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Composition of bone? (3 main components)
Matrix - 35% organic phase mainly collagen type 1 and other proteins such as osteonectin, osteocalcin, GAG’s, proteoglycan, GF’s
65% Mineral phase - HAP, calcium, phosphate
Cellular - osteoblasts, osteoclasts, osteocytes
osteoblasts - mesenchymal cells
osteoclasts - macrophage lineage
Mature osteoblasts in calcified bone matrix lying in lacunae and communicate with each other via canaliculi
Bone strucutre?
Cortical/compact bone - hard dense bone - 80-90% calcified - lamellar organisation of collagen in mature bone matrix, parallel or concentric organisation - surrounding channel centred on blood vessel known as haversion system
Cancellous/spongy bone - 15-25% - containing bone marrow/connective tissue and blood vessels in the spaces


Which is compact and which is cancellous bone?

What is the structure of alveolar bone?
comment on the turnover of bone
Cortical plates of compact bone
Trabecular bone occupies the central part of alveolar process
Bone lining the socket is bundle bone
Embedded in the bundle bone are the Sharpey’s fibres of the pDL
there is continuous turnover

Again what are the 3 bone cells?
Osteoblasts -
osteoclasts - bone lining cells
osteocytes - encased in bone matrix

Where in this photo are the osteoblasts situated?

Osteoblasts synthesis: (what type of organic protein, other proteins, an important indicator of bone metabolism and receptors for (4))
Type 1 collagen
Bone matrix proteins - ostecalcin/pontin, bone sialoprotein
alkaline phosphatase
PTH, vitamin D3, growth factors, cAMP response to PTH


Where are the osteocytes?

Osteocytes
abundance?
arrangement and role?
The most abundant cells in the bone
Network of long-lasting cells linked through canaliculi
Involved in cell signalling and response to mechanical forces


label
Osteocytes are arranged around the vascular canals forming the harversion systems


What are these? where are the osteoclasts in the top image?
Osteoclasts

Morphology of osteoclasts and where they are usually located?
Multinucleated with ruffled border
Adjacent to resorbed bone
Bone lining cells, in contact with calcified bone surface and in lacunae
4-20 nuclei, giant cells

Osteoclasts produce what important enzyme? have what receptors that reduced their activity? osteoclasts are responsive to what hormones for what response?
TRAP - differentiation, activation and proliferation of OC’s
Calcitonin receptors - reduces their activity
Responsive to calcitropic hormones - bone growth and remodelling

Mechanism of bone resorption:
Osteoclasts are recruited through?
They attach to what?
What does the osteoclast secrete?
What can the osteoclasts resorb and not resorb and how is this managed?
External stimulus
Bone matrix at clear zone to form a seal under cell
Secrete hydrogen ions across ruffled border to demineralise bone
Cannot break down unmineralized organic matrix aka osteoid so MMPs and other collagenase enzymes must remove the osteoid first to allow it to resorb the mineralised bone
Osteoclasts resorb pits of bone called lacunae


Explain how osteoclastic activation required Osteoblasts?
Formation of osteoclast progenitors or precursor cells in hematopoietic tissues from a macrophage lineage
and the development of resting pre-osteoclasts and osteoclasts in the bone itself
2 Preparation of the bone surface, osteoblasts facilitate the removal of unmineralized osteoid layer by producing enzymes such as MMPs and other collagenases
This allows osteoclasts access to the mineralised bone and ensuing resorption
Osteoblasts have receptors for certain bone resorption agents such as prostaglandins, vit D3 and PTH
Osteoblasts then transmit resorptive signals to the osteoclast to activate them:
RankL on osteoblasts connects with RANK receptor on Pre osteoclasts and promotes osteoclast differentiation
As a control mechanism, OPG is a decoy receptor and binds RANKL and inibits OC activations
Also, M-CSF - stimulates the differentiation and proliferation of pre-osteoclasts
Osteoblasts stimulated by bone resorbing hormones causes release of MMP and allow for osteoclastic activity to ensue by removing osteoid layer
3 - Osteoclasts resorb bone, ruffled border with finger like projections to create increased SA to facilitate exchanges of materials
4 - OC activity decreases and osteoblast precursor cells appear in area of resorption and differentiate locally into osteoblasts - mediated by BMPs and growth factors the cells become completely embedded to become osteocytes until which they produce collagen/osteoid
TNF released from local cells inhibit continued production of bone

Again, how do OBs regulate OCs?
what acts against the OCs but acting on the OBs?
Differentiation and function is regulated through OB derived factors (RANKL M-CSF)
RANKL stimulated formation and function of OCs
OPG by acting as a decoy receptor for the RANKligan

What is the with of the PDL?
What are some functions of the PDL? (5)
what is it primarily composed of?
What 2 undifferentiated cells does it contain and these are responsible for what 2 processes?
What property does the pdl have? (one word)
0.5 mm
Tooth support, cementum ligament and bone repair, sensory: pressure pain proprioception, orthodontic tooth movement, dissipation of forces, shock absorption
Collagen type 1
Undifferentiated fibroblasts and osteoblasts
Ligament cementum and bony socket remodelling
Fluid visco-elastic properties

What is the zone of equilibrium?
Teeth appear to lie in a position of balance between the tongue on one side and lips/cheeks on the other
How does the PDL influence this position of balance?
The PDL has an intrinsic force which needs to be overcome before teeth move
Loss of PDL e.g in periodontal disease, means less force and therefore uncontrolled movement of teeth
Lack of PDL means there is a lack of resistance to constant soft issue forces on teeth with influence on tooth position as a result


What is this picture showing?
Zone of equilibrium (depiction of forces applied to teeth externally)
What happens when light forces are applied to teeth?
1-2 sec
5 sec
minutes
hours
2-3 days
5-14 days
14-30 days
pdl fluid expressed
pdl fibres and cells compressed
altred blood flow - pg an ck released
metabolic changes - ob and oc activity
frontal resorption and slight tm
lamina dura resorption - no otm until this is removed
otm occurs again - resorption an deposition
Blood flow altered due to compression and tension forces and distortion of pdl fibres and cells
oxygen levels altered signalling proteins such as ck and pg are released
metabiotic changes occur over next few hours, enzyme levels change and chemical changes
cellular diff occurs within pdl and days later oc and ob are required and tooth movement occurs
teeth move by frontal resorption on the compression side
4 week period is required for removal of hyalinised bone and for pdl to recover
so pts are reviews on avg every 4-6 weeks to allow for tm to occur in the appropriate time required for bone and pdl turnover

What happens when heavy forces (greater than capillary pressure) areapplied to tooth?
1-5 second
minutes
hours
2-3 days
14 days
15-30 days
pdl completely compressed
blood flow completely ceases
tissue ischaemia and necrosis - hyalinisation
ob/oc requited mediating undermining resorption (in adj area)
hyalinsation zone is removed
OTM occurs
in first few seconds blood flow completely occluded to the local area
hours later ischaemia results in cell death and tissue necrosis or areas of hyalinisation
OC and OB activity cannot occur in this area
days later these cells are recruited to adjacent bone areas to initiate undermining resorption
weeks later lamina dura adjacent to pdl is removed and tooth movement finally occurs

What are the optimal forces required for OTM? as it reduces risk of what?
Just greater than resting capillary pressure
to reduce risk of tissue and cell necrosis, pulp damage, pt discomfort
for optimal OTM

force effects depend on what? (4)
Magnitude
Rate of decay of the force
Duration - Continuous vs intermittent
Type of force - tipping, intrusion, extrusion, bodily, torque


What does centre of resistance mean?
It is the point on the tooth when a single force is passed through it, would bring about its translation along the line of action of the force

What are factors that affect the centre of resistance? (3)
Number of roots/root surface area
Degree of alveolar bone loss
Degree of root resorption


What type of force is being applied in this image?
how many areas of compression?
Tipping
The force is not applied through the centre of resistance
Therefore the rotation of the tooth is around the point at which the force is applied
2 areas of compression

What types of forces are these?
how much force does each need and what is the general rule?
Bodily and intrusion forces
the more pdl surface involved the more force required to generate the desired tooth movement

What can be used to apply ortho forces? (appliances) (5)
Removable appliance
Archwires (fixed)
Headgears
Intermaxillary - elastics
Intramaxillary - push coild

Optimum force levels for tipping, bodily, intrusion, extrusion and torque?
bodily movement
torque
tipping , extrusion
intrusion

Optimum force levels are determined by what? (4)
Type of force
PDL/surface area
Bone levels
RSA and root number

What are the ideal visit intervals?
4 weeks minimum to allow repair mechanisms for hyalinisation ears

What is anchorage?
The resistance to unwanted tooth movement
based on newtons third law that for every action there is an equal and opposite action
Why is anchorage important?
what can be used (4)
To present wastage of space gained from xla not being used to align the teeth
Transpalatal arch, nance appliance, tad and headgear

Headgear
what is it attached to?
what 2 things its used for?
extra oral anchorage
Kloehn bow attaches to headgear tubes on upper 6’s bands to prevent mesial molar movement
can also be used to distalise molars by increasing the forces to create space


What are these headgears called?
cervical pull or Low pull head gear
Occipital head gear - high pull
Combination pull head gear


Temporary anchorage devices:
What type of anchorage do they provide?
How is it attached?
How is it different to an implant?
what arches can it be used in?
What is it used in?
Intraoral device used for indirect anchorage
Screwed into the alveolus at the level of the attached gingivae
It doesn’t Osseointegrate and can be easily removed when no longer needed
upper and lower
moving teeth in severe hypodontia, reducing OJs in loss of 6’s

Intraoral anchorage:
How is the anchorage value for a tooth calculated?
Anchorage value of a tooth is proportional to the surface area of the root
The tooth with larger root surface area requires greater force to move an therefore higher anchor value

anchorage value of each tooth

What 2 conditions affecting a tooth can make them good sources of anchorage?
Difference in Crown root angulation - dilaceration
ankylosis - fused to bone

What is a common risk factor associated with ortho tx?
Root resorption
How much mm of root from the apex is usually lost
1-2 mm

What are some risk factors associated with root resorption? (10)
long time
class 2 elastics
roots into cortical plate
nail biting
history of trauma
atopic pts
blunt, short and pipette roots
previous ortho tx
previous radio therapy
family history

Where does the root resorption occur
be specific about tooth structures and cells
Cementum adjacent to the hyalinised pdl undergoes resorption by cementoclasts
this can progress overtime to the extend of the dentine
Once ortho forces are removes, repair occurs by the deposition of new cementum in the aea of previous destruction
dentine once lost will not be replaced

Resorption categorisation?
Slight blunting - very common
Moderate
Severe
can either be localised or generalised

Moderate generalised resorption:
what happens in this?
risk factors?
What teeth are mostly affected?
most teeth show some loss of root length - mostly clinically insignificant
longer duration of tx
maxillary incisors and first molars

Severe generalised resorption?
risk factors?
thyroid deficiency
atopic e.g asthamtics

Severe localised resorption
causes? (3)
greater risk for what teeth?
excessive forces and prolonged duration of tx
if roots of maxillary incisors are forced against the lingual cortical plate
greater for maxillary incisors

Pulp damage?
increased risk in? (1)

What are medical inhibitions of OTM? (4 main)
NSAIDS and TAD - inhibit COZ patway meaining OC signalling is reduced
But LOX pathway can take over
Bisphosphonates - promotes bone deposition and OB activity but inhibits OC and resorption so necrotic bone is not removed
Reduced oestrogen levels - influence bone remodelling
Bone disorders: OP/osteopetrosis - impact bone remodelling
