Oral Developmental anomalies
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Faleh Sawair: BDS, FDS RCS (England), Ph.D.
Professor in Oral Pathology
& Medicine
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http://elearning.ju.edu.johttp://elearning.ju.edu.jo
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References & Supporting Material
Strongly recommended:
Oral Pathology: Soames & Southam, 4th edition 2005.
Also recommended:
• Essentials of Oral Pathology & Oral Medicine: Cawson & Odell; 8th edition
2008.
• Contemporary Oral & Maxillofacial Pathology: 2nd edition 2003.
• Oral & Maxillofacial Pathology: 3rd edition 2008.
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Developmental disturbances
of the oral regionDefinitions: Congenital, Hereditary, Genetic, Autosomal, Sex-liked, Dominant, Recessive, Developmental, Acquired.
Classification
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Prof F. SawairProf F. Sawair
Developmental Disturbances of soft tissue
Lip pits:1- Commissural: common 1-20%, ↑adults
Autosomal D: in some cases
Uni/bilateral blind tracts at angle of lip, up to 4 mm
Saliva
Preauricular pits
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2- Paramedian lip pits: as deep as 2 cm
Van Der Woude Syndrome: AD; PLP + Cleft lip/palate
Popliteal pterygium syndrome: AD
In some cases, missing teeth.
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Horizontal folds of mucosal tissue
Inner aspect of U > L lip
Ascher syndrome:
Double lip: usually
congenital
+ Goitre and edema and dropping of upper U eyelids
Blepharochalasis
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Other causes of double lip
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Frenal Tag: Autosomal D U labial
frenum Significance
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Fordyce granules: Collection of sebaceous glands
Mostly bilateral on BM
Clin: multiple yellowish structures (1-2m), puberty
Present histologically in infants
Sebaceous naevi
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Hist: superficial; no hair
Glands (1-5 lobules)
that empty into a duct
that opens on the
mucosal surface.
PrognosisHyperplasia
Tumors
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Their relation with:
• Gender
• Skin type
• Systemic disease
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Oral tonsils: Slightly elevated reddish
plaques/FOM
Foliate Papillitis:
Cancer
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Slightly raised area, about 2-4 mm, often bilaterally Commonly located lingual to the cuspids Attached gingiva ≈ incisive papilla Histologically:
A focus of fibrovascular tissue With an orthokeratinized /parakeratinized surface Covers the osseous foramen of a nutrient blood
vessel
Retrocuspid Papilla
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Ankyloglossia “tongue-tie”: Congenital Short, thick & anteriorly positioned lingual
frenum Complications:
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• Less common in
adults
• Age of surgery
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Microglossia: isolated cases or
In most reports + Malformations in the hands (no
digits) & feet (oromandibular-limb hypogenesis syndrome)
Cleft palate Dental agenesia (lower
incisors).
……Aglossia
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Macroglossia: Protruding & scalloped
Complications: Noisy breathing, snoring, drooling,
feeding difficulties.
Glossitis
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Congenital: • Idiopathic muscular hypertrophy• Down syndrome• Hamartoma• MEN III• Lingual thyroid• Transient neonatal DM • Cretinism• Rare syndromes
Acquired: • Inflammation/infection/trauma• Neurofibromatosis• Amyloidosis, Sarcoidosis• Acromegaly• Hypothyroidism • Allergy• Ca
True:
Edentulous patient
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Pseudo/relative: force the tongue to sit in an
abnormal position:
Enlarged tonsils and/or adenoids
Low palate and ↓ oral cavity volume
Transverse, vertical, or AP deficiency in the
maxilla or mandible
Severe mandibular deficiency (retrognathism)
Hypotonia of the tongue
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Bifid Tongue
Cleft tongue
Ankyloglossia
TTT: Surgery
Aetiology
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Lingual thyroid nodule:
Thyroid tissue at mid-posterior dorsum of tongue Failure of migration Clinically: 2-3cm smooth sessile mass Apparent during puberty or adolescence Complications: Hist:
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≈ 70%: no thyroid tissue in neck.
33%: Hypothyroidism (cause of enlargement)
Diagnosis:
Thyroid scan using iodine isotopes or technetium 99m.
CT & MRI: size and extent of lesion.
Biopsy: avoided (bleeding & ≈ source hormone).• Parathyroid• What happens if you give thyroxin
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Fissured tongue: Deep fissures may be seen in children or adults
but ↑ with age Clustering in families Prevalence: worldwide varies but as high as
21%. Complications: In 20% of cases associated with geographic
tongue: same gene Down syndrome & Melkersson-Rosenthal
SyndromeAcquired cases
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Geographic tongue (Benign Migratory Glossitis): Filiform papillae Clin: appearance, Prevalence (3%), age & +FH Migrate & periods of remission Asymptomatic but acidic & spicy food
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Hist: Edge: hyperparak, acanthosis & a dense AICI Centre: atrophy & CICI
Association: fissured tongue, psoriasis (in 10%), Reiter syndrome
Neutrophilic infiltration
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Other sites: Migratory stomatitis
• Tongue involved
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Median Rhomboid Glossitis: CPA
Appearance & site Origin: Tuberculum Impar vs. Candida Hist:
Not all cases improve with antifungal therapy or show initial evidence of fungal infection
Kissing lesion
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Etiology: most recent evidence
Biopsy?
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Disturbances in the size of teeth:
Developmental disturbances of teeth
Tooth size is variable among different races and between sexes
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Microdontia
Localized: Peg-shaped laterals & U 3rd Ms Generalized: True vs. relative
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Macrodontia Localized: isolated, hemifacial hypertrophy Generalized: true vs. relative
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Anodontia Hypodontia
3rd Ms (20-25%); L 2nd
PM; U 2
Symmetrical or
haphazard
Pmt > PryEtiology: unclear Hereditary component Msx1 and Pax9 control genes Maternal age, LBW, Rubella, radiation, chemotherapy,
idiopathic hypoparathyroidism
Disturbances in number
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• Prevalence of hypodontia in primary
dentition?
• Which primary teeth are most
commonly affected?
• What happen to their successional
teeth?
Oligodontia?
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Association with systemic defects
Ectodermal DysplasiaX-linked recessive trait
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Cleft lip/palate
Crouzon's Syndrome
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Other syndromes?
Multiple missing teeth→ syndromes?
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Supernumerary
Other sites: Paramolars & Distomolars
Mesiodens
Hyperdontia: single 80%, 2 in ≈ 20%, >= 3 in < 1% of cases
Pmt > Pry
1-3% of population 80-90% in maxilla 25% erupt
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How do they develop
1/3 of supernumerary teeth in primary are followed by supernumerary permanent teeth
Timing of their formation
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The presence of a supernumerary
tooth is the most common cause for the
failure of eruption of a maxillary central
incisor.
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Supplemental
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Association with systemic defects:
Cleidocranial Dysplasia Gardner Syndrome Cleft lip/palate
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Supernumerary teeth
developing in sites other
than the jaws?
Dental Transposition? and confusion hyperdontia
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Disturbances in the form of teeth:
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Double teeth (Connated teeth): Joined by C, R or both Primary mandibular incisors Aetiology:
Gemination Fusion
or
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Taurodontism Elongated crown w apically placed furcation Aetiology: Rarely: w craniofacial anomalies or XXY
syndrome
Pmt Ms
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Concrescence Acquired Upper Pmt Ms Follows hypercementosis Complications:
Before or after eruption
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Dilaceration Sharp bend of root Upper centrals Aetiology & complications
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Disturbances in the structure of
teeth:
Enamel:
Hypoplastic vs. Hypomineralized Defect depends on many factors Types depending on extent
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Focal enamel hypoplasia:
Aetiology: Idiopathic:
Infection/Trauma:
Radiotherapy Turner teeth
Enamel opacities
Labial surface
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Generalized enamel hypoplasia: Systemic disturbances
including: Nutritional deficiencies: e.g. Vit D Infections Maternal disease & premature birth Haemolytic disease of newborn Congenital heart disease Chemotherapy Excess fluoride Endocrine disease GIT disease
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Congenital syphilis
“Hutchinson incisors” “Mulberry molars”
Affect primary teeth?
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Excess Fluoride Mostly PM, U incisors & 2nd Ms Fluoride mottling:
Mild: smooth E w white patches or striations
Severe: yellow/brown/black E w pits & grooves
Optimum level of F
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Hereditary Disturbances
(genetic): Affecting only teeth:
Amelogenesis Imperfecta
Generalized defects including
teeth:
Ectodermal Dysplasia
Down syndrome
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Amelogenesis Imperfecta Inheritance: Autosomal dominant, recessive, X-
linked.
Most of …..Enamel …….on all teeth
………..in both dentitions
Other components of teeth are normal Not associated with other health problems
Mutations in the ENAM, MMP20, KLK-4 and AMELX (5%) genes cause amelogenesis imperfecta
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Researchers have described at least 16
forms of AI. Distinguished by their
specific dental abnormalities and by
pattern of inheritance.
Incidence: 1 in 700 (Sweden) to 1 in 15,000 (USA)
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Are there any reported cases of
amelogenesis imperfecta with no
family history of the disorder?
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Hypoplastic type: Thin E but normally mineralized (>D in
radiodensity)
All E smooth teeth
with needle-like cusps
Not all E general
roughness w pitting &
vertical grooves
Stains
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Hypomineralized/hypomaturation type:
Most common form
E of normal thickness Newly erupted: normal size & shape of teeth Opaque, brown-yellow E soft chalky and easily removed → gross attrition E = D in radiodensity
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Dentine:
Local causes: Turner teeth,
radiotherapy
General causes:
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Systemic disturbances:o Rickets:
preD, hypocalcified w in interglobular D
o Hypophosphataemia:
in interglobular D, large pulp chambers &
long pulp horns with cracked E
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o Hypophosphatasia:
preD, in interglobular D, large
pulp chambers
o Juvenile hypoparathyroidism:
Small teeth w hypoplastic E and short roots
Prominent incremental lines in D
o Cytotoxic agents: Prominent incremental lines in D
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Dentinogenesis Imperfecta:
Type I:
o Patients with Osteogenesis Imperfecta
o Autosomal dominant
Type III: Brandywine isolate:
Rare, isolated (Maryland)
Mutation in the DSPP gene
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Type II: (Hereditary opalescent dentine) Autosomal dominant but no OI
Bluish-gray, brown/yellowish
Both dentitions
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Radiographs:
Short, blunt root
Obliteration of pulp with D
Bulbous crowns
↑ Root fracture
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Histologically: Normal E Normal mantle D Rest of D: hypomineralized w , irregular, wide D tubules often devoid of odontoblastic processes.
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Originally it was thought that a defective DEJ was
present; SEM studies have disclosed a normal
junction.
There is a tendency for enamel loss, and the
cleavage of enamel likely occurs within defective
dentin underlying the DEJ. Soft D attrition
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Which is more
common DI or AI
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Dental Caries Tooth Sensitivity Crowning of teeth/timing
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Dentine Dysplasia:
o Autosomal dominant
o Two types:
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Type I (Radicular Dentine
Dysplasia):
Most common
Normal crowns
Radiographs:
Short, blunt, conical or absent roots
Obliterated pulp chambers & RC
Or pulp chamber is "crescent shaped".
Periapical radiolucencies but no caries
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Histologically:
Radicular dentine: Numerous calcified spherical bodies
→“water streaming round boulders”
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Complications
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Type II (Coronal Dentine Dysplasia):
Roots are normal
Primary teeth:
DI clinically
Obliterated pulp chambers
Permanent teeth:
Normal color
Thistle-tube pulp chambers w pulp
stones
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Regional Odontodysplasia: Unknown etiology Regional Anterior maxilla Delay or failure of eruption Irregular & hypoplastic enamel
D is thin with interglobular D Pulp stones and widely open apices Focal calcifications in the dental follicle Radiographs: Ghost teeth
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Hypercementosis: Periapical inflammation
Occlusal forces
Paget’s disease,
Hyperpituitarism
Idiopathic
Hypocementosis: Cleidocranial Dysplasia: CC
Hypophosphatasia: Aplasia
Cementum
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Premature
eruption: Natal & neonatal
teeth
Disturbances in eruption & shedding of teeth:
Premature loss of primary tooth
Hyperthyroidism & Gigantism
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Delayed eruption/retarded eruption: Retained primary Hypothyroidism
& hypoparath Crowding Nutritional :
vitamin D, anemia
Fibrosis Down syndrome Supernumerary/cyst/tumor Cleid Dysplasia Trauma Prematurity
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Premature loss: Caries & periodontal disease Hypophosphatasia Palmar-Plantar hyperkeratosis Juvenile onset diabetes, Cyclic neutropenia & agranulocytosis, Scurvy, and Dentin dysplasia
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3. Developmental Disturbances of Bone:
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Facial Hemihypertrophy (hyperplasia):
Significant unilateral enlargement of the face Aetiology: ↑ NV supply Associated: skin, hypertrichosis, mental
retardation (20%), Abdominal tumors 6% (Wilms tumor, adrenal, or liver).
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D. Dx: Neurofibromatosis Fib. Dysplasia A-V malformation
Intraoral: unilateral macroglossia, teeth, malocclusion
Premature formation and eruption
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Throughout life
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B. Hemifacial atrophy: (Romberg
Syndrome) Progressive unilat in face size (other parts) Onset: 1st or 2nd decade
2.5 ys 5 ys 11 ys
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Aetiology Associated: hyperpigmentation & loss of facial hair Intraoral: lips & tongue, alveolar bone, teeth
(delay, short roots)
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C) Cleft Lip & palate: Cleft lip: Median nasal & maxillary process
Nostril complete or incomplete
Complete alveolar process & teeth
M > F; 25% of cases; 80% uni; 70% on L side
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Cleft palate: Lateral portions of palate Degree F>M; 30% of cases
Cleft lip & palate: M>F; 45% of cases
Bifid uvula: • Common in Asians and native Americans.
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• Aetiology:
Hereditary: 40% of CL & 20% of CP
Environmental: Nutritional factors
Large tongue Toxins Infections Stress Ischemia
Alcohol Drugs
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What is the percentage of clefts associated with syndromes?
Which syndrome is the most common syndrome associated with Orofacial clefting?
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Median cleft of upper lip
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Lateral facial cleft