Bone Changes During Orthodontic Tooth Movement

BONE CHANGES DURINGBONE CHANGES DURING
ORTHODONTIC TOOTHORTHODONTIC TOOTH
MOVEMENTMOVEMENT
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 Bone is a specialized mineralized connective tissue made upBone is a specialized mineralized connective tissue made up
of an organic matrix of collagen fibrils embedded in anof an organic matrix of collagen fibrils embedded in an
amorphous substance with mineral crystals precipitatedamorphous substance with mineral crystals precipitated
within the matrix.within the matrix.
The main functions of bone are two fold.
Function of Support
Reservoir Function

Classification of bone
Based on Structure.
Compact Bone or cortical bone - the
dense outer shell of the skeleton.
Cancellous Bone or trabecular bone -
comprises of a system of plates, rods,
arches and struts traversing the medullary
cavity encased within the shell of compact
bone.
Based on development
Intramembranous bone – Eg.,
Bones of cranial vault, maxilla,
etc.
Intracartilagenous bone – Eg.,
Vertebra, ribs, base of the skull,
etc

Based on the arrangement of the collagenous matrix.
Immature Bone : is subdivided into :
Woven Bone : Relatively weak ,disorganized and poorly
mineralized. The first bone formed in response to orthodontic
loading usually is the woven type.
Bundle bone
Bundle bone is a functional adaptation of lamellar structure
to allow attachment of Sharpey's fibers
Mature Bone or Lamellar bone
Lamellar bone a strong, highly organized, well-mineralized
tissue. Adult human bone is almost entirely of the remodeled
variety: secondary osteons and spongiosa..

W – Woven Bone L – Lamellar Bone

HISTOLOGY OF BONE

Periosteum
Compact Bone
Circumferential lamellae
Concentric lamellae
Interstitial lamellae
Bony trabeculae
Bone Marrow
HISTOLOGY OF BONE

CELLS OF THE BONE
Any cell that forms bone.
Differentiation of Osteoblasts
Mesenchymal stem cells differentiate into osteoblasts when
they are exposed to bone morphogenic proteins (BMP). Cbfa1 is
necessary for osteoblast differentiation.
Osteoblast

Osteoblast

RECEPTOR ACTIVATION
In the nucleus, different second messengers account for immediate early
gene (IEG) expression.. The transcription of the IEGs (c-fos, c-jun, and
egr-1) has been shown to increase when cells are exposed to
cytokines, growth factors, or mechanical stimulation. Protein products
from the c-fos and c-jun genes form activator protein1 (AP1) which
regulates osteoblast differentiation.
Functions of osteoblasts
production of the proteins of bone matrix type I and IV collagen and other
non collagenous proteins
Osteoblasts secrete the growth factors.
Osteoblasts mineralize newly formed bone matrix.
Osteoblast may be required for normal bone resorption to occur.
Functional lifespan of osteoblasts may range from 3 – 4 months to 15 years

Lining Cells
Lining Cells are remnants of
osteoblasts that previously laid down
bone matrix, forming a bone
membrane that controls ion fluxes into
and out of bone.
Osteocytes
As osteoblasts secrete bone matrix,
some of them become entrapped in
lacunae and are then called
osteocytes.

Osteoclasts
Osteoclasts are multi nucleated giant cells which resorb bone.
They occupy shallow pits called ‘Howship’s lacunae’ on flat bone surfaces.
Positive staining for tartarate - resistant acid phosphatase.
The part of an osteoclast that is directly responsible for carrying out bone
resorption is a transitory and highly motile structure called its ruffled border
Their lifespan is uncertain, though it may be as long as 7 weeks.

Origin and Cell Lineage

Differentiation of Osteoclasts
•The molecule that inhibits osteoclastogenesis is OPG (osteopotegerin)
and OCIF (osteoclastogenesis inhibiting factor).OPG is secreted by
osteoblasts and blocks the formation of osteoclasts
•Osteoclast differentiation factor (ODF) or OPG-L was able to induce
osteoclastogenesis.
•The ratio of OPG/OPG-L regulates the osteoclast' s lifecycle
•Cytokines TNF, interleukin-1 [IL-1 ], prostoglandin E2 [PGE2] and
growth factors (TGF-B, BMP) are upstream signals which regulate
the OPG/ OPG-L ratio.
•When the balance favors OPG, there are fewer active osteoclasts;
when the balance favors OPG-L, there is an increased number of
active osteoclasts.
RECEPTOR ACTIVATION
Osteoclasts also express integrin receptors including the vitronectin
receptor which leads to adhesion of osteoclasts to bone surface.
Peptides containing the RGD motif have been shown to inhibit oste-
oclast-mediated bone resorption

Structural composition of bone

Organic Matrix
Organic matrix consists of 90% of collagen and remaining 10% is
composed of other non-collagenous molecules.
Bone Collagen
Collagen is defined as a molecule composed of three polypeptide chains
termed α chains which associate into a triple helical molecule.
Bone consists predominantly of type I collagen with traces of type III, V &
XI collagen.
Non-collagenous proteins
Proteoglycan & Glycoproteins
Osteonectins
RGD containing proteins (Arg – Gly – ASP) Fibronectin, Thrombospondin,
Osteopontin, Bone Sialo Protein.
Fibronectin
Thrombospondin
Osteopontin
Bone sialo protein
Bone acidic glycoprotein (B A G)
Osteocalcin & Matrix Gla Protein
Growth Factors
Inorganic Component
calcium hydroxy apatite - Ca10(PO4)6(OH)2www.indiandentalacademy.comwww.indiandentalacademy.com

ORTHODONTIC TOOTH MOVEMENT
PEIZOELECTRIC THEORY
Bone responds to an applied strain. Strain represents a change in length.
Application of small bending forces result in compression on one side and
tension on the opposite side. This produces a flow of interstitial fluid,
through the canalicular network, generating streaming potentials.
Because of the negative charge of proteoglycans, there is an excess of
positive mobile ions in the fluid.
Charges are symmetrically arranged so that no net macroscopic electric field
is present.
Compression of bone produces streaming potentials by the displacement of
mobile ions relative to charged proteoglycans en-trapped by collagen.
Fluid movement over the cell surface may directly stimulate bone cells
because it generates shear stress.

ORTHODONTIC TOOTH MOVEMENT AS RELATED TO BONE
DEFORMATION
BIOELECTRICITY: First suggested by Farrar (1888)
Piezoelectricity is a phenomenon observed in many crystalline materials in
which deformations of the crystalline materials results in the flow of electric
currents. Collagen itself is piezoelectric.
A quick decay rate
The production of an equivalent
signal, opposite in direction, when
the force is released.
Piezoelectricity signals have two
unusual characteristics:

Zengo et al (1973-74) showed that bending of bone may create negative
fields occurring in the concave aspects of the bone surface leading to bone
deposition and positive fields occuring on the convex bone surface leading
to bone resorption
Baumrind and Buck et al suggested that the major physiologic and
mechanical changes might occur not in the periodontal ligament but
rather in the alveolar bone.
A second type of endogenous electric signal, which is called the “bioelectric
potential” can be observed in bone that is not being stressed.
Electronegative charges are observed in areas of metabolically active bone
or connective tissue where bone growth or remodeling is occurring.
Inactive cells and areas are nearly electrically neutral.
The purpose of this bioelectric potential is not yet known.
Davidovitch showed that modifying the bioelectric potential, a
tooth moves faster than its control.www.indiandentalacademy.comwww.indiandentalacademy.com

ORTHODONTIC TOOTH MOVEMENT
The orthodontic response is divided into three elements of tooth
displacement: initial strain, lag phase, and progressive tooth movement.
Initial strain of 0.4 to 0.9 mm occurs in about 1 week because of PDL
displacement (strain), bone strain, and extrusion .

CHANGES IN THE PERIODONTAL LIGAMENT
Progressive displacement of the tooth relative to
its osseous support stops in about 1 week, of
PDL necrosis. This lag phase lasts 2 to 3 weeks
but may be as long as 10 weeks. After
undermining resorption restores vitality to the
necrotic areas of the PDL, tooth movement
enters the secondary, or progressive, tooth
movement phase. The mechanism of sustained
tooth movement is a coordinated array of bone
resorption and formation events.
PRESSURE TENSION THEORY

CHANGES IN THE ALVEOLAR BONE
Modeling, a change in shape or size of an
osseous structure, is achieved by
differential bone formation and resorption
along the periosteal and endosteal
surfaces. Internal turnover of osseous
tissue is termed remodeling
The remodeling process has evolved a
vascularized multicellular unit for removing
and replacing cortical bone which is called
a cutting/filling cone. Cutting cones
create resorption cavities in the cortical
bone thereby reducing the density of
cortical bone

Remodeling of dense alveolar bone may enhance the rate of
tooth movement and replace the less mature osseous tissue
formed by rapid PDL osteogenesis. These intraosseous
resorption cavities are the initial remodeling events that occur
during the first month of the remodeling cycle.

CELLULAR EVENTS
 The activation of osteoclast may occur because of the integrins on
osteoclast cell membrane with proteins in bone matrix which contain R G
D amino acid sequences such as Osteopontin.
Has a dual function of allowing osteoclastic access to mineralized bone
matrix and releasing factors from the matrix such as osteocalcin which are
chemotactic for osteoclasts or their precursors.

How do osteoclasts work?
The ruffled border area carries out the
resorption process itself.. Osteoclasts contain large
amounts of carbonic anhydrase to facilitate the
conversion of CO2 and H2O to H2CO3. The
degradation of bone matrix is presumably the result of
the activity of a number of lysosomal enzymes which
can degrade bone at low pH.
There is a correlation between activation of bone
resorption and acid phosphatase release.
A variety of cathepsins and other lytic enzymes which
are produced by the osteoclast are able to degrade
collagen at low pH.
There is a evidence that oxygenderived free radicals
are produced by osteoclasts and may be localized in
the ruffled border area.
Superoxide dismutase,, has been identified in
osteoclasts. OCL - Osteoclast

Reversal
The reversal phase lasts from 7 to 14 days
The resorption bays are now devoid of osteoclasts and are occupied by
Osteocytes, macrophage like mononuclear cells and preosteoblast..
Osteoblasts are summoned into the reversal lacuna.by growth factors

Bone matrix formation
Begins with the deposition by the osteoblasts of osteoid,. The second stage in bone
formation is mineralization of the organic matrix,).
The completed piece of new bone is termed either a basic structural unit or a bone
structural unit (BSU).

Bone mineralisation
2 mechanisms.
A) Matrix Vesicle :The matrix vesicle contains alkaline phosphatase, pyro
phosphates, CaATPase, metallo proteinases, proteoglycan and anionic
phospholipids which are able to bind to calcium and inorganic phosphate

B) Heterogeneous Nucleation : Noncollagenous proteins act as nucleators
and others may act to control crystal growth. Dephosphorylation of the
phosphoprotein provides the additional phosphate ions for nucleation
and crystal growth.
Additional crystallites may form by secondary nucleation from
mineral phase particles
Factors influencing mineralization
Local Factors
Collagen – Collagen has holes and pores in which nucleation, crystal
growth, secondary nucleation and multiplication of the solid phase can
occur.

Non Collagenous Molecules
Name Composition Possible Function
Osteopontin Phosphoprotein inhibits crystal growth
Osteonectin Phosphoprotein inhibits crystal growth
Bone Sialo Phosphorylated nucleator for mineralization
Protein glycoprotein
GLA Protein Protein & Regulator of crystal growth
rcarboxy glutamic acid
Biglycan & Chondroitan Sulfate Removed at mineralization front
Decorin Proteo glycans to permit mineralization
Phospholipids calcium binding at mineralization
front.
Pyrophosphate inhibitor of calcification

Growth Factors
FGF : Increase osteo blastic precursor population and also
increase collagen synthesis.
IGF : Increase bone cell proliferation and total protein
synthesis.
TGF, PGDF : increase proliferation of osteo-progenitor and total
protein synthesis.
Interleukin 1 : At low doses, it stimulates collagen synthesis but is
inhibitor in higher concentrations.
Tumor necrosis factor: stimulate proliferation and collagen synthesis in pre-
osteoblasts.

Systemic Factors
PTH, 1,25 - Dihydroxy Vitamin D3, estrogen
Role of alkaline phosphates
hydrolyzes phosphate ions from organic radical at an
alkaline pH
Marker of osteoblast activity.
Incremental lines
Due to variations in the degree of mineralization at the
boundaries between periods of activity and rest.

HISTOLOGICAL ASPECT
 Primary compacta is formed by
woven bone which fills in with lamellar
bone to form primary osteons.
Within weeks, the new primary bone is
remodeled to more mature secondary
osteons by a progressive wave of
cutting/filling cones .
. Supporting bone continues to adapt
to the new position of the tooth for up to
a year after the end of active tooth
movement.
 Cortical bone is formed along
periosteal and PDL/bone surfaces by
the same mechanism.
During the retention period the newly
formed bone remodels and matures..

The osteogenic layer of the suture is called
the cambium, and the inner leaf the
capsule. Between these two layers is a
loose cellular and vascular tissue.
Sutures experience, absorb, and transmit
mechanical stresses generated from either
functional activities such as mastication, or
exogenous forces such as orthopedic
loading.
Mechanical stresses transmitted through
the bone are experienced as tissue level
bone strain, interstitial fluid flow that in turn
induces cell level strain on the bone cells
and subsequent anabolic or catabolic
responses , resulting in regional
acceleration of bone adaptive activity
SUTURES

Rapid palatal expansion.- the adjacent expanded suture experienced
hemorrhage, necrosis, and a wound healing response. Chang et al
demonstrated the angiogenic capillary-budding process associated with the
propagation of perivascular osteogenic cells

Functional appliances exert the skeletal effect by inducing the action
of masticatory muscles expressed by multiple lines of stresses exerted
by the masticatory muscle attachment .
Sutural expansion within physiologic limits is a clinically viable means of
repositioning the bones of the craniofacial complex to improve esthetics
and function.

Factors Regulating Tooth movement
 Growth;
 Bone density
 Type of tooth movement
 Role of Periodontium
 Duration and force magnitude
 Circadian rhythm
 Effect of chemicals

Parathyroid hormone
- effects on bone resorption
- effects on bone formation
- effects on Ca++ homeostasis
Calcitonin
- short term regulator of Ca++
homeostasis
- inhibits osteoclastic bone
resorption
1,25 - Dihydroxyvitamin D3
- Calcium homeostasis
- bone remodeling
- bone resorption

Prostaglandins
bidirectional effect on osteoclasts - an immediate transient effect
to slow bone resorption and a sustained effect to Osteoclastic
bone resorption.
Interleukin - 1
- powerful and potent stimulator of bone resorption
Tumor necrosis factor
- Osteoclastic bone resorption
Osteoprotegrin
- inhibitor of bone resorption
Interleukin - 6
Gamma interferon
Growth factors www.indiandentalacademy.comwww.indiandentalacademy.com

Bone Changes During Orthodontic Tooth Movement

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Bone Changes During Orthodontic Tooth Movement