2. ORAL PATHOLOGY
It is the speciality of dentistry and pathology that deals
with the nature, identification and management of
Dr. Ali Tahir
diseases affecting the oral & maxillofacial regions
It is a science that investigates the causes, processes &
effects of these diseases
The practice of oral pathology includes research,
diagnosis of disease using clinical, radiographic,
microscopic biochemical or other necessary
examinations & investigations
3. DISTURBANCES IN SIZE
Microdontia
When one or more teeth are smaller than
normal
Dr. Ali Tahir
Generalized
True generalized: When all teeth are uniformly smaller
than normal
Cause: Pituitary Dwarfism, Down’s syndrome
Relative generalized: When mandible or maxilla are
somewhat larger (Macrognathia) but teeth are of normal
size
Localized
When one tooth is involved
Maxillary lateral incisors are the most common
5. DISTURBANCES IN SIZE
Macrodontia
When one or more teeth are larger than normal
Dr. Ali Tahir
Generalized
True Generalized: When all teeth are uniformly larger
Relative Generalized: When maxilla/mandible is smaller
in size (Micrognathia) but teeth are of normal size
Regional
It is localized e.g; Hemifacial hypertrophy (unilateral),
segmental odontomaxillary dysplasia
Rhizomegaly :
When only roots are larger than normal
7. DISTURBANCES IN NUMBER
Anodontia
Congenital absence of all teeth
Dr. Ali Tahir
Associated with Hereditary Ectodermal Dysplasia
Hypodontia
Congenital absence of one or more teeth
Third molars, maxillary lateral incisors are most
commonly absent teeth consecutively
9. DISTURBANCES IN NUMBER
Supernumerary Teeth
Teeth in excess of normal number
Dr. Ali Tahir
More common in maxilla (90%)
Examples
Maxilla
Mesiodens
Paramolars
Lateral incisors
Mandible
Premolars
paramolars
Multiple supernumerary teeth are seen in Cliedocranial dysplasia
and gardner sydrome
11. DISTURBANCES IN ERUPTION
Premature Eruption
Natal Teeth:
Dr. Ali Tahir
Erupted decidous teeth present at time of birth
Neonatal:
Deciduous teeth that erupt in first 30 days of life
Premature eruption of entire permanent dentition should
suspect the possibility of hyperthyroidism
13. DISTURBANCES IN ERUPTION
Delayed Eruption
Eruption later than the normal age of eruption
Dr. Ali Tahir
Usually idiopathic
Or associated with systemic conditions such as
rickets, cliedocranial dysplasia, cretinism
Gingival fibromatosis
14. DISTURBANCES IN ERUPTION
Impacted teeth
Teeth with eruption that is impeded by a
Dr. Ali Tahir
physical barrier
Causes:
Dental crowding
Supernumerary teeth
Odontogenic cysts
Odontogenic tumors (odontomas)
Most common are mandibular and maxillary
third molars followed by maxillary cuspids
15. IMPACTED TEETH
Classified according to their orientation as
Mesioangular
Dr. Ali Tahir
Distoangular
Horizontal
Vertical
According to their stage of eruption
Completely impacted (within bone)
Partially impacted (partly in soft tissue)
16. IMPACTED TEETH
Partially impacted teeth that communicate with the oral
Dr. Ali Tahir
cavity are more prone to pericoronitis
Complications
Root resorption of adjacent normal tooth
Infection & pain
Dentigerous cyst
External resorption of impacted tooth
18. DISTURBANCES IN ERUPTION
Eruption Sequestrum
A small spicule of calcified tissue that is extruded
Dr. Ali Tahir
through the alveolar mucosa that overlies an
erupting molar
19. DISTURBANCES IN SHAPE
Dilaceration
A sharp bend or
Dr. Ali Tahir
angulation involving the
root of the tooth
Causes:
Trauma during tooth
formation
Continued root
formation during a
curved or tortuous path
of eruption
20. DISTURBANCES IN SHAPE
Taurodontism
A molar with an
Dr. Ali Tahir
elongated crown and
apically placed
furcation of roots
resulting in an enlarged
rectangular pulp
chamber.
Occurs because of late
invagination of
Hertwig’s Epithelial
Root Sheath
21. DISTURBANCES IN SHAPE
Dens Invaginatus
Developmental
Dr. Ali Tahir
anomaly characterized
by a deep enamel lined
pit that extends for
varying depths into the
underlying dentin
displacing the pulp
chamber
22. DENS IN DENT AND SUPERNUMERARY
CUSP
Supernumerary
cusps
Dr. Ali Tahir
Teeth containing
additional cusp
Example: Cusp of
caribili, Talon cusp
23. DISTURBANCES IN SHAPE
Dens Evaginatus
Characterized by
Dr. Ali Tahir
cusp like
supernumerary
enamel protrusion
on occlusal or
lingual surface of
crown
24. Gemination
Single rooted tooth with
Dr. Ali Tahir
unusual wide, partly
divided crown or two
separate crowns.
Cause: Because of
partial division of a
single tooth gem
Teeth count is normal
25. DISTURBANCES IN SHAPE
Fusion
Abnormally shaped
Dr. Ali Tahir
tooth with wide crown
or a normal crown with
additional root(s)
Cause: Results from
the union of two tooth
germs
26. DISTURBANCES IN SHAPE
Concrescence
Union of the roots of
Dr. Ali Tahir
two or more normal
teeth by confluence of
their cementum.
Cause: Trauma, Inter-
septal bone loss
27. DISTURBANCES IN SHAPE
Hypercementosis
One or more teeth with excessive deposition of
Dr. Ali Tahir
cementum of roots
Causes: Increase/Decreased occlusal forces,
Paget’s disease, hyperpituitarism, chronic
inflammation
28. Cervical Enamel
Projections
Dr. Ali Tahir
Apical extension of
coronal enamel beyond
the smooth cervical
margin
29. Hemispheric structures
that may consist
Dr. Ali Tahir
entirely of enamel or
may contain underlying
dentin & pulp
Mostly present in roots
of maxillary or
mandibular molars
30. DISTURBANCES IN STRUCTURE OF ENAMEL
Acquired
Environmental factors
Dr. Ali Tahir
Bacterial (syphilis), viral infections
Inflammation
Nutritional deficiencies
Chemical injuries
Trauma
Genetic
Amelogenesis Imperfecta
31. ACQUIRED DISTURBANCES
Focal enamel hypoplasia
Localized enamel hypoplasia involving one or two
Dr. Ali Tahir
teeth
Example: Turner tooth, results from localized
inflammation or trauma during tooth development
Enamel has pitting areas or deformed with
yellowish or brownish discoloration
32. ACQUIRED DISTURBANCES
Generalized Enamel Hypoplasia
Systemic or Environmental factors inhibit
functioning ameloblasts.
Dr. Ali Tahir
Enamel has horizontal lines of small pits or
grooves
Example:
Hutchinson’s incisors and mulberry molars due to
congenital syphilis
Neonatal line
Flourosis
Can also be seen in hypocalcemia (Vit. D
deficiency), measles, chicken pox, scarlet fever, Vit
A & C deficiency
34. ACQUIRED DISTURBANCES
Flourosis (Flouride mottling)
Minimal Flourosis:
Dr. Ali Tahir
Smooth enamel surface with white flecks
Mild Flourosis:
Smooth enamel surface with white opaque areas
Moderate to severe:
Pitting and brownish discoloration
Severe:
Enamel is softer and weaker than normal, resulting
in excessive wear
Teeth are largely resistant to caries
36. HEREDITARY DISTURBANCES
Amelogenesis Imperfecta
A heterogeneous group of genetic disorders
Dr. Ali Tahir
exhibiting faulty enamel formation (affects both
primary & permanent dentition)
Normal enamel formation:
1. Enamel matrix formation
2. Mineralization of enamel
3. Enamel maturation (secondary mineralization)
Accordingly three types of AI is identified
37. TYPES
Clinical Features:
Hypoplastic (focal or generalized)
Decreased enamel formation by disturbance in function of
ameloblasts
Dr. Ali Tahir
Enamel is thinner than normal
Radiodensity is greater than that of dentin
Hypocalcified
Defect in mineralization of enamel
Enamel is off normal thickness but softer than normal
Can be easily removed with a blunt instrument
Radiodensity is lesser than that of dentin
Haypomaturation
Focal or generalized areas of immature enamel
crystallites
Enamel of normal thickness, but less harder and is
radiolucent e.g. snow capped teeth
40. DISTURBANCES IN STRUCTURE OF DENTIN
Acquired
Turner tooth
Regional odontodysplasia
Dr. Ali Tahir
Genetic
Dentinogenesis Imperfecta
Type I
Type II
Type III
Dentin Dysplasia
Type I
Type II
Familial hypophosphatemia (Vit. D resistant rickets)
41. DENTINOGENESIS IMPERFECTA
A hereditary (autosomal dominant) defect
consisting of opalescent teeth composed of
irregularly formed & undermineralized dentin
that obliterates the pulp chambers & canals
Dr. Ali Tahir
Types:
Type 1
Associated with osteogenesis imperfecta.
Characterized by bluish tint to sclera
Type 2
Hereditary opalescent dentin
Most common type
Type 3
Also called brandywine type
Clinically the same as type 1 & II
Multiple pulpal exposures of decidous dentition
42. DENTINOGENESIS IMPERFECTA
Clinical Features
Both dentitions are affected
Oplaescent teeth with bluish grey to brownish
Dr. Ali Tahir
or yellowish discoloration
Abnormally soft dentin, enamel easily chipped
off
Despite the exposure of dentin, teeth are not
prone to caries
Histopathology
The mantle dentin is normal whereas remaining
dentin is severely dysplastic
Amorphous matrix with globular & inter-globular
areas of mineralization
Irregularly widely spaced disoriented dentinal
tubules
44. RADIOGRAPHICALLY
Type I & II
Bulb shaped crowns
Dr. Ali Tahir
Constricted cemento-enamel junction
Thin roots
Varying degrees of obliteration of pulp chamber &
canals
Type III
Same features or may show extremely large pulp
chambers surrounded by thin shell of dentin
45. DENTIN DYSPLASIA
A hereditary defect in dentin formation where root
dentin is abnormal & gnarled, roots are
Dr. Ali Tahir
shortened & tapered
Also called Rootless teeth
Autosomal dominant
Two types
Type I (radicular)
Type II (coronal)
46. DENTIN DYSPLASIA
Types:
1) Radicular Dentin Dysplaisa:
Dr. Ali Tahir
Brownish or bluish translucency in cervical region
More common than type II
All teeth in both dentitions are affected
Teeth often show increased mobility & exfoliate prematurely
Histopathology:
Enamel and mantle dentin is normal
Remaining coronal and root dentin consists of nodular
masses composed of tubular dentin and osteo-dentin
Slit-like pulp remnants may be seen between nodular masses
Gives an appearance of ‘lava flowing around boulders’
48. RADIOGRAPHICAL FEATURES
Short blunt roots, may
be absent entirely
Dr. Ali Tahir
Mandibular molars
have W-shaped roots
Dentition may show
obliteration of pulp
chambers & canals
Crescent shaped
remnants of pulp may
be seen
50. DENTIN DYSPLASIA TYPE II (CORONAL)
Both dentitions affected
Deciduous teeth with bluish-grey, brownish or
yellowish discoloration
Dr. Ali Tahir
Same translucent, opalescent appearance as in DI
Permanent teeth have normal clinical appearance
Histopathology:
Deciduous teeth
Normal zone of mantle dentin that changes abruptly into
dense amorphous dentin with irregular arrangement of
tubules.
Permanent teeth
Globular and inter-globular areas of dentin in pulpal third
of dentin with atubular root dentin
Has pulp stones in pulp chamber
Narrow pulp canals
51. RADIOGRAPHIC FEATURES
Deciduous teeth show
obliteration of pulp
chambers & canals as
Dr. Ali Tahir
seen in DD type I & DI
Roots are normal
Pulp chambers of
permanent teeth are
enlarged
Thistle-tube or flame
shaped pulp chamber
Pulpal calcifications in
coronal pulp chamber
52. REGIONAL ODONTODYSPLASIA (GHOST
TEETH)
Defective formation of enamel and dentin with
abnormal pulp and follicle calcifications with
Dr. Ali Tahir
surrounding soft tissue hyperplaisa along-
with accumulations of spherical
calcifications and odontogenic rests
53. CLINICAL FEATURES
More common in maxilla
Affects several adjacent teeth in the same quadrant
Dr. Ali Tahir
Mostly in permanent dentition
Deformed teeth with soft, leathery surface
Discolored, yellowish brown
Histopathology
Dysplastic, globular and interglobular dentin
Widened predentin layer
Enlarged pulp chamber with pulp stones
54. RADIOGRAPHIC FEATURES
Ghost teeth
Decreased
Dr. Ali Tahir
radiodensity
Enamel & dentin are
very thin
Large pulp chambers
Pulp stones
56. DISTURBANCES IN STRUCTURE OF
CEMENTUM
Hypophosphatasia
Disorder of bone mineralization caused by
Dr. Ali Tahir
deficiency in alkaline phosphatase in serum and
tissues
Autosomal recessive/dominant
Delayed formation and eruption of dentition
Premature loss of primary teeth
Spontaneous loss of permanent teeth
Radiographically
Enlarged pulp chambers & pulp canals
Histopathology
Absence or marked reduction of cementum