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Bone metabolism & Biological
Theories of Tooth movementPreceptors:
Dr. Pavan Kumar Chandra
Dr. Piush Kumar
Presented by:
Dr. Anuja Aggarwal
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Bone is a specialized mineralized connective tissue
made up of an organic matrix of collagen fibrils
embedded in an amorphous substance with mineralcrystals precipitated within the matrix.
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Matrices
organicinorganic
35 % of dry wt.
Type I collagen.
10 % non collagenousproteins.ex:BMP
Non collagenousproteins are PG orGAG
Modulate cellularattachment.
6070 % of dry wt.
99% Ca, 85 % P, 40
60 % Na & Mg
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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 boneEg., Bones of
cranial vault, maxilla, etc.
Intracartilagenous boneEg., Vertebra,
ribs, base of the skull, etc
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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 boneBundle bone is a functional adaptation of lamellar structure to
allow attachment ofSharpey's fibers
Mature Bone or Lamellar boneLamellar bone a strong, highly organized, well-mineralized
tissue. Adult human bone is almost entirely of the remodeled
variety: secondary osteons and spongiosa..
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W Woven Bone L Lamellar Bone
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HISTOLOGY OF BONE
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Periosteum
Compact Bone
Circumferential lamellae
Concentric lamellae
Interstitial lamellae
Bony trabeculae
Bone Marrow
HISTOLOGY OF BONE
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Bone consists of 4 microstructural components
1. Cells
2. Organic matrix
3. Inorganic matrix
4. Soluble signalling factors
Osteoblasts
Osteocytes
osteoclasts
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According to Brighton following fracture with
in 12 hrs polymorphic mesenchymal cells
appear providing preosteoblastic cell resource.
Depending on the presence of environmental
cues such as nutrient supply, specific growth
factors, blood vessels & mechanical stability ,they can convert either to cartilage forming
chondrocytes or bone forming osteoblasts.
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Osteoblasts
Round cells with an organelle rich cytoplasm. Form boneby laying down osteoid first and then mineralizing it.
Osteoblasts are metabolically active secretory cells that
express soluble signaling factors ex: BMPs, TGF- beta,insulin like growth factor I & II , interleukin1 & plateletderived growth factor & osteoid.
Expression of these factors by osteoblasts occurs during
bone embryogenesis, maintenance(ex: remodeling) &repair.
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Osteoblasts are derived from paravascular connective
tissue cells.
Mesenchymal stem cells differentiate into osteoblasts
when they are exposed to bone morphogenic proteins
(BMP).
Cbfa1 is a transcription factor that is expressed by the
cells of osteoblastic lineage and is necessary forosteoblastdifferentiation
During remodeling , osteoid is produced at the rate of 2 - 3
micrometers per day at a thickness of 20 micrometers.
After a maturational period of 10 days, osteoid mineralises
at a rate of 1- 2 micro meters per day.
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Osteocytes
Osteocytes are former osteoblasts that have becomeentrapped in bone matrix.
These are relatively inactive cells. Their subduedmetabolic activity is crucial to bone viability & tosustain homeostasis.
The complex processes of homeostasis are regulated byphysiologic interactions among cells, tissues, organs &signaling factors such as harmones & growth factorsthat meticulously titrate intra & extra cellular levels ofcationic & anionic moieties
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Vitality of bone is maintained through a
network of osteocytic cytoplasmic processes
that traverse canaliculi.
This highway system enables osteocytes to
interact through gap junctions & permits
signal transmission to osteoblasts fromosteocytes & from osteocytes to osteoblasts.
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Osteocytes,osteoblasts & osteoclasts are the
cellular crafts men performing the
managerial roles of calcium regulation &
bone homeostasis, physiological processes
fundamental to modeling & remodeling.
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Osteoclasts
Granulocyticprecursors found in bone marrowenter the circulation as monocytes , and throughasynchronous fusion, produce a multinucleated cellwith an average of 1012 nuclei known asosteoclast. They represent the terminal stage ofdifferenciation of these cells.
Osteoclasts have a ruffled border, possess calcitonin
receptors.
They secrete a lysosomal enzyme, tartrate- resistantacid phosphatase (TRAP),which is also used as a
marker for osteoclast identification.
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Differentiation of osteoclasts
Osteoclasts differentiate from
hematopoietic cells. This pathway
of differentiation is also shared bymacrophages.
GM-CSF (granulocyte monocyte
colony stimulating factor) and M-
CSF (macrophage colony stimulatingfactor) are important in regulating
these shared stages of development.
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Another important discovery ofosteopotegerin
(OPG) or Osteoclastogenesis inhibiting factoe
(OCIF)secreted by osteoblasts and functions to
block the formation of osteoclasts and boneresorption.
SUDA et al isolated an osteoblast membrane bond
molecule called osteoclast differentiation factor
(ODF).ODF was able to induceosteoclastogenesis inbone organ cultures.
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Osteoblast regulates the differentiation of osteoclasts. TheTALK between an osteoblast and osteoclast isaccomplished through an osteoblast membrane bondRANK Ligand (RANKL) (receptor activator of nuclear
factor kB ligand)
In this situation OPG can develop to block RANKL in turnblocking the interaction between RANK and RANKL/ODF
Cytokines (TNF, interleukin-1), prostaglandins E andgrowth factors (TGF-, BMP) are upstream signals whichregulate the OPG/ODF ratio.
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How do osteoclasts work?
Osteoclasts contain large amounts of carbonic anhydrase tofacilitate the conversion of CO2 and H2O to H2CO3. Thedegradation of bone matrix is presumably the result of theactivity of a number of lysosomal enzymes which can degradebone at low pH.
There is a correlation between activation of bone resorptionand acid phosphatase release and oxygen derived free radicalslocalized in ruffled border..
A variety of cathepsins, superoxide dismutase and other lyticenzymes which are produced by the osteoclast are able todegrade collagen at low pH.
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Decreased blood Ca level
parathyroid kidney
parathormone Vitamin D
Bone
Increase in
resorption &release of Ca
Intestine
Increase in
absorption ofCa
Increased blood Ca level
thyroid
calcitonin
Bone
Inhibition of bone
resorption anddeposition of Ca
Normal calcium level
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Tooth Movement
2 types of tooth movements-
Physiologic
Under the effect of force.
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Theories explaining orthodontic
tooth movement-
Pressure tension theory
Biological electricity or bioelectrictheory
Fluid Dynamic Theory
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Why it was rejected?
Baumrind, pointed out a conceptual flaw in it.
He considered the PDL to be a continuous hydrostatic system andsuggested that any force delivered to it would be transmitted equally toall regions accoording to Pascals Law.
He further stated that the presence of fibers in the PDL does not modifythe operation of this law, because of the concomitant existence of acontinuous body of liquefied ground substance.
He recognized that only part of the periodontium where differentialpressures, as mentioned in the pressure-tension hypothesis, can bedeveloped, is solidbone, tooth, and discrete solid fractures of thePDL.
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Bone Bending & Bioelectric Theory
(Farrar 1876)Farrar was the first to suggest, that alveolar bone bending plays a pivotal role
in orthodontic tooth movement.
It has been hypothesized that mechanical deformation of the crystalline
structure of the hydroxyapetite and the crystalline structure of collagen inducemigration of electrons that generate local electric fields. This phenomenon is
calledpiezoelectricity.
Zengo et al concluded that the concave side of orthodontically treated bone is
electronegative and favors osteoblastic activity, whereas the areas of positivityor electrical neutralityconvex surfacesshowed elevated osteoclastic
activity.
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The 2 unusual properties of
piezoelectricity, which seem to notcorrelate well with orthodontic tooth
movement are(1) a quick decay rate
(2) production of an equivalent signal in the
opposite direction upon force removal
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Further, ions in the fluids surrounding the living bone interact withthese electrical fields. These currents of small voltages are called
streaming potentials.
Davidovitch et al suggested recently that piezoelectric potentialsresult from distortion of fixed structures of the periodontium
collagen, hydroxyapatite, or bone cell surface. But in hydrated
tissues, streaming potentials (the electrokinetic effects that arise
when the electrical double layer overlying a charged surface isdisplaced) predominate as the interstitial fluid moves.
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Fluid Dynamic Theory (Bein 1966)
Tooth movement occurs as a result alterations in
fluid dynamics in the PDL.
When PDL is compressed due to orthodontic
force blood vessels of the PDL get trapped
between the principal fibers and this results in
stenosis. The vessel above the stenosis then
balloons resulting in the formation of ananeurysm.
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How is ortho mvmt diff from
physiological TM
Orthodontic tooth movement is uniquelycharacterized by the abrupt creation of compressionand tension regions in the PDL.
Physiological tooth movement is a slow process thatoccurs mainly in the buccal direction into cancellousbone or because of growth into cortical bone. Incontrast, orthodontic tooth movement can occur
rapidly or slowly, depending on the physicalcharacteristics of the applied force, and the size andbiological response of the PDL.
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Biology of tooth movement due to
applied force: Current Concepts
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PATHWAYS OF TOOTH MOVEMENT
On the basis of research in basic biology and clinical observations, Mostafa et al
proposed an integrated hypothetical model for tooth movement. This model
consists of 2 pathways
I ----Physiological response
II----Generation of local inflammatory response
Pathway I
Orthodontic force creates vectors of pressure and tension
bone bending, generation of tissue bioelectric polarization, and subsequent boneremodeling
act on the cell surface cyclic nucleotide pathway, generating changes in the
levels of intracellular second messengers cAMP
cell proliferation, differentiation, and activation
electrically neutral or positive areas promote osteoclast activity, whereas
electronegativity supporting osteoblastic activity.
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Pathway II
Orthodontic forces trigger inflammatory processes inthe involved dental and paradental tissues.
Lymphocytes, monocytes, and macrophages invadethese tissues
The local elevation in prostaglandins and asubsequent increase in cellular cAMP concentrations
increase osteoclast activity. Secreted hydrolyticenzymes, such as collagenase, dissolve themechanically strained ECM.
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Recent model
Recent reports by Jones et al detailed events in bone cells immediately after the application of mechanicalstress.
Osteoblasts respond to physiologic levels of stress- increase in intracellular free calcium andmembrane potential through activation of K channels.
activation of phospholipase C, which releases inositol triphosphate within 10 seconds.
Elevated levels of phospholipase C maintain the high calcium concentration throughout stressapplication by keeping the mechanosensitve ion channels open and by further activation of proteinkinase C
Phospholipase A is activated
Arachidonic acid
Prostaglandins (10 mins)
Release of products of the lipooxygenase pathway (leucotriens and hydroxyeicosatetraenoic acids),followed by an elevation in the concentration of cAMP.
Cellular synthetic and secretory activities.
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Primary stimulus
Acts on
Pdl and bone cells
Interaction between
these cells leads to
Transient
increase in the intracellular levels of
second messengers
CAMP
IP3
Ca++
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Secondary messenger
Nucleus
Takes signal to
In the nucleus of each cell different second messengers
account for the differential patterning, protein synthesis and
Gene expression.
Recently identified Immediate Early Gene expression include
Cfos, Cjon mRNA, egr-I, SP1 growth differentiation factor 9B,
extracellular GLA protein.
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Phospholipids
Mechanical,
hormonal,
pathological,
electrical
Phospholipase A
Arachidonic acid
Leucotrienes
Lipooxygenase pathway
Cyclic peroxide
Cyclooxygenase pathway
PG E PG F
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Role of cytokines and growth factors
Cytokines are the protein factors released from cells, which
modulate the activity of other cells and have multiple actions
like bone remodelling, bone resorption & deposition.
Prominent cytokines which have been shown to stimulate bone resorption andinduce osteoclast proliferation are-
Interleukin 1
Interleukin-6
Tumor necrosis factor
Granulocyte-macrophage colony stimulating factor
Macrophage colony stimulating factor
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Growth factors are released during inflammation and
repair by the cells of PDL and bone.
These factors include
Fibroblast growth factor
Insulin like growth factor (IGF-I, IGF-II)- increase type-Icollagen and matrix synthesis by osteoblasts.
Transforming growth factor (BMP)- induce mesenchymalprogenitors to differentiate into both osteoblasts and chondrocytes
Platelet growth factors
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Role of neurotransmitters
In areas where tension or compression evolves under
the influence of the orthodontic appliance, vasoactive
neurotransmitters are released from distorted nerve
terminals that interact first with capillary endothelialcells. In response, the endothelial cells express
receptors that bind circulating leukocytes, promoting
their migration by diapedesis out of the capillaries to
secrete signal molecules, including cytokines andgrowth factors, that stimulate PDL and alveolar bone
lining cells to remodel their ECM.
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The PDL is abundantly supplied with 2 kinds of nerve terminals:
Ruffini-like endings & nociceptive endings which change theirstructures in response to external stimuli, such as orthodonticforce.
Mechanoreceptors in the apical half of the dental root have a low
threshold and respond to even minor stretching of the PDL. Incontrast, nociceptors have a high threshold and are activated byheavy forces, tissue injury, and inflammatory mediators.
The mechanoreceptors are silent in physiological conditions but
contain various neuropeptides such as substance P, vasoactiveintestinal polypeptide, and calcitonin gene-related peptide(CGRP) released when strained.
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Increased immunoreactivity (increases PG) of substanceP has been demonstrated in the PDL in the early phasesof tooth movement.
Another neurotransmitter involved in orthodontic toothmovement is CGRP.
Kvinnsland and Kvinnsland localized CGRP in the PDLand the dental pulp after 3 days of molar movement infibroblasts at PDL tension sites.
Saito et al reported finding intense reactivity tovasoactive intestinal polypeptide, in the compressed PDLand in the pulp of moving teeth in cats.
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Role of neurotransmitters in orthodontic tooth movement
Orthodontic force
Movement of tissue fluids inside and out of PDL
Distortion of nerve endings
Release of stored neurotransmitters centrally and peripherally
Pressure sensation, pain
Interaction with PDL fibroblasts and
alveolar bone cells
Increased levels ofintracellular 2nd messengers
Synthesis and secretion of cell
products- cell proliferation etc.
Interaction with endothelial cells
vasodilatation
Extrusion of plasma(prostaglandins) and
leukocytes
Synthesis and secretion of cytokines
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Pressure/tension-electrical-cell
After an orthodontic force is applied, the initialstep is the detection of a mechanical strain.
Application of small bending force to long bones
result in compression on one side and tension onthe opposite side.
This produces a flow of interstitial fluid throughthe canalicular network, generatingstreaming
potentials and/or fluid shear stress.
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Streaming potentials is the electric potential that developsbetween two components by an electrolyte flowing
between the solid surfaces.
Eg:bone is partially composed of proteoglycans, which areentrapped in a collagen network. Because of the negative
charge of proteoglycans, there is an excess of positive mobileions in the fluid. Such potentials could possibly arise invascular channels, Haversian systems, canaliculi,microporosities of the structure and as a result of the bloodflow and interstitial fluid movement.
Slow decay of signal due to relaxation of fluid flow in thestressed bone.
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Cell to Cell contact
There are two types of cellular adhesions- Cell-to-cell adhesion
Cell-to-extracellular matrix adhesion.
Integrins are cell surface receptors that mediate cell-to-cellattachment or cell attachment to ECM molecules such ascollagen, fibronectin, laminin etc.
The cytoskeleton (Microtubules, microfilaments,Intermediate filaments) presents a number of possibilitiesfor transducing mechanical forces acting on cells and/ortheir adjacent matrices.
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Many of the extracellular matrixproteins responsible for celladhesion contain a common peptidesequence Arg-Gly-Asp (RGD)
which is essential for the cell-binding properties of theseproteins.
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Classically, the second messengerassociated with mechanical forcetransduction isAdenosine 35 cyclicmonophosphate (cAMP).
It was first identified in 1960 bySUTHERLAND et al-
When liver slices were exposed toadrenalin, free glucose appeared underthese conditions and it was postulated that
adrenalin was acting as the firstmessenger, binding to a receptor andstimulating the production of a powerfulchemical second messenger.
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The G proteins act as intermediariesbetween receptors and intermediaryenzymes.
The three important G proteins
pertinent to orthodontic toothmovement are
Gs- the stimulatory regulator of adenylatecyclase
Gi- the inhibitory regulator of adenylatecyclase
Gp-the stimulatory regulator of the PIpathway.
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Early gene expression
In the nucleus different second
messengers account for the
differential pattern ofimmediate
early gene expression (I EG).
IEGs are among the earliest
responses that can be measured at
the transcription level.
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The transcription of the IEGs has
been shown to increase when cells
are exposed to cytokines, growth
factors or mechanical stimulation.
IEGs are-
c-fos
c-jun and
egr-1
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Protein products from the c-fos and
c-jun genes form a hetrodimeric
complex named activator protein-1
(AP-1).
Depending on the state of the cell or
in the presence of various stimuli
Ap-1 can produce either cellular
proliferation or differentiation.
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Signal input-genetic output
Cytoplasmic signaling proteins such
as sonic hedgehog, TGF-
superfamily and many transcriptionfactors and ions reach the nuclear
matrix and then genome- resulting in
enhanced or suppressed gene
expression.
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Input becomes output as gene
expressed proteins
Protein synthesis inhibition
Mobilize mitosis Cell motility
Secretion of other proteins
Programmed cell death (apoptosis)
all of which modify cytoskeleton, cell membrane andECM.
This process is continuous.
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Pain & Orthodontic Tooth Movement
Tooth movement-associated tissue remodeling, an
inflammatory process, might induce painful sensations,
particularly after activation of the orthodontic appliance.
After 24 hours of force application, C-fos(immunoreactive
neurons known to be involved in transmission
of nociceptive information) expression is noted
ipsilaterally in the trigeminal nuclues modulated
through serotonergic and dopaminergic systems.
D i i
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Drug interaction
Pharmacological agents manipulate toothmovement in both directions.
Factors that enhance tooth movement are vitamin
D & direct injection of prostaglandin intoperiodontal ligament.
Drugs that inhibit tooth movement areBisphosphonates used in the treatment of
osteoporosis. Ex : alendronateProstaglandin inhibitors. Ex : NSAIDS,
Corticosteroids , Parathyroid, Thyroxin.
Osteoporosis is a problem particularlyd i l f l b i
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encountered in post menopausal females but isassociated with aging in both sexes.
Estrogen therapy , which is used frequently toprevent loss of bone in older women , has noimpact on orthodontic treatment.
Bisphosphonates are synthetic analogues of
pyrophosphates that bind to hydroxyapatite inbone & act as specific inhibitors of osteoclastmediated bone resorption.
If orthodontic treatment is necessary in olderpatients it is better to switch over to estrogen atleast temporarily Or use Raloxifene (estrogenrec modulator).
Bartzela et al Am J Orthod Dentofac Orthop 2009;135:16-26
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Dietary calcium : Adults require 1000 to 1300 mg ofcalcium in their daily diet.
The effect of dietary supplemental calcium on OTM wasstudied in dogs that were fed low- or high-calcium diets for 10weeks before orthodontic premolar movement was induced witha force of 100 N for 12 weeks.
From 8 weeks on, the low-calcium regimen led to asignificantly higher rate of OTM than did the high calcium diet.
These data support bone turnover studies showing increases inthe number of osteoclasts and osteoblasts in dogs with a low-
calcium diet. The final outcome was increased bone remodelingphenotype in which excessive bone resorption prevailed overdeposition.
Bartzela et al Am J Orthod Dentofac Orthop 2009;135:16-26
P l di E i hibi
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Prostaglandin E inhibitors:
Prostaglandin E inhibitors are of two categories:
Corticosteroids & NSAIDs.
Prostaglandins are formed from arachidonic acid
which in turn is derived from phospholipids.
Corticosteroids reduce prostaglandin synthesis
by inhibiting the formation of arachidonic acid.
NSAIDs inhibit conversion of archidonic acid to
prostaglandins by acting on Cox.
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Kehoe MJ et al, 1996 suggested Misoprostol (producesanalgesia similar to morphine) has insignificant
inhibitory effect on local PGe2 production. The degree & rate of tooth movement increased
attributed to the enhanced bone resorbing activity ofPGe1.
It was found ibuprofen significantly decreases PG
synthesis in pdl of guinea pigs. There is a marked
decrease in degree & rate of tooth movement.
Acetaminophen decreases peripheral PG production.But there is no significant effect on tooth movement.
Thus by prescribing OTC analgesics with minimuminhibition of PG, the treatment time can be reduced.
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