tissue and, contribute
to prostaglandin release and hydrolytic enzyme secretion (II, H).
 Pathway II
Tissue Injury
Local inflammatory responses stimulate
Prostaglandins are generated osteoclast activity.
from membrane phospholipids
in response to certain localized
irritants or physical stimulators.

Prostaglandins and collagenase

levels increase at the site of inflamed
gingiva and periodontal ligaments.

A correlation has been noted between increased levels of prostaglandins and cAMP.
This increase in osteoclast activity is believed to be generated by local elevation of
prostaglandin (II, F) and the subsequent increase in cellular cAMP (II,G).
A second effect of changing cAMP levels is increased collagenase activity.