cell biology of orthodontic tooth movement Flashcards
which cells control orthodontic tooth movement?
- Periodontal ligament fibroblasts
- Mesenchymal stem cells
- Macrophages
- T cells
- Neutrophils
- Endothelial cells
- Neuronal cells
- Pre-osteoclast cells
- Pre-osteoblast cells
- Pre-cementoblast cells
- Osteocytes
- Remnants of HERS
- Rests of malassez
which cells orchestrate orthodontic tooth movement and on which sides?
- osteoclasts
- Bone resorption - compression side
- osteoblasts
- bone formation - tension side
- osteocytes
- communcation with osteoblasts and osteoclasts
- and with other osteocytes
signalling on the compression side during OTM
and outcome of these signalling events
- increase in
- cox2
- increase in PGE2
- increase in RANKL and MCSF
- TNFa
- MMPs
- eNOS
- IL-1beta
- cox2
outcome
- increased osteoclasts
- increased resorption
- decreased apposition
Effect of Cox2 and where it occurs
leads to increase in PGE2
therefore increase in RANKL and MCSF
activation of osteoclasts
effect of increase of IL-10 and where it
increase of OPG
inhibition of RANKL-RANK
reduction of osteoclasts
on tension side
theories for orthodontic bone resorption
which is correct
- Pressure-tension theory
- Pressure causes cascade of cellular events
- Biological piezoelectric theory
- (bone is regarded as a crystal structure that produces a short lived flow of electricity)
- Leads to signalling and activation of cells
- Biomechanical theory
- mechanical distortion of the cell membrane.
- Rounded on compression side, flatter on tension side.
a combination of all theories in reality
explain pressure-tension theory of orthodontic tooth resorption
- compression of collagen fibres
- leads to fluid movement
- compression of blood vessel endothelial cells and nerve fibre cell
- hypoxia
- leads to
- necrosis
- cytokine production
- leads to
- hypoxia
- infiltration of immune cells
- as blood vessels become ruptured
= controlled aseptic inflammation
- as there is no bacterial infection
explain the biological piezoelectric theory of orthodontic tooth resorption
- ion channels within bone may pick up electric current
- induce cell signalling cascade
- signals are short lived
- pressure on bone can also induce piezoelectric signals
- Osteocytes entombed in crystallised (hydroxyapapite) matrix of bone
- Receptors on osteocytes sense electric currents
- Signals are short lived
- Osteocytes respond to produce protein signalling factors.
explain how the mechano-responsiveness of osteocytes leads to bone resorption
- bending of bone
- osteocytes signal to stimulate osteoblasts to produce RANKL and MCSF
- RANKL-RANK interactions = activation of osteoclasts & cell fusion
- MCSF = directs haemopoietic monocytes to differentiate into osteoclasts
- large forces can lead to fractures and apoptosis of cells
- release of apoptotic signals
- leads to recruitment of osteoclasts
- = resorption of bone
explain the biomechanical theory of orthodontic bone resorption
- compressive forces on PDL and mesenchymal progenitor cells
- bind to ECM via integrins
- cells are stretched
- reorganisation of intracellular network and cytoskeleton
- changes in cytoskeleton
- Geometric remodelling of the cytoskeleton may alter cell metabolism or signal transduction by changing the relative position of different regulatory molecules, hence altering their ability to chemically interact.
what happens on the compression side on the periodontal ligament
- Osteocyte activation
- Osteoclast activation
- Cytokine activity by PDL
- Increased MMP activity
- Cell apoptosis
- Activation of blood vessels
- Provide signalling molecules to pdl
- Provide signalling molecules to activate osteoclastogenesis
- Increase in MMP
- Attempt to remodel collagen fibres
- Produces by PDL fibroblasts, immune cells, osteocytes.
what signalling occurs on the compression side on the periodontal ligament
- Periodontal ligament (PDL) cells under compressive strain synthesize interleukin-1 (IL-1), IL-6 and prostaglandins.
- Prostaglandin
- Can regulate process of osteoclastogenesis
- IL-1 & 6 - upregulate RANKL
- Prostaglandin
- IL-1 and IL-6 act to up-regulate RANKL and matrix metalloproteinase (MMP-8 and MMP-13; collagenases) expression by PDL cells and osteoblasts.
- Osteoblast-derived MMPs degrade the non-mineralized surface osteoid layer of bone, while MMPs produced by PDL cells degrade their extracellular matrix.
- RANKL stimulates the formation of active osteoclasts and degrade the mineralized matrix.
- Deformation of the alveolar bone up-regulates MMPs expression by osteocytes adjacent to the bone surface.
how are prostaglandins produced
through arachidonic pathway
- arise through activity of several enzymes that take phospholipids from the cell membrane and convert them into arachidonics
- important enzyme = Cox2
- important in prostaglandin production
roles of prostaglandins
vasodilators
- mediate orthodontic tooth movement
- produce inflammatory cytokines
which prostaglandins have roles in orthodontic tooth movement
what are their roles
Prostaglandin E2 and prostacyclin
vasodilators
increase vascular permeability and inflammatory swelling
PGE2 works with IL-1 to stimulate bone resorption & high conc. of PGE2 inhibits collagen synthesis
outline the phases of orthodontic tooth movement
Force too strong = longer hyalinisation period
Wants to be as short as possible during OTM
show timeline for orthodontic tooth movement
- Initial phase represents initial resorption of teeth following displacement of the PDL and bending of the alveolar bone and some bone resorption.
- Secondary phase of bone resorption following removal of hyalinized tissue
- almost impossible to avoid blood vessel occlusion completely,
- hyalinization always occurs to a certain degree and tooth movement is a result of combined undermining and frontal resorption
