1

Developmental disturbances of oral cavity

Dr. Kush
 Craniofacial anomalies 2

• Cranial + Facial structures

• Anomaly – Irregularity or Differing from normal
• Congenital
• Variations – Mild or Severe (require surgery)
 Etiology – 3

1. Combination of genes – Due to changes in genes at the time of

conception.
2. Environmental – Due to prenatal exposure to certain chemical or
physical environment.
3. Folic acid deficiency (B vitamin) – Present in orange juice, leafy
vegetables, cereals and enriched grain products. If not taken
during pregnancy, may lead to development of congenital
anomalies, including Cleft lip/cleft palate.
Anomalies– 4

• Cleft lip
• Cleft palate
• Craniosynostosis
• Hemifacial microsomia
• Vascular malformation
• Hemangioma
• Deformational plagiocephaly
Cleft lip 5
Cleft palate 6
Craniosynostosis
7
Hemifacial microsomia 8
Vascular malformation
9
 10

Vascular malformation
 11

Hemangioma
12
13
Deformational Plagiocephaly 14
15
Teratogenic Agents 16

 Agents that may cause birth defects when present in the fetal
environment.

 Drugs, chemicals, physical and metabolic agents can affect

intrauterine life of developing fetus.

 They exceed pathogenic mechanisms to produce alterations in

form and functions of embryo and even fetal death.
 17

Mechanism is selective

Their pattern is selective

However, the extent to which an individual may be

adversely affected by exposure to a given teratogen varies
widely.
 18

 This depends on :

1. Difference in dose
2. Developmental timing of exposure.
3. Difference in susceptibility
4. Interactions among environmental exposures.
Developmental disturbances of Jaws 19
 Agnathia
 Micrognathia
 Macrognathia
 Facial Hemihypertrophy
 Facial Hemiatrophy

Abnormality of dental arch relations

 Class I
 Class II
 Class III
 AGNATHIA 20

 Lethal anomaly

 Characterized by hypoplasia or absence of the mandible with

abnormally positioned ear.
 An autosomal recessive mode of inheritance.

 More commonly only one portion of jaw missing.

 Maxilla :- one maxillary process or pre maxilla.

 21
 Mandible Partial absence (even more common), entire mandible on one

side, only condyles (more frequently), bilateral agenesis of condyle and

ramus.

 Ear to be deformed or absent

22
MICROGNATHIA 23

• Literally means small jaw

• Many cases apparent micrognathia
• True micrognathia:- congenital and acquired
• Associated with other congenital abnormalities including
congenital heart disease and the Pierre Robin syndrome
24
25
 26

Pierre robin syndrome

Cleft palate
Micrognathia
Glossoptosis
Congenital heart defects
Ocular anomalies
Skeletal defects
 27

• Micrognathia of maxilla frequently occurs due to a deficiency of pre

maxillary area.
• Patients with this deformity (in maxilla) appear to have the middle
third of face retracted.
• Suggested that the mouth breathing is a cause.
• Owing to associated mal-development of nasal and nasopharyngeal
structures
 28

• Mandibular Micrognathia of the congenital type is often

difficult to explain.

• Agenesis of the condyles results in true mandibular

Micrognathia.
 29
• Acquired type is of postnatal type.

• Mandibular Micrognathia usually results from disturbance in

the area of TMJ.

• Characterized by severe retrusion of chin, a steep mandibular

angle and a deficient chin button
causes 30

• Pierre Robin syndrome

• Congenital syphilis
• Trisomy 18
• Turner’s syndrome
• Noonan’s syndrome
 Trisomy 18 31

• A condition that causes severe

developmental delays due to
an extra chromosome 18.
 Turner’s syndrome 32

• A chromosomal
disorder in which a
female is born with
only one X
chromosome
Noonan’s syndrome 33

 Noonan syndrome (NS) is a relatively

common autosomal dominant congenital disorder
 Male version of Turner’s syndrome.
MACROGNATHIA 34

• Condition of abnormally large jaw

• Pituitary gigantism:- Increase in size of both jaws
• More commonly only the jaw affected
• Macrognathia may be associated with
1. Paget’s Disease
2. Acromegaly
3. Leontiasis Ossea
35
 36

Mandibular protrusion or prognathism is rather clinical

occurrence.
Some follow hereditary patterns.
 37

• The true prognathic patients have long rami, less steep

angle.
• Excessive condylar growth predisposes to mandibular
prognathism.
 38

 General factors which influence and tend to favor are

1. Increased length of ramus
2. Increase mandibular body length

3. Anterior Position of glenoid fossa

4. Decreased maxillary length
 39

5. Posterior positioning of the maxilla in relation to the

cranium.

6.Prominent chin button.

7.Varying soft tissue contours

40
 41
FACIAL
HEMIHYPERTROPHY
 Rare developmental anomaly characterized by the
asymmetric overgrowth of one or more body parts.

 Hemi hyperplasia.

 Can be isolated, but may be associated with a variety

of malformation syndromes
42
 43

 Anatomic classification (by Hoyme et al 1998)

1. Complex
2. Simple
3. Hemi facial hyperplasia
Etiology 44

 Unknown
 Hormonal imbalance
 Incomplete twinning
 Chromosomal abnormalities
 Vascular or lymphatic abnormalities
 CNS disturbances
Clinical features 45

 Unilateral macroglossia, bucal mucosa also affected.

 Unilateral premature development and eruption as well as

increased size of dentition

 Females are affected more frequently

 Equally affected right and left side

Oral manifestations
46

 Abnormal dentition in three respects

1. Crown size,
2. root size and shape
3. Rate of development

 Not exceeding a 50% increase in size

 Cuspids, premolars and molars
 47

 Maxilla and mandible are also enlarged wider

and thicker with altered trabecular pattern.

 Tongue:- Enlargement of lingual papillae,

general unilateral enlargement and contra
lateral displacement.
Syndromes associated 48

 Beckwith – Weidmann syndrome

 Neurofibromatosis

 Mc-Cune Albright syndrome

 49
Treatment and prognosis

 Cosmetic surgery advised after growth cessation

Differential diagnosis
 Neurofibromatosis
 Fibrous dysplasia
FACIAL HEMIATROPHY 50
(Parry-Romberg syndrome, Romberg-Parry
syndrome, Progressive hemifacial atrophy)

 Consists of slowly progressive atrophy of the soft

tissues of essentially half of the face.

 Characterized by progressive wasting of

subcutaneous fat, sometimes accompanied by atrophy
of skin, cartilage, bone, muscle
51
 52

 Accompanied usually by contralateral Jacksonian

epilepsy, Trigeminal neuralgia and changes in the
eye and hair.

 May be form of localized scleroderma

Etiology
53

1. Cerebral disturbance leading to increased and

upregulated activity of sympathetic nervous system.

2. Extraction of teeth
3. Local trauma
4. Infection
 54

5. Genetic factors.
6. Disruption of stapedial artery.
7. Peripheral trigeminal neuritis.
8. Localized scleroderma
Clinical features 55

 Most common early sign is pain less cleft.

 Atrophy of muscle, bone, cartilages, alveolar bone and

soft palate on affected side.

 May include the ipsilateral salivary gland, hemiatrophy

of the tongue.
 56

 Unilateral involvement of the ear, larynx,

esophagus, diaphragm, kidney and brain.

 Startsin the first decade and lasts for about three

years before it become quiescent.
57
 58
 Neurological disorders :- 15%

 Ocular findings:- 10-40%

 May be accompanied by pigmentation disorders,

vitiligo, pigmented facial nevi,

 Contra lateral Jacksonian epilepsy, trigeminal

neuralgia
 59

 Female to male ration is 3:2

 Predilection for the left side
 First and second decades of life
 Progresses over a period of 2 to 10 years
 60

COUP DE SABRE
Oral manifestations 61

 Incomplete root formation, delayed eruption and

severe facial deformity

 Resulting in facial deformation and difficulty with

mastication.

 Dark pigmentation of the affected side

 62

 Atrophy of half lip and tongue.

 Shorterramus and body of mandible resulting in

malocclusion.

 Delayed eruption of teeth on affected side.

Differential diagnosis 63

 Post traumatic fat atrophy,

 Hemifacial microsomia
 Goldenhar,s Syndrome
 Partial lipodystrophy

Treatment and Prognosis

 No specific treatment
 64
Abnormalities of dental arch
relations

 Class I
 Class II
 Class III
 65

Cleft lip & Palate

Introduction 66

 Facialclefting is the second most common

congenital deformity (after clubfoot).

 Affects 1 in 750 births

 Problems are cosmetic, dental, speech,

swallowing, hearing, facial growth,
emotional
67
Epidemiology 68

 Cleft Lip - 2 Male: 1 Female

 Cleft Palate - 2 Female: 1 Male

 Cleft Lip - Native Americans > Oriental ,

Caucasians > Blacks

 Cleft Palate- Same among ethnic groups

Anatomy 69

 Hard Palate

 Bones: Maxilla( Palatine Processes) +

Palatine Bones(Horizontal Lamina)

 Blood Supply: Greater Palatine Artery

 Nerve Supply: Anterior Palatine Nerve

Anatomy 70

 Soft Palate
 Fibro muscular area attached like a shelf to
posterior portion of hard palate.

 Muscles: Tensor Veli Palatini(CNV), Levator

Veli Palatini(Primary Elevator), Musculus
Uvulae, Palatoglossus, Palatopharyngeus(CN IX
and X)
Etiology 71

 Hereditary – One of the most important factor.

 Genetic –

 Single mutant gene

 Number of genes (polygenic inheritance)
(each producing small effects which together
create this condition)
 72

 Nutritional disturbances – Riboflavin deficiency

 Developmental – Physiological, emotional and

traumatic stress during developmental stages.

 Defective vascular supply – causes ischemia

 Mechanical disturbances – size of tongue may

prevent union of parts.
 73

 Infection

 Miscellaneous – steroid therapy during

pregnancy, alcohol, and toxins in circulation.
Cleft Lip 74
75
76
 Cleft Formation 77

 Cleft result in a deficiency of tissue.

 Cleft lip occurs when an epithelial bridge fails to fuse.

 Cleftsof primary palate occur anterior to incisive

foramen.

 Clefts
of secondary palate occur posterior to incisive
foramen.
Cleft Formation 78

Cleftof lip increases likelihood of cleft of palate

because tongue gets trapped.
 79
 Classification

Unilateral incomplete

Unilateral complete

Bilateral incomplete

Bilateral complete
 Clinical features: 80

o M>F
o Direct communication between nasal and
oral cavity
o Speech problem
o Regurgitation of food
o Esthetics
o Proper development of arches is hampered
Syndromes associated 81
 Pierre robin syndrome

 Oral facial digital syndrome

 Apert’s syndrome

 Nagar syndrome

 Down’s syndrome

 Marfan syndrome
82
Management 83

 Cheiloplasty – surgical closure of lip.

 Obturator – provides cross arch stability

 Bone grafting

 Orthodontic therapy
Management 84

 Cleft Rhinoplasty – improves nasal function and

correct distortion

 Speech therapy

 Psychotherapy

 Feeding plate – prevents regurgitation and nasal reflux

 85

Developmental Disturbances
ORAL LYMPHOID
TISSUE
Reactive lymphoid aggregate 86

Also called Reactive lymphoid hyperplasia.

Lingual tonsil located on the posterior portion of
tongue on dorsolateral aspect.
One of the largest oral lymphoid.
Gets inflamed / enlarged and becomes clinically
evident.
87
Etiology: 88

•Associated with aging (up to 13%), autoimmune

disease, inflammatory conditions, infectious disorders.
•Occasionally reported in association with tobacco use
and certain medications
•Benign aggregates also seen in patients with chronic
myeloid neoplasms
• Usually bilateral 89

• If unilateral, might be mistaken for early carcinoma.

• Surrounded by crypt lined by stratified squamous
epithelium.
• Can also occur in Buccal mucosa.
• Lymph node presents as firm, nodular sub-mucosal
mass with tenderness positive.
 90

Hyperplastic lymphoid polyps also described as

polypoid tissue.
Occurs on gingiva, buccal mucosa, tongue and floor
of mouth.
Mean age 57 years (12 to 99 years)
 91

• Incidence increases with age.

• Many cases associated with HIV, hepatitis B or C,
fungal or bacterial infections (immune mediated
disorder or inflammatory condition).
Lymphoid Hamartoma 92

• Synonyms – Angiofollicular lymph node

hyperplasia, Angiomatous lymphoid, Castleman’s
tumor, Giant benign lymphoma, Giant lymph
node hyperplasia
• Types of Castleman’s disease:-
1. Hyaline vascular type
2. Plasma cell type
93
 94
1. Hyaline vascular type:-
• Common site – Chest, Stomach and Neck. (localized
hyaline type)
• Less common sites- Armpits, Pelvis and Pancreas.
• Abnormal enlargement of lymph nodes.
• Generally asymptomatic.
• May develop as non-cancerous growth of lymph node
95
96
97
Plasma cell type – 98

•Rare disorder
•Non cancerous benign growth developing in lymph
node throughout the body.

•May be associated with fever, weight loss, skin rash,

hemolytic anemia, Hypergammaglobulinaemia.
 99
Multicentric/generalized castleman’s disease:-

•Newly reported in medical literature

•Affects multiple area
•Exhibit as Hepatosplenomegaly
 10
0
Etiology:
•Exact cause unknown
•Might be due to increased production of interlukin 6
(produced in lymph node)
Angiolymphoid hyperplasia 10
with Eosinophilia 1

• Synonyms – Epitheloid hemangiomas,

Inflammatory angiomatous nodules, Histiocytoid
hemangioma.
• Idiopathic & uncommon
• Presents as isolated, grouped plaques or nodules in
skin of head and neck.
10
2
 10
Clinical features: 3
•Uncommon but not rare
•Common in Japan
•F>M
•Age – 20-50 years, mean onset 30-33 years
•Rare in elderly.
 10
• Most patient present lesions in 4
periauricular
region, forehead or scalp.
• Appear as dome shape, smooth surface.
• Pain or pruritis present
• Diameter – 0.5-2 cm with range between 0.2- 8
cm.
• Benign, persistent and difficult to eradicate.
 10
5
• Benign but with unusual reactive process.
• Multifocal condition
• May occur following trauma or infection
• Faster lesional growth during pregnancy or oral
contraceptive use.
 10
6
• Approx. 20% patients have blood eosinophilia
• No malignant transformation
• Similar to KIMURA DISEASE.
Histology: 10
7
•Proliferation of endothelial lined small blood vessels.
•Enlarged endothelial cells.
•Infiltrations primarily of lymphocytes and
eosinophils
•Eosinophils – 5-15%
 10
8

Endothelial cells have cobblestone appearance.

10
9
11
0
 11
1
Treatment –
•Not mandatory
•Corticosteroids (not very effective)
•Surgical removal – best results
•Might RECUR.
Lymphoepithelial cyst 11
2

• Develops within a benign lymphoid aggregate or

accessory tonsil of oral or pharyngeal mucosa.

• Other than head and neck, found in pancreas and

testes.
11
3
 11
Clinical features: 4
•Movable, painless submucosa nodule with yellow or
yellow white discoloration.

•Occasionally cyst are transparent.

•Commonly found in oral cavity, at floor of mouth.

 11
5
• May occur on lateral, ventral tongue, soft palate,
mucosa over pharyngeal tonsil.

• Diagnosed usually during teen years or third

decade of life.
11
6
 11
7

• Generally diameter is less than 0.6 cm.

• Surface of cyst is indented with tonsillar crypts.

• Superficial cysts may rupture and release foul tasting,

cheesy keratinaceous material.
11
8
 11
9

• Clinically similar to Epidermoid, dermoids cysts

• Less growth potential.

• Never occur on oral mucosa.

 12
Histology:- 0
•Atrophic and degenerated stratified squamous
epithelium.
•Lacks rete pegs.
•Minimal granular cell layer.
•Orthokeratin is seen to be sloughing from epithelial
surface into cystic lumen.
 12
1
• Sometimes dystrophic calcification seen.
• Rarely mucous filled goblet cells seen.

• Cyst is entrapped within well demarcated aggregate

of mature lymphocytes.
• Lymphoid aggregate may be hyperplastic.
12
2
 12
3
Treatment:
•No treatment is required unless its location is such that
it can be traumatized.
•Surgical excision
•No malignant transformation
 12
4

Developmental Disturbances

SALIVARY GLANDS
Aplasia 12
Congenital absence of salivary glands 5

Xerostomia – Dry mouth

Oral mucosa appears dry, smooth, pebbly

Lips are crackled and fissures at corner of
mouth.
Rampant caries and early loss of teeth
No specific treatment
12
6
 Atresia 12
7

• Congenital absence of salivary gland duct

• Salivary gland atresia is congenital blockage or
absence of the orifice of a major salivary gland
duct or part of the duct itself.

• Retention cysts
• Severe Xerostomia
Treatment 12
8

Chemical ablation of the salivary gland used to

treat traumatic rupture of the duct.

Effective and practical method of resolving the

problem. 
Aberrancy 12
9

 Presence of salivary glands in abnormal locations

 Leads to formation of retention cyst

 Neoplasm like Central mucoeidermoid carcinoma

 13
0
Site– Cervical region near the parotid gland or
body of the mandible.
Posterior to first molar.
Xerostomia 13
1

Dry or burning sensation of mucosa.

Mucosa may become atrophic, inflamed, pale &

translucent.

Atrophy of lingual papillae.

 13
2

Fissuring, cracking, areas of denudation.

Rampant caries.

Lack of tolerance of appliances.

13
3
 Etiology 13
4

Temporary Xerostomia is due to emotional reaction, blockage of ducts,

drugs.

Salivary gland Aplasia

X Ray radiation
 13
5
Vitamin deficiency

Sjogren’s syndrome (incurable)

Miscellaneous causes
Hyperplasia of Palatal Glands 13
6
Hyperplasia of minor salivary glands

Etiology :
Endocrinal disorders, Diabetes mellitus,
menopause, hepatic disease, starvation,
alcoholism, inflammation, sjogren’s syndrome,
etc.
13
7
 13
8
Clinical features
 Small localized swelling, usually on hard palate or
junction of hard and soft palate.

 Intact surface, sessile, normal color, asymptomatic

 13
9

Histopathology:
Closely packed collection of normal
mucous acini, normal ducts.
Treatment
Surgical excision
14
0
 14
Stafne cyst 1
Due to inclusion of glandular tissue adjacent to lingual
surface of the body of mandible.
Radiographic features:
Ovoid radiolucency between mandibular canal and
inferior border of mandible in the molar region
Should be differentiated from traumatic bone cyst
 14
The 2
Stafne defect is thought to be a normal anatomical
variant.

The depression is created by ectopic salivary gland

tissue associated with the submandibular gland.

Does not represent a pathologic lesion as such.

14
3
14
4
 14
5

Developmental Disturbances
LIPS & PALATE
Congenital lip and commissural 14
pits and fistulas 6

Etiology
 Notching of lips in early stages of development.

 Failure of complete union of embryonic lateral

sulci of lip

 Pitsof lower lip with cleft lip or palate is

known as Van der woude’s syndrome
 14
 Clinical 7
features
 Unilateral or bilateral depression on either lip.

 Lip may appear swollen.

 Commissural pits appear as unilateral or bilateral pits

at the corners of the mouth.

 Treatment
 Surgical excision
14
8
 Double lip 149

 Characterized by excess tissue fold on the inner

mucosal aspect of lips

 Lower lip as well as upper lip is involved

 When the upper lip is tensed it appears as Cupids Bow.

15
0
 Double lip, Non toxic thyrotoxicosis and
blepharochalasis constitutes Aschers 15
syndrome. 1

 Surgical excision of excess tissue

Chelitis Glandularis 15
2

 Clinically descriptive diagnosis

 Refers to an uncommon, poorly understood

inflammatory disorder of the lower lip.

 Characterized by progressive enlargement and

eversion of the lower labial mucosa that results in
obliteration of the mucosal-vermilion interface.
 15
3
 With chronic exposure, lower labial mucosa gets
secondarily altered by environmental influences,
leading to erosion, ulceration, crusting, and,
occasionally, infection.

 Therefore, cheilitis glandularis can be considered a

potential predisposing factor for the development of
actinic cheilitis and squamous cell carcinoma.
15
4
15
5
Etiology 15
6

 Chronic exposure to sun, wind and dust

 Tobacco

 Stress

 Hereditary
 15
7
 Cheilitis glandularis has been sub classified into 3
types:

Simple, Superficial Suppurative, and Deep

Suppurative.

 The Deep Suppurative type has also been variously

referred to as myxadenitis labialis or cheilitis
apostematosa.
 15
8

 The Superficial Suppurative type has been termed

Baelz disease.

 Ifthe simple type is not treated, it could become

secondarily infected and progress to become the
superficial or eventually, the deeply suppurative
type.
 15
Clinical Features: 9
 Enlarged lower lip, firm and finally becomes
everted.

Simple type - Multiple painless pinhead sized lesions,

with central depressions and dilated canals.

SuperficialSuppurative type- (Baelz’s disease) painless

swelling, induration, crusting, superficial and deep
ulcerations
 16
0
 Deep supparative type- (Chelitis glandularis apostematosa,
Myxadenitis labialis) deep seated infection, abscess, fistulous
tracts, scar formation

 Treatment & Prognosis

 No treatment

 Malignancy associated as some consider it as premalignant

lesion

 Surgical stripping of lip

Chelitis Granulomatosa 16
(Miescher-Melkersson-Rosenthal 1
syndrome)
 Diffuse swelling of lip

 Soft swelling, no pitting on pressure

 Surrounding skin normal in color or erythematous

 Fissuring, vesicles or pustules are seen

16
2
 16
3

 Melkersson Rosenthal syndrome- Involves the

association with facial nerve palsy and plicated tongue.

 Facial paralysis, scrotal tongue and chelitis

granulomatosa, recurrent facial swellings, oral swellings
and gingival enlargements.
 16
4

Chronic inflammatory cell infiltrate, focal non caseating

granuloma formation, epitheloid cells and langhans giant
cells
Hereditary intestinal polyposis 16
5
Peutz-Jehgers syndrome, Intestinal polyposis with
melanin pigmentation
Clinical features
 Pigmentation of lips and oral mucosa
measuring 1-5 mm
 Buccal mucosa, gingiva and hard palate,
mucosal surface of lips
 Intestinalpolyps of small intestine, abdominal
pain, minor obstruction
16
6
 16
Labial & Oral Melanotic macules 7

 Any age, single or multiple.

 Small, flat, brown, black asymptomatic lesion of lip near

midline

5 mm or less in diameter.

 Oral macules are seen on gingiva, buccal mucosa and palate.

16
8
Histopathology: 16
9

 Variable thickness of epithelium.

 Increased amount of melanin in basal layer

 Chronic inflammatory cells are seen

Treatment
 No Treatment
17
0
17
1
 17
2

DEVELOPMENTAL DISTURBANCES OF
TONGUE
1. Microglossia
2. Macroglossia
3. Ankyloglossia
4. Cleft tongue
5. Fissured tongue
6. Median rhomboid glossitis
7. Benign migratory glossitis
8. Hairy tongue
9. Lingual varices
10. Lingual thyroid nodule
 MICROGLOSSIA

 It is a rare congenital anomaly manifested by the

presence of Rudimentary or small tongue

 The condition when tongue is completely absent is

known as Aglossia.

 Patient finds difficulty in eating and swallowing

 CLASSIFICATION

I. True microglossia
II. Relative microglossia

TREATMENT

I. Orthognathic correction
II. Speech & language development

175
microglossia
 MACROGLOSSIA
 It is a condition when patient has an enlarged tongue
 May be congenital or acquired

ETIOLOGY FOR CONGENITAL MICROGLOSSIA

 Congenitalmacroglossia is due to an over development of

the musculature
 Down syndrome
 Beckwith-Wiedemann syndrome
CAUSES FOR ACQUIRED MICROGLOSSIA

1. Tumors in tongue such as lymphangioma,hemagioma

and neurofibroma

2. Acromegaly

3. Amyloidosis

4. Angioedema
Macroglossia
 CLINICAL FEATURES
 Noisy breathing
 Difficulty with chewing/ swallowing
 Drooling
 Slurred speech
 Widened interdental space
 Open bite/ mandibular prognathism
 Dry/ cracked tongue
 Ulceration/ secondary infection/ hemorrhage
 TREATMENT

Surgical reduction or trimming may be required when

macroglossia disturbs the oro-pharyngeal function

181
ANKYLOGLOSSIA
 Itcan be defined as a developmental condition
characterized by fixation of tongue to the floor of
the mouth,causing restricted movement

 Itcan be either complete ankylogssia or partial

ankyloglossia (tongue tie)
 Partial ankyloglossia occurs as a result of short
lingual frenum or due to a frenum which attaches
too near to the tip of the tongue

Complete ankyloglossia occurs as a result of fusion

between the tongue and the floor of the mouth
CLINICAL FEATURES
 Speech disorders
 Deformities in dental occlusion
 Difficulties in swallowing

TREATMENT
 Partial ankyloglossia are self corrective
 Complete ankyloglossia can be surgically treated by
frenulectomy.

184
CLEFT TONGUE SYNDROME

A complete cleft tongue occurs due to lack of

merging of lateral lingual swellings of this organ.

 Partiallycleft tongue occurs more common and is

manifested as deep groove in the midline of dorsal
surface
 18
7

 Partialcleft tongue occurs due to incomplete

merging and failure of groove obliteration by
underlying mesenchymal proliferation.

 Food debris and microorganisms collect in base of

cleft and cause irritation
Cleft tongue
 18
9

 The initial surgery is usually performed by the

time a baby is 3 months old.

 About 20% of children with a cleft palate require

further surgeries to help improve their speech
FISSURED TONGUE

 Its a malformation manifested clinically by

numerous small grooves on dorsal surface along
the midline of tongue.

ETIOLOGY
 It also occurs as a sequel to geographic tongue

 Hereditary factors
 Clinical Features

 Grooves / furrows – 2-6mm

 Asymptomatic / mild burning sensation rarely

 Melkersson Rosenthal syndrome

 Facial paralysis, scrotal tongue.

191
 The lesions are ususally asymptomatic unless
debris is entrapped within the fissure, causing
irritation.

 Fissured tongue affects the dorsum surface and

often extends to the lateral borders of the tongue
and form lobules.
 MEDIAN RHOMBOID GLOSSITIS

 Synonyms- Central papillary atrophy of the

tongue / posterior lingual papillary atrophy

 It is an asymptomatic elongated erythematous

patch of atrophic mucosa on the mid-dorsal
surface of the tongue
 ETIOLOGY 19
5
 Ithas been described as a congenital abnormality of
tongue due to failure of tuberculum impar to retract
before fusion of lateral halves of tongue.

 So that structure devoid of papillae is interposed

between them.

 It is a focal area which is susceptible to chronic

infections by candida albicans.
19
6
 CLINICAL FEATURES

 Lesion appears Ovoid, diamond rhomboid shaped

reddish patch on dorsal surface of tongue immediately
anterior to circumvallate papillae.

 It appears as a flat or slightly elevated area and stands

out distinctly from rest of tongue because it has no
filiform papillae.
 19
8

 Seenmostly in females in a ratio 3:1 when

compared with males

 Kissing lesions are seen.

 19
9
 Is thought to be created by a chronic fungal
infection.

 Usually is a type of oral candidiasis

TREATMENT

 Antifungal agents-amphotericin B or nystatin

20
1
BENIGN MIGRATORY
GLOSSITIS
Synonyms- Geographic tongue, erythema migrans and
wandering rash of tongue.

ETIOLOGY
 The exact etiology remains unknown. It may be genetic.

 However many investigators believe that emotional

stress may precipitate this condition
 CLINICAL FEATURES
 The lesion occurs in about 1 to 3 % of population

 Females are affected more frequently than males

by a 2:1 ratio

 Geographic tongue is usually seen on the anterior

two third of the dorsal tongue mucosa

 
 20
4

 Characterized by
Multiple, well-demarcated, erythematous,
depapillated patches.

Typically surrounded by a slightly elevated yellow

white scalloped border, and usually restricted to
the dorsum of the tongue.
TREATMENT AND PROGNOSIS
 There is no specific treatment for erythema
migrans.

 Heavy doses of vitamins and topical steroids may

produce some results in few cases
HAIRY TONGUE
 Synonyms- Black hairy tongue, lingua nigra, lingua
villosa.

 Hairy tongue is characterized by marked

accumulation of keratin on filliform papillae of the
dorsal surface resulting in a hair like appearance.
 ETIOLOGY
 Chronic smokers

 It occurs due to microorganisms such as candida albicans

 Systemic disturbances like anemia, gastric upset.

 Oral use of certain drugs like sodium perborate, sodium

peroxide and antibiotics such as penicillin.

 Extensive x-ray radiation

20
9
21
0
 CLINICAL FEATURES
 Formation of a pigmented thick matted layer on the
tongue surface heavily coated with bacteria and fungi.

 Hair like appearance

 Halitosis

 Irritation of tongue due to accumulation of food debris.

 Candidal over growth may cause glossopyrosis (burning

tongue)
 TREATMENT

 Cleaning and scrapping of tongue

 Reducing the adminstration of long term

antibiotics
 LINGUAL VARICES

 It is a dilated , tortuous vein which is often

subjected to increased hydrostatic pressure but is
poorly supported by surrounding tissue.
 CLINICAL FEATURES
 Varices usually involves the lingual ranine veins.

 The involved veins appear red or purple shot like

clusters of vessels on the ventral surface and lateral
borders of tongue as well as in the floor of the mouth.

 Presence of lingual varices before the ages of 50

indicates premature ageing.
 21
5

Treatment
 There is no specific treatment for lingual
varices
LINGUAL THYROID
NODULE
 Itis an anomalous condition in which follicles of
thyroid tissue are found in the substance of the
tongue.

ETIOLOGY
 Itoccurs when thyroid failed to migrate to its
predestined position or it’s remnants become
detached and were left behind.
 CLINICAL FEATURES

 Itappears as a nodular mass in or near the base of

tongue just posterior to foramen caecum.

 Deeply situated and has a smooth surface

 The size varies from 2 – 3 cm

 Chief symptoms are dysphagia, dyspnoea, dysphonia

or fullness of throat
21
9
CT scan of the neck, showing the lingual
thyroid at the base of the tongue.
 HISTOPATHOLOGY

 Lingual thyroid nodule consist of normal mature

thyroid tissue.

 Occasionally thyroid nodules may exhibit colloid

degeneration or goitre.
22
3
DIFFERNTIAL DIAGNOSIS
 Thyroglossal tract cyst
 Neoplasms

TREATMENT
 Surgical excision
 Suppresive therapy iwht supplemental thyroid
hormone can reduce the size of the lesion
 22
5

DEVELOPMENTAL DISTURBANCES OF
ORAL MUCOSA
Fordyce’s Granules/Spots 22
6
 Sebaceous Prominence, are small raised, pale red,
yellow-white or skin-colored bumps or spots that
appear on the scrotum, or the vermilion border of
the lips.

 The vermilion border ?

 Fordyce spots are a type of ectopic sebaceous gland

 22
7

Vermilion border : Fordyce’s granules

 22
8

Buccal Mucosa : Fordyce’s Granules

 22
9

Shows a single sebaceous gland lesion consisting of single or a group of

small but mature sebaceous lobules around small sebaceous duct
extending to the surface epithelium.
 23
0
Ectopic = In an abnormal location or position
Sebaceous - Relating to oil and fat
Glands = Organs or collection of cells that secrete things.

Endocrine glands secrete things, such as hormones, into

the body.
Exocrine glands secrete things outside the body, such
as sweat or mucus
 23
1
 Sebaceous gland = a small skin gland that secretes
sebum (oily matter) into the hair follicles to
lubricate the hair and skin.

 Ectopic sebaceous gland = a sebaceous gland that

is on the skin but not in the hair follicle.
 23
2
 Not associated with any disease or illness
 Cosmetic concern only
 Not infectious
 Often mistaken for cancer or herpes simplex
 They are painless and do not itch.
 They are simply abnormally dilated blood vessels that
are covered by thickened skin.
Treatment 23
3

 Electro desiccation (CO ) laser

2

 Pulsed dye lasers

 Micro punch technique

Focal Epithelial Hyperplasia 23
4
(Heck’s disease)
 One of the most contagious oral papillary lesions.

 Discrete, recurrent papillary lesions on oral mucosa.

 Multiple nodular lesions with sessile base

 23
5
 Commonly seen on lips, buccal mucosa and

tongue.
 Native American and Eskimo children, affected.
 1-5mm diameter
 Same color as adjacent mucosa
 Children between 3-18 years affected commonly
 Undergoes regression in 4-6 months
 23
6

Etiology –
Common amongst Americans
Irritation

Vitamin Deficiency
HPV 1, 13, 32
 23
7

Well-circumscribed, sessile and pale elevation of buccal

mucosa
23
8
 23
9

Squamous epithelium with parakeratosis, acanthosis

and marked papillomatosis
 24
0

Typical nuclear changes produced by HPV. Ballooning spinous

cells are seen in this microscopic field
 24
1
Treatment
 Successful topical treatment with interferon-beta
(Fiblaferon gel).

Effective, simple, non-invasive, cheap and low-risk

alternative to other invasive or surgical therapeutic
modalities.
 24
2

DEVELOPMENTAL DISTURBANCES OF
GINGIVA
Fibromatosis Gingivae 24
3

 Elephantiasis gingivae, hereditary gingival

Fibromatosis, congenital macrogingivae

 A condition characterized by multiple fibromas,
with relatively widespread distribution.

 Abnormal hyperplasia of fibrous tissue.
 24
4
  The presence of multiple FIBROMAS.

 The formation of a fibrous tumor like nodule

arising from the deep fascia.

 Locally recurrent

 It is non inflammatory
 24
5
 Usually inherited as an autosomal dominant trait.

 But some cases are idiopathic and others are produced by 
drugs.

 Palmar Fibromatosis-palmar fascia (tissue in the palm of

the hand covering the finger tendons thickens and scars)
24
6
 24
7
• Plantar Fibromatosis-plantar fascia (Ledderhose's disease)

• Uncommon non-malignant thickening of the feet's deep

connective tissue, or fascia.

• In the beginning, nodules start growing in the fascia of the foot.

• The disease is minor.
24
8
 24
9
 Most frequently present on the medial border of the sole, near
the highest point of the arch. 

 The
lump is usually painless and the only pain experienced is
when the nodule rubs on the shoe or floor. 

 The overlying skin is freely movable

 25
0

It is an inherited disease
The genes necessary for it, may remain
dormant for a generation or more and then
surface in an individual, or be present in
multiple individuals of the same generation
with varying degree.
25
1
 25
2
 Problem in chewing & eating.

 Increased mobility of teeth.

 Abnormal shape & movement of teeth.

 Inflammation and/or swelling of the gums/gingiva.

 25
3
 Not necessarily any signs of pain but experiencing
pain is possible.

 Difficulties in speaking, oftentimes can lead

to speech disorders.

 Other dental and oral problems

Histopathology 25
4
The epithelium may be somewhat thickened with
elongated rete pegs.

The bulk of the tissue is composed of dense fibrous

connective tissue.

The bundles of collagen fibres are coarse and show

few interspersed fibroblasts or blood vessels.

No inflammation mostly

25
5
Treatment 25
6

 Oral prophylaxis
 Gingivectomy followed by Gingivoplasty
 Retrocuspid papilla 25
7
 Small, elevated nodule

 Located on the lingual mucosa of the mandibular

cuspid.

 Soft, well-circumscribed, sessile, commonly

bilateral.

 Between the free gingival margin and the

mucogingival junction
 Common in children
25
8
 Mainly between 8 to 16 years

 Appears to regress with maturity

 Females > Males

 25
9
 Appears as an elevated mucosal tag often showing
mild hyperorthokeratosis or hyperparakeratosis,
with or without acanthosis.

 The underlying connective tissue is sometimes

highly vascularized and may exhibit large stellate
fibroblasts as well as occasional epithelial rests.
Treatment 26
0

 Regresses with age

 Frequently seen, so considered normal

Disturbances in teeth

 (1) Size

 (2) Number and Eruption

 (3) Shape/Form

 (4) Defects of Enamel and

Dentin
 26
2

DEVELOPMENTAL DISTURBANCES IN
SIZE OF TEETH
 Microdontia

 Macrodontia
 Size
 Microdontia

 True Generalized Microdontia

 Relative Generalized Microdontia

 Focal or Localized Microdontia

 True Generalized
 All teeth are smaller than
normal

 Occur in some cases of

pituitary dwarfism

 Very rare

 Teeth are well formed

 Relative Generalized

 Normal or slightly smaller than normal teeth

 Are present in jaws that are somewhat larger than

normal
 Focal/localized
 Common condition

Affects most often maxillary lateral incisior + 3rd

molar

These 2 teeth are most often congenitally missing

 Commonly affects
maxillary lateral incisior

 Peg laterals

 sides converge or taper

together incisally
 Forms cone-shaped
crown.

 Root is frequently shorter

than usual
 Macrodontia

 True Generalized Macrodontia

 Relative Generalized Macrodontia

 Focal or Localized Macrodontia

 True Generalized
 All teeth are larger
than normal

 Associated with
pituitary gigantism

 Very rare
27
2
Relatively Generalized
 Normal or slightly larger than normal teeth in small
jaws

 Results in crowding of teeth

 Insufficient arch space

 Focal/ localized
 Uncommon condition

 Unknown etiology

 Usually seen with mandibular 3rd molars

27
5
 Number & Eruption

 Supernumerary

 Anodontia

 Impaction
 Supernumerary

 Results from continuous proliferation of permanent

or primary dental lamina to form third tooth germ

 Teeth may have:

• Normal morphology
• Rudimentary
• Miniature
27
8
27
9
 More often in permanent dentition than primary
dentition

 More in the maxilla than in mandible

May be impacted erupted or impacted

 Because of additional tooth bulk, it causes:

• Malposition of adjacent teeth

• Prevent their eruption

 Many are impacted

•Characteristically found in Cleidocranial
dysostosis
28
3
 Supernumerary

 Mesiodens

 Fourth molar

•Maxillary Paramolar
• Distomolar or Distodens

 Mandibular Premolar

 Maxillary lateral incisors

 Mandibular central incisors

 Maxillary Premolars
Mesiodens
 Most common supernumerary tooth

 Tooth situated between maxillary central incisors

 Single

 Paired

 Erupted or impacted

 Inverted
28
7
 Small tooth

 Cone-shaped crown

 Short root

Small + rudimentary
 Situated bucally or lingually to one of the maxillary
molars

Interproximally between 1st+ 2nd or 2nd + 3rd maxillary

molars
Distomolar/ Distodens
 Molar located distal to molar
Anodontia

 lack of tooth development

 absence of teeth
Types:

 Complete Anodontia

 Partial Anodontia
• Hypodontia
• Oligodontia

 Pseudoanodontia

 False Anodontia
Complete Anodontia
 when all teeth are missing

 rare

 often associated with a

syndrome known as
hereditary ectodermal
dysplasia.
Hypodontia
 lack of development of one or more teeth
Oligodontia
 Lack of development of six or more teeth
Pseudoanodontia

 When teeth are absent clinically because of

impaction or delayed eruption.
False Anodontia

 when teeth have been exfoliated or extracted

Impaction
 Most often affects the mandibular 3rd molars +
maxillary canines.

 Less commonly:
• premolars
• mandibular canines
• second molars
29
9
 Occurs due to obstruction from crowding

 From some other physical barrier

 Occasionally, may be due to an abnormal

eruption path, presumably because of unusual
orientation of tooth germ
Ankylosis

 Fusion of a tooth to surrounding bone

 With focal loss of periodontal ligament, bone +

cementum become inextricably mixed

 Cause fusion of tooth to alveolar bone

30
2
Developmental Disturbances
 (1) Size

 (2) Number and Eruption

 (3) Shape/Form

 (4) Defects of Enamel and Dentin

Shape & Form
 Crown

 Root
 Crown

 Fusion

 Gemination

 Taurodontism

 Talon’s Cusp

 Leong’s Cusp
 Crown 30
6
 Dens Invaginatus

 Peg-shaped Lateral

 Hutchinson Incisor

 Mulberry Molar
 30
 Root 7

 Concrescence

 Enamel Pearl

 Dilaceration

 Flexion

 Ankylosis
Fusion 30
8
30
9
 31
Tooth gemination is a dental phenomenon that0
appears to be two teeth developed from one.
Taurodontism 31
1
Body of the tooth and pulp chamber is enlarged
vertically at the expanse of the roots.

As a result, pulpal floor and the furcation of the tooth

is moved apically down the root.

Aetiology - is the failure or late invagination

of Hertwig's epithelial root sheath, which is
responsible for root formation.
 31
2

Taurodontism is most commonly found in permanent

dentition although the term is traditionally applied to
molar teeth.

Sometimes autosomal dominant trait is seen

.
Taurodontism is found in association
with Amelogenesis Imperfecta, ectodermal dysplasia.

The term means "bull like" teeth

 31
3

 Associated with syndromes

such as

 Down syndrome

 Klinefelter’s syndrome
31
4
 31
5
Hypotaurodont – Mild form with slight apical
displacement of pulpal floor
 31
6
Mesotaurodont – Moderate form & pulpal floor
displacement is about midline of the tooth.
 31
7
Hypertaurodont – Severe form & pulpal floor
displacement is maximum, near the apex.
 31
Dens Evaginatus 8
Talon’s cusp 31
9
• Also known as eagle’s talon.

• Extra cusp on lingual side of anterior teeth.

• 55% occur on permanent maxillary laterals

• 33% occur on permanent maxillary centrals

• Rarely affecting deciduous

• When it interferes with normal occlusion,

endodontic treatment should be done
32
0
32
1
Leung’s cusp 32
2
• A Leung's premolar is a premolar with an extra
cusp on the top surface of the tooth.

• A Leung’s molar will look like there is an extra

tiny tooth growing on top of your tooth.

• It is also known as an evaginated tooth and is

common among people of oriental descent. 
 32
3

• A Leung's premolar may consist entirely of

dentine, enamel, and pulp which is very fragile
and is prone to fracturing.

• With fractures, the pulp inside can easily become

infected or even result in abscess formation.

• When this happens, it can only be removed

through a root canal procedure
32
4
 Dens Invaginatus
Dens In Dente
 Deep surface invagination of crown or root that is
lined by enamel.

“Tooth within a tooth”

 2 forms:

 Coronal
 Radicular
 Depth varies from slight enlargement of cingulum
to a deep in folding that extends to apex.

 Historically, it has been classified into 3 major types:

 Type I
 Type II
 Type III
 32
 Type I 7

• Confined to the crown

 Type II
• Extends below cemento-enamel junction

•May or may not communicate with adjacent

dental pulp.
32
8
 32
9

 Type III

• Extends through the root

• Perforates in the apical or lateral radicular

area without any immediate communication
with pulp
 Peg laterals 33
0
 Undersized lateral incisor

 Smaller than normal

 Occurs when permanent lateral incisors do not

fully develop
33
1
33
2
 Hutchinson’s incisor 33
4

 Characteristic of congenital syphilis

 Lateral incisors are peg-shaped or screwdriver-

shaped

 Widely spaced

 Notched at the end

 With a crescent-shaped deformity

 33
5

 Notches on their biting

surfaces
 Mulberry molars
 Dental condition usually associated with congenital
syphilis.

 Characterized by multiple rounded rudimentary

enamel cusps on permanent 1st molars.

Dwarfed molars with cusps covered with globular

enamel growths.

Giving the appearance of a mulberry.

33
8
33
9
 Root

 Concrescence

 Enamel Pearl

 Dilaceration

 Flexion

 Ankylosis
 Concrescence

 2 fully formed teeth.

 Joined along the root surfaces by cementum.

 Noted more frequently in posterior and maxillary

regions.
34
2
 May occur before or after the teeth have erupted.

 Usually involves only 2 teeth.

 Diagnosis can frequently be established by X-ray

examination

 Often requires no therapy unless union interferes with

eruption; then surgical removal may be warranted
34
4
 Enamel Pearl 34
5

 Droplets of ectopic enamel (pearls).

 May occasionally be found on roots of teeth.

 Uncommon, minor abnormalities, which are

formed on normal teeth.
Occur most commonly at bifurcation or
trifurcation of teeth.

Maxillary molars > Mandibular

molars
 May cause stagnation at gingival margin but, if they
contain pulp, this will be exposed when pearl is
removed.
 Dilaceration 348

 Angulation or a sharp bend or curve in root or

crown of a formed tooth.

 Trauma to a developing tooth.

Can cause root to form at an
Angle to normal axis of tooth.

 Rare deformity.
350
 Hereditary factors are believed to be involved in
small number of cases.

 Eruption generally continues without problems.

 Flexion
 Deviation or bend restricted just to the root portion.

 Usually bend is less than 90 degrees.

 May be a result of trauma to the developing tooth.

35
3
 Ankylosis
 Also known as “submerged teeth”

 Fusion of a tooth to surrounding bone

Deciduous teeth, most commonly, mandibular 2nd

molars.

 Undergo variable degree of root resorption

Become ankylosed to bone

 This process prevents their exfoliation +

subsequent replacement by permanent teeth

 After adjacent permanent teeth have erupted,

ankylosed tooth appears to have submerged below
level of occlusion
35
6
35
7
 35
8

Defects in Enamel & Dentin

Amelogenesis Imperfecta 35
9
 Also known as:

 Hereditary Enamel Dysplasia

 Hereditary Brown Enamel

 Hereditary Brow Opalescent teeth

36
0
 Group of conditions caused by defects in the genes
encoding enamel matrix proteins

 Genes that encode for enamel proteins:

 Amelogenin mutated in
 Enamelin in patients
 Others with this
condition
 Affects both dentition

 Deciduous
 Permanent

 Classified based on pattern of inheritance:

 Hypoplasia
 Hypomaturation
 Hypocalcified
 No treatment except for improvement of cosmetic
appearance
Hypoplastic Amelogenesis
Imperfecta
 Inadequate formation of matrix.

 Enamel is randomly:
 Pitted
 Grooved or very thin
 Hard + translucent

 Stained, but teeth are not susceptible to caries

unless enamel is scanty and easily damaged.
36
5
 Reduced enamel thickness

 Abnormal contour
 Absent interproximal contact points

 Radiographically:

 Enamel reduced in bulk

 Shows thin layer over occlusal + interproximal
surfaces
 Dentin + pulp chambers appear normal

 No treatment is necessary
 Hypomaturation
Amelogenesis Imperfecta
 Enamel is normal in form on eruption:

 Opaque

Normal
shape
Defect in maturation of enamel crystals.
36
Mottled
9
appearance

Enamel is soft

White, yellow or brown discoloration

Vulnerable to attrition
 37
0

Loss of tooth structure due to mechanical masticatory forces

 Radiographically:

 Affected enamel exhibits radiodensity similar

to dentin
Hypocalcified Amelogenesis
Imperfecta
 Enamel matrix is formed in normal quantity

 Poorly calcified

 When newly erupted:

 Enamel is normal in thickness

 Normal form
 But weak
 Opaque or chalky in appearance
37
3
 With years of function:

 Coronal enamel is removed

 Radiographically:

 Density of enamel + dentin are similar

 Dentinogenesis Imperfecta
 Also known as “Hereditary Opalescent Dentin”

 Due to clinical discoloration of teeth

 Mutation in the dentin sialophosphoprotein

 Affects both primary + permanent dentition

 37
6

With distinctive translucence

37
7
 Have blue to brown discoloration

 Enamel frequently separates easily from underlying

defective dentin
 Radiographically:

 Bulbous crowns
 Cervical constriction
 Thin roots
 Early obliteration of
Roots canals + pulp
chambers
 Treatment:

 Prevent loss of enamel + subsequent loss of

dentin through attrition

 Cast metal crowns on posterior

 Jacket crowns on anterior teeth

 Classification:

 Type I
 Type II
 Type III
 Dentinogenesis Imperfecta
Type I

 Occurs in families with Osteogenesis Imperfecta

 Primary teeth are more severely affected than

permanent teeth
 Radiographically:

 Partial or total obliteration of pulp chambers +

root canals

 By continued formation of dentin

 Roots may be short + blunted

 Cementum, periodontal membrane + bone

appear normal
 Dentinogenesis Imperfecta
Type II
 Never occurs in association with Osteogenesis
Imperfecta unless by chance.

 Most frequently referred to as hereditary opalescent

dentin

 Only have dentin abnormalities and no bone disease.

 Dentinogenesis Imperfecta
Type III
 Radiographically:

 Partial or total obliteration of pulp chambers +

root canals by continued formation of dentin.

 Roots may be short + blunted

 Cementum, periodontal membrane + bone

appear normal.
 Brandywine Type Dentinogenesis Imperfecta

Males>Females

 Periapical radiolucencies

Enamel appears normal

 Large size of pulp chamber occurs not due to
resorption but rather to insufficient + defective dentin
formation
Dentin Dysplasia

 Also known as “Rootless Teeth”

 Rare disturbance of dentin formation

 Normal enamel
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 Atypical dentin formation

 Abnormal pulpal morphology

 Hereditary disease
 Classification:

 Type I (Radicular Type)

 Type II (Coronal Type)

 Type I Radicular
Dentin Dysplasia

 Both dentitions are of

normal color

 Periapical lesion

 Premature tooth loss may occur because of short roots

or periapical inflammatory lesions
 Radiographically:

 Roots are extremely short

 Pulps almost completely obliterated
 Periapical radiolucencies:
• granulomas
• cysts
• chronic abscesses
Type II Coronal
Dentin Dysplasia
 Color of primary dentition is opalescent

 Permanent dentition is normal

 Coronal pulps are usually large.

 Filled with globules of abnormal dentin

 Radiographically:

(Deciduous)
 Roots are extremely short
 Pulps almost completely obliterated

(Permanent)
 Abnormally large pulp chambers in coronal
portion of tooth
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Regional Odontodysplasia
Also known as:

 Odontogenic Dysplasia

 Odontogenesis Imperfecta

 Ghost Teeth
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 One or several teeth in a localized area are affected

 Maxillary teeth are involved more frequently than

mandibular area

 Etiology is unknown
 Teeth affected may exhibit a delay or total failure in
eruption

 Shape is altered, irregular in appearance

 Radiographically:

 Marked reduction in radiodensity

 Teeth assume a “ghost” appearance

 Both enamel + dentin appear very thin

 Pulp chamber is exceedingly large

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 Treatment:

 Poor cosmetic appearance of teeth

 Extraction with restoration by prosthetic
appliance
Shell Tooth
 Normal thickness enamel

 Extremely thin dentin

 Enlarged pulps

 Thin dentin may be involve entire tooth or be

confined to the root

 Most frequently in deciduous

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