Odontodysmorphogenesis

1) Tooth size

1. Microdontia

Teeth measurably smaller than normal

Clinical types:

Absolute – smaller than normal
Relative – gigantism
Generalized – entire dentition
Focal – usually 7’s & 8’s

Etiology:

Genetic (AD) – Downs syndrome
Irradiation therapy of 10 Gy or more
Drawfism
Congenital heart disease

2. Macrodontia

Enlarged teeth

Clinical types:

Absolute – pituitary drawfism
Relative – hypognathia of maxilla/ mandible
Generalized – entire dentition
Focal – some teeth eg. hemifacial hypertrophy

2) Tooth form

1. Double teeth

a) Germination – single enamel organ – 2 teeth develop

2 crowns share same root canal
Aet: Trauma

b) Fusion – 2 tooth germs fuse by dentine ± pulp – forms single large tooth structure

Aet: Trauma

c) Concrescence – adjacent formed teeth join by cementum

Aet: Trauma, overcrowding

d) Twinning – Mirror image teeth. Complete germination

One tooth germ – develops into 2 teeth

Tooth anomaly - concrescence, fusion, germination

2. Dilaceration

Bending of roots at an angle at long axis of tooth

Aet: Trauma during root development

3. Dens invaginatus

Abnormal exaggeration of lingual pit

Type I:
- Enamel lined cavity confined to tooth crown, not extending beyond CEJ
- Mx: Pit sealing

Type II:
- Enamel lined cavity into tooth (± communication with pulp)
- Mx: XLA

Type III:
- Invagination extends beyond CEJ
- Perforating apically or laterally at a foramen (no pulpal communication)
- Mx: XLA

4. Dens evaginatus

Anomalous tubercle/ cusp projecting from occlusal surface – usually premolar

Extra cusp worn down, predispose to tooth decay

5. Taurodontism

Bull teeth

Elongated crowns with increased apico-occlusal height of pulp chambers
Failure of Hertwig’s root sheath to invaginate at proper horizontal level

6. Talon cusp/ talon cingulum

Exaggeration of cusp shaped cingulum esp. Max. anteriors

Mx: Fissure sealing & pulpotomy

7. Transposition

One tooth in place of another

8. Supernumerary

Roots: Mand. canine, premolar, molar (8)
Cusps:
- Cusp of carabelli
- Enamel pearl (root furcation)
- Dens evaginatus

3) Tooth number

1. Anodontia

Absence of teeth

Complete
Partial:
- Hypodontia (<6 teeth)
- Oligodontia (>6 teeth)

Aet:
- 1. Failure to form dental lamina
- 2. Failure to develop tooth buds
- 3. Premature breakdown of dental lamina
- 4. Autosomal dominant inheritance

High prevalence in:
- Females
- Hereditary ectodermal dysplasia
- Orofacial cleft
- Down’s syndrome

Hereditary Ectodermal dysplasia

X – Linked recessive
Nail dystrophy
Hypotrichosis
Hyperkeratosis
Oligodontia

2. Pseudodontia

Clinical absence of teeth

Aet:

Impaction
Delayed eruption

3. False anodontia

Teeth exfoliated or extracted

4. Hyperdontia

Excess teeth

Supplemental – Normal dental series
Supernumerary – Abnormal morphology

Mesiodens – In maxillary midline
Paramolar/ distodens – 4th molar
Natal – Present at birth
Neonatal – Immediately after birth (30 days)

Syndromes associated with hyperdontia

1. Cleidocranial dysplasia

Multiple supernumeraries
Aplasia of one or both clavicle
Delayed closure of fontanelles & sutures
Wormian bones in suture lines
Short sagittal diameter of cranial base
Large transverse diameter of cranium

2. Gardner’s syndrome

Multiple unerupted supernumeraries & dentigerous cysts
Multiple osteomas of facial bones
Multiple adenomatous polyposis of colon
Desmoid tumors
Cutaneous epidermoid cyst
Fibrous hyperplasia of skin & mesentery

4) Tooth colour

1. Extrinsic staining

Not incorporated into tooth substance

Chromogenic bacteria (green, black, yellow orange)
Restorative materials:
- Silver amalgam (gray black)
- Resins (yellow brown)

2. Intrinsic staining

Incorporated into tooth structure

Changes in structure/ thickness of dental tissues:

Enamel hypoplasia
Fluorosis
Caries
Dentine dysplasia II
Amelogenesis imperfecta
Dentinogenesis imperfecta
Enamel opacity
Age changes

Diffusion of pigments during/ after dental development:

Tetracycline – cross placental barrier – yellow/ grey, brown
Bilirubin – green/ brown
Liver disease/ neonatal hepatitis – Yellow brown
Porphyrins
Pulp necrosis products
RH incompatibility (erythroblastosis fetalis)
Endodontic materials

5) Tooth eruption

1. Accelerated eruption

Symmetrical:

Adrogenital syndrome
Cerebral gigantism

Unilateral:

Facial hemihypertrophy
Sturge – Weber syndrome
Vascular anomalies of bone (+ macrodontia)

2. Delayed eruption

Symmetrical:

Congenital hypothyroidism/ hypopituitarism
Cleidocranial dysplasia
Downs syndrome

Unilateral:

Regional odontodysplasia
Ankylosing of primary predecessor
Dilaceration
Severe enamel hypoplasia:
- Nutritional deficiancy
- Traumatic displacement of tooth germs
Obstruction by impaction:
- Rare in 1ry teeth, except 1st molar – Ankylosis/ submergence
- Multiple impactions – Cleidocranial dysplasia
- Single impaction:
  - Supernumeraries
  - Odontomes
  - Cysts
  - Crowding

3. Reimpaction of teeth

Previously erupted tooth becomes submerged in tissues

Aet:

Deficient development of alveolar process
Root ankylosed + Lack of growth of alveolar process

4. Premature loss

Juvenile & prepubertal periodontitis
Hypophosphatasia
Leukemia
Chronic neutropenia
Acrodynia (pink disease) – Hg poisoning
Dental caries
Hereditary palmer – planter hyperkeratosis
Langerhans cell histiocytosis – proliferation of abnormal histiocytes
- Tooth mobility
- Floating teeth in multiple quadrants
- DI
- Short stature
- Neurosensory deafness

5. Prolonged retention

Deciduous teeth not shed

Mand 1’s – Lingual eruption esp. Down’s syndrome
Max 6’s – Path of eruption further anterior than normal

6. Occlusal defects

Deep/ increased overbite:
- Over eruption of ant. teeth
- Infra eruption of post. teeth
Open bite:
- Usually ant. region
- Post. mandibular growth disorder
- Macroglossia

6) Degenerative changes (acquired)

1. Attrition

Physiologic wearing of teeth due to mastication
Abnormal occlusion habits: bruxism, tobacco/ betel chewing, abnormal tooth structure (AI, DI)
Histology: Reactionary dentine, dead tracts, translucent zones

2. Abrasion

Pathologic wear of teeth – abnormal habit, abnormal use of abrasives orally
Eg. Pipe smoking, tobacco chewing, aggressive tooth brushing, abrasive dentifrices, pins & nails (carpenters)

3. Erosion

Loss of tooth substance due to non-bacterial chemical process:
- Occupational – car battery acid
- Dietary – acidic drinks
- Chronic vomiting – anorexia, bulimia

4. Resorption

Physiological – shed deciduous teeth
Pathological:
- Periapical inflammation
- Iatrogenic – excess orthodontic force
- Neoplasms
- Impacted teeth
- Transplanted/replanted teeth
- Idiopathic

External resorption: 2ry to pathology (or idiopathic)
Internal resorption: 2ry to pulpitis (or idiopathic)

internal resorption — Internal resorption

7) Tooth structure

A) Enamel

1. Enamel hypoplasia

Quantitatively defective – ameloblast fail to produce normal volume of matrix
Enamel normal hardness
Clinical:
- Pit/ grooves on enamel surface
- General decrease in enamel thickness
Ground section: Decreased prisms than normal + abnormal direction

2. Enamel hypocalcification

Qualitatively defective – hypomineralized
Normal amounts of enamel
Clinical:
- White & opaque – after eruption – orange brown
- Quickly chips off & wears off
Ground section: Surface layers = normal

Classification

1. Local causes

Trauma
Irradiation
Infection – single tooth
- eg. Turner’s tooth – hypocalcified permanent tooth due to abscess overlying deciduous tooth (yellow/ brown)
Idiopathic (enamel opacities) – hypocalcification of 1ry & 2ry teeth esp. 11 and 21

2. Generalized causes

a) Environmental (chronological hypoplasia)

Birth to 6 years ie. period of crown formation of permanent teeth – ameloblast dysfunction

Prenatal:
- Maternal disease
- Rubella
- Syphilis (T. pallidum):
  - Hutchinson’s incisors – tapered crown + notched incisal edge
  - Mulberry molars – Lobulated occlusal surfaces

Neonatal:
- Hemolytic disease of new born
- Prolonged labour
- Premature birth
- Hypocalcemia:
- Hypercalcemia:
  - Hypothyroidism
  - Hypophosphatasia

NB: Disorders in calcium metabolism cause dysfunction of ameloblasts

Postnatal:
- Measles
- Chicken pox
- Scarlet fever
- Whooping cough
- Pneumonia
- Congenital heart disease
- GIT disease
- Hyperparathyroidism
- Fluorosis – > 1ppm, incorporates into maturation stage (not in utero due to placental barrier)
- Vitamin A, C, D deficiency
- Rickets

b) Genetic

Only teeth affected: Amelogenesis imperfecta

Mutation on distal short arm of x chromosome – codes for amelogenin protein
Classification:
- 1. Hypoplastic:
  - Areas of tooth enamel fail to form normal contour
  - Enamel is normal hardness but thin
  - Sharp needle like cusps/ pitting/ vertical grooving & wrinkling
  - Yellow + gross attrition with time
- 2. Hypomaturation:
  - Enamel of normal thickness but wears away easily
- 3. Hypocalcified:
  - Soft enamel lost easily after eruption
  - Yellow – brown plus gross attrition
  - Chalky consistence – Chips off

Teeth + generalized disease:

Ectodermal dysplasia
Down’s syndrome
Epidermolysis

B) Dentine

1. Dentinogenesis imperfecta (hereditary opalescent dentine)

Autosomal dominant (AD)
Mutations in structural genes for collagen type 1
Therefore occur with osteogenesis imperfecta
On eruption – normal contour but opalescent amber like appearance – becomes translucent + grey/brown + bluish reflection from enamel
Rapidly lost attrition

Radiological:
- Short, blunt roots
- Partial/ total obliteration of pulp chamber & root canal by dentine

Histology:
- Normal mantle dentine
- Decreased tubules – wide & irregular
- Straight DEJ (not scalloped)
- Vascular inclusions in dentine – remnants of odontoblasts + pulp tissue

Biochemical:
- Increased water content
- Decreased mineral content
- Decreased microhardness

Classification:

I	II	III	IV
AD	AD	AD	AR
Opalescent dentine in 1ry & 2ry	Discoloured teeth	Opalescent teeth	Brown opalescent teeth
White sclera	Blue sclera	Blue/ white sclera	White sclera
	Bone fragility	Bone fragility Severe long bone deformity	Rapid dentine abrasion Severe bone fragility Skeletal deformity Growth retardation

Dentinogenesis imperfecta classification

2. Shell teeth

Rare
Homozygote form of DI – No pulp chamber obliteration
Thin dentine, forms shell around pulp
Short roots

3. Dentinal dysplasia (rootless teeth)

Rare AD
Normal crown + dysplastic dentine in roots having many calcified, spherical bodies
Obliterated root canals & pulp chamber
Roots are stunted

2 types caused by fragmentation of Hertwig’s root sheath:

Radicular DD:
- Abnormal root formation
- Periapical resorption
- Therefore teeth exfoliate prematurely
- X-ray: Short roots & obliterated pulp
Coronal DD:
- Discolouration of 1ry teeth
- Obliteration of pulp chamber
- Distorted crowns of permanent teeth
- X-ray: Enlarged pulp chambers

NB: Metabolic disturbances affecting dentinogenesis:

Rickets
Vitamin D resistant rickets
Hypophosphatasia
Dentine dysplasia I & II

4. Regional odontodysplasia (enamel & dentine defect)

Involves ectodermal (enamel) & mesodermal (dentine + cementum)
Results from disorderly proliferation of dental epithelium at an early stage – of formation of hard tissues – in each affected
Etiology: Local vascular deficiency during tooth development
Clinical:
- Delayed eruption
- Irregular shape – hypoplastic and irregularly mineralized enamel
- Dentine – thin + large interglobular dentine
- Affects a region/ quadrant of maxilla/ mandible
- Usually anterior maxilla and unilateral

X-ray:
- Ghost teeth
- Decreased radiopacity
- Loss of distinction between enamel and dentine

Histology:
- Abnormal odontogenic epithelial cells
- Abnormal globular dentine

C) Cementum

1. Hypercementosis

Increased cementum deposition