Biology of tooth movement

Biology of tooth
movement
Presented by:
Dr.Fazal ur Raheman
Guided By:
Dr.Vishwanath Patil
Prof. H.O.D, H.K.E’s
S.Nijalingappa Institute of
Dental Sciences and Research
GULBARGA. 2

• To treat malocclusion,
“ Man only has to
help nature, when she
cannot complete her task
alone.”
-Delabarre
3

Introduction
• Throughout their natural history, teeth
move and migrate.
• Prior to their eruption into the oral
cavity, changes in the position of tooth
buds occur primarily due to the growth
of dental structures, and the
concomitant remodeling of
neighboring tissues, i.e., alveolar bone,
gingiva, and periodontal ligament
(PDL), including the dental follicle.
4

• Following their emergence into the oral cavity, teeth
reach a position in the dental arch, dictated by the
forces of the surrounding muscles of the tongue,
cheeks, and lips, and by contact with teeth of the
opposite jaw.
5

• During mastication, teeth can move slightly in the
vertical and horizontal directions, within the
constraints of the soft tissues of the PDL, and the
bendability of the alveolar bone.
• Bone bending in response to normal function
generates piezoelectric currents which is an important
stimulus to skeletal regeneration and repair.
• Despite their large magnitude, masticatory forces do
not alter the position of teeth, due to their short
duration.
6

Piezoelectric current
• Piezoelectricity is a phenomenon observed in
many crystalline materials in which a
deformation of the crystal structure produces
a flow of electric current as electrons are
displaced from one part of crystal lattice to
another. Organic crystals can be piezoelectric,
and collagen in the PDL is an excellent sample.
7

• However, in the presence of periodontal disease,
when paradental tissues are gradually destroyed, teeth
can migrate into new positions, where the masticatory
and parafunctional forces reach equilibrium.
• Often, these new positions are aesthetically
undesirable.
8

• In large measure, orthodontic treatment depends on
skeletal modeling (surface apposition and
resorption) within specialized, mechanically
responsive tissues i.e. sutures and periodontal
ligament (PDL).
Treatment Philosophy
9

• Orthodontic treatment is based on the principle that if
prolonged pressure is applied to a tooth, tooth
movement will occur as the bone around the tooth
remodels.
• Bone is selectively removed in some areas and added
in some.
• Tooth moves through bone carrying its attachment
apparatus with it, as the socket of the tooth migrates.
• This bone response is mediated through the
periodontal ligament.
10

Historical Review
• The first recorded recommendation to use force for
orthodontic reasons was made around the year 1 A.D.
by Celsus, who suggested the application of finger
pressure to teeth for alignment purposes.
• Seventeen centuries later, Fauchard was the first to
publish a description and an illustration of an
orthodontic appliance, which generated forces by
using ligatures to tie teeth to a rigid arch.
11

• In the 18th century, Hunter provided the first
biological explanation for orthodontic tooth
movement:
"To extract an irregular tooth would answer but little
purpose, if no alterations could be made in the
situation of the rest; but we find that the very
principle upon which teeth are made to grow
irregularly is capable, if properly directed, of
bringing them even again. This principle is the power
which many parts (especially bones) have of moving
out of the way of mechanical pressure."
12

• In 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.
13

• In 1888, Farrar hypothesized that tooth movement is
due, at least in part, to bending of alveolar bone by
applied forces.
• This notion was supported by Wolff’s proposition in
1892 that the internal architecture of bone is dictated
by the mechanical forces that act upon it.
14

• The first report on the histomorphology of tissues
surrounding orthodontically treated teeth was
published by Sandstedt in 1904 to 1905.
• That landmark experiment, performed in one dog,
concluded that force-induced tissue changes are
limited to the PDL and its alveolar bone margin.
15

• At the end of 3 weeks of treatment, Sandstedt
observed new 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).
16

• Six years later, Oppenheim reported on a histologic
examination of the jaws of one juvenile baboon
whose teeth had been treated by orthodontic forces.
• In contrast to Sandstedt, Oppenheim saw no
demarcation between the old and new alveolar bone
near the moving teeth, but rather a trabecular
structure that strongly suggested a complete
transformation of the entire alveolar bone in that
region.
17

• The bony trabeculae were all rearranged in the
direction of the force.
• However, Oppenheim's conclusions that orthodontic
forces were capable of transforming the entire
alveolus were rejected by his contemporaries as
misinterpretations.
• He was also criticized for using an animal with
deciduous teeth for his experiment, suggesting that
the transformation he had seen was related to growth
and development rather than being the outcome of
applied mechanical forces.
18

• Oppenheim's "transformation" hypothesis might have
supported Farrar's earlier contention that orthodontic
forces bend the alveolar bone, and thus are able to
stimulate all the cells in and around this bone.
• However, Farrar's clinical approach also was not
popular, because he advocated the use of heavy forces
that could indeed bend the bone.
19

• Schwarz then recommended the use of light
orthodontic forces. He defined those forces as being
"not greater than the pressure in the blood
capillaries" (15 to 20 mmHg, or about 20 to 26 g/cm2
of root surface).
20

• A 1957 publication by Fukada and Yasuda attracted
wide attention. They observed that bending of bone
by mechanical means evokes the generation of
measurable electric potential spikes in areas of
compression and tension.
• While this observation caused the rebirth of the field
of applied exogenous electricity to bone nonunion
fractures, it also precipitated the reintroduction of the
concept of alveolar bone bending by orthodontic
forces!
21

Periodontal Ligament
• The PDL is a connective tissue interface separating
the tooth from its supporting bone.
Cells Extracellular matrix
Synthetic (osteoblast, fibroblast,
cementoblast)
Resorptive (osteoclast, fibroclast,
cementoclast)
Progenitor
Epithelial rests of Malassez
Defence (mast cell, macrophages)
Fibres (collagen, oxytalan)
Ground substance
(proteoglycans,
glycoproteins)
23

• It contains an intricate network of
blood vessels and nerve endings,
and is very cellular.
• The majority of the PDL cells are
fibroblasts, but some of these
fibroblast-like cells are actually
osteoprogenitor cells.
• It has an inherent eruptive
potential.
24

• 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.
• 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. Cells may also migrate
into the PDL from neighboring marrow spaces in the
alveolar bone.
25

Neural system
• The PDL contains an elaborate network of neural
filaments that arise from the trigeminal nerve.
• Myelinated and unmyelinated fibers are found in the
PDL.
• Nerve impulses resulting from tooth movement can
be detected in afferent fibers. These impulses
originate primarily in the PDL and not in the dental
pulp, as proved by experiments.
26

• In force-induced tooth movement, the PDL nerve
fibers perform two main functions:
1. transmission of nociceptive impulses centrally and
2. release of neuropeptides peripherally.
• The latter may have an important role in regulating
the local inflammatory response, primarily by
interacting with cells of the vascular system.
27

28
Nociception (also nocioception or nociperception) is the encoding and
processing of harmful stimuli in the nervous system, and, therefore, the
ability of a body to sense potential harm. It is the afferent activity in
the peripheral and central nervous systems produced by stimulation of
specialized free nerve endings called nociceptors or "pain receptors" that
only respond to tissue damage caused by intense chemical (e.g., chilli
powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat
and cold) stimulation. Once stimulated, a nociceptor sends a signal along a
chain of nerve fibers via the spinal cord to the brain. Nociception triggers a
variety of autonomic responses and may also result in a subjective
experience of pain in sentient beings. Nociceptive neurons generate trains
of action potentials in response to intense stimuli, and the frequency of
firing determines the intensity of the pain.
Nociception

PDL Space
• It is a narrow space between tooth & alveolar
bone.
• Average width:
0.30-0.35 mm in young individuals
0.25-0.15 mm as age advances
• No space in ankylosis
• ‘Hourglass’ in shape i.e. narrowest in midroot
region, near fulcrum about which the root moves
when an orthodontic load (tipping load) is
applied.
29

PDL fluid
• The vascular system contributes to its fluid
composition.
• Bien thoroughly analyzed the dynamics of PDL fluid
in relation to tooth movement, and identified three
sources of fluid in the PDL:
1. cellular,
2. vascular, and
3. interstitial.
30

• The latter is localized in the ground substance and
acts as a thixotropic gel, which is jelly-like when not
in motion, and flows quite easily under pressure.
• 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.
31

Physiologic response to heavy
pressure against a tooth
Time
(seconds)
Event
< 1 PDL fluid incompressible, alveolar bone
bends, piezoelectric signal generated
1 – 2 PDL fluid expressed, tooth moves within
PDL space
3 – 5 PDL fluid Squeezed out, tissues compressed,
immediate pain if pressure is heavy
32

• This fluid motion and rearrangement signifies the
onset and progress 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.
33

Significance of Viscoelasticity of
PDL
• Viscoelasticity is attributed to cell protoplasm,
vascularity and the investing ground substance.
• Because of this nature, load duration is a critical
factor in effecting tooth movement.
34

• Occlusal trauma produces mobility and often root
resorption.
• Parafunction (bruxism) is usually associated with
excessive wear and hypertrophy of the surrounding
alveolar bone.
• However, neither bruxism nor occlusal trauma are
effective in moving teeth, because each loading event
is of relatively short duration.
35

• Other intermittent forces, like mastication (1 sec or
less), speech and deglutination also fail to change
tooth position.
• The tooth support mechanism effectively resists even
heavy transient loads (1-50 kg).
• On the other hand, light continuous forces (habits,
tongue posture, lip contact, supracrestal fiber traction
and orthodontic therapy) are highly efficient in
displacing PDL and moving tooth.
36

• Continuous functional loads (soft tissue posture,
eruption) produce physiologic drift, while orthodontic
forces produces therapeutic tooth movement.
• Approximal drift maintains the integrity of the arch
and prevents interdental spaces from opening as
contact areas abrade.
37

• The adaptability of PDL is important in maintaining
optimal occlusion at proper vertical dimension.
• Physiologically or therapeutically 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.
38

Role of PDL in eruption and
stabilization of teeth
• There is an inherent potential of the PDL to
continuously erupt the teeth.
• The process continues at a slower rate throughout
life.
• The continuing presence of this mechanism indicates:
1. Continuous eruption of teeth
2. Active stabilization of teeth against prolonged light
forces
39

• There are light prolonged unequal pressures from the
lip, tongue and cheeks against the teeth; but no tooth
movement occurs.
• This is due to active stabilization.
• It also implies a threshold for orthodontic force, since
forces below the stabilization level would be expected
to be ineffective.
• The current concept is that active stabilization can
overcome prolonged forces of a few grams at most,
perhaps up to 5-10 gm/cm2 often observed as the
magnitude of unbalanced soft tissue resting pressures.
41

Biologic control of tooth
movement
• Two possible control mechanisms in tooth movement:
1. Biologic electricity
2. Pressure-Tension theory
42

43
The response to sustained force against the teeth is a function of force
magnitude :
Heavy forces leads to rapidly developing pain, necrosis of cellular elements
within the PDL, and the phenomenon of undermining resorption of
alveolar bone near the affected tooth.
Lighter forces are compatible with survival of cells within the PDL and a
remodelling tooth socket by a relatively painless “frontal resorption” of
the tooth socket . This is what we want in our day to day Orthodontic
practice. Knowing that necrosis of PDL and undermining resorption will
occur despite efforts to prevent this.
Periodontal Ligament and bone response to
sustained force.

Bioelectric theory
(Biologic electricity)
• This theory relates to the changes in bone metabolism
controlled by electric signals which are produced due
to the bending & flexing of the alveolar bone.
• Electric signals which were thought to cause tooth
movement were assumed to be piezoelectric.
44

Piezoelectricity
• Bone is a mineral having crystal structure &
piezoelectric properties.
• It is a phenomenon observed in many crystalline
materials in which a deformation of the crystal
structure produces a flow of electric current as
electrons are displaced from one part of the crystal
lattice to another.
45

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.
46

47
When a force is applied to a crystalline structure such as bone or
collagen, a flow of current is produced that quickly dies away. When the
force is released, an opposite current flow is observed. The piezoelectric
effect results from migration of electrons within the crystal lattice.

• The crystal lattice is distorted due to the applied
pressure.
• Due to this deformation of the structure, electrons
migrate and electric charge is observed.
• The crystals return to their original shape after the
force is released.
• Thus reverse flow of electrons occurs.
48

• 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.
• These are called streaming potential.
49

• Stress generated signals are important in the general
maintenance of the skeleton.
• Without these signals bone mineral is lost and atrophy
occurs.
• Bones of astronauts no longer flex in a weightless
environment as they would under normal gravity.
• Stress generated electric signals do not cause
significant tooth movement as these are short lived
signals.
50

• Vibrating kind of force was used over sustained force
to see the effect on tooth movement.
• No change in results were seen after the application
of both types of forces.
-Shapiro E. AJO-DO 73:59-66,1979
51

Bioelectric potential
• This is observed in a bone which is not being
stressed.
• Metabolically active bone produces electronegative
charges that are generally proportional to how active
they are. Signals generated by the bending of alveolar
bone during normal chewing are important for
maintenance of the around the teeth.
• Inactive cells are electrically neutral.
52

• Bioelectric measurements in alveolar bone have
demonstrated that the compressed (concave) side of
the orthodontically treated bone is electronegative
with respect to the tension (convex) side, suggesting
that negative potentials during bone bending can
generate bone deposition, while positive potentials
are responsible for bone resorption.
53

• Animal & human experiments indicate that when low
voltage direct current is applied to the alveolar bone,
modifying the bioelectric potential, a tooth moves
faster than its control response to an identical spring.
-Giovanelli S et al 1996
54

Electromagnetic field
• In animal experiments, a pulsed electromagnetic field
increased the tooth movement by shortening the “lag
phase” before tooth movement begins.
Stark TM:AJO-DO 91:91-104,1987
• Electromagnetic fields can be induced by within
tissues by adjacent magnets, without the contact of
electrodes.
• This movement could be used to enhance the
55

• To summarize,
Tooth
PDL fluid & bone stimulated
Deformation of collagen/hydroxyapatite crystals
Electrical energy created
Electric field created ions in the fluid that bathe living
bone interact with the complex electric field generated
Force/pressure
56

Temperature changes / Electric signals /Alterations of
Oxygen tension / cAMP / Ca++ / Hormones
Development of conduction & convection currents
Bone Metabolism
• Without such signals, bone mineral is lost and
general skeletal atrophy ensues.
Bending of alveolar bone
57

• Experiments have been performed in animals
showing influence of piezoelectricity on tooth
movement; but they do not explain tooth movement
in humans. However, it can modify bone remodelling.
• Concluding ,we could say even if the stress generated
signals do not explain tooth movement, bioelectric &
electromagnetic influences can modify the bone
remodeling on which the tooth movement depends.
58

• Role of periodontal ligament in tooth movement.
• Role of periodontal ligament in eruption and
stabilisation of teeth.
• Bioelectric theory (piezoelectric current).
60

Physiologic Tooth Movement
It is the naturally occurring tooth movements
that take place during and after tooth eruption
1. Tooth eruption
2. Migration or drift of teeth
3. Changes in tooth position during mastication
61

Tooth Eruption
• Axial or occlusal movement of the
tooth from its developmental
position within the jaw to its
functional position in the occlusal
plane
62

Theories Of Tooth Eruption
• Vascular pressure theory
• Root formation
• Bone Remodeling
• Periodontal ligament traction
This theory states that the periodontal ligament is rich in
fibroblasts
that contain contractile tissue. The contraction of these
periodontal fibers (mainly the oblique group) result in
tooth eruption.
63

Migration Or Drift Of Teeth
• Teeth have the ability to drift through the
alveolar bone
• Human teeth have a tendency to migrate in
mesial or occlusal direction
• This maintains the inter-proximal and occlusal
contact
• Aided by bone resorption and deposition by
osteoclasts and osteoblasts respectively
64

65
Mesial or Distal - due to
proximal caries (loss of tooth
structure) or exfoliation of
mesial or distal tooth.
Occlusal - Due to premature
exfoliation or absence of
opposing tooth (supra-eruption)

• This classic theory of tooth movement relies on
chemical rather than electric signals for the stimulus
for cellular differentiation & tooth movement.
• In this theory, an alteration in blood flow within the
PDL is produced by pressure sustained at some sites
& tension at some. Chemical messengers are
important in the cascade of events that lead to
remodeling of the alveolar bone & subsequent tooth
movement.
67

• An alteration in the blood flow is produced within the
PDL , by sustained pressure.
• PDL is stretched in some areas whereas it is
compressed in some areas.
• Blood flow is decreased in areas of PDL compression
& it is maintained in areas where PDL is under
tension.
• In areas where PDL is overstretched blood flow
decreases transiently.
68

• Depending on the physiologic drift pattern, the adjacent
bone surface may be resting, resorbing or forming.
71

Application of light
sustained forces
72

Application of light sustained
force
Pressure side TENSION side
Compression of blood vessels
Blood flow altered
Oxygen tension ↓
PGs & Cytokines released (primary messengers)
Metabolic changes occur
↑ cAMP levels detectable (secondary messengers)
Stimulates circulating monocytes
OSTEOCLASTS
Frontal resorption
[3-5 sec]
[mins]
[hours]
[≈4 hours]
73

Prostaglandins
• In 1930s, a substance was found in the human semen
which could contract smooth muscles & cause fall in BP in
animals
• This active principle was termed ‘prostaglandin’, thinking
it was derived from prostrate.
• Bergstrom, Samuelsson and Vane got Nobel prize in 1982
for their work on PGs & Leukotreines [LTs].
• Changes in cell shape probably play a role. There is
evidence that PGs are released when cells are mechanically
deformed.…primary mediator/messenger (because they
bring messages regarding what is done by the target cell).
74

• Most cells in the body and osteoblasts in bone secrete
PGs.
• They can be called ‘local hormones’ that act locally
at the site of generation & then rapidly spontaneously
decay, or are enzymatically destroyed.
• PGs are Arachidonic acid [AA] metabolites
• AA is a polyunsaturated fatty acid present in
esterified form as a component of cell membrane
phospholipids
75

Cell membrane phospholipids
AA
Mechanical,
chemical or
physical stimuli
Cell
phospholipases
Cyclooxygenase Lipoxygenase
PGG2
PGH2
Prostacyclin
PGI2
Thromboxane A2
TXA2
PGD2 PGE2 PGF2
Platelet aggregation,
vasoconstriction
Anti-Platelet
aggregation,
vasodilatation
LTs
NSAIDs
Steroids
76

• PGE2 is an important mediator of the cellular response.
• Glucocorticoids inhibit AA formation & therefore PGs.
• NSAIDs inhibit cycloxygenase enzyme & therefore PGs.
• Several cytokines & hormones induce PGE2 secretion in
bone which in turn effects cytokine activity, stimulating
osteoclast activation (Schelling et al, 1980) & loss of
osteoblastic junctional complexes (Shen et al, 1986).
• Oppositely, PGs can stimulate bone formation.
• PGs stimulate osteoprogenitor cells to proliferate and
differentiate so that osteogenesis is increased. (Chyun &
Raisz, 1984).
77

• Of the many investigations emerged the hypothesis that
osteoblasts regulate the resorptive activities of
osteoclasts [Rodan & Martin]
• This hypothesis was based on the findings that osteoblasts
carry receptors to all hormones involved in the
maintenance of Calcium homeostasis, such as PTH,
calcitonin & Vit D3.
• Osteoblasts respond to these endocrine molecules, as well
as to locally produced agents such as growth factors, with
elevations in cAMP contents & PG synthesis.
• Thus PGs could serve as a stimulatory link or a coupling
factor between osteoblasts and osteoclasts.
78

Cytokines
• These are polypeptide products of many cells. (initially
it was thought to be produced by leukocytes only)
• These include:
1. Interleukins
2. Tumor necrosis factors
3. Colony stimulating factors
4. Growth factors
79

Interleukins
• It is synthesized by many cells including osteoblasts,
chondrocytes, etc.
• With respect to bone metabolism, cytokines with
demonstrated effects are IL-1, IL-2, IL-3, IL-6, TNF-
α and IFN-γ
• Most potent stimulator of bone resorption is IL-1
• Types: IL-1α & IL-1β
80

• Locally, IL-1 attracts leukocytes, stimulates
fibroblastic proliferation and enhances bone
resorption
• TNF & IL-1 act synergistically & simultaneously
• IL-1 & PTH act synergistically to stimulate bone
resorption
• IL-2 are associated with active osteoclasts
• Experiments have shown that PGs and IL-1 beta
levels increase within the PDL within a short time
after application of pressure.
81

Tumor necrosis factor [TNF]
• Secreted by various cells including osteoblasts
• Stimulated by other cytokines and infectious
microflora
• Types: TNF-α & TNF-β
• TNF- α is more resorptive
• They have the ability to create multinucleated cells,
such as osteoclasts, by stimulating monocytes to
proliferate and coalesce
82

Colony stimulating factors
• These include IL-3, granulocyte/macrophage colony
stimulating factors, stem cell growth factor, etc
• These help in differentiation into osteoclasts i.e. in
osteoclasts embryogenesis and not in resorption
directly
83

Growth factors
• Heterogeneous group of polypeptides:
1. Fibroblast GF [FGF] (vascularisation & fracture
repair)
2. Platelet derived GF [PDGF] (role in wound healing)
3. Insulin-like GF [IGF] (stimulate collagen &
proteoglycan synthesis)
4. Transforming GF [TGF] (inhibit osteoclast as well
as promote PGs production)
84

• Other messengers are Nitric Oxide, membrane
phospholipids, neuropeptides (e.g. Substance P),
metalloproteinases, phosphatases, vasoactive
peptides, etc.
85

• PGE₂ have an interesting property of stimulating
osteoclastic and osteoblastic activity, making it
particularly suitable as a mediator of tooth movement.
• If parathyroid hormone is injected, osteoclasts can be
induced in only a few hours, but the response is much
slower when mechanical deformation of the PDL is the
stimulus, and it can be up to 48 hrs before the first
osteoclasts appear within and adjacent to the compressed
PDL.
• Studies of cellular kinetics indicate that they arrive in two
waves; implying that some (1st wave) may be derived
from a local cell population, while others (the larger 2nd
wave) are brought in from distant areas via blood flow.
86

• These cells attack the adjacent lamina dura, removing
the bone in the process of “frontal resorption”, and
tooth movement begins thereafter.
• cAMP ,the second messenger, is important for many
important cellular functions appears after 4 hours of
applied force.
• Hence a removable appliance needs to be worn at
least 4-6 hours a day to produce tooth movement..
87

cyclic AMP
• It is the 2nd messenger as the message from the
primary messenger is handed over to it via a series of
chemical events
• It now continues the mediation of activities initiated
by primary messengers
• It is not normally present within the cell
• It is formed from its precursor ATP within the cell
only after the 1st messenger has acted
• The osteoclasts are activated by mechanical forces via
these primary & secondary messengers
88

Dilatation of blood vessels
Blood flow altered
Oxygen tension ↑
Metabolic changes
Stimulation of undifferentiated mesenchymal cells
OSTEOBLASTS
TENSION side
Deposition of organic matrix i.e. OSTEOID TISSUE
Osteoid tissue is more resistant to resorption
Later on, deposition of Calcium salts
90

• While all this is occuring, fibrous supporting
apparatus is remodelled by FIBROBLASTS.
• Ten Cate et al who studied the PDL and cranial
sutures in rats, observed that fibroblasts were
apparently engaged in synthesizing as well as
degrading collagen.
91

• With light sustained orthodontic forces, frontal
resorption and deposition at the pressure and tension
sites culminates in tooth movement beginning in
about 2 days.
• The force has to be maintained for 24 hrs for
optimum tooth movement. If stopped at 6-8 hrs,
chemical activity is cut off leading to stoppage of
cascade of events. Thus, if a removable appliance is
worn less than 4-6 hrs per day, it will produce no
orthodontic effects. Above this threshold, tooth
movement does occur.
92

Application of heavy
sustained force
93

Application of heavy sustained
force
Pressure side TENSION side
PDL tissue fluid is expressed out
PDL compressed more
Blood vessels occluded
Blood flow cut off, Oxygen tension ↓
Cell death (STERILE NECROSIS)
Cell differentiation in adjacent marrow spaces
due to blood vessels stimulation in spongiosa
Osteoclast formed in spongiosa & not against PDL
UNDERMINING RESORPTION
Hyalinisation
(1-2 days)
(3-5 days)
(3-5 sec)
(mins)
94

• When the blood vessels are totally occluded, rather
than cells within the compressed area of the PDL
being stimulated to develop into osteoclasts, a sterile
necrosis ensues within the compressed area.
• This avascular area in the PDL traditionally has been
referred to as hyalinized.
• Despite the name, the process has nothing to do with
formation of hyaline connective tissue but represents
the inevitable loss of all cells when the blood supply
is totally cut off.
97

• The name has been derived from light-microscopy,
where the tissue appears glass-like when
hematoxylin-eosin staining is used.
• In humans, it takes about 1-2 days to develop.
• Tooth is not capable of further movement until this
local tissue damage is removed & adjacent alveolar
bone is resorbed.
98

• After a period of several days, cellular elements begin
to invade the necrotic area of PDL.
• Osteoclasts appear from within the adjacent bone
marrow spaces and begin to attack the underside of
the bone adjacent to the necrotic PDL (since there are
no living cells) .
• This is termed as "undermining resorption”.
99

Phases of hyalinization
• The PDL tissue changes associated with a
hyalinization process follows a complex sequential
pattern.
1. Tissue degeneration
2. Elimination of damaged tissue; and
3. Reconstruction of the supporting tissue
101

Tissue degeneration
• Degeneration of vascular & cellular elements are 1st
signs of beginning of hyalinization
• Under Electron Microscope, one is able to recognize
degenerative changes in the endothelial cells lining
the blood vessels.
Breakdown of vessel wall
Spillage of contents i.e. compressed RBCs, blood fluid
Increased pressure in the area
Cell differentiation & phagocytosis is hampered
102

• Studies on human premolars have shown that most of
the cells in the hyalinized zone are reduced to isolated
nuclei after 2 day’s exposure to continuous force
between 70g & 120g.
103

Elimination of damaged tissue
• Elimination of hyalinized tissue occurs by two
mechanisms:
1. Resorption of alveolar bone by osteoclasts
differentiating in the peripheral intact PDL and in
adjacent marrow spaces
2. Invasion of cells & blood vessels from the periphery
of the compressed zone by which the necrotic tissue
is removed
104

Hyalanized area
Slow cellular invasion
Penetration of cells through hyalinized area is by pushing
cellular extensions
Collagenolytic enzymes released
Collagen breakdown
Phagocytosis
105

Reconstruction of the supporting
tissue
• Reconstruction of fibrous apparatus gradually occurs
following elimination of hyalinized remains.
• New collagen fibrils are produced & attached to
cementum & alveolar bone.
• Hyalinized zones seen during treatment with modern
orthodontic appliances & moderate forces are usually
small [1mm-1½ mm in diameter] & do not last
beyond 3 weeks.
106

• Hyalinization & undermining resorption delay the
tooth movement.
• First delay is caused due the differential stimulus of
cells in the marrow spaces.
• Second delay is caused due to the fact that a
considerable amount of bone needs to be removed to
cause tooth movement.
• Tooth movement progresses more smoothly when the
applied force is light.
107

PDL following hyalinization
• When compared with PDL before tooth movement
started, posthyalinized area is wider, richer in cells
& with increased blood circulation.
• If original orthodontic force is not reactivated, PDL
will soon adopt previous appearance & width.
• If force is reactivated, alveolar bone wall toward
which tooth is moving will probably undergo direct
resorption.
108

Dilatation of blood vessels
Blood flow altered
Oxygen tension ↑
Metabolic changes
Stimulation of undifferentiated mesenchymal cells
OSTEOBLASTS
TENSION side
Deposition of organic matrix i.e. OSTEOID TISSUE
Stretching of PDL
109

• The tooth is not able to move unless the hyalinised area
is removed along with the adjoining alveolar bone
resorbed. Within 2-3 weeks this hyalinised area is
removed.
• With heavy forces, tooth movement occurs within 7-14
days.
• At this time, if original force is reactivated, PDL will
soon adopt its original appearance and width. However,
if force is reactivated, the alveolar wall towards which
the tooth is moving will probably undergo direct
resorption.
110

• Role of periodontal ligament in tooth movement.
• Role of periodontal ligament in eruption and
stabilisation of teeth.
• Bioelectric theory (piezoelectric current).
• Theories of tooth eruption.
• Migration or drift of teeth.
• Pressure tension theory.
• Role of PGs.
• Resorption : Frontal and undermining
111

Histomorphology of
tooth movement
112

• Reitan studied paradental tissues of animals subjected
to orthodontic forces.
• He concluded that PDL cells in sites of tension
proliferate, and that newly formed osteoid in these
areas resorb slowly when subjected to pressure.
113

• Storey conducted a series of experiments in rodents
and used a range of force magnitudes that could be
termed optimal.
• Near teeth treated with such a force, newly formed
bone appeared more mature, while heavy forces were
associated with the formation of a highly cellular,
poorly calcified matrix.
• Heavy forces caused periodontal necrosis and other
destructive changes in the PDL.
114

• Based on these observations, Storey, concluded that
the process of tooth translation through bone consists
of three different phenomena:
bioelastic, bioplastic, and biodisruptive.
• The PDL and alveolar bone, due to their fluid-fiber
composition, can be deformed elastically by external
stresses, which also evoke cellular activities.
• When the tissue elastic limit is reached, it starts to
deform plastically, with adaptive proliferative and
remodeling reactions.
115

• Prolonged forces that exceed the bioplastic limit
result in biodisruptive deformation, with ischemia,
cell death, inflammation, and repair.
• Clinically speaking, Storey asserted that light forces
within the bioplastic range would cause slow tooth
movement, while optimal forces that cause teeth to
move faster are within the boundaries of the
biodisruptive range.
• He concluded that within the optimum range, tooth
movement is rapid, but the quality of remodeling
bone is poor, increasing the potential for relapse, once
external force application ceases.
116

Effects of force distribution &
types of tooth movement
117

• Types of tooth movement:
• Tipping
• Translation
• Root uprighting
• Rotation
• Extrusion
• Intrusion
118

• Tipping is the simplest tooth movement.
• The tooth rotates around the center of resistance.
• During tipping one half of the PDL area could be
loaded, also pressure is high in two areas where it is
concentrated in relation to the applied force.
119

• If two forces are applied simultaneously to the crown
& the tooth, the tooth translates.
• In this case the entire PDL area is uniformly loaded.
• Twice as much force is required for translation than
required in tipping a tooth.
121

• Extrusive movements ideally would produce no areas
of PDL compression, only tension areas.
• Extrusive forces should be of the same magnitude of
tipping so that the whole tooth can come down with
the alveolar bone.
• Very light forces are required for intrusion as the
force is concentrated only at the apex.
123

• Animal experiments suggests that only after force is
maintained for approximately 4 hours, the cyclic
nucleotides levels increase in the PDL.
• Fixed appliances produce more efficient tooth
movement due to their constant force application
rather than the removable appliance which should be
worn by the patient at all times.
126

Effects of force duration &
force decay
127

• Decay of force or a decrease in the magnitude of
force is a characteristic of any appliance.
• Orthodontic force duration can be classified as:
1. Continuous force
2. Interrupted force
3. Intermittent force
128

Continuous force
• Leads to gradual compression of PDL on the pressure
side of tooth
• If force is within limits, reconstructional changes of
fibrous element & direct resorption of alveolar bone
occur
• If force is unnecessarily reactivated, vascular supply
is easily compromised and results in “damage-repair”
effect
• E.g. ideal spring in lab only
129

Interrupted force
• The continuous force that is applied to the tooth is
effective over only a small amount of tooth
movement, after which it stops and needs to be
reactivated
• Even if hyalinized zones are established, the PDL has
the time to become reconstructed
• There is an increase in cell proliferation which is
suitable for further tissue changes following
reactivation of force
• Seen in fixed appliances
130

Intermittent force
• Affects the tooth periodically or over a time when
many interruptions of the force occur
• Patient operated appliances like elastics, head gears,
removable plates
• On pressure side, circulation not easily hindered or
disturbed unless very high force is applied
• Increase in cell number & direct bone resorption
along alveolar bone are characteristic.
131

• Considering all these forces, we can believe that if the
force is light & continuous, a smooth progression of
tooth movement occurs due to frontal resorption.
• In case of heavy forces, the tooth movement will
delay till the undermining resorption can remove the
bone.
133

Effect of hormones on tooth
movement
134

• Parathyroid hormone:
↓ Serum Ca⁺⁺
PTH secretion
Multinucleated osteoclasts respond to PTH by activating
dormant osteoclasts or by developing new osteoclasts
Bone resorption
↑ Serum Ca⁺⁺
135

• PTH binds to cell membrane receptors on
osteoprogenitor cells, osteoblasts & osteocytes to
increase metabolism, osteolytic activity, release
ostoclastic activating factors like PGs
136

• Calcitonin
↑ Serum Ca⁺⁺
Calcitonin secretion by parafollicular cells of thyroid
Binds to osteoclastic cell receptors
Osteoclasts reduce size & shape of ruffled borders & inhibit
cell adhesion thus increasing motility
↓ Osteoclasts on bone surface
↓ bone resorption
137

• Vitamin D3
Potent stimulator of bone resorption by increasing
number of osteoclasts, increase size of ruffled
border, lysosomal enzymes, intestinal absorption of
Ca⁺⁺ ----↑ Serum Ca⁺⁺
• Glucocorticoids
↓ intestinal absorption of Ca⁺⁺
↓ Serum Ca⁺⁺
PTH secretion
↓ Bone mass
138

• Sex hormones
Estrogens, progestins and androgens all have stimulatory
effect on osteoblasts
• Thyroid hormones
Increase bone growth and development, stimulate
osteoprogenitor cells to proliferate & differentiate into
osteoblasts
However, thyroid hormone therapy & hyperthyroidism
leads to bone resorption
139

Drug effects on the response to
orthodontics force
140

141
• At present, drugs that effects the tooth
movement are right now not available, but
efforts produce them is going on.
• A major problem is how they would be
applied to the local area where an effect on
tooth movement is required.

• Tooth movement stimulation:
o Vit D administration can enhance tooth movement
o Direct injection of PGs into PDL can increase tooth
movement but is quite painful
• Relaxin a pregnancy hormone that facilitates birth by
causing a softening and lightening of the cervix and
pubic symphysis is suppose to stimulate the tooth
movement by reducing collagen synthesis and
increasing collagen breakdown.
• It seems that at some point in future, drugs to facilitate
tooth movement will be available—but there is no way
to know how long it will take to develop them.
142

• Tooth movement inhibition:
o Biphosphonates e.g. alendronate, risendronate used
in treatment of osteoporosis [are taken up by active
osteoclasts, precipitates at the ruffled border, prevents
enzymatic release, thus inhibits tooth movement]
o NSAIDs(inhibit conversion of AA to PGs) & Steroids
(inhibit production of AA): inhibit PG synthesis, thus,
inhibit primary mediators
o Common analgesics like ibuprofen, paracetamol have
little or no effect; centrally acting acetaminophen too
have no effect; potent ones like indomethacin can
inhibit tooth movement
143

• Other agents that have
agonist/antagonist effects on PGs:
o Tricyclic antidepressants (doxepin, amitriptyline,
imipramine)
o Antiarrhythmic agents (procaine)
o Antimalarials (quinine, quinindine, chloroquine)
o Methylxanthines
o Anticonvulsants (phenytoin)
o Tetracyclines (doxycycline)
144

• Histomorphology of tooth movement
• Effects of force distribution and Types of tooth
movements.
• Effects of force duration and decay.
• Effects of hormones on tooth movement.
• Effects of drugs on tooth movement.
145

Effect of Local Injury: Corticotomy and
Accelerated Tooth Movement.
• Remodeling of alveolar bone is the key
component of Orthodontic tooth movement
and bone remodeling is accelerated during
wound healing.
• The idea that teeth could be moved faster
after local injury to the alveolar process first
given by the pioneer American Oral Surgeon
Hullihan in late nineteenth century.
146

147
• The Idea was not adopted for several reason, like
concerns about infection and bone loss in that pre-
antibiotic era.
• In mid-century , the German surgeon Kole revived
the idea that cut between the tooth could faster the
tooth movement.
• This idea is presented again in 1978 by Gunderson et
al but it was viewed as unnecessarily invasive and
was not widely accepted.
• It was again presented in late 1990s and has
achieved some acceptance as its mechanism has
better understood.

Modified dento-alveolar Distraction
Osteogenesis for rapid tooth movement
• The process of conventional tooth movement
takes certain amount of time and it usually
lasts for 1 to 2 years.
• Preservation of anchorage is another major
concern to orthodontists which is critical to
ensure predictable and successful treatment.
148

With the advent of dental distraction osteogenesis the
two above concerned are eased off because.
1. Dental distraction is completed in three
weeks.
2. There is minimal loss of anchorage.
Dental distraction can be of two types.
1. Periodontal distraction.
2. Alveolar bone distraction.
149

Surgical technique.
• After giving LA and elevation of flap.
• With a round carbide bur buccal cortical holes
are made both mesial and distal to canine and
are continued 2 to 3mm beyond the root apex
of the canine, and they are joined together.
• In the next step the first premolar is extracted
and buccal bone is removed up to the second
premolar with the large round burs.
150

Disadvantage.
• Invasive procedure as lots of bone has to be
trimmed leading to post operative swelling
and discomfort.
• In order to reduce this post operative
discomfort some modifications are made in
the surgical procedure
151

Modified surgical technique for dento-
alveolar distraction.
• They have modified the above technique to
overcome the shortcomings of conventional
method.
• After making canines as bone transport
segment similar buccal cortical holes were
made mesial and distal to first premolar and
the holes are connected and premolar is
extracted so the buccal cortical plate came
along with the extracted premolar.
152

Biological principles of distraction
osteogenesis.
• Based on clinical experience lizarov discovered
two biological principles, “Lizarov effects”:
1. Tension-stress effect on the growth and genesis
of the tissues. This suggested that when two
bone plates are separated, there is pressure
acting on one side and tension on the other side
of the device in situ. Due to physiological
changes osteoblasts are stimulated to grow thus
helping in new bone formation.
2. The influence of blood supply and loading on
the shape of bones and joints.
153

Distraction osteogenesis consists of
five sequential periods.
• Osteotomy
• Latency
• Distraction
• Consolidation
• Remodelling
154

Osteotomy
• Osteotomy is the surgical separation of bone
into two segments. Osteotomy causes loss of
mechanical integrity, triggering fracture
healing, which involves recruitment of
osteoprogenitor cells, followed by cellular
modulation(osteoinduction) and
establishment of environment template
(osteoconduction).
155

Remodelling
• It is the time after the removal of the
distraction device.
• Although this period usually continues for
approximately 1 year after the completion of
distraction, remodelling of the newly formed
bone begins at the completion of distraction
and continues throughout the consolidation
period.
156

Histological aspect of distraction osteogenesis
• The effect of osteodistraction on bone
Latency phase
The latency phase allows for the initial trauma
response to take place. Following osteotomy a
hematoma is formed that encircles the
osteotomised bone segments. Granulation tissue
that consist of soft tissue cells, neutrophils and
invading capillaries replace the hematoma after
several days this tissue transform into soft
callous.
157

Distraction phase
• During distraction phase, tensile forces are
applied to the callous with a specific rate and
rhythm.
• Callous is stretched and, a central fibrous zone
called fibrous interzone forms. It is rich in
chondrocyte like cells, fibroblasts and oval cells .
• The differentiating osteoblasts and fibrous
interzone deposit osteoid along collagen bundles.
• They undergo mineral crystallization parallel to
the collagen bundles.
158

Consolidation phase.
• Once the desired bone length is achieved,
distraction ceases.
• Consolidation phase begins, where bone and
extensive amount of osteoid undergo
mineralization and eventual remodelling.
159

The effect of osteodistraction on
gingiva.
• Distraction forces applied to bone also create
tension in the surrounding tissues, initiating a
sequence of adaptive changes termed as
Distraction histogenesis.
• Under the influence of tensional stress produced
by gradual distraction, active histogenesis has
been reported in various soft tissues surrounding
the distracted bony segments.
• The primary mechanism by which gingiva
undergoes adaptation during osteodistraction is
by neohistogenesis.
160

Bone morphogenic proteins (BMPs).
• They play an important role in signalling
pathways that link the mechanical forces
created by distraction to biological responses.
They accelerate and differentiate the
precursor cells into chondrogenic osteogenic
cells.
161

Transforming Growth factor Beta (TGF-β)
• They suppresses osteoblast maturation by
delaying differentiation of osteoblasts during
the mineralization stage of distraction
osteogenesis.
162

Interleukin-1, Interleukin-6 (IL-1,IL-6)
• They have been hypothesized to contribute to
intramembranous ossification, by enhancing
the differentiation of cells committed to
osteoblastic lineage.
163

Insulin-like growth factors (IGF-1) and
Basic Fibroblast growth Factor (bFGF)
• They account for osteoblast proliferation and
formation from precursor mesenchymal cells
in the distracted area.
Vascular Endothelial Growth Factor (VEGF).
• They induces neoangiogenesis during
distraction osteogenesis.
164

165
• The surgery was conceptualized as creating blocks of bone around the teeth that
could be repositioned without depending on remodeling created by the PDL
responses .
• An orthodontic appliance placed before surgery was activated using relatively stiff
archwire.
• The method therefore would be considered as variation of distraction osteogenesis
from current perspective.

166
• Recently, rapid tooth movement after Corticotomy has come
to be viewed as a demineralization/remineralization
phenomenon.
• That produces regional acceleration of bone remodeling that
allows faster tooth movement, rather than movement of
blocks of bone that contains a tooth.
• Now light forces are used to move the teeth physiologically
while taking the advantage of more widespread remodeling of
alveolar bone.
• This is known as “Accelerated osteogenic Orthodontics” AOO
or Wilkodontics.

Treatment outcomes in corticotomy assisted
tooth movement.
• In order to evaluate corticotomy assisted
tooth movement an analysis of benefit versus
cost and risk is needed.
• The primary benefit claimed is reduction in
treatment time, with facilitation of arch
expansion via AOO as a secondary benefit.
168

169
• After a fracture, bone healing takes about 6
weeks, 2 months of stabilization is
recommended and mature bone in the bone
regenerate area is seen after 4 months.
• So one would expect that bone remodelling
after corticotomy could be accelerated for 2
to 4 months.
• Alignment is the first phase of comprehensive
orthodontic treatment.

170
• Its duration depends on the extent of crowding ,
• But even severe crowding rarely requires more
than 5 months with super elastic arch wires.
• If corticotomy reduced that to 1 month, the 4
month reduction in total treatment time would
represent about 20%of the typical treatment of 18
to 21 months. Can such a greater reduction
possible if so what is the mechanism.
• Does the corticotomy reduces treatment time for
tooth movement other than alignment.

171
• What about intrusion which requires remodelling of denser
bone that lies beneath the tooth roots and requires several
months.
• The rate of intrusion is 1mm per month.
• One recent paper which is a case report, reported that after
an osteotomy beneath the incisors and application of AOO in
conjunction with skeletal anchorage still took several months
to obtain the desired intrusion.
• In cost and risk side of the evaluation include,
• All aspects of the burden of treatment .
• In addition economic cost of the surgery.

Modified corticotomy.
• Since the Corticotomy/AOO is quite extensive
surgery.
• This has lead to modifications of the
corticotomy technique .
• It typically involves incision in interproximal
gingiva without reflecting a flap, and less
extensive cuts in the bone.
172

Other proposed approaches to the
faster tooth movement.
• Three other methods to accelerate the tooth
movement have been proposed quite
recently.
1. Vibration of the teeth.
2. Application of therapeutic ultrasound to the
teeth and alveolar bone.
3. Application of light to the alveolar bone.
174

175
Device-assisted treatment Another approach in accelerating
tooth movement is by using device-assisted therapy . This
technique includes direct electric currents, pulsed
electromagnetic field, static magnetic field, resonance
vibration, and low level laser which was mostly investigated
and gave the most promising results. The concept of using
physical approaches came from the idea that applying
orthodontic forces causes bone bending (bone bending
theory) and bioelectrical potential develops. The concave
site will be negatively charged attracting osteoblasts and
the convex site will be positively charged attracting
osteoclasts as detected by Zengo in his measurements on
dog alveolar bone.

176
The bioelectrical potential is created when there is
application of discontinuous forces, which leads to
the idea of trying cyclic forces and vibrations. It has
been found that applying vibrations for different
duration per day accelerated tooth movements
between 15% and 30% in animal experiments

177
Cyclical force device effect on tooth movement We have also
used this concept by using the cyclical force device with
patients and achieved 2 to 3 mm/month of tooth movement.
The vibration rate was 20 to 30 Hz and used for 20 min/day.
Further results needed to be investigated to clearly identify
the range of Hertz that can be used in these experiments to
get the maximum desired results.

179
Low-level laser therapy Photobiomodulation or low level
laser therapy (LLLT) is one of the most promising approaches
today. Laser has a biostimulatory effect on bone regeneration,
which has been shown in the midpalatal suture during rapid
palatal expansion , and also stimulates bone regeneration
after bone fractures and extraction site . It has been found
that laser light stimulates the proliferation of osteoclast,
osteoblast, and fibroblasts, and thereby affects bone
remodeling and accelerates tooth movement.

181
Direct electric current effect on tooth movement Another
approach is to use direct electric current. This technique was
tested only on animals by applying direct current to the
anode at the pressure sites and cathode at the tension sites
(by 7 V), thus, generating local responses and acceleration of
bone remodeling as shown by group of investigators . Their
studies were more successful than the previous attempts
because electrodes were placed as close as possible to the
moving tooth. The bulkiness of the devices and the source of
electricity made it difficult to be tested clinically

Effect of tooth movement on
other dental tissues
182

• Pulp:
-mild forces cause hyperemia of pulp tissue
-sometimes sensitivity to thermal changes after
adjustments of appliances
-severe forces can lead to partial or total pulp
degeneration
-usually in case of mild to moderate forces, pulp
reaction returns to normal after completion of
orthodontic therapy
183

• Cementum:
-when orthodontic forces are applied, cemental
surface may be perforated and semilunar resorption
areas appear
-if forces are intermittent or after completion of
treatment cementoblasts appear and usually fill the
resorption bays
184

• Dentine:
-with severe pressures, a breakthrough of the
cementoid layer occurs followed by dentine
resorption in some cases
-if dentine resorption is less then it gets filled in by
cementum-like substance produced by cementoblastic
repair
185

• Enamel:
-no tissue changes are observed in enamel as a result
of tooth movement per se
-decalcification around bands as a result of debris not
removed and an etching of the enamel rods may be
seen by naked eye
186

• Mobility:
- combination of wider PDL space & somewhat
disorganized PDL means that some increase in
mobility is observed in every patient
- heavier the force more is the mobility
- if excessive mobility develops all forces should be
discontinued & the tooth should be taken out of
occlusion until mobility reduces
187

• Pain:
• If heavy pressure is applied to a tooth, pain develops
due to crushing of PDL
• There is no excuse for using force levels that produce
such pain immediately
• If appropriate force levels are used, the patient feels
little or no pain
188

• Several hours later mild aching sensation appears,
and the teeth are sensitive to pressure, so biting hurts
• This pain typically lasts for 2-4 days, then disappears
until appliance is reactivated
• If light forces are being used, this pain can be
decreased by having the patients engage in repetitive
chewing (sugarless gum) during first 8 hrs after
appliance activation
189

Advances in biology of tooth
movement.
• Osteoblasts which are lining the bony socket are now
believed to be directly responsive to the strain such
as orthodontic force.
• one of the proteins in the membrane of osteoblast is
the integrin, it translate mechanical strain into a
signal which in turn stimulates a gene to make the
cell develop ligans. Ligans allow intracellular
communication, which stimulates undermining
resorption allowing orthodontic tooth movement.
190

191
• The second type of cells are osteocytes.
• They were histologically thought to be trapped
osteoblasts in the matrix and whose function was
considered to provide support and sustenance to
the bone.
• It has been demonstrated that an intermittent
force within physiologic limits has an effect in
increasing the expressions of glucose-6-phosphate
dehydrogenase , 3H-uridine, c-fos, and insulin like
growth factor in the osteocytes within six hours
after intermittent loading at physiological strain
magnitude.

192
• The third type of cells are osteoclasts which
differentiate from monocyte-haemopoetic cells.
Active osteoclasts exhibit high content of a specific
chemical marker, tartrate resistant acid phosphatase
(TRAP), which participates in signalling active bone
resorption.
• Many chemical mediators of macrophage family are
known to influence osteoclast differentiation, they
are cytokines (e.g. : tumour necrosis factor TNF
interlukin-1 alpha, 6-alpha), certain growth factor,
(macrophage colony stimulating factor, and
prostaglandins.

193
• Apart from above there is osteoprogenitor cells and
bonelining cells.
• Osteoprogenitor cells are mesenchymal, fibroblast
like cells, regarded to form a stem cell population to
generate osteoblasts.
• They are situated in the vicinity of blood vessels of
PDL.
• Bone lining cells are the undifferentiated flattened
cells lining the bone surface.

194
• In essence, bone remodelling is orchestrated
by cells of osteoblast linage and involves a
complex network of cell to cell and cell to
matrix interactions involving systemic
hormones, locally producing cytokines,
growth factors, many of which are
sequestrated within the bone matrix, as well
as the mechanical environment of cells.

195
• Comparison of CT examinations permits three-
dimensional evaluation of osteoclastic and
osteoblastic periodontal remodelling .
• The picture showed orthodontically induced bone
dehiscence that was partly repaired by osteoblastic
periodontal remodelling in the retention period.

Role of prostaglandins in OTM
• PGs are synthesized from fatty acids by a Microsomal
enzyme complex (PG synthetase) found in all
mammalian tissues.
• Prostaglandins acts as one of the mediators of
inflammation cause an increase in intracellular C
AMP and calcium accumulation by Monocytic cells,
which then modulates and activates osteoclastic
activity.
• Studies indicates that Prostaglandins increase the
number of osteoclasts as well as stimulate
osteoblastic cell differentiation and new bone
formation.
196

Cytokines and growth factors in OTM
• The early phase of OTM involves an acute
inflammatory response characterized by
periodontal vasodilatation and migration of
leukocytes out of PDL capillaries.
• Cytokines secreted by leukocytes may interact
directly with bone cells or indirectly, via
neighbouring cells, such as monocytes /
macrophages etc.
• Cytokines have multiple activities, which include
bone remodelling , bone resorption and new
bone deposition.
197

Detection of mechanical strain by bone cells.
• OTM involves application of forces and
moments from wires through brackets to
teeth, with a goal of repositioning them in
dental arches.
• The system of forces and movements is
applied to the tooth which is a rigid body. The
PDL and alveolar bone houses the teeth.
• After application of Orthodontic force, the
initial step is the detection mechanical strain.
198

199
• Three theories have been suggested on how these
cells sense mechanical strains and how then the
stimuli are passed into the cell and from one cell to
another.
a) Strain released potentials
b)Activation of ion channels
c) Extracellular matrix and cytoskeleton
reorganization.

1) Strain released potentials
• Application of small bending forces is known
to produce flow of interstitial fluid through
the canalicular network, generating streaming
potentials.
• The in vitro and in vivo experiments of Crown
et al indicates that osteocytes are more
sensitive to mechanical stress than osteoblasts
which in turn are more sensitive than
fibroblasts.
200

201
• In vivo studies conducted in Amsterdam Dept. of
Oral cell Biology, Academic centre for dentistry
indicates that application of forces to bone results
in several potential stimuli to bone cell function,
including time dependent changes, hydrostatic
pressure, direct cell strain, fluid flow induced
shear stress and electric fields resulting from
electrokinetic effects accompanying fluid flow.
• These events effects osteocytes, which are
mechanosensor cells of bone these in turn,
activates osteoblasts or osteoclasts to produce
adaptive bone remodelling.

2) Activation of ion channels.
• Ion channels are tunnel shaped proteins that
cross the width of cell membrane, and serve
as selective conductive pathways for ions that
cross the membrane as well as membranes
surrounding intracellular organelles.
• Ion channels are divided into two groups,
depending upon types of stimulus needed to
activate the channel.
202

203
• They are voltage gated ligand gated and mechanosensitive
(stretch) ion channels.
• The voltage gated channels have channel proteins that
undergo conformational changes in response to changes in
transmembrane potential.
• Ligand gated channels responds to specific ligands that may
attach to the cell membrane near channel opening.
• Stretch ion channels react to structural perturbations.
• The stretch ion channels, response (gated in an open or
closed positions) to mechanical stimuli are relevant to OTM.

204
• The stretch activated ion channels allow passage of
cat ions i.e. calcium and potassium .
• Continuous mechanical load similar to an
orthodontic force affects the mechanosensitive ion
channels of osteoblastic cells in culture, thereby
producing large increase in intracellular calcium.

3) Extra cellular Matrix and Cytoskeleton
Reorganization
• The principle elements of ECM of either PDL
or the bone may be considered as collagen
fibrous network embedded in, and interacting
with a non collagenous matrix consisting of
proteoglycans and various glycoproteins.
• The macromolecules, which make up the ECM
are collagen and glycose amino glycans.
• They are secreted at local levels by fibroblasts
in PDL and osteoblasts in the bone.
205

206
• The growth and repair of connective tissue is a
delicately balanced process of ECM removal and
replacement with significant control by Matrix
megaloproteins and primary natural inhibitors or
Tissue inhibitors of metalloproteinases (TIMPS).
• Cytoskeletons represents a framework attaching cell
to cell or cell to extracellular matrix, thereby
presenting a possibility of transducing mechanical
forces acting on the cells or on their adjacent
matrices.

Clinical application of knowledge of histological aspects of OTM
• Enhancing rate of tooth movement pharmaco-
therapeutically or electro physiologically or
genetically would be an ultimate goal for all present
day researchers.
• But till now only two human studies have been
reported one by yamasaki et al, wherein a total of
40µg of PGE1, was injected in the vestibular region at
the upper right canine area during orthodontic tooth
movement. The result showed almost twice faster
tooth movement.
207

• The other study was reported by Anand K. Patil, S.D.
Gaitonde et al. this was the second human trial till
date.
• They injected, 1µg/ml PGE2 along with lignocaine as
vehicle was injected in vestibular region on the right
side of the upper quadrant in 14 patients during
separate canine retraction stage on the 1st, 3rd , 6th
day. After the 60 days the result showed 1 ½ time
more tooth movement.
208

209
• The other experimental studies have been conducted
mainly in animals.
• It shows increased tendency of root resorption with
exogenous application of PGs.
• The tendency of root resorption is dose dependent.
• As the PG dose increases root resorption tendency also
increases.
• J. leiker has suggested application of minimal dosage of PGs
(1-3µg) in animal experiments during orthodontic tooth
movement.

210
• The dis advantage of local injection PG is pain
and root resorption and leakage of drug at the
site and anchor loss.
• A study reported by Massound Seifi et al shows
injection of PGE2 supplemented orally with
calcium in rats shows no tendency of root
resorption.
• Ali Raza Shekhawat et al have reported injection
of stable PGE1 analogue such as misoprostol in
rats have shown faster tooth movement with
minimal tooth resorption.

211
• Other ways of modifying OTM include injection of Vit.D
metabolites as reported by Takano-Yamamoto et al in 1992.
• Selin Kale et al 2004 reported comparison of effect of 1, 25
dihydrocalciferol (biologically active form Vit.D) and PGE2 on
OTM.
• In this rat experimental study both of the above enhanced
the enhanced the amount of tooth movement significantly.
• The number of osteoblasts on the external surface of
alveolar bone on the pressure side was significantly greater
in 1, 25 DHCC group than PGE2 group.
• They have suggested that 1, 25 DHCC more effective in
modulating bone turnover during OTM, because of its
effect on formation and resorption is well balanced.

212
• Application of steroid therapy in the rats reported by Colin
et al suggests that steroid treatment reduces clastic activity.
• Injection of parathyroid hormone in experimental tooth
movement in rats by soma et al showed increase in clastic
activity.
• An injection of L-arginine (nitric oxide precursor) in
experimental tooth movements shows that increase in nitric
oxide production increases bone remodelling and

• In the mid-18th century, John Hunter explained that
orthodontic tooth movement is an outcome of the
habit of the bone “to move out of the way of
pressure”
• In recent years, extensive investigations have
confirmed that physical and chemical alterations
occur concomitantly in the paradental tissues,
resulting in cellular activities that culminate in tissue
remodeling and tooth movement
214

References
1. Proffit, WR. Contemporary Orthodontics.
2. Moyers, RE. Handbook of Orthodontics, 3rd ed. Force systems
and tissue responses to forces in orthodontics and facial
orthopedics.
3. Graber, TM. Orthodontics Principles & Practice.
4. Dixon, AD. Fundamentals of craniofacial growth.
5. Davidovitch, Z. Tooth Movement. Critical Reviews in Oral
Biology and Medicine, 2(4):411-450 (1991).
6. Norton, L. The biology of tooth movement.
7. Robbins. Textbook of General Pathology
8. Anad K Patil, V.P. Jayde. Advances in Biology of tooth
movement- A Review.
9. Mahajan et al. journal of regenerative medicine and tissue
engineering 2013. 216

217
10. Nimeri et al. Progress in Orthodontics 2013, 14:42

Biology of tooth movement

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