This document provides an overview of oral pathology and abnormalities of teeth. It discusses various histological staining techniques used in oral pathology as well as abnormalities in tooth shape, number, enamel, dentin, pulp, and color. Some key points include descriptions of taurodontism, supernumerary teeth, amelogenesis imperfecta, dentinogenesis imperfecta, regional odontodysplasia, pulp calcification, internal and external resorption, and endogenous and exogenous staining. The document serves as a guide for oral pathology laboratory procedures and identifying various dental abnormalities.

1. Oral Pathology I. Lab.
BDS-231
.Aiman A. Ali DDS, PhD

2.  Slide preparation for histopathological
examination
Routine H & E
Ground sections
Decalcified
sections

3. Macroscopic description

4. Old machine [Processing]

5. Computerized machine [Processing]

6. Paraffin bath

7. Microtome

8. Staining

9. Mounting

10. HP Diagnosis

11. Archiving

12. Ground sections

13. Decalcified sections

14. Periodic Acid Schiff (PAS)
 This technique identifies a number of polysaccharides
and carbohydrate-containing compounds

15. Masson Trichrome Stain
 Collagen fibers stain an intense green

16. Aldehyde Fuchsin
 Stains elastic fibers purple to black.

17. Verhoeff's Hematoxylin
 This method stains elastic fibers black in
addition to nuclei

18. Wright's/Giemsa Stain
 Stains for blood and bone marrow smears

19. Immunohistochemical staining

21. February 19, 2005
Oral Pathology I
Abnormalities of Teeth I & II

22. Alteration in Shape
Taurodontism
 It is a variation of tooth form.

Elongated crown

Apically displaced furcation

Increased height of pulp
chamber

Associated with Down
syndrome

23. Alteration in Shape
Taurodontism
 11%
occurrence in middle
east
 It
is of little clinical
significance
 No
treatment is required

24. Alterations in Shape
Supernumerary root
 Accessory roots are most
commonly seen in:
 Mandibular
canines
 Premolars
 Molars
(thirds)
 Recognition of extra-root numbers
is important for extractions or
endodontic treatment

26. Alterations in Shape
Enamel pearls
 Droplets of ectopic enamel, they
occur most commonly on

The bi-or tri-furcation of teeth

Maxillary & mandibular molars

It may be detected on
radiographic examinations

It is of significance when
periodontal disease is present

27. Alterations in Shape
Enamel pearls

28. Attrition, Abrasion & Erosion
 Attrition: The loss of tooth structure from tooth
to tooth contact
 Abrasion: The loss of tooth structure due to
repeated mechanical contact with objects other
than teeth
 Erosion: Non-carious loss of tooth structure
due to chemical dissolution not related to acid
produced by dental plaque

29. Attrition, Abrasion & Erosion

30. Alterations in Shape
Attrition
 It is a physiologic wearing of
teeth as a result of
mastication

It is an age related process
& varies from one
individual to another

Diet, dentition,
musculature & chewing
habits can influence the
pattern of attrition

31. Alterations in Shape
Abrasion
 It is the pathologic wearing of teeth
as a result of abnormal habit
(abrasive substance)

Pipe smoking

Tobacco chewing

Aggressive toothbrushing

Abrasive dentifrices

32. Alterations in Shape
Erosion
 It is a loss of tooth structure
from a non-bacterial chemical
process
 Acids
 External: work
environment or in the diet
 Internal: regurgitation of
gastric contents (chronic
vomiting)
 In many cases of tooth
erosion, no cause is found

33. Alterations in Number
Anodontia
 It is an absence of teeth that is
often associated with hereditary
ectodermal dysplasia
 It is caused by polygenic
(enviromental & genetic
factors)
 The prevalence of hypodontia is
4.6%
Complete anodontia:
All teeth are missing

34. Alterations in Number

35. Alterations in Number
Anodontia
 Partial
anodontia (hypodontia):
one or several teeth are missing
 Pseudoanodontia:
when teeth
are absent clinically
 Most
commonly seen in third
molars, second premolars &
maxillary lateral incisors

36. Alterations in Number
Impaction
 It is most commonly seen in
mandibular third molars &
maxillary cuspids, it occurs
because of:

Crowding

Physical barrier

Abnormal eruption path

Ankylosis (fusion of tooth to
alveolar bone)

37. Alterations in Number
Supernumerary teeth
 It results from continued
proliferation of permanent or
primary dental lamina

The tooth can be rudimentary
& miniature

It can be an isolated event,
familial or associated with
syndromes

38. Alterations in Number
Supernumerary teeth
 Clinical significance:
 Occupy space
 Block eruption
 Delay or mal-eruption
 Natal teeth
 Post-permanent dentition
 Maxilla>mandible: 10:1
 Anterior midline of maxilla
(mesiodens)
 Fourth molar

39. Defects of Enamel
Environmental defects of enamel
 Severe metabolic injury can cause:

Defects in the quantity & shape

Enamel hypoplasia

Defects in the quality and color

Enamel hypocalcification
Enamel hypoplasia

40. Defects of Enamel
Environmental defects of enamel
 The extent of the defect is
dependent on:

The intensity of the etiologic
factor

The duration

The time of occurrence
Enamel hypoplasia

41. Defects of Enamel
Environmental defects of enamel
 Etiologic factors can be

Local: (Turner’s tooth)



Trauma
Abscess
Clinical signs

Hypocalcification or hypoplasia

42. Defects of Enamel
Environmental defects of enamel
 Systemic

should occur after birth and
before age 6

It commonly affect anterior
teeth and first molars

Defects in primary teeth and
possibly the tips of central
incisors and first molars

43. Defects of Enamel
Environmental defects of enamel

Research have shown that causes are
attributed to

infectious diseases

Nutritional defects (rickets)

Congenital syphilis

Birth trauma (neonatal line)

Fluoride (hypoplasia or
hypocalcification)

Idiopathic factors

44. Amelogenesis Imperfecta
 It is a hereditary disorders affects both
primary and permanent dentitions
 It can be hypocalcified or hypoplastic

Hypoplastic type


Insufficient amount of enamel
(pits & grooves to aplasia)
Hypocalcified type:

Soft & friable enamel (wears
readily)

45. Amelogenesis Imperfecta
 The color varies from white
opaque to yellow to brown
 Dentin & pulp chamber appear
normal
 Cosmetic problem

46. Defects in Dentin
Dentinogenesis imperfecta

It is an autosomal dominant trait

It affects dentin in both primary
and permanent dentitions

Type I: Occurs in pts. With
osteogenesis imperfecta

Type II: Only dentin but no bone
abnormalities

47. Defects in Dentin
Dentinogenesis imperfecta

Type III: Only dental defects occur

Pulp exposures

Periapical radiolucencies

Variable radiographic appearance

48. Defects in Dentin
Dentinogenesis imperfecta
 Clinical features:

Both dentitions exhibit translucent
appearance

Yellow-brown to gray

The enamel fractures easily

Excessive constriction at the
cementoenamel junction

Roots are shortened and blunted

49. Defects in Dentin
Dentinogenesis imperfecta
 Radiographically, Type I & II exhibits
identical changes:

Opacifications of dental pulps

Short roots and bell shaped crowns
 Type III:

Dentin appears thin

Pulp chambers and root canals are
extremely large (Shell teeth)

50. Defects in Dentin
Dentinogenesis imperfecta
 Microscopically:

The dentin contains fewer but larger and irregular dentinal
tubules

Pulp replaced by irregular dentin

Enamel appears normal but dentinoenamel junction is
smooth
 Treatment is directed toward protecting tooth from wear
and esthetic appearance

51. Defects in Dentin
Dentin dysplasia
 It is a hereditary rare condition that
has been subdivided to:
 Type I (radicular type)
 The color of both dentition is
normal
 Periapical lesions are regular
features
 Premature tooth loss (short roots)
 Pulps are completely obliterated

52. Defects in Dentin
Dentin dysplasia
 Type II (coronal type)
 Primary dentition is opalescent and
permanent dentition is normal
 The coronal pulps are large and
filled with globules of abnormal
dentin
 Periapical lesion are not regular
features
 Primary teeth appeared similar to
type I but permanent teeth exhibit
enlarged pulp chamber

53. Defects in Dentin
Dentin Dysplasia
 Microscopically:

Enamel and immediately subjacent dentin appear normal

Deeper layers of dentin shows atypical tubular patterns &
amorphous, atubular areas and irregular organization
 Treatment is directed toward retention of teeth but
prognosis is poor

54. Defects of Enamel & Dentin
Regional odontodysplasia
 It is a dental abnormality that
involves the hard tissues that
are derived from both epithelial
(enamel) and mesenchymal
(dentin & cementum)
components of the tooth
forming apparatus

55. Defects of Enamel & Dentin
Regional odontodysplasia
 A region or quadrant of the maxilla
or mandibule are affected

Short roots

Open apical foramina

Enlarged pulp chambers

Poor mineralization of enamel &
dentin (ghost teeth)

56. Defects of Enamel & Dentin
Regional odontodysplasia
 Permanent teeth>primary teeth
 Maxillary anterior teeth are more affected
 Eruption is delayed or does not occur

57. Defects of Enamel & Dentin
Regional odontodysplasia
 Cause in unknown, however:
 Trauma
 Nutritional deficiencies
 Infections
 Metabolic abnormalities
 Systemic diseases
 Local vascular compromize
 Genetic influences
 Treatment: teeth removal because of poor quality

58. Abnormalities of the Dental Pulp
Pulp calcification
 Occurs with increasing age
 No apparent reason
 Microscopic size
 Large
 Linear (diffuse)
 Nodular (pulp stones)

True denticle

False denticle

Not source of pain

59. Abnormalities of the Dental Pulp

60. Internal Resorption
 It may be seen as
 Inflammatory response to pulpal
injury
 No apparent trigger
 It occurs as a result of osteoclasts
activation on internal surfaces

61. Internal Resorption
 The root or crown can be perforated
 In advanced cases teeth may appear pink
 Treatment is root canal therapy before perforation

62. External Resorption
 It may be a result of an adjacent pathologic process

Chronic inflammatory lesion

Cysts

Benign tumors

Malignant neoplasms

63. External Resorption
 The cause has been related to:

Release of chemical mediators

Increased vascularity

Pressure

64. External Resorption
 It may be associated with:

Trauma

Reimplantation

Impactions

Idiopathic
 The lesion can occur on root
surfaces below the gingival
epithelial attachment
 It can occur at the apex

65. Alterations in Color
Exogenous stain
 It is the stain that can be
removed by abrasives

Dietary substances

Colored by-products of
chromogenic bacteria

66. Alterations in Color
Endogenous stain
 It results from deposits of
systemically circulating substances
during tooth development
 Tetracycline
 Bright yellow color
 The color change with time due
to oxidization
 Minocycline
 It stains the root of adult teeth
 Skin & mucosa

67. Alterations in Color
Endogenous stain
 Congenital porphyria (hereditary)

Errors in porphyrin metabolism

Deposition of porphyrin in
developing teeth which appear red
to brown
 Liver disease, biliary atresia & neonatal
hepatitis

It may cause discoloration of the
primary teeth