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Paediatrics > Chapter 11: Dental Anomalies > Flashcards

Chapter 11: Dental Anomalies Flashcards

1
Q

5 different classifications of dental anomalies are:

A
  • number anomalies
  • size anomalies
  • shape anomalies
  • color anomalies
  • structure anomalies
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2
Q

What type of anomaly does this statement describe?
“ they occur in the earliest periods of development (Dental lamina disorganisation)”

A

Number anomalies

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3
Q

The two types of number anomalies are:

A

Agenesis and supernumerary

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4
Q

Agenesis: classification from more severe to less severe

A
  • anodontia: the total absence of the tooth germ
  • temporary teeth: agenodontia
  • permanent teeth: ablastodontia
  • oligodontia: half or more of the tooth germs are missing
    *10 or fewer teeth germs are present in primary dentition (instead of 20): oligogenodontia
    *16 or fewer teeth germs are present in permanent dentition (instead of 32): oligoblastodontia
  • hypodontia: less than half of the tooth germs are missing
  • less than 10 primary teeth are missing: atelogenodontia
  • less than 16 permanent teeth are missing: ateloblastodontia
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5
Q

Agenesis: frequency

A
  • more frequent in permanent teeth
  • more frequent in females
  • 75% of patients with agenesis in temporary teeth will have agenesis in permanent teeth
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6
Q

Agenesis: location
- in temporary teeth it’s more common in the ___ (maxilla/mandible) and is usually ____ (bilateral/unilateral) and in these teeth ____
- in permanent teeth it’s more common to affect ___ (more teeth/one tooth), and is usually ___ (bilateral/unilateral) and in these teeth _____

A
  • maxilla, unilateral, upper LI, lower CI, lower LI
  • more than 1 tooth, bilateral, 3rd molars, upper LI, 2nd lower PM, 2nd upper PM, lower CI (in that order)
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7
Q

Agenesis: aetiology

A
  • By a physical obstruction at the dental lamina (oral-facial-digital syndrome)
  • functional abnormalities of the dental epithelium ( ectodermal dysplasia)
  • bud developers but there is no induction of the mesenchyme
  • space problems
  • non syndromic agenesis: genes MSX1, PAX8, and AX1N2
  • drugs (thalidomide)
  • infections: rubella in the mother
  • radiotherapy in children
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8
Q

Agenesis: diagnosis
- clinical
- radiographical

A
  • clinical: absence of a tooth for around 1 year—> suspected diagnosis
  • radiographical: absence of 2nd PM at 9-10 years old
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9
Q

Agenesis: treatment (multidisciplinary)

A

Orthodontic, prosthetic, or restorative

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10
Q

Supernumerary (hyperdontia): frequency
- infrequent in ?
- more frequent in ____ (boys/girls)
- more frequent in ?

A
  • infrequent in temporary and permanent dentition (1-4% of the population)
  • more frequent in boys
  • more frequent in upper incisors
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11
Q

Supernumerary (hyperdontia): aetiology (different theories)

A
  • hyperactivity of dental lamina
  • tooth germ division
  • hereditary (especially in syndromes)
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12
Q

Supernumerary (hyperdontia): classification according to the morphology

A
  • supplemental: similar to the adjacent, normal shape, most common in permanent upper LI
  • rudimentary: different to the adjacent, (short-barrel shaped —> palatal to upper CI
    most common shapes:
  • tuberculate (short barrel shaped): palatal to upper CI, unilateral or bilateral
  • conical shaped (peg- shaped): most typical is mesiodens
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13
Q

Supernumerary (hyperdontia): classification according to the location

A
  • mesiodens: between upper CI, single or multiple, variable size and shape but typically conical rudimentary, can be suspected when there’s an asymmetry in the eruption of the CI
  • paramolars: extramolars
  • distomolars: distal to 3rd molars
  • peridens: premolar area
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14
Q

Supernumerary (hyperdontia): alterations caused by mesiodens

A
  • eruptive delay
  • deviation of the permanent successor teeth or adjacent tooth
  • root resorption by contact
  • radicular cyst formation
  • eruption in nostrils
  • sometimes causes diastemas
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15
Q

Supernumerary (hyperdontia): diagnosis and treatment

A
  • always radiographic
  • extraction and orthodontic treatment
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16
Q

Which type of anomaly does this statement describe?
“ they are produced in the morphodifferentiation period of germs”

A

Size and shape anomalies

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17
Q

Size anomalies: classification

A
  • macrodontia
  • microdontia
  • rhizomegaly
  • rhizomicry
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18
Q

Size anomalies: bigger than normal anomalies

A
  • macrodontia
  • rhizomegaly
  • fusion
  • germination
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19
Q

Size anomalies: macrodontia aetiology

A
  • hereditary associated with endocrine disorders
  • generalised form associated with congenital syndromes
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20
Q

Size anomalies: macrodontia frequency

A
  • more in permanent teeth
  • upper CI, C, M
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21
Q

Size anomalies: rhizomegaly frequency

A

Lower permanent canines and molars

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22
Q

Size anomalies: fusion

A
  • F22
  • joining of 2 teeth germs that gives rise to a single larger tooth
  • it can have 1 or 2 pulp chambers
  • different than macrodontia because there’s a tooth missing in the arch
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23
Q

Size anomalies: fusion frequency

A
  • autosomal dominant inheritance
  • more frequent in primary teeth in the anterior area
  • if we see fusion in primary teeth, there is often agenesis of 1 of the 2 permanent successors
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24
Q

Size anomalies: germination

A

G12
- an incomplete division of a germ resulting in an abnormally large tooth
- 1 root and 1 canal
- common in anterior sector of the maxilla
- differs from fusion because the number of teeth in the arch is not altered

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25
Q

Size anomalies: smaller than normal anomalies

A
  • microdontia
  • rhizomicry
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26
Q

Size anomalies: microdontia

A
  • due to the weakening of the enamel organ during differentiation
  • generalised clinical forms are rare and are usually associated with different diseases (Down syndrome, pituitary dwarfism, antihydrotic ectodermal dysplasia)
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27
Q

Size anomalies: microdontia frequency

A
  • most frequently localised and bilateral
  • most affected tooth: maxillary LI
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28
Q

Size anomalies: rhizomicry
- mainly in?
- frequent with which diseases?

A
  • mainly in CI and 3rd molars
  • frequent in osteopetrosis —> generalised rhizomicry
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29
Q

Size anomalies: treatment
- 2 main problems
- macrodontia treatment
- microdontia treatment

A
  • space and aesthetics
  • macrodontia: lack of space and malocclusion: Ortho
  • microdontia: multiple diastemas, if many teeth affected: prosthetic, if few: CR restoration
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30
Q

Shape anomalies: types

A
  • dens evaginatus (Talon cusp)
  • dens in dente
  • taurodontism
  • cynodontia
  • dilaceration
  • radicular divergence
  • radicular convergence
  • pyramidal root
  • enamel pearl
  • accessory root
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31
Q

Shape anomalies: dens evaginatus (talon cusp)

A
  • a tooth with an extra cusp or tubercle
  • frequency form more to less: I, C, PM, M
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32
Q

Shape anomalies: dens evaginatus treatment

A

Not necessary unless the occlusion is affected, in that case:
- We carve the tubercle carefully because the pulp extension can exist, and the root canal treatment could be necessary if a pulp exposure takes place
- Caries are frequent in the groove surrounding these tubercles—> conservative treatment (it is advisable to do sealants)

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33
Q

Shape anomalies: dens in dente aetiology

A

Invagination of the inner enamel epithelium during tooth formation

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34
Q

Shape anomalies: dens in dente frequency

A
  • in permanent teeth
  • most affected teeth: upper LI, CI, C , supernumerary (unilateral)
  • there might be contact between the pulp and oral environment
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35
Q

Shape anomalies: dens in dente treatment

A
  • as the pulp communicated with the oral environment, we have frequent early pulpitis —> pulp treatment
  • if pulp treatment fails, extraction
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36
Q

Shape anomalies: taurodontism

A
  • only molars are affected
  • larger crowns and shorter roots
  • elongated pulp chamber and the furcation is shifted towards apical compared to a normal tooth
  • no clinical disturbance, radiographic diagnosis
37
Q

Shape anomalies: taurodontism frequency

A
  • both dentitions can be affected, more common in permanent teeth
  • generalised may be associated with 2 syndromes: tricho dento osseous syndrome and orodigitofacial syndrome
38
Q

Shape anomalies: taurodontism treatment.

A
  • No treatment is needed, but the diagnosis is useful
  • It is useful to know if we ever need to do a pulp treatment (important to know
    that the anatomy is different: large pulp chamber and short roots)
39
Q

Shape anomalies: cynodontia

A
  • The converse situation of taurodontism
  • Due to the early invagination of Hertwig’s epithelial root sheath
  • Short crowns with short pulp chambers and long roots
  • The furcation will be located more occlusal
  • More often in permanent molars
  • No treatment is required but its diagnosis is useful
40
Q

Shape anomalies: dilaceration

A
  • Abnormal root curvature at the level of the crown-radicular union
  • A variant of dilaceration is root angulation when the curvature occurs at any point of the root and bayonet root which is a double angulation.
  • aetiology: Thought to be due to trauma in primary teeth (incisors intrusion)
41
Q

Shape anomalies: radicular divergence

A

Teeth having a steeper divergence than normal

42
Q

Shape anomalies: radicular convergence

A
  • The opposite of divergence
  • If convergence is so big that the roots are joined—> synostosis
  • The roots are joined in their apical portion by apposition of secondary cement
43
Q

Shape anomalies: pyramidal root

A
  • Molar having a single root (when it should have multiple)
  • 2nd and 3rd molars
44
Q

Shape anomalies: enamel pearl

A
  • Enamel formations, rounded, in locations where the enamel is not supposed to be
  • Usually in furcation of molars
  • Where the pearl is formed there is no cement, the enamel is deposited directly into the dentin
45
Q

Shape anomalies: enamel pearl aetiology

A
  • Atrophic supernumerary tooth germs
  • Groups of hypertrophic ameloblasts
46
Q

Shape anomalies: accessory roots

A
  • They exceed in number and can have a normal shape or as appendices
47
Q

Color anomalies: when do intrinsic stains occur ?

A

During tooth development, pigments are included in the structure of the tooth, they’re difficult to remove

48
Q

Color anomalies: intrinsic staining: tetracycline staining:

A
  • Due to the administration of tetracycline in periods of enamel and dentin mineralisation
  • Tetracycline binds to Ca molecules and remains attached to dental tissue
  • Tetracyclines can cross the placental barrier, so the temporary teeth could be affected if taken by the mother during pregnancy
  • Colour: from yellowish to dark grey, with diffuse bands of different widths at different levels of the crown
  • Location of the band: depends on the moment of the development of the tooth at the time of the administration of the drug
49
Q

Color anomalies: intrinsic staining: tetracycline staining critical periods

A
  • from the 4th month of gestation to the 9th month after birth (primary dentition)
  • from birth to 7-8 years old (permanent dentition)
50
Q

Color anomalies: intrinsic staining: dental fluorosis

A
  • Due to the systemic administration of more than 1.8 ppm of fluoride per day
  • The degree depends on the moment of the development of the enamel and dentin, and the magnitude of the ingestion
  • Colours range from chalk white to brown
  • In severe cases, there are structural defects (hypoplasia and hypocalcification of the enamel)
51
Q

Color anomalies: intrinsic staining: staining by blood pigments

A
  • In children with blood disorders that lead to hemolysis and release blood pigments, which bind to enamel and dentin in formation
52
Q

Color anomalies: intrinsic staining: staining by blood pigments is caused by?

A

a. Congenital erythropoietic porphyria
b. Fetalerythroblastosis
c. Post-transfusional hemolysis
d. Congenital hyperbilirubinemia

53
Q

Treatment of intrinsic staining?

A

It depends on the degree of alteration (intensity and number of affected teeth)
- Mild pigmentation in a few teeth—> restoration with composite resins
- Severe and extensive pigmentation—> porcelain veneers or crowns

54
Q

Color anomalies: extrinsic staining

A
  • Outside the dental structure, and lies on tooth surface or in acquired pellicle
  • Plaque deposits with chromogenic bacteria
  • More common: deposits of ferric compounds, excess food, or pigmented drinks
  • Incorporated into the surface of the teeth once the tooth finishes its formation
  • Eliminated with a correct brushing or professional cleaning (dental scaling or dental hygiene)
55
Q

Structure anomalies: enamel anomalies
- quantitative
- qualitative
- two types

A
  • Quantitative defects: hypoplasia
  • Qualitative defects: hypomaturation, hypocalcification, MIH (molar-incisor
    hypomineralisation)
  • Enamel anomalies are either:
    a. Hereditary enamel disturbances: amelogenesis imperfecta
    b. Acquired enamel disturbances: due to general or local factors
56
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta:

A
  • The main hereditary enamel disturbance
  • Alteration in the calcification of the enamel due to an abnormal function of ameloblasts
  • Both dentitions may be affected
  • Frequent anterior open bite
  • Low caries due to few interdental contacts
57
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta: 3 types

A

a. Hypoplasia: quantity is affected
b. Hypomaturation: quality is affected
c. Hypocalcification: quality is affected

58
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta: hypoplastic type:

A
  • Quantity: reduced enamel thickness but relatively well-mineralised
  • Both dentitions are affected (temporary and permanent)
  • Altered colour of the enamel from yellowish to dark brown
  • Hard consistency
  • Dentin hypersensitivity: 60% lingual interposition with open bite
59
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta: hypomaturation type:

A
  • Both dentitions are affected
  • The final stage of the mineralisation process is abnormal
  • The quality of the enamel is affected, and the mineral context of the enamel is altered
  • The enamel is brittle, porous, very permeable, and rough
  • Colour from white to brown and tends to fall off easily
  • Many subtypes, one of them is “snow-capped teeth”: white spots on incisal edges and the buccal surfaces near the occlusal surface
  • X-ray observation: no contact points, lost enamel
60
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta: hypocalcified type:

A
  • The quality of the enamel is poor as calcification of the interprismatic substance of the matrix is altered, instead of the mineral content (hypomaturation type)
  • The enamel formed in adequate amounts, but poorly calcified: fragile, easily detaching, exposing the dentin
  • Radiographically: the dentin is usually more radiopaque than the enamel
  • Clinically: cannot be differentiated from the hypomaturation type
61
Q

Structure anomalies: enamel anomalies: hereditary enamel disturbances: amelogenesis imperfecta: treatment

A
  • Objective: to prevent teeth from breaking, suppress sensibility and achieve aesthetics and prevent caries
  • Oral hygiene techniques
  • Fluoride (that hardens the enamel)
  • Composite restorations and crowns (need to be changed very often because the adhesion is very bad)
  • If left untreated: may have sensitivity and might need pulp treatments
  • Severe cases end up needing prosthetic restorations
62
Q

Structure anomalies: enamel anomalies: acquired due to general or systemic causes: neonatal disorders

A
  • Hypoxia
  • Hypocalcemia
  • Premature birth
  • Stress at birth: neonatal lines or Retzius lines in the temporary dentition
63
Q

Structure anomalies: enamel anomalies: acquired due to general or systemic causes: nutritional deficiency:

A
  • Hypovitaminosis A, C, D, K
  • Deficiency of Ca and P
  • Teeth appear with horizontal rows that coincide with the matrix area formed
    at the time of vitamin deficiency
  • The extension depends on the duration of the process/deficiency
64
Q

Structure anomalies: enamel anomalies: acquired due to general or systemic causes: maternal diseases

A
  • Maternal diabetes: frequency of dysplasia in temporary teeth
65
Q

Structure anomalies: enamel anomalies: acquired due to general or systemic causes: severe postnatal diseases

A
  • With high fevers (febrile hypoplasia)
  • Exanthematic diseases: chicken pox, measles, salmonellosis
  • Neuropathies
  • Congenital alterations of the metabolism
  • Due to some diseases like asthma
66
Q

Structure anomalies: enamel anomalies: acquired due to general or systemic causes: prenatal infections

A
  • Congenital syphilis: enamel and dentin hypoplasias
  • The permanent maxillary incisors have spots and are pyramidally shaped (Hutchinson’s teeth) and mulberry molars
  • Rubella in the first trimester of pregnancy: affects the temporary dentition
67
Q

Characteristics of acquired enamel anomalies due to general causes:

A
  • Enamel defects due to systemic causes are characterised by their tendency to symmetry and by affecting the same dental groups
  • We try to relate the time of the cause with the teeth that have had the malformation
  • Once the tooth is formed with the stain, preventive treatments are not a solution
68
Q

Structure anomalies: enamel anomalies: acquired due to local causes: radiation

A

pregnant women undergoing radiation therapy

69
Q

Structure anomalies: enamel anomalies: acquired due to local causes: apical infections

A

from temporary to permanent teeth.
The temporary tooth damaged at the apical level produces a spot in the permanent tooth (Tumer’s tooth) from temporary to permanent teeth.

70
Q

Structure anomalies: enamel anomalies: acquired due to local causes: iatrogeny

A

in patients with cleft lip or pathologies requiring surgical treatment that may affect the dental germ

71
Q

Structure anomalies: enamel anomalies: acquired due to local causes: maxillary infections

A

maxillitis or osteomyelitis

72
Q

Structure anomalies: enamel anomalies: acquired due to local causes: trauma

A

when the temporary teeth impact with the next permanent germ (diente de Carlos)

73
Q

Treatment of acquired enamel anomalies:

A
  • Application of fluoride
  • Restoration with composite resins
  • in some cases, performed crowns
74
Q

Dentin anomalies: hereditary: dentinogenesis imperfecta

A
  • An inherited disorder affecting dentin with defective dentin
  • Autosomal dominant inheritance
  • Both dentitions are affected
  • The deepest dentin (closest to the pulp) is more affected
  • 3 types (according to Shields): type I, II and III
75
Q

Dentin anomalies: hereditary: dentinogenesis imperfecta features

A
  • Bulbous crowns (very rounded)
  • Short roots
  • Small or obliterated (nonexistent because filled with dentin) pulp chamber and narrow or non-existent canals
  • No sensitivity
  • Vertical dimension is lost very soon → one of the objectives of the treatment is to preserve the vertical dimension
76
Q

Dentin anomalies: hereditary: dentinogenesis imperfecta type I:

A
  • Always associated with osteogenesis imperfecta
  • All teeth in both dentitions are affected
  • The teeth have an amber colour, are soft and have frequent fractures
77
Q

Dentin anomalies: hereditary: dentinogenesis imperfecta type II or hereditary opalescent dentin:

A
  • Both primary and permanent dentitions are equally affected
  • Translucent bluish-brown colour
  • Rapid wear and loss of vertical dimension due to abrasions
78
Q

Dentin anomalies: hereditary: dentinogenesis imperfecta type III or Brandywine Maryland:

A
  • Rare
  • Shell-like appearance, very fragile and multiple pulp exposures
79
Q

Dentin anomalies: hereditary: dentin dysplasia:

A
  • A rare group of dentin alterations
  • Autosomal dominant inheritance
  • Affects the dentin next to the pulp and the root
  • 2 types: type I and II
80
Q

Dentin anomalies: hereditary: dentin dysplasia: type I or radicular dentin dysplasia

A
  • Crown: normal colour and shape in both primary and permanent dentitions. Only affects the root (both dentitions)
  • Root: tends to be short or absent. Obliterated pulps and multiple periapical radiolucencies (X-ray)
81
Q

Dentin anomalies: hereditary: dentin dysplasia: type II or coronal dentin dysplasia:

A
  • Root: normal
  • Pulp chamber: altered
  • Obliterated pulp chambers in temporary teeth, thistle shape in permanent teeth
  • Amber teeth
  • Sometimes: pulpitis (calcifications, X-ray)
82
Q

Dentin anomalies: acquired

A

All are due to systemic factors:
- Nutritional deficiency (hypovitaminosis A, C and D)
- Alterations in metabolism

83
Q

Enamel and dentin anomalies: odontogenesis imperfecta:

A
  • Hereditary
  • Linked to osteogenesis imperfecta and enamel disorders
  • Clinically: type I dentinogenesis and enamel hypoplasia
84
Q

Enamel and dentin anomalies: regional odontodysplasia (ghost teeth):

A
  • Localised dentition of the development of the enamel and dentin in a particular tooth
  • X-ray observation: normal teeth and some are blurred with very large chambers and short roots
  • Early loss
  • Does not trespass the midline
85
Q

Cementum anomalies: hereditary: hereditary cementosis:

A
  • Autosomal dominant inheritance
  • Radiographic diagnosis: usually casual when observing periapical diffuse radiopaque masses
86
Q

Cementum anomalies: hereditary: cleidocranial dystosis:

A
  • Autosomal dominant inheritance
  • Cement dysplasia
  • Delayed eruption and supernumerary
87
Q

Cementum anomalies: hereditary: hypophosphatasia

A
  • Autosomal recessive inheritance
  • Inability to produce alkaline phosphatase
  • 3 clinical forms: infantile, juvenile, adult
  • The cementum is not formed so the tooth has mobility and early exfoliation (periodontal problems)
88
Q

Cementum anomalies: acquired: concresence:

A
  • The union of 2 or more teeth by root cementum
  • True concrescence: occurs when the teeth are forming (typically between the 2nd and 3rd molars)
  • Acquired: produced by hypercementosis secondary to local factors, trauma, or mechanical pressure
  • Also, in Paget’s bone disease (due to hyperproduction of cement)

Paediatrics (11 decks)

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