Biology of Tooth Movement

By Dr. Aslam Hisam Qasmi

 Cytokines
ECM
POL Fluids shifted in GF
OTM Bone cell and matrix Remodelling
distortion CSF
Vascular
Neural Vaso Active
Neurotransmitters Movement of Teeth
 MECHANOSENSING, TRANSDUCTION AND RESPONSE :- (KRISHNAN AND DAVIDOVITCH)

Mineralised
Tissue
Non-Mineralised
OTM ECM Remodelling Tissue
Blood Vessel
Neural
 Osteoblasts Formation
Mineralised Tissue Osteocytes
Osteoclasts Resorption

Non-Mineralised Tissue PDL Fibroblasts Reorganisation Ortho-

movement
Endothelial Bone
Blood Vessels Reorganisation Remodelling
cells

GF
Neural SP & CGRP Cytokines Inflammation
CSF
 Phases of Tooth Movement

Lag Initial

1962 Burstone 3 Phases Lag

Log

1st 24 hrs – 2 days Bony socket

2nd 20 – 30 days Arrest

4 Phases
After 30 days Removal of Necrotic
3rd
tissues

4th Next movement Proper Orthodontic

Movement
 Alveolar bone response to Orthodontic force
Increase in osteocytes &
OTM G-6-PO4 DHGS
bone surface lining cells
2 hrs C-fos mRNA

TGF β
Insulin-like GF 4 hrs
(ILGF mRNA)

Flow of bone Sheer stress in Deformation of osteocytes

OTM interstitial fluid mineralised ECM in lacunae & dendrites in
Pertubs integrin
molecules
canaliculi

Pass through gap Hemi-channels opened

Acts of signals Release of PG’s
junction in strained osteocytes
Adjacent
Osteocytes Strength
Synthesis & deposition Osteocalcin
of osteoid matrix in Structure Non-collagen
Bone surface TP1 Collagen
cells osteocytic lacunae wall Elasticity protein Osteopontin
& bone surface
Osteoblasts Express/secrete Osteonectin
 Cytokine
GF
TF Osteoblasts Bone Formation
Inflammatory

Or persist as an
Osteocyte Rank Rank L OPG Apoptosis

Osteoclastogenesis More
Osteoblasts
Monocyte Rank Micro Secrete protons via
Macrophage Rank L Environment electrogenic H+ ATPase
(Proton pump)

Creates intracellular
Cl enters via channel Prevented by alkalinity
Generating HCl (because of massive
in H+ ATPase HCO3/Cl exchange
proton transport)

Acidity mobilises Later degraded by

pH- 4.5 mineral component collagenolytic lysosomal
exposing organic protease, (cathepsin)
matrix from osteoclasts
 Provide gases ECM provide support for
Blood vessels
and nutrients vascular endothelium OTM Cytokines
through integrin

Angiogenesis
Generate mechanical 3D Capillary
contractile forces Proliferation Protein Kinase
Network
within ECM Migration of
endothelial cells

Tension based Interconnected

Endothelial cells Strain
guidance pathways cords

Actin polymerisation, TP1

Shape changes by collagen genes, Signal Integrin
endothelial cells neovascularisation,
Maturation remodelling of BV’s
 <72 Hrs Decrease in BV’s
OTM
>72 Hrs
Increase in BV’s

Neural Response:
Trigeminal
ganglia Dental and
Neurons
paradental tissues
Mesencephalic
trigeminal nucleus
Nerve from Trigeminal ganglia
Mechanoreceptors
Nerve from Mesencephalic and nosiceptors Neuropeptides CGRP & SP
trigeminal nucleus (ruffini like endings)

MR CGRP & SP
OTM CNS
Release Bioactive
(also act as
Neurogenic
Proteins Inflammation
NR vasodilators)
Bind to circulating
Inflammation Leukocytes and Endothelial
migrate out of cells
capillaries into PDL

Monocytes
Lead to tissue
Cytokines/neuropeptides Lead to the release remodelling
Lymphocytes /direct actions of GF and CSF process
Mast Cells