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6 Craniofacial Growth II
6 Craniofacial Growth II
CRANIOFACIAL
GROWTH II
L.M CHAPTER 4
DR.REEM ALDHURGHAM
ASSISTANT PROFESSOR
DCLINDENT, UK
MORTHRCS (EDINBURGH)
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Force
Compression
Tension
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more less
more less
Bone deposition more less Bone resorption
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more less
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3. Osteoclasts:
Large multinucleate cells
Responsible for resorption of bone.
Found on bone surfaces undergoing active resorption in pits
called Howship’s lacunae.
DR. REEM ALDHURGHAM
The organic matrix of bone consists of type 1 collagen fibres, proteoglycans, and many growth
factors.
Bone contains more growth factors than any other tissue, which may in part explain its
capability for regeneration, repair, and remodeling.
Many of the growth factors and signaling molecules shown to be associated with bone
homeostasis play an active role in the bone remodeling associated with ortho tooth
movement.
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In areas of tension, the osteoblasts are flattened and the osteoid remains unexposed.
Cells in the PDL increase the amount of a specific secondary messenger (extracellular signal-
related kinase (ERK)) in response to tension.
ERK signaling induces the expression of RUNX-2 which in turn causes an increase in
osteoblast number, possibly by inducing differentiation of fibroblasts into osteoblasts.
Osteoblasts clump into groups, secreting collagen and other proteins composing the organic
matrix, then produce hydroxyapatite, which mineralizes the matrix resulting in new bone.
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If the force applied to a tooth exceeds the pressure in the capillaries (30 mmHg, or around 50
g) blood vessels will be occluded nutrient supply to the PDL will reduce cell death in
the compressed PDL ‘hyalinized’ (as it takes on a glass-like appearance due to sterile necrosis)
There are no osteoblasts to recruit osteoclasts to resorb the bone in the expected way It
takes several days for cells to migrate from undamaged areas.
Eventually osteoclasts appear in the adjacent marrow spaces and resorb the bone from
underneath the necrotic area (Undermining resorption).
Where hyalinization and undermining resorption occur, there is a delay in tooth movement of
10–14 days.
The clinical implications of excessive force are more discomfort for the patient, an increased
risk of root resorption, and the risk of loss of anchorage.
DR. REEM ALDHURGHAM
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External apical root resorption is a complex inflammatory process that occurs in virtually all pts undergoing
tx with ortho appl’s
Odontoclasts are the cells responsible for the resorption of mineralized dental tissue, they are similar, but
not identical to, osteoclasts.
In mild cases of orthodontically induced root resorption (OIRR), only small areas of cementum are resorbed
and these areas are repaired with cellular cementum once the ortho force has stopped.
In more severe cases, the apical portion of the root is removed by odontoclast activity and the root length is
decreased. The remaining dentine will be recovered by cementum, but the root will remain shortened.
There is increasing evidence to suggest that OIRR is more likely where force levels are excessive, especially in
areas of compression.
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Summary
Cellular basis of tooth movement
Ortho tx would not be possible without the ability of the alveolar bone to remodel.
The cells of the PDL are responsible for the bone remodeling and, hence, tooth movement.
The osteoblast is the bone-forming cell and is responsible also for the recruitment and activation of osteoclasts (bone-
resorbing cells).
Many different growth factors and signaling molecules are now known to be involved in bone turnover during ortho tooth
movement with the RANK/RANKL/OPG osteoclast programme being the most important.
Excessive force can cause cell death and hyalinization of the PDL. This leads to a time delay (10–14 days) before the bone is
removed by undermining resorption and then tooth movement can continue. Clinically this can lead to pain, root resorption,
inefficient tooth movement, and anchorage loss.
Root resorption
Root resorption occurs in most pts undergoing ortho tx.
The cell responsible for the removal of cementum and dentine is the odontoclast.
DR. REEM ALDHURGHAM
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Any Questions?
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