1. Bone Pattern

2. Outline Normal bone pattern Localized change in bone pattern
Radiographic changes in diseases affecting bone
Systemic Diseases affecting bone
Hyperparathtroidism
Rickets Osteomalacia
Osteopetrosis
Paget’s disease
Sickle cell anemia and Thalasemia
Conclusion

3. Normal Bone Pattern * Cortical plates Cancellous bone
To understand what abnormal bone looks like we must fully understand what normal bone pattern looks like.
Normal: cancellous bone which lies between well defined cortical plates (dense compact bone).
Important cortical plates look for:
Inferior boarder of the mandible which is made of robust cortical bone
Cotex of the anterior and posterior boarders of the ramus of the mandible
IAN cotex
Cortical boundries of the maxillary sinus *

4. Normal Bone Pattern Cancellous Bone:
Trabeculae------thin radiopaque plates and rods, surrounding many small radiolucent pockets of marrow.
The radiographic pattern of the trabeculae show intrapatient and interpatient variability
Or Trabecular bone

5. Normal Bone pattern Maxilla Mandible Anterior Posterior
Trabeculae: Thin, numerous---Fine granular dense pattern, random orientation.
Marrow spaces: small, numerous
Trabeculae: Thick, coarse, horizontally orientation
Marrow spaces: Larger
Posterior
Same as above
Larger marrow spaces
More horizontally oriented trabeculae
Larger marrow spaces in the periradicular area

6. Normal Bone Pattern
The distribustion and size of the trabeculae throughout both jaws show a relationship to the thickness (and strength) of the adjacent cortical plates.
So where the cortical plates are thick (posterior mandible), internal bracing by the trabeculae is not needed…….so there are fewer trabeculae. By contrast in the maxilla and anterior mandible were the cortical plates are less rigid trabeculae are more numerous----more internal bracing

7. Localized Change in bone Pattern

8. Dense Bone Island Or enostosis, internal counterpart of exostoses
Localized growth of compact bone in the cancellous bone.
Well-defined but may blend with the surrounding bone.
No trace of a radiolucent margin or capsule.
RARELY may cause external root resorpsion
Or enostosis, internal counterpart of exostoses
Seen more in the mandible

9. Marrow space Or Focal Osteoporotic Bone marrow
Normal area of hematopoietic or fatty marrow, etiology is unknown but has be postulated to be:
Bone marrow hyperplasia
Persistent embryonic marrow remnants
Site of “ abnormal” healing following extraction, trauma, or local inflammation.
Or Focal Osteoporotic Bone marrow

10. Generalized Change in Bone Pattern

11. General radiographic changes of diseases affecting bone:
Change in size or shape of bone.
Change in number /size/ orientation of trabeculae.
Altered thickness and density of cortical structures.
Increase or decrease in overall density of bone
Systemic disorders affect the entire bode, so the radiographic changes in the jaws are generalized.
In most cases it is not possible to to identify diseases based on radiographic characteristics.

12. Mature are immune to systemic demineralization.
Some Systemic diseases that occur DURING tooth formation may result in dental alterations
Accelerated or delayed eruption.
Hypoplasia
Hypocalcification
Loss of lamina dura
Mature are immune to systemic demineralization.

13. Diseases affecting Bone
Diseases that cause
DECREASE in bone
density
Diseases that cause
INCREASE in bone
density
Teeth stand out
Against a radiolucent
jaw
Loss contrast of
Inferior cortex of
madndible
Cortical structures
Thin, less defined
IAN canal stands
out

14. Systemic Diseases Manifested in the Jaws
Endocrine
Disorders
Metabolic Bone
Diseases
Others
Hyperparathyroidism
Osteoporosis
Scleroderma
Hypoparathyroidism
Rickets
Sickel cell anemia
Hyperpituitarism
Hypophosphatasia
Thalassemia
Hypophosphatemia
Hypopituitarism
Osteopetrosis
Hyperthyroidism
Hypothyroidism
Diabetes
Cushing’s Syndrome

15. Hyperparathyroidism
Excess of serum PTH:
Increases bone remodeling (osteoclastic resorption)
Increases renal reabsorption of calcium
Increases renal production of active vitamin D.
Could be primary due to an adenoma in one of the glands
Or secondary as a result of a compensatory increase in PTH in response to hypocalcemia.
Condition of older patients 30-60
Increase serum
calcium

16. Hyperparathyroidism
Radiographic Features: (1 in 5 have obvious radiographic changes)
CHANGES IN THE JAWS:
Loss and thinning of cortical boundaries
Decrease in density of jaw *
Trabeculae: small, numerous, randomly oriented, Ground glass appearance, *
Teeth stand out in contrast to the radiolucent jaws.
Ground glass

17. Hyperparathyroidism Brown Tumours:
Brown tumours regress spontaneously when the condition is treated.
Resemble central giant cell granuloma. Histologically its identical to a giant cell granuloma.
If giant cell granuloma occurs later than the second decade, patient should be screened for hyperparathyroidism.

18. Hyperparathyroidism
CHANGES IN THE TEETH:
Loss of lamina dura
loss of lamina dura may give the root a tapered appearance because of decreased image contrast.

19. Rickets (infants) and Osteomalacia (adults)
Inadequate serum and extracellular levels of calcium and phosphate (minerals required for normal calcification of bone and teeth).
They result from a defect in the normal activity of vitamin D metabolites which is required for normal reabsorption of calcium from the intestines.

20. Rickets may result in hypoplasia of the dental hard tissues.
These changes may manifest as:
Large pulp chambers and widened root canals.
Thinning or loss of tooth follicle cortices and laminae durae.

21. Osteopetrosis
Is a disorder that results from a defect in the differentiation and function of osteoclasts
Abnormal formation and remodelling of primary skeleton and generalized increase in bone mass.
Dense, fragile bones susceptable to fracture and infection
Obliteration of marrow---compromises hematopoiesis and compresses cranial nerves

22. Bones show great increase in density, which is bilaterally symmetrical
Osteopetrosis
It is homogeneous and diffused.
Loss of Contrast between the outer cortical boarder and the cancellous bone
Entire bone may be mildly enlarged
Bones show great increase in density, which is bilaterally symmetrical

23. Osteopetrosis Increased radiopacity of the jaws.
The radiographic image may fail to reveal any internal structure.
Roots may fail to appear.
Delayed eruption of teeth
Malformed teeth

24. Paget’s Disease
A condition of abnormal resorption and apposition of osseous tissue in one or more bones.
Affects late middle and old age.
Males>Females (2:1)
Frequent in Great Britain and Australia.
Ds may involve many bones simultaneously, but it is not a generalized skeletal ds.

25. Paget’s Disease Clinical Features: Enlargement of the skull
Jaws
Enlargement of the Jaws:
Separation and movement of teeth
Tight or ill fitting dentures
Curvature of the spine
“buffalo hump”
Bowing of the legs
Neurologic Pain– due to bone impingement on foramina and nerve canals

26. Paget’s Disease
Three radiographic phases:
Early radiolucent resorptive stage:
Decrease density of bone.
Decrease number of trabeculae.
Granular second stage:
Short, random distribution of trabeculae.
Granular pattern of bone
Dense radiopaque appositional late stage:
Cotton-wool appearance
Basically an intense wave of osteoclastic activity. Which results in irregular shaped resorption cavities.
Vigorous osteblastic phase trying to for woven bone

27. Increase in dimension between the internal and outer cortex of skull
Hypercementosis
Cotton-wool pattern

28. Paget’s Disease Complications: Extraction sites heal slowly.
Higher incidence of osteomyelitis.
Development of osteosarcoma (10%).

29. Sickle Cell Anemia Hemolytic blood disorder. Abnormal hemoglobin:
Under low oxygen tension results in sickeling of the RBCs.
These RBCs have a reduced ability to carry oxygen.
Because of their abnormal membrane proteins, they adhere to vascular endothelium and obstruct capillaries.
Abnormal RBCs are destroyed by the spleen.
Hematopoietic system responds to the anemia by increasing the production of RBCs.
Which requires hyperplasia of the bone marrow.
Sickle cell crisis

30. Thalassemia
Defect in hemoglobin synthesis. It involves either alpha of beta globulin genes
Resultant RBCs have reduced hemoglobin content and have a shortened life span.

31. Radiographic Changes:
The hyperplasia of the bone marrow at the expense of cancellous bone is the primary reason for the radiographic manifestations of sickle cell anemia and thalassemia.

32. Radiographic Changes:
General osteoporosis.

33. Radiographic Changes:
Widening of the diploic space.
Outer table of skull will not be apparent and a hair-on-end appearance.
Linear alteration of the trabeculae.

34. Drugs That Affect Bone Density
Corticosteroids
Heparin
Antiepileptic drugs
Cytotoxic drugs
Ciclosporin (immunodepressant)

35. Radiograph at a later time
What do you do if you suspect the presence of disease (apparent absence of trabeculae)?
Examine previous
radiographs
Change
No Change
Most probably
abnormal
Repeat R with lower
exposure
Change
No Change
Presence of expected but sparse trabecular pattern that was over exposed----Normal
Follow up with a
Radiograph at a later time