Generalised radiopacities /prosthodontic courses

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 Florid cementoosseous
dysplasia
 Pagets disease-mature
stage
 Osteopetrosis
 Rarities
 Albrights syndrome
 Caffeys disease
 Camurati-engelmann
disease
 Craniometaphyseal
dysplasia
 Osteogenesis imperfecta
 Familial adenamatosis coli
(gardners syndrome)

 It is the most common cause of pathologic generalised
radiopacity of the jaws .
 It is benign condition usually involves mutiple
quadrants of the tooth bearing regions of the jaws.
 It belongs to spectrum of benign reactive fibro
cemento osseous lesions of periodontal ligament in
origin.

 In united states ,it is seen in middle aged –elderly black
women
 It also develops in chinese and japanese and least in india
 The lesions usually restrictes to the tooth bearing areas of
the jaw bones.
 Bilateral and symmetrical
 Hypercementosis may be feature

 Asymptomatic
 Cortical expansion
 Secondary osteomyelitis-denture wearing prosthesis-
pain ,swelling,mucosal ulceration,sequestra.
 Ulceration-due to alveolar resorption and pressure
points over the expanding mass.

 It demonstrate pagetoid ,cotton wool appearance with
multiple irregularly shaped radiopaque areas with well
defined radiolucent rims.
 3 stages - Radiolucent
- Mixed
-Radiopaque
 Root clubbing with hypercementosis

 Multiple cemento osseous dysplasia
 Familial gigantiform cementomas
 Diffuse sclerosing osteo myelitis
 Pagets and osteopetrosis

Multiple
cementoosseous
dysplasia
Familial
gigantiform
cementomas
Diffuse
scleroisng
osteomyelitis
Pagets and
osteopetrosis
•More common
•Multiple Small
lesions of pcod
and fcod
•Donot cause
cortical expansion
•Not suceptable to
osteomyelitis
•Rare
•m=f
•Early age group
•Involves only one
segment
•It does not have
well defined
radiolucent rim
•It does not show a
prediliction to
black females
•Additional
involvement of the
skeleton and jaws.
•Serum chemistry
levels.
Management- no treatment is required

 Paget's disease is a condition of abnormal resorption
and apposition of osseous tissue in one or more
bones.
 The disease may involve many bones simultaneously,
but it is not a generalized skeletal disease.
 It is initiated by an intense wave of osteoblastic
activity, with resorption of normal bone resulting in
irregularly shaped resorption cavities.

 It is a chronic disease of bone that may occur in 3
stages –
 1)the early -osteoclastic stage
 2)the intermediate stage- osteoblastic- osteoclastic
 3)mature stage -osteoblastic stage

 Age-middle age
 Cortical expansion
 Progressive enlargement of the maxilla
 Alveolar ridge is widened
 Palate is flattened and teeth undergo
migration,tipping , loosening and increased
interproximal spacing
 It is difficult for edentulous patients to wear
removable prosthesis which must be periodically
remade to accomadate alveolar expansion.

1. Trebeculae are reduced in number , but these
remaining are coarse and tend to run in the direction
of bone with minimum intersection –post to bicuspids
2. Increase In the number of trebecula which are finer in
texture-greater density of bone
3. Coarse and sparse trebecula some times tend to
converge towords the midline of the mandible –highly
suggestive of pagets disease
4. Cortex at the inferior border of the mandible to loose
density and reveals laminated structures

 A common radiographic manifestation is structure of the
bone is altered in such a way that trebaculae are replaced
by dense bone which is granular in nature
 With in the radiolucent bone areas of greatly increased
density -Cotton wool appearance

 Loss of lamina dura
 Hypercementosis
 Some root resorption may present
 Osteogenic sarcoma has increased incidence in pagets
disease

Disease Lab findings
Pagets •Serum calcium and phosphate levels-
normal
•Serum alkaline phosphatase levels
•Urinary hydroxy proline levels
•Urinary excretion of bone specific
pyridinium collagen cross links
•Urinary n –telopeptide
•Urinary alpha c- telopepetide

 The bone is dense with massive trabeculae due to
fusion of small trabeculae
 Mosaic pattern-reversal lines from increased
resorption and apposition of bone
 Osteoblasts and osteoclasts are seen rimming the
trabeculae

 Osteopetrosis
 flcod

 Other names-albers schonberg disease ,marble bone
disease
 It is group of diseases that affect the growth and
remodelling of bone
 It is charecterised by overgrowth and sclerosis of bone
with resultant thickening of bony cortices and
narrowing of marrow cavities
 It is due to failure of bone resorption related to
defective osteoclasts

 3 types of osteopetrosis
Osteopetrosis tarda
Osteopetrosis congenita
Marble bone disease

Variant
Inheritance
pattern Pathophysiology Clinical features
Age of
onset Prognosis
Osteopetrosis
tarda
Autosomal
dominant
Abnormal
osteoclastic bone
resorption
No bone marrow failure; brittle
bones; increased susceptibility to
fractures but with normal healing;
degenerative joint disease; 50%
of patients are asymptomatic
Adulthood Good
Osteopetrosis
congenita
Autosomal
recessive
Abnormal
osteoclastic bone
resorption
Severe bone marrow failure;
pancytopenia; bleeding; infection;
failure to thrive; growth
retardation; proptosis; blindness;
deafness; hydrocephalus
Infancy Poor
Marble bone
disease
Autosomal
recessive
Abnormal
osteoclastic bone
resorption
No bone marrow failure; renal
tubular acidosis; intracranial
calcifications; sensorineural
hearing loss; psychomotor
retardation
Childhood Poor

 Increased density of the entire skeleton –diffuse
homogenous ,symmetrically sclerotic appearance of all
bones
 Pathologic fractures – most common clinical sign
 The normal land marks are lost in the dense ,diffuse
radiopacity
 Diploe is effaced
 Narrowing of cranial foramina-nerve and vessel
compression
 Hearing loss ,impairement of vision and facial palsy

 Bone is dense –roots of the teeth obscure
 Density is generally homogenous ,increased
thickening of trabeculae with reduction of marrow
spaces
 Lamina dura is lost
 Dental findings-
 Delayed tooth eruption
 Partial anodontia
 Unerupted teeth
 Malformed teeth
 Enamel hypoplasia
 Abnormal pulpchambers,early decay.thickened lamina
dura

Malignant osteopetrosis Benign osteopetrosis
Serum calcium
Parathyriod hormone
Serum acid phosphatase
Creatine kinase BB
Serum acid phosphatase
Creatine kinase BB
Serum bone specific alkaline phosphate
Lab findings

 Flcod
 Pagets disease

Gardeners syndrome

CONCLUSION

Polyostotic fibrous dysplasia Pagets disease
•It involves localised bone
•Age-<20yrs
•Unilateral
•Radiographic-ground glass pattern
•Serum chemistry not significant
•Abnormal trabeculae of
immature(woven bone ) in fibrous
marrow
•It involves complete bone
•Middle age
•Bilateral
•Radiographic-cotton wool appearance
• Serum chemistry changes present
•Extensive osteoclastic and osteoblastic
activity (woven) bone in a fibrous
marrow. surrounding “mosaic”
trabeculae with vascular dilation and
lymphocytic infiltration of marrow

flcod osteopetrosis pagets
•Mandible and maxilla
•Black women
•>30yrs
•Radiolucent rim present
•Serum chemistry –not
significant
•Involves all skeletal
bones
•Benign-older persons
•Malignant-childhood
•Absent
•Serum chemistry values
•Involves
skull,pelvis,vertebrae,fem
ur ,maxilla,mandible
•Middle age
•Hypercementosis is seen
•Absent
•Serumchemistry values

 Principles practice oral radiologic interpretation H.m
worth
 Oral radiology principles and interpretation 5th edition
white & pharaoh
 Differential diagnosis of orol and maxillofacial lesions
5th edition norman.k and wood,paul w.goaz

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