Cortical bone /certified fixed orthodontic courses by Indian dental academy


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Cortical bone /certified fixed orthodontic courses by Indian dental academy

  1. 1. CORTICAL BONE INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Clinical considerations 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.
  3. 3. Clinical considerations 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.
  4. 4. Clinical considerations 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.
  5. 5. Clinical considerations 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 mandible. • 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.
  6. 6. Clinical considerations Why do I have to be careful with cases suffering from periodontitis? Moving teeth when progressive periodontal disease is present invites disaster. 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.
  7. 7. 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 renal osteodystrophy. Orthodontics:Current principles & techniques T.M. Graber & R.L. Vanarsdall;225,3rdEd
  8. 8. Osteoporosis: Generic term for low bone mass. Risk factors: • Age (after 3rd decade). • Long term glucocorticoid therapy. • Slight stature. • Menopause. • Excessive smoking,alcohol. • Low physical activity. • Low calcium,vit. D diet. • Kidney failure,liver disease. Features: Low bone mass,low radiographic density of jaws, thin cortices, excessive bone resorption
  9. 9. 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.
  10. 10. Adult rickets Only flat bones & diaphysis of long bones are affected.Seen in postmenopausal women with low calcium intake and little exposure to UV light. Features:softening,distortion,increased tendency towards fracture.stress bearing bones have asymmetric deformities & long bones have hairline fracture.
  11. 11. 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.
  12. 12. 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. Hypophosphatasia Low alkaline phosphatase levels.Results in rachitic deformity.
  13. 13. Vitamin C 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).
  14. 14. Hyperparathyroidism 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.
  15. 15. Leader in continuing dental education