Physiology of tooth movement 1 /certified fixed orthodontic courses by Indian dental academy

Physiology of tooth movement -I

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com


Contents
- Overview of tooth supporting structures.
- Response to normal functions
- Biologic response to orthodontic forces
- of the bone and periodontium
- Clinical response, histologic response, cellular
and molecular mechanisms.
- Theories of tooth movement.


- Bone physiology
bone structure, modelling and remodelling,
osteoblast histogenesis and bone formation,
osteoclast recruitment and bone resorption.
- Wolff s law , bone metabolism
- Effects of force magnitude, direction, duration
decay.
- Drug effects.

- Anchorage aspects
- Deleterious effects of force on tooth movement.
- Skeletal effects of force

- Future applications
- Conclusion


Tooth supporting structures
Tooth movement involves changes in the periodontium
depending upon the force applied. The following is a
brief description of the characteristics of the normal
periodontium.
GINGIVA –The gingiva is differentiated into the free and
attached gingiva. The connective tissue of the gingiva
consisits of 60 pc of collagen fibres, 5pc of
fibroblasts and 35 pc of vessels, nerves and matrix.
The gingival collagen fibres exhibit cross banding
with a periodicity of 700 nm.

- The gingival fibres which comprise the dentogingival
unit are
CIRCULAR FIBRES.
DENTOGINGIVAL FIBRES.
DENTOPERIOSTEAL FIBRES.
TRANSSEPTAL FIBRES.


PERIODONTAL LIGAMENT – The pdl is approx
0.25mm in width, soft richly vascular and celluar
connective tissue that surrounds the roots of the teeth.
The major component is a network of parallel
collagenous fibres inserting into the cementum of the
root surface and lamina dura. The other components
are cellular elements and the tissue fluids. Blood
vessels and nerve endings (proprioception) are also
found. The true periodontal fibres ,the PRINCIPAL
FIBRES are grouped as follows.

- ALVEOLAR CREST GROUP
- HORIZONTAL GROUP
- OBLIQUE GROUP
- APICAL GROUP
- INTERRADICULAR GROUP


CEMENTUM –it is a specialised mineralized tissue
covering the root surfaces and has many features
common with the bone. It contains no blood
vessels ,no innervation ,does not undergo physiologic
resorption but continuous deposition occurs
throughout life.
Primary cementum – no cells, formed during erruption.
Secondary cementum - cells present, formed in response
to functional demands.

Response to normal functions
- Tissue reactions in the tooth supporting structures
take place with the erruption of teeth and
development of occlusion. Contrary to the relatively
short erruption period the teeth and the supporting
tissues have a life long ability to adapt to functional
demands and drift through alveolar bone called
physiologic migration.
-When the teeth migrate they bring the supraalveolar
fibre system with them, implying remodelling of the
alveolar bone and PDL.

-The cells are more active on the bone side than near the
root cementum. Hence major remodelling takes place
near the alveolar bone. Unlike the osteoclastic
resorption of bone to provide the space for tooth
movements, the corresponding remodelling of the
fibrous attachment is not clearly understood .But the
presence of a mesh work of collagen fibres of small
diameter is sufficient to explain the rapid
reorganization process.


-A slow apposition occurs on the cementum surface
throughout life, a fact that is of great importance for
the resorptive mechanism in the bone and cementum.
The unmineralized precementum layer has special
importance as a resorption resistant coating layer thus
protecting the root surface during physiologic
migration.
-Along with the mesio distal migration teeth also exhibit
continued erruption even after full emergence ,
accompanying growth in alveolar height .

-The interest in continued erruption of teeth has taken a
new turn in recent years with the introduction of
implants inserted directly into the alveolar process.
-The need is ever increasing for more information about
the use of dental implants in young individuals,
whether they should be used at all ,and if so, how and
when.
-Moreover tooth wear is a common occurrence and may
counteract the continuous tooth erruption.

Physiologic response to heavy pressure
- During mastication teeth and PDL are subjected to
intermittent heavy forces. Tooth contacts last for 1
sec or less and forces range from 2 kg to 50 kgs. In
this situation quick displacement of the tooth within
the PDL space is prevented by the tissue fluids and
the force is transmitted to the alveolar bone which
bends in response.
< 1 sec –PDL fluid incompresible ,bone bends.
1-2 sec –PDL fluid expressed, tooth moves in PDL
space

- 3 -5 sec –PDL fluid squeezes out, tissues compressed

immediate pain if pressure is heavy.
- Role of PDL in erruption and active stabilization of
teeth.
- The phenomenon of erruption makes it plain that
forces generated within the PDL itself can produce
tooth movement (metabolic changes in PDL). This
also produces active stabilization of teeth against
prolonged forces of light magnitude.

The current concept is that active stabilization can overcome
prolonged forces of a few gms (5 -10)observed as the
magnitude of unbalanced soft tissue resting pressures.

Response to orthodontic forces
Basically no great difference exists between the tissue
reactions observed in physiologic migration and those
seen in orthodontic tooth movement. The changes are
just more marked and extensive.
Application of a continuous force on the crown of a
tooth leads to its movement within the alveolus. The
duration of tooth movement can be divided into an
initial period and a secondary period.


INITIAL PERIOD -In this crucial stage compression in

limited areas of the pdl impedes vascular circulation
and cellular differentiation causing degradation of
cells and vascular structures .Degradation starts
where the pressure is highest, near the bony spicules.
Retardation of blood flow is followed by
disintegration of vessel walls, degradation of blood
elements. The tissue assumes a glass like appeareance
termed HYALINIZATION.


Hyalinization is caused partly by anatomic and partly by
mechanical factors and is almost unavoidable in the
initial period of tooth movement in clinical
orthodontics. It represents a sterile necrotic area
generally limited to 1 or 2 mm in diameter. This
process displays three stages.
DEGRADATION.
ELIMINATION OF DESTROYED TISSUE.
REESTABLISHMENT OF A NEW TOOTH ATTACHMENT .


- In hyalinized zones the cells cannot differentiate into

osteoclasts and no bone resorption can take place.
Tooth movement stops until the necrotic areas have
been removed. A limited hyalinized zone is expected
to persist for two weeks with the use of light forces.
- Now the invasion of macrophages from the adjacent
undamaged PDL helps in the elimination of the
necrotic zone. Recent evidence shows invasion of
multinucleated giant cells belonging to the
mononuclear phagocytic system.

- Reestablishment of the tooth attachment in the

-

hyalinized area starts by the synthesis of new tissue
elements as soon as the degenerated tissues have been
removed. The ligament space is now wider than
before and rich in cells.
SECONDARY PERIOD – The PDL is considerably
widened and the osteoclasts attack the bone surface
over a much wider area now. As long as the force is
kept gentle further bone resorption is predominantly
direct.

-A large number of osteoclasts are seen along the bone
surface and the tooth movement is rapid. Extensive
breakdown of the fibres takes place on the pressure
side followed by complete reorganization of the
fibrous system.
-The main feature is the bone deposition on the tension
side. Osteoblast proliferation is usually seen after 30
to 40 hours shortly after which osteoid tissue is
deposited . (depends on the fibre bundles )


- Concomitantly with the resorption and apposition on

the pdl surfaces an accompanying apposition and
resorption on the spongiosa surface of the alveolar
bone takes place .This tends to maintain the
dimensions of the supporting bone.
- Thus the orthodontic tooth movement involves many
inflammation like reactions ( a process occuring in a
local area when a rapid response is needed for a stress
that is felt by the cells to be heavy). No unwanted
sequale occurs as long as this sterile necrosis is of
short duration and not complicated by local infection.

- Finite element in the past was used to describe
stressed situations within the pdl and alveolar bone.
The present study sought to determine the impact of
the modelling process on the outcome of FE analyses
and rate it to the current theories on tooth movement.
Results demonstrate that loading of the pdl cannot be
explained in simple terms of compression and tension
along the loading direction. Tension in the alveolar
bone was far more predominant than compression.
Cattaneo, Melsen B. J Dent Res 2005

Theories of tooth movement
The two possible control elements, biologic electricity
and pressure-tension in the PDL that affects blood flow
are contrasted in the two major theories of orthodontic
tooth movement.
Pressure tension theory –This classical theory of tooth
movement relies on chemical rather than electrical
signals as the stimulus for cellular differentiation and
tooth movement. Chemical messengers are important
in the cascade of events leading to tooth movement.

Sustained pressure
Areas of compression, tension
Blood flow alterations
Changes in oxygen tension, changes in other
metabolites
Release of biologically active agents
Stimulation of cellular differentiation activity

The Bioelectric Theory
This theory relates tooth movement to changes in bone
metabolism controlled by the electric signals that are
produced when alveolar bone flexes and bends.
Electric signals that might initiate tooth movement
initially were thought to be piezoelectric.
Piezoelectricity is a phenomenon observed in many
crystalline materials. Deformation of crystal structure
causes a flow of electric current due to electron
displacement.

- These signals have two unusual characteristics.
-a quick decay rate
-the production of equivalent signal opposite in
direction when the force is released.
- The ions in the extracellular fluids interact with the
electric fields generated due to bone bending and give
rise to small voltages called STREAMING
POTENTIALS.
- Reverse piezoelectric effect can also be seen.

- Stress generated signals are important for the

maintenance of the skeleton. Signals generated by the
bending of alveolar bone during normal chewing are
surely important for the maintenance of bone around
teeth.
- On the other hand sustained forces in orthodontics do
not produce prominent stress generated signals.


BIOELECTRIC POTENTIALS.-These are a type of

endogenous electric signals observed in bone not
being stressed.
Metabolically active bone cells – electronegative
charges.
Inactive areas – electrically neutral.
- Although their purpose is unknown, cellular activity
can be modified by adding exogenous electric signals.


- Their combined affect is noted at the cell membrane
level affecting the membrane receptors and
membrane potential along with cellular responses.
- Electromagnetic fields can also cause the above
affects.
- Perhaps a fair conclusion is that even though the
stress generated electric signals do not explain tooth
movement ,electric and electromagnetic influences
can modify the bone remodelling on which tooth
movement depends.

- Studies by Karanth, Shetty (2001) have shown that

application of an electric current may alter the
electrolytic environment allowing changes in the type
and rate of ions that move across the cell membrane.
- Changes of the flux of K, Na, Ca, Mg, Cl can
mediate cellular changes.
- Micropulsed electrical stimulation- can reach
osteoblasts – increase cAMP, cGMP – can cause
efficient remodelling- enhanced tooth movement.

- Tengku, Joseph (2000) incorporated a ststic

magnetic field into an orthodontic appliance and
noted that the tooth movement was not significantly
enhanced than the controls but in contrast the root
resorption was significantly increased.
- Davidovitch et al (1980) studied the effects of DC
electric currents on the pdl tissues. It was concluded
that electric stimulation enhances cellular enzymatic
phosphorylation activities in pdl tissues and may be a
potent tool in accelerating bone turnover.

- The effect of electric-orthodontic treatment on the pdl

cyclic nucleotides was studied. It was seen that teeth
treated by both force and electric currents moved
faster as compared to teeth treated by force alone.
Anode – bone resorption ( compression side)
Cathode –bone deposition ( tension side)
- Hence it was concluded that orthodontic treatment
can be accelerated by the use of locally applied
electric currents.

CLINICAL RESPONSES TO ORTHODONTIC
FORCES
- From a clinical perspective orthodontic tooth
movement has three distinct phases.
DISPLACEMENT PHASE.
DELAY PHASE.
ACCELERATION AND LINEAR PHASE.

DISPLACEMENT PHASE. –the initial reaction of the
tooth to force is almost instantaneous within a
fraction of a second. It reflects the immediate
movement of the tooth within the viscoelastic PDL.

- There is no extensive amounts of tissue or bone
remodelling. The fluid compartments of the pdl help
in the transmission and dampening of forces acting
on the teeth. The magnitude of the displacement
response is dependent on the root length , alveolar
bone height and age.
DELAY PHASE.- This phase of the tooth movement
cycle is characterised by absence of clinical
movement and is referred to as the delay or latency
phase.

- Although there is no tooth movement extensive
remodelling occurs in all the tooth investing tissues.
The absolute amount of force applied is not as
relevant as the relative force applied per unit area.
- There can be partial or absolute occlusion of blood
vessels. In absolute occlusion tooth movement is
slower and starts approximately after 1 – 2 weeks.
- Aging has been shown to effect the proliferative
activity of the cells of the pdl and tooth movement
subsequently during the delay phase.

- It has been seen that in young subjects there is faster

initial tooth movement. But once the linear phase is
reached the tooth movement rate becomes equal in
both the groups. This indicates that the clinically
observed increase in treatment time for adults can be
primarily attributed to the delay phase prior to the
onset of tooth movement, but the rate of migration is
equally efficient once tooth movement has started.
- Ren Y, Maltha. J Dent Res 2003.


ACCELERATION AND LINEAR PHASE.- The third
phase is characterized by rapid tooth displacement
Tooth movement is initiated in deference to the
adaptation of the supporting pdl and alveolar bone
changes. Studies have shown that following
orthodontic appliance reactivation, along with the
presence of activation osteoclasts a second cohort of
osteoclasts can be recruited immediately. This causes
immediate significant tooth movement with no
greater risk of root resorption. King, Archer AJO
1998

- The force magnitude directly affects the rate of tooth
movement. High forces used in excess of 100 gms
(canine retraction) have shown to produce a lag phase
of about 21 days before tooth movement. Lower
forces can induce tooth translation without a lag
phase at rates that are still clinically significant.
Iwasaki, Nickel, Morton AJO 2000.


- Equally as important as magnitude, however is the
timing of the force application .The force regimen has
more influence on the rate of movement than the
force magnitude. Light forces are more conducive to
tooth movement because the cell biology system
remains in a constantly responsive state .Conversely
the application of intermittent forces creates a
fluctuating environment of cellular activity followed
by quiescence.


CELLULAR MECHANISMS
- When a force is applied the tooth moves in the

direction of the force. Resorption of alveolar bone
takes place and a little distance behind the alveolar
wall a new bony lamella is laid.
- There is transmission of mechanical influence into
cellular response.
- How do different cells know that they should react
and in a special way? Several mechanisms have been
proposed for these cellular reactions.

- The perturbation of pdl cells as a result of forces may
change the influx of calcium and sodium ions into
the cells which in turn alters the production of second
messengers –cAMP and cGMP .Low levels of these
may influence the differentiation of cells for bone
production.
- Also mechanical stress may induce localized cells to
produce prostaglandins which stimulate osteoclastic
bone resorption.


- Another mechanism can be piezoelectricity. When a

long bone is bent the concave surfaces become
negatively charged which is believed to stimulate
bone formation.
- Orthodontic forces also puts into motion both the
nervous and immune systems. Increase in secondary
messengers is not just solely from the direct effects of
stresses but also due to endogenous signalling agents.


- Neurotransmitters – substance P, vasoactive

intestinal polypeptide VIP, calcitonin gene related
peptide CGRP and others act as from sensory nerve
fibres in the pdl and supply a link between the
physical stimulus and the biochemical response.
- Orthodontic forces cause a marked increase in the
staining intensity of interlukin 1-alpha and interlukin
1-beta particularly in osteoblasts and osteoclasts.
Saito M et al AJO 1991

- Changes in cell shape may also play a role. There is
some evidence that prostaglandins are released when
cells are mechanically deformed. Prostaglandin
release may be a primary rather than a secondary
response to pressure .It is likely that mobilization of
membrane phospholipids , which leads to formation
of inositol phosphates is another pathway towards the
eventual cellular response. Changes in cell shape
produce effects mediated by membrane integral
proteins (integrins).
Sandy, Farndale AJO 1993

- Kaku M, Kohno (2001) have studied the effects of

vascular endothelial growth factor and concluded that
local administration of rhVEGF enhances the number
of osteoclasts and may increase the rate of tooth
movement.
- AlhashimiN, Brudvik (2004) have concluded that the
CD4O- CD40L interaction appears to be an active
process and that force induces T-cell activation .Such
activation may be involved in the induction of
inflammatory mediators and bone remodelling.

MOLECULAR MECHANISMS
- Skeletal integrity is the result of dynamic interactions
between osteoblasts and osteoclasts. The rate of
remodelling is dependent however on the cells of the
osteoblast lineage which in addition to bone
formation are also responsible for the activation and
recruitment of osteoclast precursors.
- However the basis of communication between these
cells was unclear untill the intermediary factor was
identified. It has been named as the receptor activator
of nuclear factor kB ligand. RANKL

- Binding of RANKL to its cognate receptor, the RANK
expressed on the surface of osteoclast progenitor cells
leads to induction and activation of osteoclasts.( bone
resorption )
- RANKL however can bind to osteoprotegerin OPG,
and can inhibit activation of osteoclasts and reduce
bone resorption.
- This ratio of RANKL /OPG expression by osteoblasts
is believed to be a key determinant of the rate of
recruitment and activation of immature osteoclasts.

- From an orthodontic perspective , it is very likely that

pressure changes in the microenvironment of the
tooth socket may cause up and down regulation of the
RANKL and OPG genes as a means of modullating
protein production and ultimately bone remodelling.
- Local mechanisms – inflammatory cytokines like
interlukins , TNFs, growth factors that have biologic
activities influencing individual phases of the cycle.
- Endocrine mechanisms include the calciotropic
hormones and the sex steroids

- These factors act on osteoblasts to regulate osteoblast
osteoclast equilibrium and can either up- or downregulate a cascade of downstream signalling
pathways that ultimately affect the expression of
specific genes necessary to synthesize specific
proteins involved in bone remodelling.


- Studies by Kanzaki ,Chiba (2004) have shown that

when local OPG gene transfer was done, OPG
production was enhanced and osteoclastogenesis was
inhibited. Local OPG gene transfer significantly
diminished tooth movement.
- Recent studies by Kanzaki, Chiba (2006) have shown
that local RANKL gene transfer significantly
enhanced osteoclastogenesis and hence lead to
increased tooth movement.


- Tooth movement was enhanced and no systemic
effects were seen. Local RANKL gene transfer might
be a useful tool not only for shortening treatment time
but also for moving ankylosed teeth where teeth fuse
to the surrounding bone.
- Wise GE, Yao S, Liu. Clin Anat 2006 have proposed
that local injections of OPG may help in delaying
tooth erruption.


References
- Kanzaki H, Chiba M, Takahashi – Local RANKL

gene transfer to the pdl tissues accelerates orthodontic
tooth movement. Gene Thera 2006 jan5 (epub ahead
of print)
- Wise GE, Yao S, Liu: Injections of OPG and PMA
delay tooth erruption. ClinAnat 2006;jan19-1:19-24
- CattaneoPM, Dalstra M, Melsen B: The finite element
model – a tool to study orthodontic tooth movement.
J Dent Res 2005 may 84:428-433

- Kanzaki H,Chiba M, Takahashi: Local OPG gene

transfer to the pdl tissues inhibits orthodontic tooth
movement.J Dent Res2004 dec 83:12:920-5
- Von Bohl M, Maltha JC .Focal hyalinization during
experimental tooth movement in beagle dogs. AJO
may 2004 125(5):615-23.
- Alhaimi N, Fritiof, Brudvik .CD40- CD40L
expression during orthodontic tooth movement in
rats. AO 2004 feb 74(1) 100-5.

- Ren Y, Malhata JC. Age effect on orthodontic tooth

movement in rats. J Dent Res 2003;82:38-42.

- Karanth H S, Shetty KS. Orthodontic tooth

movement and bioelectricity. Ind J Dent Res 2001 oct
–dec 12,4-212-21.
- Kaku M, Kohno S, Kawata. Effect of vascular
endothelial growth factor on osteoclast induction
during orthodontic tooth movement in mice. J Dent
Res 2001 oct 80,10 1880-3.

- Iwasaki LR, Haack JE, Morton. Human tooth

movement in response to continuous stress of low
magnitude. AJO 2000;117:175-183.
- Davidovitch Z et al: Electric currents, bone
remodelling and orthodontic tooth movement. I and II
AJO1980;jan 77:14-32
- King GJ, Archer , Zhou. Late orthodontic appliance
reactivation stimulates immediate appearance of
osteoclasts and linear tooth movemnt. AJO
1998;114:692-677.

- Nakagawa N, Kinosaki, Yamaguchi .RANK is the

essential signaling receptor for osteoclast
differentiation factor in osteoclastogenesis. Biochem
Biophy Res Commun 1998:253;395-400.
- Zengo, Pawluk, Bassett: Stress induced bioelectric
potentials in the dentoalveolar complex. AJO
1973:64:17.
- Roberts W, Chase ;Kinetics of cell proliferation and
migration assosciated with orthodontically induced
osteogenesis. J Dent Res 1981:60:174

- Thilander et al; Osseointegrated implants in

adolescents. An alternative in replacing missing
teeth? EJO 1994: 16:84.
- Sandy JR, FarndaleRW, Meikle: Recent advances in
understanding mechanically induced bone
remodelling. AJO 1993:103;212-222
- Saito M et al: Interlukin 1 beta and PGE are involved
in the response of pdl cells to mechanical stress in
vivo and in vitro. AJO 1991 ,99:226


- Tengku BS, Joseph –Effect of a static magnetic field

on orthodontic tooth movement in rats. EJO 2000
oct22 ,5 ;475-87.
- Orthodontics – current principles and techniques.
third edition. Graber , Vanarsdall.
- Contemporary orthodontics. third edition, Proffit.
- Biomechanics and esthetic strategies in clinical
orthodontics. Ravindra Nanda. first edition.


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Physiology of tooth movement 1 /certified fixed orthodontic courses by Indian dental academy

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