This document discusses the development of teeth from initiation to eruption. It begins with an overview and introduces the key tissues involved - epithelium and ectomesenchyme. It then covers the molecular signaling pathways, formation of the primary epithelial band and dental lamina, and the sequential developmental stages from bud to bell stage. Defects at each stage like anodontia, fusion and macro/microdontia are also summarized. Finally, it discusses the processes of amelogenesis and root formation in detail.

1. Development of Teeth
Kavisha Mahajan
MDS I
Department of Pediatric and Preventive Dentistry, BVDUCH
1

2. Contents
• Introduction
• Molecular aspects
• Primary epithelial band
• Developmental stages
– Morphologic stages
– Physiologic processes
• Defects in development
• Root formation
• Development of teeth in-vitro
• References
2

3. Introduction
• Tooth development: Process of tooth formation, eruption and integration
with its surrounding tissues.
– Includes both deciduous and permanent teeth development
• The entire primary dentition is initiated between 6-8 weeks of
embryonic development;
• The successional permanent teeth between 20 weeks in utero and 10
months after birth; and
• The permanent molars between 20 weeks in utero (first molar) and 5
years of age (third molar).
3

4. Molecular Aspects
• Before starting with the process – the molecular signals that control
cell growth, migration, and differentiation should be studied to
better understand morphogenesis.
• The molecular aspect of tooth development shares many similarities
with the development of various other organs (e.g., lung and kidney)
and the limbs.
• Thus, studying about tooth development helps us to know about the
developmental pathways, in general as well.
4

5. Molecular Aspects
• The five major conserved signalling pathways that are involved are
1. Bone morphogenetic protein (BMP)
2. Fibroblast growth factor (FgF)
3. Sonic hedgehog (Shh)
4. Wingless-related integration site (Wnt)
5. Ectodysplasin A (Eda).
• The core of the molecular program is formed by the reciprocal and
sequential interactions between dental mesenchyme and epithelium
5

6. Molecular Aspects
• Example: MSX1 and PAX9 genes are involved in the mediation of BMP,
Wnt, and FGF signalling in early dental mesenchyme.
• If there is a loss of function of these genes:
– Mice: Tooth development is arrested
– Humans: Oligodontia or hypodontia.
6

7. 7

8. Molecular Aspects
• Genes regulate the development of many different organs and are
not specific to teeth.
• The gene mutation behind a dental defect can affect other tissues
and organs as well, and thus the teeth can be an indicator of a
malformation syndrome.
• This can form the basis for new ways to prevent and treat other
dental defects.
8

9. Development of Teeth
• The primitive oral cavity (stomodeum), is lined by stratified squamous epithelium
called the oral ectoderm or primitive oral epithelium.
• The oral ectoderm contacts the endoderm of the foregut to form the
buccopharyngeal membrane which ruptures on the 27th day of gestation and forms
a connection between the stmatodeum and foregut.
• Most of the connective tissue cells underlying the oral ectoderm are of neural crest
or ectomesenchyme in origin.
• These cells are thought to induce the ectoderm to start tooth development.
9

10. Development of Teeth
• Tissues that take part:
– Epithelium
– Ectomesenchyme
• Instruct each other in a sequential and reciprocal manner to start tooth
development
• NCC – derived from ectoderm – give rise to mesenchymal cells 10

11. Primary Epithelial Band
• 6th week - primary epithelial bands - continuous bands of odontogenic
epithelium formed around the mouth in each jaw
11
 A change in orientation of the
mitotic spindle & cleavage
plane of dividing cells.
 Increased proliferative
activity within the epithelium

12. Developmental Stages
12

13. Initiation
• 7th week: primary epithelial band divides into
– Dental lamina: inner (lingual) process
– Vestibular lamina: outer (buccal) process.
• Deciduous teeth - develop from the dental lamina
• Permanent molars - a distal extension of the dental lamina
• Successors of deciduous teeth – lingual extension of the dental lamina
(successional lamina)
13

14. Initiation
14

15. Initiation - Dental Lamina
• Activity extends for at least 5 years
• As the teeth continue to develop, it degenerates
• Remnants of the dental lamina persist as epithelial pearls or islands
within the jaw as well as in the gingiva - cell rest of Serres.
15

16. Initiation - Vestibular lamina
• Develops labial and buccal to the dental lamina
• Also known as the lip furrow band
• It subsequently hollows and forms the oral vestibule between
the alveolar portion of the jaws and the lips and cheeks
16

17. • Certain points along the dental lamina develop additional
growths protruding into the underlying mesenchyme – dental
placodes. 10 maxillary and 10 mandibular (future deciduous
teeth)
• They form the enamel organ of the tooth bud of deciduous
teeth.
• The first to appear: those in the anterior mandibular region
• The balance between stimulatory (FGFs, Wnts) and inhibitory
(BMPs) signals is important in determining the site of
placodes
17
Initiation

18. 18

19. Initiation
• The enamel organ increases in size
(differential proliferation of cells),
sinks deeper into the
ectomesenchyme and now
resembles a cap
• Convex surface facing the oral
cavity
• Inner concavity – ectomesenchymal
cells proliferate and form the dental
papilla
• Combined dental papilla and
enamel organ are surrounded by the
dental sac / dental follicle
19

20. Tooth germ
1. Ectodermal component
• Enamel organ – Enamel
2. Ectomesenchymal component
• Dental papilla – Dentin & pulp
• Dental follice – Cementum, PDL, alveolar bone
20

21. Initiation - Defects
1. Anodontia
– Lack of initiation
– True (congenitally missing) or false (after extraction of all
teeth)
– Partial anodontia: Absence of either a single tooth or multiple
teeth. Most frequently involved:
• Permanent mandibular 2nd premolars, maxillary lateral
incisors, maxillary 2nd premolar, third molars.
• Primary maxillary lateral incisor
– Complete anodontia
– Permanent > Deciduous teeth
– Close correlation between congenitally missing deciduous
teeth and their permanent successors; suggesting involvement
of a genetic factor – commonly ankylosed mandibular E
which is replaced by permanent 2nd premolar
21

22. Initiation - Defects
2. Supernumerary teeth
– Abnormal initiation (hyperactivity of the DL) or
– Develop from a third tooth bud arising from the dental lamina near the
permanent tooth bud, or from splitting of the permanent bud itself
– Single or multiple
– Commonly associated with cleft lip and palate, cleidocranial
dysplasia, and Gardner syndrome
22

23. 23
Mallineni S. Supernumerary Teeth: Review of the Literature with Recent Updates. Hindawi Publishing
Corporation Conference Papers in Science Volume 2014. Article ID 764050

24. Initiation - Defects
3. Ectopic eruption:
– Teeth may develop in abnormal locations such as the ovary
(dermoid tumors or cysts) or in the hypophysis.
– May be seen in the palate, maxillary sinus, condyle, orbit, or
even through skin
– The tooth undergoes normal stages of development.
– Causes: trauma, infection, cyst, the presence of supernumerary
tooth, and crowded dentition
24

25. Initiation - Defects
• Treatment: removal of cause followed by orthodontic repositioning within
the arch, if required. Elsewhere in the body - extraction
25

26. Proliferation – Bud Stage
• Enamel organ – small bud
• Surrounding mesenchymal cells proliferate which results in their condensation in
two areas:
– dental papilla: immediately below the enamel organ
– dental sac: surrounds the enamel organ & dental papilla
(not very well defined in this stage)
• Poorly morphodifferentiated and histodifferentiated
26

27. Proliferation – Cap Stage
• Differential proliferation of cells: central cells
proliferate slower than peripheral cells – cap shape
• Outer Enamel Epithelium (OEE) – cuboidal
peripheral cells
• Inner Enamel Epithelium (IEE) – tall columnar
cells
• Basement membrane separates
– OEE & dental sac
– IEE & dental papilla
• Stellate reticulum
27

28. Proliferation – Cap Stage
• Stellate reticulum
– water enters the enamel organ from the dental papilla
– Polygonal cells separate
– Become star shaped but still maintain contact with each other via
cytoplasmic processes
28

29. Proliferation – Cap Stage
Transitory structures (temporary, disappear before enamel formation begins)
• Enamel knot:
– Cluster of non dividing cells in the center of enamel organ
– Signalling center for growth factors
– Their no. & location determines no. & location of cusps in the developing
tooth
• Enamel cord: Vertical extension of the enamel knot
29

30. Proliferation – Cap Stage
• Enamel septum: Where the enamel cord to meet the outer enamel
epithelium – as it divides the stellate reticulum into two parts.
• Enamel navel: A small depression at the point of meeting of enamel septum
and outer enamel epithelium – resembles umbilicus.
• Enamel niche: The enamel organ may seem to have a double attachment of
dental lamina to the overlying oral epithelium enclosing ectomesenchyme
called enamel niche between them.
30

31. Proliferation - Defects
1. Microdontia
– True generalised microdontia
• all the teeth are smaller than normal
• Extremely rare except a few cases of pituitary
dwarfism
– Relative generalised microdontia
• normal or slightly smaller than normal teeth are
present in jaws that are somewhat larger than
normal
• Hereditary
– Microdontia involving a single tooth
• Common: Maxillary lateral incisor and the third
molar
• Peg lateral: sides converge or taper together
incisally, forming a peg-shaped or cone-shaped
crown. The root is frequently shorter than usual. 32

32. Proliferation - Defects
2. Macrodontia
– True generalised macrodontia
• all the teeth are larger than normal
• Extremely rare except a few cases of pituitary
gigantism
– Relative generalised macrodontia
• common
• normal or slightly larger than normal teeth are
present in jaws that are somewhat smaller than
normal
• Hereditary
– Macrodontia involving a single tooth
• Relatively uncmommon
• Variant: seen in cases of hemihypertrophy of the
face, in which the teeth of the involved side may
be considerably larger than those of the
unaffected side. 33

33. 34

34. 35

35. 36

36. 37

37. Histodifferentiation – Early Bell Stage
38

38. Morphodifferentiation – Advanced Bell Stage
39

39. Morphodifferentiation – Advanced Bell Stage
• Fragmentation of the dental lamina
– Usually degenerate
– Persist to form supernumerary teeth, odontogenic
cysts & tumors
• Tooth continues its development within the tissues of the
jaw
• Before the tooth can function, it must re-establish a
connection with the oral epithelium and penetrate it to
reach the occlusal plane - unique example of a natural
break in the epithelium of the body.
• Integrity is re-established by formation of the junctional
epithelium around the tooth
40

40. Morphodifferentiation – Advanced Bell Stage
Crown Pattern Determination:
• Folding of the crown – as a result of its intrinsic growth
• Point at which the growth stops and differentiation of cells occurs – site of the future
cusp development
• Followed by the deposition of dentin and enamel first at the cusp tip: face-to-face,
thereby defining the DEJ.
• More zones of cell differentiation – more cusps
• Zones are determined by molecular signals from the enamel knot - primary &
secondary
41

41. Morphodifferentiation – Defects
1. Gemination
– An attempt at division of a single tooth germ by an
invagination
– Appearance of two crowns that share the same root canal
– Trauma is a possible cause
42

42. Morphodifferentiation – Defects
2. Fusion
– Complete or incomplete.
– Some physical force or pressure
produces contact of the developing
teeth
• Early (before calcification): teeth
might be completely united
• Late: only a portion of the root
might be united
– Dentin is always confluent in cases of
true fusion.
– Deciduous > permanent
– Can also occur between a normal and
supernumerary
43

43. Apposition
• Apposition is the deposition of the matrix of the hard dental
structures.
• Appositional growth of enamel and dentin is a layer like
deposition of an extracellular matrix
• Additive growth
• Characterized by regular and rhythmic deposition of the
extracellular matrix.
• Alternate periods of rest and activity.
44

44. Apposition - Amelogenesis
• Process of enamel formation
– Deposition of enamel matrix by ameloblasts
– Mineralisation of the matrix
45

45. Apposition - Amelogenesis
• Stages:
1. Pre-secretory stage
• IEE differentiate to form ameloblasts
2. Secretory stage
• Ameloblasts secrete organic matrix – full thickness of
enamel
3. Maturation stage
• Ameloblasts cause degradation of enamel matrix
• Followed by replacement with inorganic material
46

46. Amelogenesis – Pre-secretory Stage
• Pre-secretory stage
1. Morphogenetic phase
2. Differentiation phase
1. Morphogenetic Phase
– Enamel organ is in bell stage
– Crown shape is established
– IEE cells are low columnar
47

47. Amelogenesis – Pre-secretory Stage
– Golgi apparatus
– Other organelles are scattered
48

48. Amelogenesis – Pre-secretory Stage
2. Differentiation Phase
– IEE cells differentiate into ameloblasts
– Cell elongates
49

49. Amelogenesis – Pre-secretory Stage
2. Differentiation Phase
– IEE cells differentiate into ameloblasts
– Cell elongates
50

50. Amelogenesis – Pre-secretory Stage
2. Differentiation Phase
– IEE cells differentiate into ameloblasts
– Cell elongates
51

51. Amelogenesis – Pre-secretory Stage
2. Differentiation Phase
– IEE cells differentiate into ameloblasts
– Cell elongates
52

52. Amelogenesis – Pre-secretory Stage
2. Differentiation Phase
• Simultaneously, dental papilla cells differentiate – odontoblasts – dentin
• This is because of signalling molecules from the IEE: TGF, BMP
• Ameloblasts are attached to each other by junctional complexes proximally
and distally
53

53. Amelogenesis – Pre-secretory Stage
54

54. Amelogenesis – Secretory Stage
55
• Ameloblasts develop tome’s process
– Distal extension of ameloblasts
– Proximal and distal
– Responsible for rod and inter rod enamel formation
• In the beginning, only proximal part is present

55. Amelogenesis – Secretory Stage
56
• Ribosomes help in synthesising proteins –
secreted by the tome’s process
• Initial layer of enamel matrix is laid down on
mantle dentin
– Immediately mineralised
– Doesn’t have enamel rods
• As more matrix is laid out, ameloblasts move
away from the enamel
• Tome’s process develops its distal extension
• Now, enamel formation
– Proximal end – inter rod
– Distal end – enamel rods

56. Amelogenesis – Secretory Stage
57
• Eventually, distal process becomes thinner and disappears
• Leaves behind small space between the rod and inter rod
enamel – filled with inorganic material to form the enamel
sheath

57. Amelogenesis – Secretory Stage
58
• Last increment of enamel formed doesn’t have enamel rods
• Final enamel:

58. Amelogensis – Maturation Stage
59
• Maturation Stage
1. Transitional phase
2. Maturation proper
1. Transitional Phase
– Ameloblasts reduce in height and volume
– Undergo apoptosis
2. Maturation Proper
– Bulk of protein and water in organic material is replaced by
inorganic material (modulation)

59. Amelogensis – Maturation Stage
60
• Modulation – the cyclic creation, loss and recreation of an
invaginated ruffle ended apical/distal surface in an ameloblast
• Ameloblasts cyclically alternate in having a ruffle ended and
smooth ended border

60. Amelogensis – Maturation Stage
61

61. Amelogensis – Maturation Stage
62

62. Apposition – Dentinogenesis
• Process of dentin formation by odontoblasts
• First predentin is formed (organic matrix/proteins), then
mineralisation takes place
1. Organic matrix (20%)
2. Water (10%)
3. Inorganic material (70%) - hydroxyapetite
63

63. Apposition – Dentinogenesis
• Begins in bell stage
• IEE
Signalling molecules (TGF, BMP)
Dental papilla cells
Differentiate into
Pre-odontoblasts
Increase in size
Odontoblasts
64
Nucleus becomes polarised ,
shifts away from IEE

64. Apposition – Dentinogenesis
1. Mantle dentin
– First formed
– 15 to 20mm thick
– Confined to the upper layers, near enamel
2. Circumpulpal dentin
– Forms rest of the dentin
65

65. Apposition – Dentinogenesis
• Odontoblasts secrete collagen & non collagenous proteins in
the extracellular region, towards the IEE
• Hence, initial mantle dentin matrix has
– Type I collagen
– Von korff’s fibres (type III collagen)
66

66. Apposition – Dentinogenesis
• Then, odontoblasts develop odontoblastic processes – tome’s
fiber
– Extend towards extracellular matrix
– Keeps elongating
– Odontoblasts move towards pulp
– Finally, the processes are embedded in dentinal tubules
67

67. Apposition – Dentinogenesis
• Organic matrix is secreted
• Mineralisation occurs, leaving an unmineralised portion between the cell
body and mineralised portion – predentin (15-20 microns thickness)
68

68. Apposition – Dentinogenesis
• Once mantle dentin secretion and mineralisation is complete,
circumpulpal dentin matrix deposition begins
• Consists of
– Type I collagen
– Non collagenous proteins (NCP)
– Proteoglycans (PG)
69

69. Apposition – Dentinogenesis
• Deposition takes place from 2 points:
– Near the cell body
– Mineralisation front (via odontoblastic processes)
70

70. Apposition – Dentinogenesis
• Mineralisation starts from the mantle dentin – towards circumpulpal dentin
71

71. Apposition – Dentinogenesis
• When an odontoblast secretes mantle dentine, it buds off many membrane
bound vesicles – matrix vesicles
• Present in the matrix below the IEE
72
• Crystal growth initiated
within the vesicles
• Rupture
• Crystals are deposited
in the matrix
• Fuse with each other
• Mineralise the entire
matrix

72. Apposition – Dentinogenesis
• Circumpulpal dentin:
73

73. Apposition - Defects
1. Dens in dente (Dens invaginatus, dilated composite odontome)
– as a result of an invagination in the surface of tooth crown before
calcification has occurred
– Possible causes: increased localized external pressure, focal growth
retardation, and focal growth stimulation in certain areas of the
tooth bud.
– Most commonly involved: permanent maxillary lateral incisors, as
an accentuation in the development of the lingual pit
– Radicular variety: infolding of the HERS after root completion
74

74. 75
Mild form:
- deep invagination in the lingual pit area.
- R/F: pear-shaped invagination of enamel and dentin with a
narrow constriction at the opening on the surface of the tooth
and closely approximating the pulp in its depth
Apposition - Defects

75. Apposition - Defects
– Severe form: invagination extends nearly to the apex of the
root, and these present a bizarre radiographic picture
Treatment: Prophylactic restoration
76

76. Apposition - Defects
2. Dens evaginatus (Occlusal tuberculated premolar, Leong’s
premolar, evaginated odontome, occlusal enamel pearl)
– Seen as an accessory cusp or a globule of enamel on the
occlusal surface between the buccal and lingual cusps of
premolars, unilaterally or bilaterally. Occurs rarely on
molars, cuspids, and incisors.
– Cause: proliferation and evagination of an area of the IEE
and subjacent odontogenic mesenchyme into the dental
organ during early tooth development.
– May lead to incomplete eruption, displacement of teeth
and/or pulp exposure with subsequent infection following
occlusal wear or fracture 77

77. Apposition - Defects
3. Taurodontism (bull like teeth)
– Possible causes:
• a specialized or retrograde character,
• a primitive pattern,
• a mendelian recessive trait,
• an atavistic feature,
• a mutation resulting from odontoblastic deficiency during dentinogenesis
of the roots.
– Permanent teeth > primary teeth 78

78. Apposition - Defects
4. Talon’s cusp
– There is deep developmental groove where the cusp blends with the
sloping lingual tooth surface
– Composed of normal enamel and dentin and contains a horn of pulp
tissue.
– Treatment: Prophylactic restoration of the groove to prevent caries.
79

79. Apposition - Defects
5. Amelogenesis Imperfecta
(Hereditary enamel dysplasia,
hereditary brown enamel, hereditary
brown opalescent teeth)
– Structural defect
– 3 types, depending on the C/F
& stage of enamel formation
affected
– Hereditary: Alteration in the
genes involved in enamel
formation & maturation - also
the general location of
amelogenin (the principal
protein in developing enamel)
80

80. Apposition - Defects
• Hypoplastic Amelogenesis
Imperfecta (AI)
• Hypomature AI
• Hypocalcified AI
81
• Hypomature-hypoplastic AI
• Hypocalcified-hypoplastic AI

81. Apposition - Defects
82
R/F:
Enamel may be totally absent present as a very thin layer, mainly over the
cusp tips and on the interproximal surfaces
H/F:
• Hypoplastic: Disturbance in the differentiation or viability of
ameloblasts – defects in matrix formation or total absence of matrix.
• Hypocalcific: Defects of matrix structure and of mineral deposition.
• Hypomaturation: There are alterations in enamel rod and rod sheath
structures.
Treatment: none, except to improve cosmetic appearance

82. Apposition - Defects
6. Environmental Enamel Hypoplasia
– an incomplete or defective formation of the organic
enamel matrix of teeth.
– Two basic types of enamel hypoplasia:
1. A hereditary type (described previously under
amelogenesis imperfecta)
• Deciduous and permanent dentition, both
involved
• Generally only enamel affected
2. An environmental type
• Either dentition
• Both enamel and dentin
83

83. Apposition - Defects
• Causes:
1. Nutritional deficiency (vitamins A, C, and
D), exanthematous diseases (e.g. measles,
chickenpox, scarlet fever);
2. Hypocalcemia/tetany;
3. Congenital syphilis;
4. Birth injury, prematurity, Rh hemolytic
disease;
5. Local infection or trauma (turner’s tooth);
ingestion of chemicals – fluoride;
6. Idiopathic causes 84

84. Apposition - Defects
• Hypoplasia results only if the injury occurs during the time the
teeth are developing - during the formative stage of enamel
development.
• Thus, by knowing the chronologic development of the deciduous
and permanent teeth, it is possible to determine from the location
of the defect on the teeth the approximate time at which the
injury occurred.
85

85. Apposition - Defects
7. Dentinogenesis Imperfecta
• Both dentitions
• Etiology: chromosome number 4 is involved. It encodes a protein called
dentin sialophosphoprotein (DSPP). constitutes about 50% of the
noncollagenous component of dentin matrix
86

86. Apposition - Defects
Revised classification:
A. Dentinogenesis imperfecta I:
– Dentinogenesis imperfecta without osteogenesis imperfecta
(opalescent dentin)
– Corresponds to dentinogenesis imperfecta type II of Shields
classification.
B. Dentinogenesis imperfecta II:
– Brandywine type dentinogenesis imperfecta
– Corresponds to dentinogenesis imperfecta type III of Shields
classification.
– Rare and paradoxically characterized by too little rather than
too much dentin resulting in ‘shell teeth.’
• There is no substitute in the present classification for the category
designated as DI type I of the Shield’s classification. 87

87. Apposition - Defects
A. Dentinogenesis imperfecta I (Opalescent dentin, DI without osteogenesis
imperfecta, DI, Shields type II, Capdepont teeth)
• Cause: Mutation in the DSPP gene, encoding dentin phosphoprotein and dentin
sialoprotein
• C/F: Teeth are blue-gray or amber brown and opalescent.
88

88. Apposition - Defects
• R/F: Teeth have bulbous crowns, roots are narrower, pulp chambers and
root canals are smaller than normal or completely obliterated.
• H/F: Dentinal tubules are larger in diameter, less numerous or may be
completely absent. Pulp chamber almost obliterated with continued dentin
depostion
• The enamel may split readily from the dentin when subjected to occlusal
stress
89

89. Apposition - Defects
B. Dentinogenesis imperfecta II (Shields type III, Brandywine
type DI)
• The crowns of the teeth wear rapidly after eruption
• The dentin is amber and smooth
• Constriction of the cervical area resulting in a ‘tulip’ shape
• R/F:
– Deciduous dentition show very large pulp chambers and root
canals, at least during the first few years, may become reduced
in size with age.
– The permanent teeth have pulpal spaces that are either smaller
than normal or completely obliterated
– Classic ‘shell teeth’ appearance.
• MacDougall et al (1999): Multiple pulp exposures, normal
nonmineralized pulp chambers and canals, and a general
appearance of ‘shell teeth.’
90

90. Apposition - Defects
• Treatment: directed primarily towards preventing the loss of
enamel and subsequent loss of dentin through attrition -
crowns
91

91. Apposition - Defects
8. Dentin Dysplasia (rootless teeth)
• Rare disturbance
• Normal enamel but atypical dentin formation & abnormal pulpal
morphology.
• Hereditary
• Shields classification: type I (dentin dysplasia) and type II (anomalous
dysplasia of dentin).
• Witkop classification: radicular dentin dysplasia (type I) and coronal dentin
dysplasia (type II). Type I more common
92

92. Apposition - Defects
C/F:
• Type I (radicular):
– Both dentitions affected
– Normal clinical appearance
– Extreme mobility
– Premature exfoliation / after only
minor trauma due to abnormally short
roots.
• Type II (coronal):
– Both dentitions
– Deciduous teeth have the same
appearance as DI
– Permanent teeth appear normal
93

93. Apposition - Defects
R/F:
• Type I (radicular):
– Roots are short, blunt, conical, or similarly malformed
– Deciduous teeth: Pulp chambers and root canals are usually completely
obliterated
– Permanent dentition: a crescent-shaped pulpal remnant may still be seen in the
pulp chamber.
– Periapical RL representing granulomas, cysts, or abscesses in apparently intact
teeth can be seen.
• Type II (coronal):
– Deciduous teeth: Obliterated pulp chambers
– Permanent teeth: Abnormally large pulp chamber - ‘thistle-tube’ in shape. Pulp
stones may be found.
94

94. Apposition - Defects
H/F:
• Type I (radicular):
– Most of the obliterations of the pulp are
calcified tubular dentin, osteodentin, and
fused denticles.
– Characteristic ‘lava flowing around
boulders’ appearance: Normal dentinal
tubule formation is blocked so new
dentin forms around the obstacles
– Sauk et al: ‘cascades of dentin’ result
from repetitive attempts to form root
structure.
– Dentin itself is normal but is simply
disoriented.
95

95. Apposition - Defects
• Type II (coronal):
– Deciduous teeth: Amorphous and atubular dentin in the radicular
portion, while coronal dentin is relatively normal
– Permanent teeth: Relatively normal coronal dentin, but the pulp has
multiple pulp stones or denticles.
96

96. Apposition - Defects
9. Regional Odontodysplasia (Odontodysplasia, odontogenic dysplasia,
odontogenesis imperfecta, ghost teeth).
• One or several teeth in a localized area are affected in an unusual manner
• Maxillary teeth >
• Permanent central and lateral incisors, canines
• Etiology
– Genetic mutation
– Latent virus in the odontogenic epithelium which gets activated during
tooth development
– Involvement of vascular defects
97

97. C/F:
• Delayed/failure of eruption of teeth
• Altered/irregular shape
• Defective mineralisation
R/F:
• Ghost teeth appearance: reduced radiodensity
• Very thin enamel and dentin
• Large pulp
98
Apposition - Defects

98. Apposition - Defects
H/F:
• Reduced amount of dentin
• Wide predentin layer
• Irregular tubular pattern of dentin
• REE around the nonerupted teeth shows irregular calcified bodied
Treatment: Extraction – poor cosmetic appearance
99

99. Apposition - Defects
10. Dentin hypocalcification
• Normal dentin calcification:
– Deposition of calcium salts in the form of globules
– Further peripheral deposition of salts
– Entire mass becomes homogenous
• Hypocalcification:
– Globules fail to unite
– Normal C/F, detected in histologic sections
– Etiology: same as that of enamel hypoplasia and hereditary enamel
hypocalcification.
100

100. Root formation
• Mineralisation of enamel and dentin
• Stellate reticulum collapses
• Ameloblasts + OEE cells fuse – Reduced Enamel
Epithelium (REE)
• Cervical loop gives rise to a double layer of cells -
Hertwigs Epithelial Root Sheath (HERS)
101

101. Root formation
• HERS bends at a 45 degree angle
towards the pulp, narrowing the
cervical opening – epithelia
diaphragm – future apical foramen
• Free end of diaphragm doesn’t grow,
HERS grows coronal to it
• Inner layer cells of HERS – induces
adjacent dental papilla cells –
odontoblasts – dentin
• When dentin is being formed, adjacent
root sheath cells disintegrate
• HERS never continuous, keeps
disintegrating as it grows
102

102. Root formation
• Most disintegrated cells move away,
dental follicle cells take their place
• Interaction – cementoblasts –
cementum
• Some disintegrated cells don’t
migrate, persist in that area –
epithelial rests of Malassez
103

103. Root formation
104

104. Root formation
• Multirooted teeth
105

105. Root formation
106

106. Root formation
107

107. Root formation
108

108. Root formation - Defects
1. Concrescence
• A form of fusion which occurs after root formation has been completed
• Teeth are united by cementum only
• Cause: traumatic injury or crowding of teeth – roots in close approximation
• Before or after the teeth have erupted
• Diagnosis – generally radiographic
109

109. Root formation - Defects
2. Dilaceration
• An angulation, or a sharp bend or curve, in the root or crown of a formed
tooth
• Cause – trauma during tooth formation
• Difficulty during extraction, obtain radiographs
110

110. Root formation - Defects
3. Supernumerary roots
• Common in single rooted teeth – mandibular canines and premolars – 2
roots
• Maxillary and mandibular molars (mainly third molars)
• Significance – in exodontia, one of these roots may be broken off during
extraction and, if unrecognized and allowed to remain in the alveolus, may
be the source of future infection.
111

111. Development of Teeth in-vitro
• Advantages over current restorations:
– These teeth would functionally integrate into the jaws
– Maintain the health and integrity of the associated
periodontal tissues
– Hopefully last longer
112

112. Development of Teeth in-vitro
• Tissue engineering:
– Functional restoration of the living tissues that are
impaired/damaged/absent
– Involves the induction of organ specific cells and then seeding
them into an extracellular matrix or scaffold.
– Process is carried out in the lab, prior to transplantation of the
engineered tissue into the recipient donor site.
113

113. Development of Teeth in-vitro
• Stem cells are undifferentiated cells, capable of self renewal
• Sources
– Embryonic SC
– Somatic/Adult SC
– Induced pluripotent SC (iPSC)
• A fertilised egg/zygote is totipotent – capable of differentiating into
all cell types
• Human embryonic stem (ES) cells in the inner cell mass are
pluripotent – can give rise to all cells types except the extra
embryonic membranes
114

114. Development of Teeth in-vitro
• Human ES cells – ultimate stem cells in terms of tissue regeneration
• Potential problems associated with their usage - ethical and moral
dilemmas
• Human adult stem (AS) cells – undifferentiated cells in a mature
tissue/organ
• Also have the ability to self renew
• Experiments have shown that the ES cells that are normally required
for tissue regeneration can be replaced by the AS cell lines
115

115. Development of Teeth in-vitro
• Tissue engineering for replacement of the dentition – two principle
strategies
1. Using the stem cell lines to recapitulate the inductive events that
occur during early odontogenesis
2. Using biodegradable scaffolding to support disassociated
odontogenic cells harvested from tooth germs
116

116. Development of Teeth in-vitro
Problems:
• A supply of epithelial stem cells will be required if the tooth is to be
generated entirely artificially
• These SC will need to be engineered to express the correct genes
required to initiate the tooth development
• Human teeth take several years to develop – long time for a
potential recipient to wait
117

117. Applied Aspect
Dental age estimation
118

118. • Nolla’s stages of tooth development
119

119. References
• Ten Cate’s Oral Histology, 9th edition
• Orban’s Oral Histology & Embryology, 13th edition
• Shafer’s Textbook of Oral Pathology, 7th edition
• Gugnani N, Pandit I K, Gupta M, Gugnani S, Vishnoi A, Sabharwal O,
Manhas S. Ectopic eruption of maxillary central incisor through abnormally
thickened labial frenum: An unusual presentation. J Indian Soc Pedod Prev
Dent 2017;35:94-7
• Farias D, Pinto A, Garjardo P. Diversity of clinical, radiographic and
genealogical findings in 41 families with amelogenesis imperfecta. J. Appl.
Oral Sci. vol.27 Bauru 2019 Epub Apr 01, 2019
• Onyekwelu O, Seppala M, Zoupa M, Cobourne M. Tooth development: 2.
Regenerating teeth in the Laboratory. Dent Update 2007; 34: 20-29
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