Cortical bone offer good anchorage / fixed orthodontics training
Why does cortical bone offer good anchorage?
The marrow space contains a large surface area for cellular activity which is
indispensable for tooth movement.On the other hand if bone involved in tooth
movement is of a compact character the surface area where the cellular reaction
can take place is greatly reduced.
When one is planning orthodontic treatment ,the tooth should remain in spongy
bone during movement.On the other hand when teeth are pitted against cortical
bone they can be used to our advantage to provide more anchorage.
INDIAN DENTAL ACADEMY
Leader in continuing dental education
How soon after extraction can we start treatment ?
Extraction spaces contain tissue undergoing reconstruction which is rich in
cells & vascular supply.Such an area is ideally suitable for tooth
movement & due advantage should be taken of this by commencing
treatment as soon as possible following extraction. Thereby one avoids
atrophy & narrowing of the alveolar process,resulting in bone loss &
cortical bone formation at the extraction site.
Why do teeth move faster in the upper arch?
A common example is space closure in a Class I four premolar extraction
case.It is often necessary to use headgear on the maxillary 1st molars
to maintain the Class I relationship.The relative resistance of the
mandibular molars to mesial movements is well known.
Why do teeth move faster in the upper arch…
Why are mandibular molars more difficult to move mesially than
maxillary molars ?
2 physiologic factors hold the answer:
• Thin cortices & trabecular bone of the maxilla offer less resistance to
resorption than thick cortices & more coarse trabeculae of the
• The leading root of mandibular molars being translated mesially
forms bone that is far more dense than the bone formed by translating
maxillary molars mesially.Why this occurs is not known.
Why do I have to be careful with cases suffering from
Moving teeth when progressive periodontal disease is present
Osteoclasts thrive in the diseased tissue environment.
On the other hand osteoblast histogenesis is suppressed
by inflammatory disease.
When teeth are moved in the presence of active periodontal disease resorption is
normal or even enhanced & bone formation inhibited.this may exacerbate the
disease process,resulting in a rapid loss of supporting bone.
However if the metabolic problems (particularly –ve calcium balance) are
resolved with medical treatment, these patients can be treated orthodontically
assuming sufficient skeletal structure remains.
No age limit is specified for orthodontic treatment; however the clinician must
carefully assess the probability of metabolic bone disease.In addition to
osteoporosis orthodontist must be particularly vigilant for osteomalacia and
Orthodontics:Current principles & techniques
T.M. Graber & R.L. Vanarsdall;225,3rdEd
Osteoporosis: Generic term for low bone mass.
• Age (after 3rd decade).
• Long term glucocorticoid therapy.
• Slight stature.
• Excessive smoking,alcohol.
• Low physical activity.
• Low calcium,vit. D diet.
• Kidney failure,liver disease.
Low bone mass,low radiographic density of jaws, thin cortices, excessive
Vitamin D deficient rickets
Any disorder in the vit.D-Calcium phosphorus axis which results in
hypomineralized bone matrix.
Cessation of calcification of epiphysial growth plate cartilage.however the
cartilage continues to grow.since unmineralized bone canot bear
weight they bow.
Effects on teeth:developmental anomalies of dentin & enamel,delayed
eruption,misaligned teeth,high caries index,eruption rate retarded.
Only flat bones & diaphysis of long bones are affected.Seen in
postmenopausal women with low calcium intake and little exposure to
Features:softening,distortion,increased tendency towards fracture.stress
bearing bones have asymmetric deformities & long bones have
Vitamin D resistant rickets
(familial hypophosphatemia,refractory rickets,phosphate diabetes)
• Hypophosphatemia & hyperphosphaturia associated with decreased
renal tubular reabsorption of inorganic phosphates.
• Familial occurrence,X-linked dominant trait.
• Do not respond to the usual doses of vit. D.
• Normocalcaemia with high normal PTH levels.
• Diminished intestinal calcium & phosphate absorption.
• Decreased growth & short stature.
• Normal vit. D metabolism.
Renal rickets(renal osteodystropy)
Common finding in patients with chronic renal disease.Results from the
inability of diseased kidneys to convert 25-hydroxy cholecalciferol to
the active form of vit.D.
Low alkaline phosphatase levels.Results in rachitic deformity.
It has a role in the hydroxylation of proline in collagen synthesis.
Vit C furthers the normal development of intercellular ground substance
in bone,dentin & connective tissue.
Daily requirements: 35-60mg
Effects on bone:
Osteoblasts fail to form osteoid.Calcified cartilage(scorbutic lattice) is
formed but no bone develops.The calcified cartilage is liable to
fracture(trummerfeld zone or zone of complete destruction).
Bone pain,pathologic fractures,gerneralized osteoporosis,giant cell
tumours of the jaw.
Malocclusion caused by sudden drifting with definitive spaces.Lamina
dura is lost.
Histologically: The most characteristic change in bone is osteoclastic
resorption of the trabeculae of the spongiosa & along the blood vessels
in the haversian system of the cortex.Fibroblasts are found as a mass
in some areas.
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