Opi 1-introduction-tooth abnormalities

Oral Pathology I
Aiman A. Ali DDS, PhD.

Oral Pathology
Oral Pathology I
 Abnormalities
 Dental caries
 Inflammatory jaw lesions
 Ulcerative lesions
 Vesiculo-Bullous lesions
 White lesions

Oral Pathology II
 Cysts of head and neck
 Odontogenic tumors
 Non-Odontogenic tumors
 Salivary gland diseases
 ---

 Red blue and pigmented L.
--Aiman A. Ali DDS, PhD.

Oral Pathology I
Course director: Dr. Aiman A. Ali
Course contributors:
Dr Louay Jaber
Dr Wael Swelam

Theory: Saturday 1-2 pm
Laboratory: OP Lab. Saturday 2-5 pm


Course content
Week

Date

Lecturer

Topic

1

Introduction to oral pathology

2

Abnormalities of teeth

3

Dental caries

4

Inflammatory jaw lesions I

5

Inflammatory jaw lesions II

6

Pathological bases of the periodontal diseases

7

Vesiculo-Bullous disease I

8

Vesiculo-Bullous disease II

9

Ulcerative conditions I

10

Ulcerative conditions II

11

White lesions I

12

White lesions II

13

Red-Blue lesions

14

Pigmentation of oral and perioral tissues

15

Advanced diagnostic methods in oral and maxillofacial pathology


Evaluation
Attendance ………………………………………………………....
Quizzes ………………………………………………….………………....
Midterm ……………………………………………….………………....
Continuous practical evaluation ……....
Final practical exam ……… …………..……………....
Oral interview …………………………………………………....
Final Written exam ……………………….……………....
Total

5
10
20
10
10
5
40
100


Abnormalities of teeth & oral tissues
Reference book:
• Regezi & Sciubba. Oral Pathology: clinico-pathological correlation.
• Cawson: Oral Pathology and Oral Medicine

Recommended book:
• Shafer, Hine & Levy. A text book of Oral Pathology. Chp 1.


Alteration in size
Alteration in shape
Alteration in number
Alteration in structure
Alteration in color


Abnormalities of oral structures
Developmental disturbances of the jaws
Developmental disturbances of the tongue
Developmental disturbances of lip and palate
Developmental disturbances of oral mucosa
Developmental disturbances of salivary glands



Alterations in size
Microdontia
Macrodontia


Microdontia
Generalized
– True
– Relative

Focal or localized
– Maxillary lateral incisor
– Maxillary third molar


Macrodontia
Generalized
– True
– Relative

Focal or localized
– Mandibular third molar
– Hemifacial hypertrophy



Alterations in shape
Gemination
Fusion
Concrescence
Dilaceration
Dens Invaginatus
Dens Evaginatus
Taurodontism
Supernumerary roots
Enamel pearls


Gemination


Fusion


Concrescence


Dilaceration


Dens Invaginatus


Dens Evaginatus


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


Alteration in Shape

Taurodontism
 11%

occurrence in middle east



It is of little clinical significance



No treatment is required


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

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

Enamel pearls


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


Attrition, Abrasion & Erosion


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

Abrasion


It is the pathologic wearing of
teeth as a result of abnormal habit
(abrasive substance)


Pipe smoking



Tobacco chewing



Aggressive toothbrushing



Abrasive dentifrices


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

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)



Complete Anodontia:
All teeth are missing

The prevalence of hypodontia is 4.6%
Partial Anodontia:
some teeth are missing

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


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)

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




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


Alterations in tooth structure

Enamel

Hereditary: Amelogenesis Imperfecta

Environmental: Trauma, Fluoride, Syphilis …etc.

Dentine

Hereditary: Dentinogenesis Imperfecta

All dental hard tissues

Dentine dysplasia
Hereditary: Regional odontodyslasia
Environmental: Resorption

Pulp


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


Defects of Enamel


The extent of the defect is dependent on:


The intensity of the etiologic factor
Enamel hypoplasia



The duration



The time of occurrence


Defects of Enamel


Etiologic factors can be


Local: (Turner’s tooth)





Trauma
Abscess

Clinical signs


Hypocalcification or hypoplasia


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


Environmental Defects of Enamel


Due to Syphilis


Local infection or trauma
Turner’s teeth


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)


Amelogenesis Imperfecta



The color varies from white
opaque to yellow to brown



Dentin & pulp chamber
appear normal



Cosmetic problem


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


Defects in Dentin

Type III: Only dental defects occur
• Pulp exposures

• Periapical radiolucencies
• Variable radiographic appearance


Defects in Dentin


Clinical features:


Both dentitions exhibit
translucent appearance



Yellow-brown to gray



The enamel fractures easily



Roots are shortened and blunted


Defects in Dentin


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)



Periapical radiolucencies

Defects in Dentin


Microscopically:




Pulp replaced by irregular dentin





The dentin contains fewer but larger and irregular
dentinal tubules

Enamel appears normal but dentinoenamel junction is
smooth

Treatment is directed toward protecting tooth from
wear and esthetic appearance

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


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


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


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




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)






Permanent teeth>primary teeth
Maxillary anterior teeth are more affected
Eruption is delayed or does not occur




Cause is unknown, however:










Trauma
Nutritional deficiencies
Infections
Metabolic abnormalities
Systemic diseases
Local vascular compromize
Genetic influences

Treatment: teeth removal because of poor quality


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




Abnormalities of the Dental Pulp


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


Internal Resorption


The root or crown can be perforated



In advanced cases teeth may appear pink



Treatment is root canal therapy before
perforation


External Resorption


It may be a result of an adjacent pathologic process


Chronic inflammatory lesion



Cysts



Benign tumors



Malignant neoplasms


External Resorption



The cause has been related to:


Release of chemical mediators



Increased vascularity



Pressure


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

Alterations in Color
Exogenous stain


It is the stain that can be
removed by abrasives


Dietary substances



Colored by-products of
chromogenic bacteria




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

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

Tetracycline


Developmental disturbances of the
jaws
Agnathia
Micrognathia
Macrognathia
Facial Hemihypertrophy
Facial Hemiatrophy


Developmental disturbances of
the tongue
Aglossia
Microglossia
Macroglossia
Ankyloglossia
Cleft, bifid and fissured tongue
Lingual thyroid nodule
Median rhomboid glossitis


lip and palate
Lip and commissural pits
Clefts
Double lip


oral mucosa
Fordyce’s granules
Focal epithelial hyperplasia


salivary glands
Aplasia
Atresia
Aberrancy
Mandibular salivary gland depression


Opi 1-introduction-tooth abnormalities

Opi 1-introduction-tooth abnormalities

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