BIOLOGY OF ORTHODONTIC TOOTH

MOVEMENT

PRESENTED BY :Dr.MANJUNATH
GUIDED BY: Dr.CHANDRIKA
SAROVAR
 CONTENTS
• INTRODUCTION

• HISTORY

• STRUCTURE OF PDL

• BONE MODELING AND REMODELING

• ORTHODONTIC TOOTH MOVEMENT

• PHASES OF TOOTH MOVEMENT

• BIOLOGICAL CONTROL MECHANISMS

• THEORIES OF TOOTH MOVEMENT

• ORTHODONTIC FORCES

• MAGNITUDE AND DURATION OF FORCES

• TYPES OF TOOTH MOVEMENTS & TISSUE REACTIONS

• DRUGS AND HORMONES EFFECTING ON TOOTH
MOVEMENT

• METHODS TO ACCELERATE OR DECELRATE TOOTH

MOVEMENT

• RELASE OF TOOTH MOVEMENT

• CONCLUSION

• REFRENCES
 INTRODUCTION
• Orthodontic treatment is made possible by the fact
that teeth can be moved through alveolar bone by
applying appropriate force

• Bone remodelling occurs around the tooth as the force

is applied resulting in tooth movement

• As a rule of thumb, bone subjected to the area of

pressure as a result of PDL compression ,resorb while
bone form as a result of stretching of PDL
• These tissues when exposed to varying degrees of
force in terms of their magnitude direction and
duration, express extensive microscopic and
macroscopic changes

• The force induced strain induce the pdl vascularity

and blood flow resulting in local synthesis and release
of key molecules such as neurotransmitters cytokines
growth factors etc

• These cellular response provide a favorable

microenvironment for deposition and resorption of
bone.
 HISTORY
• First histological examination of tissues surrounding
orthodontically treated teeth were reported by
Sandstedt(1904-1905)

• He subjected teeth in a dog for increasing period of time

and observed stretching of periodontal ligament in
tension sites and narrowing of tissues in pressure sites

• New alveolar bone formation was seen in the tension

side and necrosis and bone resorption were seen in the
pressure side
• Multiple osteoclasts in howships lacunae were seen at
the pdl alveolar bone interface

• According to Sandstedt these osteoclasts where

responsible for the force induced tooth movement

• Oppenheim reported that tooth movement in one

preadolescent baboon resulted in complete remodeling
of the alveolar process indicating that orthodontic force
effects spread beyond limits of the pdl
• Schwarz in 1932 from his study conclude that
occlusion of blood vessels during force
application would lead to necrosis of surrounding
tissue which would be harmful and would reduce
the velocity of tooth movement

• Reitan in1971 supported this and he favoured the

use of light intermittent force because they cause
minimum tissue damage and cell death
 Periodontal Ligament
• The Periodontal Ligament (PDL), approximately
0.25mm wide, is the soft, richly vascular and cellular
connective tissue that surrounds the roots of the
teeth and joins the root cementum with the lamina
dura or alveolar bone proper.

The presence of a PDL makes it possible to distribute

and resorb the forces elicited into the alveolar process
through the alveolar bone proper.

The true periodontal fibres, the Principal Fibres,

develop in conjunction with the eruption of the tooth.
• When the tooth has reached contact in occlusion and
is functioning properly, the principal fibres associate
into the following well-oriented groups:

Alveolar Crest Fibres(ACF),Horizontal Fibres(HF),

Oblique Fibres(OF) and Apical Fibres(APF).

The fibrils of PDL are embedded in a ground

substance which contains connective tissue
polysaccharides (Glycosylaminoglycans), and water.
 Groups of periodontal fibers

• Alveolar crest group

– From cementum just below CEJ –
run downward and outward –
insert into rim of alveolus

• Horizontal group
– Apical to the alveolar crest group
– run at right angles to the long
axis of the tooth till the bone just
below the alveolar crest

• Oblique group
– Most numerous group of fibers –
run from cementum in an
oblique direction to insert into
bone coronally
• Apical group

– Radiate from the cementum

around apex of root to bone –
forming the base of the socket

• Interradicular group

– Found only between roots of

multirooted teeth – run from
cementum into bone, forming
the crest of the interradicular
septum
Transseptal group of fibers

– Run interdentally from

cementum just apical to the
base of the junctional
epithelium of one tooth over
the alveolar crest and insert
into a comparable region of
the cementum of the adjacent
tooth

– Collectively, they form an

interdental ligament
connecting all the teeth
• CELL TYPES :

– Synthetic cells
• Fibroblasts
• Osteoblasts
• Cementoblasts

– Resorptive cells
• Fibroblasts
• Osteoclasts
• Cementoclasts
 Fibroblasts

–Principle cells of the PDL

–Characterized by an ability to achieve

an exceptionally high rate of turnover
of the extracellular compartment, in
particular collagen

–Large cells with an extensive

cytoplasm containing in abundance all
the organelles associated with
synthesis and secretion ( eg. Rough
ER, several golgi complexes, many
secretory vesicles )
– They also have a well developed
cytoskeleton with a particularly
prominent actin network ( indicates
functional demands placed on them,
requiring change in shape and
migration

– Lined along the general direction of

the fiber bundles and with extensive
process that wrap around the fiber
bundles

– In PDL, the remodeling of collagen is

achieved by a single cell - the
fibroblast, which is capable of
simultaneously synthesizing and
degrading collagen.
• One probable main reason of alveolar bone remodeling
and tooth movement takes place because of the
unique property of the PDL

• A healthy PDL always tries to maintain a width and

orientation of fibers that would best enable the tooth
to maintain an equilibrium state

• The fibroblast cells of the PDL tightly cling along the

principle fibers

• These fibroblasts are very sensitive to the mild

variations in vascular flow or fiber orientation
• Bone and cementum cells

– Even though situated within the periodontal ligament, bone and

cementum cells are associated with the hard tissues they form

– Osteoblasts/osteoclasts
• Line the bone surface of the ligament
• May be either functional or resting, depending on the functional
state of the ligament
• This variation in the distribution of bone cells along the socket wall
reflects the constant rate of flux of the alveolus
 OSTEOBLAST

• Derived from Pleuripotent

mesenchymal stem cells.
• Uninucleated
• Synthesize osteoid.
• Increase level of alkaline
phosphatase.
• Express PTH receptor &
release RANKL ,OPG &
other cytokines.
 OSTEOCLAST

• Bone resorbing,
multinucleated.
• Occupy shallow hollowed
out depressions called
Howship’s lacunae.
• CSF-1 (M-CSF) & RANKL are
critical cytokines for its
differentiation.
 BONE MODLING AND REMODLING
During OTM

Relase of inflammatory cytokines (pGs,interlukins

1b,)

T cells produce RANKL

RANKL converts preosteoclast into osteoclast

Bone reabsorption take places

• Growth factors produced and they stimulate
preosteoclasts to produce osteoprogerin

Osteoprogerin deactivates osteoclasts

Mononuclear cells coat irregular resorbing surface

with cementing substance

Perivascular cells migrate and differentiate to

preosteoblasts

Osteoblasts form new bone

 PHASES OF TOOTH MOVEMENT
• Three stages –according to Burstone
1. Initial phase
2. Lag phase
3. Post lag phase
 INITIAL PHASE
• When an orthodontic therapy begun,rapid
tooth movement occur for a short period of
time, which then stops
• By displacement of tooth in pdl space & also
by bending of alveolar bone
• 0.4-0.9 mm occur in a week time
 LAG PHASE

• Immediately after the initial phase, there is a lag period, with

relatively low rates of tooth displacement or no displacement

• It has been suggested that the lag is of the PDL in areas of

compression

• No further tooth movement occurs until cells complete the

removal of all necrotic tissues.
• Duration depends upon the amount of force applied 2-
3 weeks
 POST LAG PHASE
• The third phase of tooth movement follows the
lag period, during which th rate of movement
gradually or suddenly increases.

• Frontal resorption in the PDL, and initial

remodeling events in the cortical bone ahead of
the advancing tooth allow for progressive tooth
movement at a relatively rapid rate
LIGHT FORCES
VS
HEAVY FORCES
 TOOTH MOVEMENT

• UNDER LIGHT FORCES UNDER HEAVY FORCES

• DIRECT RESORPTION
INDIRECT RESORPTION
 Application of light sustained force
• PRESSURE SIDE
Compression of blood vessels

Blood flow altered

Oxygen tension ↓
PGs & Cytokines released (primary messengers)

Metabolic changes occur

OSTEOCLASTS

FRONTAL RESORPTION
 APPLICATION OF LIGHT SUSTAINED FORCE

• TENSION SIDE
Dilatation of blood vessels

Blood flow altered

Oxygen tension

Metabolic changes occur

Stimulation of undifferentiated mesenchymal cells

OSTEOBLAST

Deposition of organic matrix i.e. OSTEOID TISSUE

Osteoid tissue is more resistant to resorption

 Application of heavy sustained force
• PRESSURE SIDE
PDL tissue fluid squeezed out

PDL tissue compressed

Blood vessels occluded

Cell death (Sterile Necrosis)

Cell differentiation in adjacent marrow spaces

UNDERMINING RESORPTION
APPLICATION OF HEAVY SUSTAINED FORCE

• Tension side
Stretching of PDL
Dilatation of blood vessels
Blood flow altered
Oxygen tension ↑
Metabolic changes
Stimulation of undifferentiated mesenchymal cells

OSTEOBLASTS
Deposition of organic matrix i.e. OSTEOID TISSUE
 forces
TISSUE RESPONSE

STRONG/ HEAVY FORCE PDL on pressure side ischemia &

(Forces far exceeding capillary blood degeneration of PDL = hyalinization = more
pressure) delay in tooth movement
MODERATE FORCE PDL strangulation resulting in delay in bone
(Force exceeding capillary blood resorption
pressure)
LIGHT FORCE PDL ischemia with simultaneous bone
(Force less than capillary blood resorption and formation = more continuous
pressure ) tooth movement
 Optimal Orthodontic Force

• Schwarz ( 1932 ) forces being "not greater than the

pressure in the blood capillaries" (15 -20 mmHg, or about
20-26 g/cm2 of root surface)

Storey ( 1973 ) : Classified forces as

• Bioelastic : light forces that mainly distorts tissues

depending upon degree of elasticity

• Bioplastic : greater forces resulting in remodelling without

tissue damage

• Biodisruptive : large enough to cause extensive damage to

teeth and surrounding tissues
OPTIMUM FORCES REQUIRED FOR DIFFERENT
TYPES OF ORTHODONTIC TOOTH MOVEMENT
 PDL following hyalinization
3 main stages:
• 1) Degeneration – changes in blood flow and cells
• 2) Elimination of destroyed tissue
• 3) Establishment of new tooth attachment

• Physiologically strained PDL has an inherent ability to

maintain its width by influencing surface adaptation of
adjacent alveolar bone

• The osseous response of the PDL to applied loads is the

physiologic basis of orthodontic practice
Types of forces
 CONTINOUS
• Force is maintained at some appreciable
fraction of the original from one patient visit
to next
 INTERRUPTED
• Force level decline to zero between activation
 INTERMITTENT
• Force level declines abruptly
to zero intermittently
• When the orthodontic
appliance is removed by the
patient or when the fixed
appliance is temporarily
de activated,and then return
to original level some time
later
 Areas of pressure

Impeding vascular circulation

and cell differentiation

Rupture and Changes in cells ( swelling

discoloration of of mitochondria and ER)
cytoplasmic
membrane

Occurrence of mild
inflammation
Hyalinization zone Cells unable to No bone resorption
differentiate into from Periodontal
osteoclasts membrane

Peripheral areas of hylanized Tooth movement halts until

tissue are removed by invasion adjacent bone has resorbed
of cells and blood vessels from and hyaline structure is
adjacent undamaged PDL removed and areas
repopulated by cells

Hyalinized material Adjacent bone removed

Reestablishment of
ingested by phagocytic by cells that have
tooth attachment –
activity of macrophages differentiated into
wider ligament space
and removed osteoclasts
Secondary period of
PDL widened Osteoclasts attack the
tooth movement
considerably bone surface over a
much wider area

Reorganization of fibrous Further bone resorption – Light force

attachment apparatus maintained
predominantly direct

Complete reorganization of
the fibrous system
throughout the membrane
Areas of tension

Stretching of PDL fibers

Cell proliferation
 THEORIES OF TOOTH MOVEMENT

• THE PRESSURE TENSION THEORY

• BONE BENDING THEORY
• BIOELECTRIC SIGNALS IN ORTHODONTIC
TOOTH MOVEMENT
• PIEZOELECTRICITY
 THE PRESSURE TENSION THEORY

• Most accepted theory of tooth movement

• Relies on chemical rather than electric signals as the

stimulus for cellular differentiation and tooth movement

• Sustained pressure causes tooth to shift position within

the pdl space

• Some areas of the ligament get streched, some

compressed
• Blood flow decreases in the compressed areas and
increases or is maintained in the areas under tension

• Blood flow alteration leads to quick changes in the

chemical environment ( eg. reduced Oxygen levels in
compressed region )

• These chemical changes act either directly or by

stimulating the release of other biologically active
agents that stimulate cellular differentiation and activity
 Pressure side ( osteoclast formation )
• ORTHODONTIC FORCE
Partial compression of blood vessels in PDL

• Mechanical distortion of PDL cells and fibers

• Alteration of blood flow and oxygen levels

• INFLAMMATION

• Cascade of chemical mediators

 Chemical Mediators
• Histamine
• Serotonin
• Plasma proteases
• neuropeptides
• Kinins
• Eicasonoids ( prostaglandins , interleukins )
• Nitrous oxide
• Cytokines
 What triggers osteoclasts
• Osetoclasts may get activated directly by the action of
chemical mediators like interleukins

• But latest research shows that the cells responsible for both
recruiting and restraining of osteoclasts are osteoblasts

• Osteoblasts contain receptors for PTH, PGE2, Vit D3 etc

• Once these attach to their respective receptors, osteoblasts

release secondary messengers called “RANKL” and “M-CSF”
• Osteoclasts have on their surfaces, receptors for
RANKL and M-CSF

• Recent research reveals that the main cytokine

responsible for activation of osteoclasts is RANKL
and also that the major source of RANKL are the
osteoblast cells

• Under the influence of RANKL, ostoclasts get

recruited and start to function
• Research also shows that not only are Osteoblasts
responsible for recruiting osteoclasts, they are also
responsible for restraining them

• This occurs when the osteoblasts get activated and in

turn release the secondary messenger “OPG”

• OPG has a strong affinity for and gets attached to the

RANKL molecules which in turn prevents the activation
of osteoclasts
 Bone bending theory
• Farrar ( 1888 ) : 1st to suggest that alveolar
bending plays a pivotal role in tooth movement

• Later confirmed by Baumrind ( 1969 ) in rats and

Grimm ( 1972 ) in humans

• Orthodontic forces produce bending of bone &

tooth as well as of solid structures of PDL.
• The active biological processes that follow
bone bending involve bone turnover and
renewal of cellular & inorganic fractions.

• Reorganization proceeds not only at the

lamina dura of alveolus but also on surface of
every trabeculum within the corpus of bone
 Bioelectric signals

• Bassett ( 1962 ) & Zengo et al ( 1974 ): proposed that

in response to mechanical forces, there is generation
of electric potentials within the stressed tissues.

• Enhanced cellular activity in PDL and alveolar bone.

• The bioelectric responses ( piezoelectric & streaming

potentials ) propogated by bone bending function as
pivotal cellular first messengers
• Bioelectric measurements in alveolar bone have
demonstrated that the tension (convex) side is
electronegative with respect to the compression
(concave) side, suggesting that negative potentials
during bone bending can generate bone
deposition, while positive potentials are
responsible for bone resorption
 PIEZOELECTRICITY

• Bone is a mineral having crystal structure &

piezoelectric properties

• Phenomenon observed in many crystalline

materials in which deformation of the crystal
structure produces a flow of electric current as
electrons are displaced from one part of the
crystal lattice to another
 Characteristics of piezoelectric signals
• A quick decay rate (a
piezoelectric signal created
due to a force applied dies
off quickly even if the force
is maintained).

• An equal & opposite signal

is produced when the force
is released.
• Ions in the fluid around the bone interact with this
complex electric field which is generated due to
bone bending

• This bending causes temperature changes and

electric signals

• These voltages have rapid onset and alterations

with the change in stresses on the bone
 Streaming Potential
• Borgens ( 1984 ) : induced electric current in bone
fracture sites for healing purposes – no piezoelectric
effect

Observed endogenous ionic currents –

Classified these currents as
stress generated potentials /streaming potentials
rather than piezoelectric currents

• They have long decay periods

• Davidovitch ( 1980 ) : suggested that potentials
result from distortion of fixed structures of
periodontium.
E.g : collagen, hydroxyapatite

• In hydrated tissues, however streaming potentials

predominate as the interstitial fluid moves
 To summarize,

PDL fluid & bone stimulated

Deformation of collagen/hydroxyapatite crystals

Electrical energy created

Ions in the fluid that bathe living bone interact with the complex
electric field generated
Temperature changes / Electric signals /Alterations of
Oxygen tension / cAMP / Ca++ / Hormones

Development of conduction & convection currents

 MESSENGERS OF TOOTH MOVEMENT
1. PROSTAGLANDINS
2. LUEKOTRIENS
3. CYTOKINES
4. NEUROTRANSMITTERS
 • Mechanical, chemical or physical stimuli
• Cell phospholipases
• AA

Prostaglandins and thromboxane A2 LEUKOTRIENES

 PROSTAGLANDINS (PGE2)

• Local hormones

• Mode of action : cause an increase in

intracellular cAMP & calcium accumulation by
monocytic cells which then modulates
osteoclastic activity
• Klein & Riasz (1970) : reported for the 1st time the involvement
of PGE2 in OTM

• Osteoclastic action : Several cytokines & hormones induce

PGE2 secretion in bone which in turn effects cytokine activity,
stimulating osteoclast activation (Schelling et al, 1980)

• Osteoblastic action : PGs stimulate osteoprogenitor cells to

proliferate and differentiate so that osteogenesis is increased.
(Chyun & Raisz, 1984)
 LEUKOTRIENS

• Metabolite of arachdonic acid > stimulates bone

resorption > tooth movement

• Originally demonstrated in leukocytes

• Also produced by mast cells, lung, heart, spleen etc.
• Contraction of smooth muscle
• Vasoconstriction
• Release of lysosomal enzymes
• Participate in inflammatory reactions
 CYTOKINES
• Proteins that act as signals between cells of the immune system.

• Davidovitch et al (1988): implicated the involvement of

cytokines in bone remodeling

• These include:
1. Interleukins
2. Tumor necrosis factors
3. Colony stimulating factors
4. Growth factors
 Interleukins (IL )
• Synthesized by many cells including osteoblasts,
chondrocytes, etc.

• Cytokines which demonstrated effects are IL-1, IL-

2, IL-3, IL-6, TNF-α and IFN-γ

• Locally, IL-1 attracts leukocytes, stimulates

fibroblastic proliferation & enhances bone
resorption
 Tumor Necrosis Factor [TNF]
• Pro inflammatory cytokine secreted by various cells
including osteoblasts

• Types: TNF-α & TNF-β

TNF- α : more resorptive

• Ability to create multinucleated cells, such as osteoclasts

• Bletsa et al (2006), Garlet et al(2007) : demonstrated that

TNF- α was expressed during OTM
ROLE OF NEUROTRANSMITTERS IN ORTHODONTIC
TOOTH MOVEMENT
 Second Messengers

• Sutherland & Rall ( 1958 ) : estabilished the 2nd

messsenger basis for hormone secretion
• They proposed that the 1st messenger binds to a specific
receptor on the cell membrane and produces an
intracellular 2nd messenger

• 2nd messengers : cAMP & cGMP

• This 2nd messenger then interacts with cellular enzymes

evoking a response
 CLINICAL SIGNIFICANCE OF INFLAMMATORY
MEDIATORS OF OTM
• All inflammatory mediators i.e, the primary and the
secondary mesengers activate specific genes in the
nucleus of strained paradental tissues

• Release of neuropeptides from the paradental afferent

nerve endings

• Diapedesis of leukocytes - signalling molecules -

cellular differentiation of precursor cells - osteoblasts
& osteoclasts - remodelling
 RANK, RANKL & OPG

• The receptor activator of nuclear factor kappa

B ligand (RANKL ) & its receptor ( RANK ) &
osteoprotegrin ( OPG ) were found to play
important roles in regulation of bone
metabolism

• RANKL : promoted osteoclastogenesis

• OPG : inhibited this effect
• Nakao et al (2007) : concluded that cells exposed to
compressive forces intermittently expressed higher levels of
RANKL than cells treated continuously

• Kim et al (2007) : demonstrated presence of RANKL in vivo

in compressed PDL by immunohistochemistry

• Kanzaki et al (2004) : attempted to inhibit RANKL

expression to prevent teeth from moving. Constructed mouse
OPG expression plasmid & injected into palatal Pdl of
maxillary 1st molar
 MECHANOTRANSDUCTION

• - is mechanism by which mechanical signals

are converted into biological signals.

• The process of mechanotransduction plays a

key role in tooth movement due to
orthodontic forces
 Extracellular matrix and cytoskeleton reorganization

– There are two types of cellular adhesions-

 Cell-to-cell adhesion
 Cell-to-extracellular matrix adhesion.

– Several families of adhesion receptors have been

identified, including integrins.

– Integrins are cell surface receptors that mediate cell-to-

cell attachment or cell attachment to ECM molecules
such as collagen, fibronectin, laminin etc.
 – The cytoskeleton presents a number of possibilities
for transducing mechanical forces acting on cells
and/or their adjacent matrices.

– The three main components of the cytoskeleton are

 Microtubules
 Microfilaments – major subunit protein ‘actin’
 Intermediate filaments
Microfilament bundles terminate at specialized sites of the cell membrane forming a junctional complex with the extracellular matrix.

These tight adhesions are known as FOCAL CONTACTS, ADHESION PLAQUES or FOCAL ADHESIONS.
– Many of the extracellular matrix proteins
responsible for cell adhesion contain a common
peptide sequence Arg-Gly-Asp (RGD) which is
essential for the cell-binding properties of these
proteins.

– These RGD “sites” are recognized by a family of

membrane integral proteins termed integrins that
span the cell membrane from the cytoplasm to
the extracellular matrix.
Cell signaling via chemical pathway
 Cascade of events following application of orthodontic force
• Movement of PDL fluids from areas of compression into areas of
tension

• A gradual development of strain in cells & ECM in the paradental

tissues involved

• Release of phospholipase A2 & cleavage of phospholipids leading to

release of PGE2 & leukotrienes

• ECM remodelling & signal transduction through integrin trans-

membrane channels

• Cytoplasmic alterations & release of 2nd messengers of tooth

movement- cAMP & cGMP, ionositol phosphates, calcium & tyrosine
kinases
• Direct transduction of mechanical forces to the
nucleus of strained cells through the
cytoskeleton, leading to activation of specific
genes

• Release of neuropeptides (nociceptive and

vasoactive) from paradental afferent nerve
endings.

• Interaction of vasoactive neuropeptides with

various cells in strained paradental tissue
• Adhesion of circulated leukocytes to activated endothelial
cells

• Migration by diapedesis of leukocytes into the

extravascular space

• Synthesis & release of signalling molecules by leukocytes

that have migrated into the strained paradental tissues

• Interaction of various types of paradental cells with the

signal molecules released by the migratory leukocytes.

• Activation of the cells to participate in the modeling and

remodeling of the paradental tissues.
 FROST MECHANOSTAT THEORY
• Frost [1990] suggested that survival of the skeleton (but also of other
tissues, such as fibrous tissue, hyaline cartilage,
fibrocartilage,cementum, or dentin) requires the functional coordination
of modeling and remodeling.

• He clearly distinguished modeling and remodeling as two biologically

different activities, which differ in their anatomical locations, effects, and
responses to mechanical usage, disease, and aging.

• As a useful rule of thumb he perceived that modeling adapts a bone to

gross overloading but remodeling adapts it to gross underloading. Where
modeling appears to be enabled by overloading, remodeling increases in
response to underloading
• compressed side of the tooth, the concentration of
RANKL increases

• RANKL promotes osteoclast formation

• In contrast, on the tensile side of an orthodontically

moving tooth the concentration of OPG increases
the relative concentrations of OPG and RANKL on the
tensioned and the compressed sides of the tooth and
the OPG/RANKL ratio in the periodontal ligament
(PDL) cells regulate bone modeling, remodeling, and
root resorption during the application of orthodontic
forces.
• In another study, Nishijima et al. [2006] revealed
that the ratio of OPG/RANKL concentrations in the
PDL fluctuate in a non linear mode in relation to
time, during orthodontic tooth movement

• The ratio of OPG/RANKL concentrations may control

the initiation and termination of the bone modeling
and remodeling process, as well as root resorption,
in a non-linear mode, as was first described by Frost.
Martin and Burr proposed that
(1) subthreshold loading of less than 200 ue results in
disuse atrophy, manifested as a decrease in modeling
and an increase in remodelling
(2) physiologic loading of about 200 to 2500 uE is
associated with normal, steady-state activities
(3) loads exceeding the minimal effective strain (about
2500 uE) result in a hypertrophic increase in modeling
and a
concomitant decrease in remodelling
(4) after peak strains exceed about 4000 ue, the structural
integrity of bone is
threatened, resulting in pathologic overload
 Methods to accelerate
or decelerate orthodontic tooth movement

physical approaches
 low-level laser therapy
 pulsed electromagnatic field
 vibratory stimulus
 photobiomodulation

surgical approaches
 Corticision
 piezocision
• Low-level laser therapy

• Taking into consideration the fact that low-level laser irradiation can augment
bone fracture healing, as well as wound healing,

• Saito and Shimizu (1997) experimented with the same in rats to augment
bone regeneration in the midpalatal suture, along with rapid maxillary
expansion.

• The successful outcome of this investigation lead

them to experiment further on the effects of low-level laser on the speed of
tooth movement and bone remodeling (Kawasaki and Shimizu, 2000), again in
the rat model.

• They observed a 1.3 times increase in the rate of tooth movement, and
augmented response in
both osteoblasts and osteoclasts in bone remodeling.
• Long et al., 2013b concluded in their meta-analysis that
laser irradiations at the wave length of 780nm at the
influence of 5J/cm2 and output power of 20mW, could
accelerate tooth movement within 2–3 months.

• Emphasizing the low dose (5J/cm2 and 8J/cm2 in

comparison to 20 and 25J/cm2) was the
result of the systematic review and meta-analysis by( Ge et
al.) (2014),who reported that acceleration, is seen during
seven days’, as well as two months’ observation periods
 Direct electric currents pulsed
electromagnetic fields
• beeson et al. (1975) were the first to try application of constant direct
electric current (10uA) in cats for five weeks during tooth movement
but were unsuccessful in increasing the rate of tooth movement.

• The concept was revived by Davidovitch et al. (1980a and b), who looked
into the levels of cyclic nucleotides in cats in the PDL and alveolar
bone, and observed enhanced phosphorylation activities in these
tissues during tooth movement.

• They proposed the application of direct current for 7 and 14 days, to determine
whether electricity can serve as a modality for accelerating tooth movement. The
resultsconfirmed the hypothesis that electric currents could be utilized for
this purpose.
 pulsed
electromagnetic fields
• . Stark and Sinclair (1987) evaluated the effect of
pulsed electromagnetic fields (PEMF) in guinea
pigs and observed almost double the rate of tooth
movement (0.42± 0.17 mm) in comparison
to the control group (0.28 ± 0.08 mm).
• They also recorded significant increases in the
number of osteoclasts and raised levels of uricacid,
creatinine and creatinine phosphokinase,
indicating increased
protein metabolism in the experimental group
 Vibratory stimulus

• The credits for the initial efforts to accelerate

tooth movement with a vibratory stimulus goes
to Krishtab et al. (1986) following which,
Ohmae et al. (2001) successfully increased the
rate of tooth movement with ultrasonic vibration

• However, considering the damaging effects

that ultrasonic vibration holds on dental pulp
• Nishimura et al. (2008) developed a vibration-
imposed system through which a vibratory
stimulus (61.02±8.375Hz) can be added to an
expansive force applied on maxillary molars of
male rats.
• They observed a significant increase in the rate
of tooth movement with resonance
vibration and a greater number of osteoclasts in
comparison to the control group, thus providing
a solid foundation to the efficacy of vibrational
stimulation.
• immunochistochemistry revealed increased
RANKL expression in the resonance vibration
group, indicating an increase in osteoclast
formation, function, and survival
 photobiomodulation

• Recently, two research groups have reported successful results

with photo biomodulation in increasing the rate of tooth movement.

• Ekizer et al. (2013) tried light emitting diode (LED) mediated

photobiomodulation therapy in rats and found the experimental
group tooth movement to be 1.55 ± 0.33 mm, in comparison to
1.06±0.35mm in the control group.

• The main advantage was the smaller amount of root resorption in

the experimental group.
• At the same time, Kau et al. (2013) evaluated the efficacy of near
infrared light with 850nm wavelength, which was again applied
through standard LED in 90 subjects (73 test subjects and 17
controls).
• They also observed significantly faster crowding resolution
(1.12mm/w) in comparison to 0.49mm/w in the control group.
 surgical approaches
• The first efforts to move teeth with
combined orthodontics and surgery is
credited to Kole .
• He identified the main tissue layer to
resist tooth movement as the cortical
bone, and corticotomies as the means to
cause teeth to move faster.
• He advocated the use of labial as well as
lingual/palatal surgical cuts, extending to
the entire alveolar height
• He also suggested horizontally
osteotomizing bone well above the apex,
which can further enhance the tooth
movement
• In 2009, two more surgical techniques were introduced,
which are modifications of corticotomy:
corticision (Kim et al., 2009) and piezocision (Dibart et al.,
2009).

• Park (2006) proposed corticision through a local

publication, this technique received greater attention in
2009, when the experiment in cats was published in the
Angle Orthodontist (Kimet al., 2009).
• They used a reinforced scalpel as a thin chisel to separate
the interproximal cortices transmucosally without flap
reflection
• they used a reinforced scalpel as a thin chisel to separate the interproximal
cortices transmucosally without flap reflection.

• Histologic analysis at day 14 revealed large resorption

cavities filled with osteoclasts, which accelerated tooth movement ,and the
healing process was initiated at this site by day 21, suggesting remodeling
of bone with this procedure .

• .The mildcrowding was completely relieved in three weeks, while moderate

crowding took nine weeks to complete.
 hormones promoting tooth movement

• Parathyroid hormone

The initial report on the effect of parathormone

(PTH) on tooth movement was published by Kamata
(1972),

• where he encountered difficulties in moving teeth

after parathyroidectomy in rats, which was
overcome by injecting parathyroid extract
• Davidovitch et al. (1972) compared the effect of
systemic administration of PTH and cortisone acetate in cats, to
consider the possibility of combining clinical orthodontics with
hormonal treatment

• they observed a greater rate of tooth

movement with PTH (50μm daily) followed by the control and
cortisone groups.

• Histologic examination of the cat jaws revealed

intense osteoclastic activity in the PDL, with the highest levels of
both resorptive and formative activities found in the PTH group,
while these were least evident in the cortisone-treated group.
 (Vitamin D3)

• It acts on precursors of both osteoclasts and osteoblasts

,promoting their differentiation, to increase the number of
mature osteoclasts involved in bone resorption (Merke et
al., 1986)

• Taking into consideration the fact that low systemic doses

of1,25-(OH)D3 are capable of activating osteoclastic activity,

• Collins and Sinclair (1988) tried it as a local injection at the

sitecof canine retraction in cats, and observed a 60%
increase in the rate of tooth movement
• Takano-Yamamoto (1992) tried submucosal
injection of vit-D3 into the palatal area of the
bifurcation of the first molar in rats,
• and demonstrated increase in the number of
osteoclasts and bone resorption when used
along with orthodontic forces.
 Corticosteorids
• Corticosteroids (CS) are a class of chemicals that
includes steroid hormones naturally produced in the
adrenal cortex.

• Storey (1958) was the first to evaluate the effect of

cortisone and ACTH on the rate of tooth movement in
rabbits and guinea pigs.

• He found an increase in the amount of bone and

connective tissue resorption following cortisone
administration in rabbits, which
could not be observed with ACTH
• Davidovitch et al. (1972),while evaluating in cats
the role of cortisone acetate in tooth
movement, found no accelerating effect on tooth
movement following a short-term administration

• Ashcraft et al. (1992)studied the effect of cortisone

acetate-induced osteoporosis in rabbits and found
that the teeth in the experimental group moved
approximately three to four times faster than in the
control group
• Ong et al. (2000) evaluated the effect of prednisolone
(1 mg/kg)administered for a period of 23 days in rats,
and concluded that it does not affect the rate of tooth
movement.

• these studies on CS suggest, that when administered

short term, will not affect the magnitude of tooth
movement,

• whereas long-term administration tends to induce

bone resorption and accelerate tooth movement.
 DRUGS USED IN PAIN MANAGEMENT

• Non-steroidal anti-inflammatory Drugs

(NSAIDs)

• Non-opioid, peripherally acting analgesics, COX inhibitors

• Studies related to NSAIDs like Ibuprofen, Acetyl salicylic

acid, Paracetamol, Misoprostol, Indomethacin, Naproxen
sodium not only reduced pain & discomfort but also
interfered with tooth movement
• Celecoxib & Parecoxib : effective in pain
management compared to Rofecoxib without
delaying OTM
 DRUGS USED IN OSTEOPOROSIS

• Osteoporotic drugs : Anti-resorptive

• Bisphosphanates (alendronate, risedronate, etidronate,

pamidronate, zoledronic acid), Estrogen & Calcitonin

• Because of their antiresorptive action,

they interfere with OTM
• Bisphosphanates : In rats, 40%
reduction in OTM
(Liu et al 2004)

• Pamidronate : Fewer osteoclasts in

alveolar bone next to PDL & reduced OTM
(Keles et al 2007)
 DRUGS USED IN RHEUMATOID ARTHRITIS

• Include immunomodulatory
agents(leflunomide), TNF
antagonists, & Interleukin
antagonists.
• Leflunomide : modulates nuclear
factor kappa B, tyrosine kinases
in signaling pathway, IL-6, MMPs
& PGE-2 resulting in delayed
OTM
 Drugs used in Asthma

• Primed leukocytes derived travel through

circulation into extravascular space of
tissues surrounding orthodontically treated
teeth

• Patients with history of asthma seem to be

at high risk for developing excessive Root
resorption during OTM (Davidovitch et al
2000)

• Clinical implications : Light forces should be

applied to reduce adverse effects like
RootResorption
 CORTICOSTEROIDS

• Kalia et al (2004) : Short term

administration of Corticosteroids in rats
reduced OTM while Long term
administration increased OTM

• Ong et al (2000) : Prednisolone treated

rats showed no significant difference in
OTM but had a decrease in amount of
RR
 HEMOPHILIA

• Hemophiliacs experience more episodes

of oral bleeding than healthy people

• Athonosios et al (2009) :compared

2controls,patients with hemophilia have
significant higher serum levels of RANK-L
& osteocalcin and significantly
decreased levels of OPG

• Clinical Implication : Increased rate of

OTM seen
 DIABETES MELLITUS
• Kaval et al : showed significantly elevated
levels of
• mRNA expression for TNF-α,M-CSF, RANKL,
and
• VEGF-A in the diabetic group
• Clinical Implications :
 Diabetes properly controlled :
Satisfactory orthodontic result
 Diabetes poorly controlled : Orthodontic
treatment contraindicated
• (risk of accelerated PDL breakdown
 HYPOTHYROIDISM
• TH deficiencies : delayed / inhibited OTM

• Insufficient growth due to

hypothyroidism can negatively affect
orthodontic treatment especially with
functional appliances (Teng et al 2004)

• Implications : Orthodontic treatment in

such patients should be combined with
hormone replacement therapy to achieve
optimum results (Verna et al 2000)
• PTH: its effects on osteoclasts occur through production
of RANKL

• Hypoparathyroidism : increases bone mineral density &

increase in bone mineralization secondary to suppressed
bone turnover

• Clinical implications : delayed tooth movement on

application of orthodontic forces
 biological background of relapse
of orthodontic tooth movement
Collagen fibers and relapse after translational
tooth movement

• Reitan(1960, 1967) was the first to describe the process of relapse

• According to Reitan (1960, 1967), these fibers are more or less

permanently elongated, and the rearrangement of the fibers and
the alveolar bone after withdrawal of the force would lead to
relapse
• Boese (1969) agreed that relapse in the first four
weeks is caused, to a large extent, by the PDL fibers.
Gingival fibers, however, would be the most
important cause of relapse thereafter.

• Thilander, During orthodontic tooth movement, PDL

fibers at the tension side only develop in the
direction of the movement.
• As long as no new bone is deposited between these
fibers, they may be able to stimulate immediate
relapse after force withdrawal
• In contrast to these ideas, Yoshida et al. (1999) are of
the opinion that immediate relapse after force
withdrawal is not caused by the elongated fibers, but
rather by the rapid remodeling of the PDL and the
surrounding alveolar bone.

• In recent years,several investigations have provided

information to support this notion.

• Administration of bone inductive proteins in sheep and

in rats have shown stimulating bone formation effect
and reduction of relapse in all experimental animals
(Hanet al.,)
• Boese (1969)who concluded that initial
relapse is caused mainly by principal
fibers of the PDL, and that after about a
month the gingival fibers systems become
most important for continuing relapse in
translational tooth movement
 Collagen fibers and relapse after rotational
tooth movement
• Studies on the stability of teeth after rotational
tooth movement focusmainly on the role of the
gingival fibers, which are anchored in the
cervical region of the rotated tooth.

• These fibers remain attached tothe teeth and

become stretched during rotation. This stretching
leads to the development of tension in the fiber
system (Reitan, 1967).
• According (Reitan, 1967; Edwards 1968 )to these authors,
the PDL fibers and the dento periosteal fibers are rapidly
reorganized during and after rotation,

• but transseptal and other gingival fibers are persistent in

remaining stretched. Such an imbalance is present for at
least five months.

• They concluded that the persistence of stretched transseptal

and other gingival fibers has long been considered the main
cause for relapse after rotational tooth movement
 collagen fibers and relapse after closure
of extraction space or midline diastema

• A special situation seems to exist when an

extraction space or diastema is closed.
• After completion of orthodontic treatment,
extraction spaces tend to reopen.
• Bcz both teeth will become separated after
removal of the mechanical retaining device, by the
action of the coiled and compressed transseptal
fibers (Erikson et al., 1945).
• It has also been shown that compressed gingival tissues
in a closed extraction site may lead to an epithelial fold,

• These epithelial folds might lead to reopening of the

extraction site even in cases in
which crowding in the anterior region was present

• histological studies have shown that extraction leads to

disruption of trans septal and other gingival fibers, but
that these fibers are restored in the diastema during
healing.
 CONCLUSION
• Though, commanding knowledge of mechanics, material
science & metallurgy have prevailed, while biological
sciences continue to play a minor role in clinical
orthodontics.

• Recent research into the biologic basis of tooth movement

has provided deep & detailed insight into the molecular,
cellular & tissue level reactions to orthodontic forces

• Future efforts in dental research will include genetic

engineering focusing on bone regeneration.
 REFERENCES
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Proffit, WR. Contemporary Orthodontics, 5 th edition. The
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Moyers, RE. Handbook of Orthodontics, 3 rd edition. Force
systems &tissue responses to forces in orthodontics & facial
orthopedics
Graber, Vanersdall, Vig. Orthodontics: current principles &
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Vinod Krishnana and Ze’ev Davidovitch , Cellular, molecular,
and tissue-level reactions to orthodontic force Am J Orthod
Dentofacial Orthop 2006;129:469e.1-460e.32
Oppenheim A (1911/12) Tissue changes, particularly of the bone,
incident to tooth movement, American Journal of Orthodontics, 3,
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Schwarz AM (1932) Tissue changes incidental to orthodontic
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•Thank you