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Faleh Sawair: BDS, FDS RCS (England), Ph.D.
Professor in Oral Pathology
& Medicine
http://elearning.ju.edu.johttp://elearning.ju.edu.jo
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.
Developmental disturbances
of the oral regionDefinitions: Congenital, Hereditary, Genetic, Autosomal, Sex-liked, Dominant, Recessive, Developmental, Acquired.
Classification
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
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.
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
Other causes of double lip
Frenal Tag: Autosomal D U labial
frenum Significance
Fordyce granules: Collection of sebaceous glands
Mostly bilateral on BM
Clin: multiple yellowish structures (1-2m), puberty
Present histologically in infants
Sebaceous naevi
Hist: superficial; no hair
Glands (1-5 lobules)
that empty into a duct
that opens on the
mucosal surface.
PrognosisHyperplasia
Tumors
Their relation with:
• Gender
• Skin type
• Systemic disease
Oral tonsils: Slightly elevated reddish
plaques/FOM
Foliate Papillitis:
Cancer
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
Ankyloglossia “tongue-tie”: Congenital Short, thick & anteriorly positioned lingual
frenum Complications:
• Less common in
adults
• Age of surgery
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
Macroglossia: Protruding & scalloped
Complications: Noisy breathing, snoring, drooling,
feeding difficulties.
Glossitis
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
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
Bifid Tongue
Cleft tongue
Ankyloglossia
TTT: Surgery
Aetiology
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:
≈ 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
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
Geographic tongue (Benign Migratory Glossitis): Filiform papillae Clin: appearance, Prevalence (3%), age & +FH Migrate & periods of remission Asymptomatic but acidic & spicy food
Hist: Edge: hyperparak, acanthosis & a dense AICI Centre: atrophy & CICI
Association: fissured tongue, psoriasis (in 10%), Reiter syndrome
Neutrophilic infiltration
Other sites: Migratory stomatitis
• Tongue involved
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
Etiology: most recent evidence
Biopsy?
Disturbances in the size of teeth:
Developmental disturbances of teeth
Tooth size is variable among different races and between sexes
Microdontia
Localized: Peg-shaped laterals & U 3rd Ms Generalized: True vs. relative
Macrodontia Localized: isolated, hemifacial hypertrophy Generalized: true vs. relative
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
• Prevalence of hypodontia in primary
dentition?
• Which primary teeth are most
commonly affected?
• What happen to their successional
teeth?
Oligodontia?
Association with systemic defects
Ectodermal DysplasiaX-linked recessive trait
Cleft lip/palate
Crouzon's Syndrome
Other syndromes?
Multiple missing teeth→ syndromes?
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
How do they develop
1/3 of supernumerary teeth in primary are followed by supernumerary permanent teeth
Timing of their formation
The presence of a supernumerary
tooth is the most common cause for the
failure of eruption of a maxillary central
incisor.
Supplemental
Association with systemic defects:
Cleidocranial Dysplasia Gardner Syndrome Cleft lip/palate
Supernumerary teeth
developing in sites other
than the jaws?
Dental Transposition? and confusion hyperdontia
Disturbances in the form of teeth:
Double teeth (Connated teeth): Joined by C, R or both Primary mandibular incisors Aetiology:
Gemination Fusion
or
Taurodontism Elongated crown w apically placed furcation Aetiology: Rarely: w craniofacial anomalies or XXY
syndrome
Pmt Ms
Concrescence Acquired Upper Pmt Ms Follows hypercementosis Complications:
Before or after eruption
Dilaceration Sharp bend of root Upper centrals Aetiology & complications
Disturbances in the structure of
teeth:
Enamel:
Hypoplastic vs. Hypomineralized Defect depends on many factors Types depending on extent
Focal enamel hypoplasia:
Aetiology: Idiopathic:
Infection/Trauma:
Radiotherapy Turner teeth
Enamel opacities
Labial surface
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
Congenital syphilis
“Hutchinson incisors” “Mulberry molars”
Affect primary teeth?
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
Hereditary Disturbances
(genetic): Affecting only teeth:
Amelogenesis Imperfecta
Generalized defects including
teeth:
Ectodermal Dysplasia
Down syndrome
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
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)
Are there any reported cases of
amelogenesis imperfecta with no
family history of the disorder?
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
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
Dentine:
Local causes: Turner teeth,
radiotherapy
General causes:
Systemic disturbances:o Rickets:
preD, hypocalcified w in interglobular D
o Hypophosphataemia:
in interglobular D, large pulp chambers &
long pulp horns with cracked E
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
Dentinogenesis Imperfecta:
Type I:
o Patients with Osteogenesis Imperfecta
o Autosomal dominant
Type III: Brandywine isolate:
Rare, isolated (Maryland)
Mutation in the DSPP gene
Type II: (Hereditary opalescent dentine) Autosomal dominant but no OI
Bluish-gray, brown/yellowish
Both dentitions
Radiographs:
Short, blunt root
Obliteration of pulp with D
Bulbous crowns
↑ Root fracture
Histologically: Normal E Normal mantle D Rest of D: hypomineralized w , irregular, wide D tubules often devoid of odontoblastic processes.
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
Which is more
common DI or AI
Dental Caries Tooth Sensitivity Crowning of teeth/timing
Dentine Dysplasia:
o Autosomal dominant
o Two types:
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
Histologically:
Radicular dentine: Numerous calcified spherical bodies
→“water streaming round boulders”
Complications
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
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
Hypercementosis: Periapical inflammation
Occlusal forces
Paget’s disease,
Hyperpituitarism
Idiopathic
Hypocementosis: Cleidocranial Dysplasia: CC
Hypophosphatasia: Aplasia
Cementum
Premature
eruption: Natal & neonatal
teeth
Disturbances in eruption & shedding of teeth:
Premature loss of primary tooth
Hyperthyroidism & Gigantism
Delayed eruption/retarded eruption: Retained primary Hypothyroidism
& hypoparath Crowding Nutritional :
vitamin D, anemia
Fibrosis Down syndrome Supernumerary/cyst/tumor Cleid Dysplasia Trauma Prematurity
Premature loss: Caries & periodontal disease Hypophosphatasia Palmar-Plantar hyperkeratosis Juvenile onset diabetes, Cyclic neutropenia & agranulocytosis, Scurvy, and Dentin dysplasia
3. Developmental Disturbances of Bone:
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).
D. Dx: Neurofibromatosis Fib. Dysplasia A-V malformation
Intraoral: unilateral macroglossia, teeth, malocclusion
Premature formation and eruption
Throughout life
B. Hemifacial atrophy: (Romberg
Syndrome) Progressive unilat in face size (other parts) Onset: 1st or 2nd decade
2.5 ys 5 ys 11 ys
Aetiology Associated: hyperpigmentation & loss of facial hair Intraoral: lips & tongue, alveolar bone, teeth
(delay, short roots)
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
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.
• Aetiology:
Hereditary: 40% of CL & 20% of CP
Environmental: Nutritional factors
Large tongue Toxins Infections Stress Ischemia
Alcohol Drugs
What is the percentage of clefts associated with syndromes?
Which syndrome is the most common syndrome associated with Orofacial clefting?
Median cleft of upper lip
Lateral facial cleft