chronology of tooth eruption

1. Chronology of tooth
eruption

2. CONTENTS
• Overview of prenatal development
• Facial development
• Dentition period - primary, mixed, permanent
• Tooth development & eruption (odontogenesis)
• Common dental disturbances

3. OVERVIEW OF PRENATAL DEVELOPMENT
• In human, prenatal development begins at the start of
pregnancy & continues until birth of the child
**pregnancy → birth
• Prenatal development consists of 3 periods :
1. Preimplantation period
2. Embryonic period
3. Fetal period

4. Periods of prenatal development
Preimplantation period
(1st week)
Embryonic period
(2nd-8th week)
Fetal period
(3rd-9th month)

5. 3 embryonic layers (embryonic period)

6. Developmental disturbances during prenatal development
• preimplantation & embryonic period (1st trimester of pregnancy) is the most
critical period of development
• developmental disturbances during this period may cause major congenital
malformations of embryo (birth defects) which evident at birth
• any teratogens can cross placenta & present during active differentiation of
organ or tissue which may lead to tissue malformations
• tissue malformations can be due to :
*genetic factors → chromosome abnormalities
*environmental factors → infections (:rubella, syphilis), radiation, chemicals,
drugs (alcohol, thalidomide, tetracycline)

7. FACIAL DEVELOPMENT
• Facial development begin to form during 4th week of prenatal period
(within embryonic period)
• During 4th week, face & neck begin to develop with the primittive
eyes, ears, nose, oral cavity & jaw areas
• Facial development derives from 5 facial processes that form during
4th week :
→single frontonasal process
→paired maxillary & mandibular processes

8. • These facial processes become centers of facial growth :
*frontonasal process → upper part of face
*maxillarry processes → midface
*mandibular processes → lower part of face

10. 5 facial processes

12. Pharyngeal / branchial arches
• structures seen during embryonic
development that are precursors for
many structures
• in human embryo, the arches are first
seen during 4th week of
development
• derived from 3 embryonic layers :
→ ectoderm, mesoderm, endoderm
• development of pharyngeal arches
relies on contribution from
ectoderm, mesoderm, endoderm &
neural crest cells
• failure of pharyngeal arches
correctly develop results in
anatomical, developmental defects

13. Pharyngeal arch

14. 1st pharygeal arch
• a.k.a. mandibular arch
• develop during 4th week of prenatal
period
• located bw stomodeum & 1st pharyngeal
groove
• this arch divides into maxillary &
mandibular process :
*maxillary process → maxilla
*mandibular process → mandible
• Meckel's cartilage (located in mandibular
process) act as a “template” of mandible
formation (perichondral ossification)

16. TOOTH DEVELOPMENT & ERUPTION
• Odontogenesis = process of tooth development, eruption & integration with
its surrounding tissues
• 2 types dentitions :
→ primary
→ permanent
• Primary dentition develops during prenatal period - consists of 20 teeth
which erupt & are later shed
• As primary teeth are shed - jaws grow & mature - permanent dentition
(consists of 32 teeth) gradually erupt & replaces primary dentition
• Overlapping period bw primary & permanent dentition → mixed dentition

17. • during odontogenesis, many physiological processes occurs -
initiation, proliferation, differentiation, morphogenesis & maturation
• not all teeth in each dentition begin to develop at the same time
• initial teeth for both dentitions develop in anterior mandibular region
→ anterior maxillary region → progresses posteriorly in both jaws
• this posterior mvt of odontogenesis allows time for the jaws to grow
accomodate the increased number of primary teeth, larger primary
molars & finally overall larger permanent teeth

18. Primary dentition
• Primary tooth buds formation → 6th week of prenatal period
• Primary teeth begin to erupt → 6 mth
• Eruption time for primary teeth → 6 mth – 3 yo

19. • Sequence of primary teeth eruption :
A → B → D → C → E
• Sequence of primary teeth loss :
A → B → D → C → E
Primary dentition

21. • tooth formation occurs as early as 6th week of prenatal period when jaws
have assumed their initial shape - but during this time jaws are small
• development of primary & permanent teeth continues in this period ; jaws
grow follows the need for additional space posteriorly for additional teeth
• alveolar bone height ↑ to accomodate the ↑ length of teeth
• growth of anterior parts of jaws is limited after 1st year of postnatal life
• at birth, usually no teeth visible in mouth

22. Interdental spacing
• Primary teeth generally shows some
degree of interdental spacing
• Spacing in primary dentition is important
for proper alignment of permanent
dentition
• Absent of spaces in primary dentition
can cause crowding in permanent
dentition

23. • Interdental spacing of primary teeth determines chances of
crowding in permanent dentition
,,,,

24. Mixed (transitional) dentition
• Transition from primary to permanent dentition begins with
emergence of :
→perm.mand.central incisors (6 yo)
→1st perm.molars (6-7 yo)

25. Early mixed dentition in a child with full set of primary teeth
& first permanent molars
A. Maxilla B. Mandible

26. Arch dimensions & tooth size
• Important part of dental arch in development occlusion of permanent dentition is
the premolar segment
• In this section, the erupting premolars are smaller in mesiodistal dimension
than primary molars, which they replace
• The difference is related to the Leeway space or amount of space gained by
difference in the mesiodistal dimensions of the premolars and the primary
molars

28. Leeway space = difference in mesiodistal width bw primary teeth (C,D,E) &
permanent teeth (3,4,5)
Arrows indicate mesial movement of the perm.molars after loss of primary molars &
eruption of 2nd perm.premolar

29. Permanent dentition
• Sequences of eruption in maxilla :
6-1-2-4-3-5-7-8 & 6-1-2-4-5-3-7-8
• Sequences of eruption in mandible :
(6-1)-2-3-4-5-7-8 & (6-1)-2-4-3-5-7-8

31. Mechanisms of tooth eruption
• 4 main factors :
-eruption path
-eruption force
-PDL capacity to adapt with eruptive movement
-quality of alveolar bone

32. Eruption path
-available, sufficient, no obstruction
-regulated by dental follicle
-alveolar bone formation & resorption occuring around
erupting tooth are regulated by dental follicle
-disturbance of dental follicle can cause failure / delay /
deflected path of tooth eruption

33. Eruption force
-comes from elongation of roots
*tooth normally erupt when they have reached 2/3 rd root length
-root elongated & pushing against immovable base
*root formation will increase tooth length - must be accommodated by
increase in jaw height & tooth crown moving occlusally

34. PDL capacity to adapt with eruptive movement
-PDL must be able to adapt with eruptive tooth mvt
-in certain conditions (-ankylosis, hypercementosis),
PDL unable to adapt with eruptive tooth mvt causes failure
of tooth eruption

35. Quality of alveolar bone
-alveolar bone malformation can disturb tooth eruption
Eg : osteopetrosis (marble bone disease)
Bones harden, denser

36. Tooth movement
• For teeth to become functional, movement is required to
bring them into occlusal plane
• 3 types of tooth mvt :
1. Pre-eruptive mvt
2. Eruptive mvt
3. Post-eruptive mvt

37. Pre-eruptive movement
• Occurs in primary & permanent tooth germs before they
begin to erupt
• Is a movement required to place teeth within jaw in a
position for eruptive movement
• Combinations of 2 factors :
1. Bodily mvt of tooth germs
2. Jaw growth

38. • When deciduous tooth germs first differentiate, they are
small
• Then, they grow rapidly & become crowded
• This crowding is alleviated by jaw growth
• Permanent tooth germs develop on lingual aspect of
primary teeth in the same bony crypt

39. Eruptive movement
• Tooth move from its position within jaw bone to its
functional position in occlusion
• During eruptive phase, significant developmental
changes occur – formation of roots, PDL, DEJ
• Once tooth erupt into oral cavity, it continues to erupt at
same rate of about 1mm every 3 mths & slowing as it
meets its antagonist in opposing arch

40. • Once it appears in oral cavity, it is subjected to
environmental factos that will determine its final position
in dental arch
Eg : muscle forces from tongue, cheeks, lips
forces of contact of erupting tooth with other erupted teeth
thumbsucking habit

41. Post-eruptive movement
• 3 types :
1. Movements to accommodate with growing jaws
-to keep pace with increasing jaws height
2. To compensate for continued occlusal wear
-compensation occurs by continuous deposition of cementum around tooth apex
3. To accommodate interproximal wear
-compensated by mesial or approximal drift

42. A. Crown formation :
1. Initiation stage
2. Bud stage
3. Cap stage
4. Bell stage
5. Apposition & maturation
stages
B. Root development :
1. Root dentin formation
2. Cementum & pulp formation
3. Periodontal ligament &
alveolar bone development
ODONTOGENESIS

43. *stomodeum → future oral cavity

44. INITIATION STAGE : (6-7th weeks of prenatal period)
-ectoderm (lining stomodeum) gives
rise to oral epithelium
-oral epithelium grows deeper into
mesenchyme & produce layer called
dental lamina
*ectoderm → oral epithelium → dental lamina
ectoderm (oral epithelium)
mesenchyme
basement
membrane
*basement membrane → separate epithelium & connective tissue

45. INITIATION STAGE
*developing mandibular
arch is lined by oral
epthelium, with the
deeper mesenchyme
influenced by neural
crest cells

46. INITIATION STAGE
*development of
dental lamina from
oral epithelium in the
mandibular arch

47. -dental lamina grow /proliferate
into bud, penetrating into
growing mesenchyme
-at the end of proliferation
involving primary dentition's
dental lamina, both future max
& mand arch will each have
10 buds
-each of these buds +
surrounding mesenchyme
→ tooth germ & supporting
tissues
BUD STAGE : (8th week of prenatal period)
mesenchyme
ectoderm (oral epithelium)
dental lamina (bud)

48. BUD STAGE
*proliferation of dental
lamina into growing
mesenchyme in the
form of buds, the
future tooth germs

49. -depression in the deepest part of dental
lamina forming cap or enamel organ
*enamel organ → future enamel
*enamel organ derived from ectoderm
-enamel organ will surround mass of
mesenchyme (dental papilla)
*dental papilla → future dentin & pulp
-basement membrane still exists bw enamel
organ & dental papilla → future DEJ
(dentinoenamel juction)
-mesenchyme surrounding enamel organ
→ dental follicle / dental sac
*dental follicle → periodontium (PDL,
cementum, alveolar bone)
CAP STAGE : (9-10th weeks of prenatal period)
enamel organ (cap)
dental papilla
basement
membrane
dental follicle (sac)

50. CAP STAGE
*Tooth germ :
-enamel organ
-dental papilla
-dental sac (follicle)
*developing primordium
of permanent
succedaneous tooth
lingual to primary tooth
germ (in bud stage)

51. -enamel organ differentiate into bell & consists of
4 types of cells :
*OEE (outer enamel epithelium)
*IEE (inner enamel epithelium)
*stellate reticulum
*stratum intermedium
-dental papilla differentiate & consists of
2 types of cells :
*outer cells of dental papilla
*central cells of dental papilla
**outer cells of dental papilla → odontoblasts (secrete dentin matrix)
**central cells of dental papilla → pulp
BELL STAGE : (11-12th weeks of prenatal period)

52. BELL STAGE : (11-12th weeks of prenatal period)
-basement membrane
remains bw IEE & dental
papilla
-dental sac will increases
in amount of collagen
fibers & differentiate into
periodontium during later
period than enamel organ
& dental papilla

53. APPOSITION STAGE :
-enamel, dentin, cementum are
secreted in successive layers as a
matrix
APPOSITION & MATURATION STAGE
MATURATION STAGE :
-dental tissues (matrix) fully
mineralize to mature form

54. Formation of Preameloblasts
• IEE will diffrentiate → preameloblasts
• premaeloblasts will later on secrete
enamel matrix

55. Formation of Odontoblasts & Dentin Matrix
• preameloblasts will induce outer
cells dental papilla to
differentiate into odontoblasts
• odontoblasts will begin
odontogenesis → apposition of
dentin matrix (predentin)
• odontoblasts secrete dentin
matrix before production of
enamel matrix

56. Formation of Ameloblasts, Dentinoenamel Junction &
Enamel Matrix
• after apposition of predentin, basement membrane bw
preameloblasts & odontoblasts disintegrates
• preameloblasts will come into contact with predentin -
will induce preameloblasts diffrentiate into ameloblasts
• ameloblasts begin amelogenesis (apposition of enamel
matrix)
• enamel matrix is secreted from Tome's process (of
ameloblasts)
• enamel matrix in contact with predentin
• mineralization of disintegrating basement membrane
forming DEJ (dentinoenamel junction)
• odontoblasts will leave odontoblastic process in
predentin area - each odontoblastic process is contained
in dentinal tubules
• calcification or maturation of matrix occurs later (different
process for both enamel & dentin)

57. ROOT DEVELOPMENT
• root development takes place after crown is completely
shaped & tooth starting to erupt into oral cavity
• structure responsible for root development is the cervical loop
• cervical loop is the most cervical portion of enamel organ,
consists of IEE (inner enamel epithelium) & OEE (outer
enamel epithelium)

58. • cervical loop will grow deeper into mesenchyme of dental
sac, elongating & moving away from crown area to enclose
more of dental papilla tissue & form Hertwig's root sheath
(HERS)
**cervical loop → HERS
• function of this sheath is to shape the root & induce dentin
formation in root area, so that it is continuous with coronal
dentin

60. ROOT DENTIN FORMATION
• root dentin forms when outer cells of dental papilla (in root
area) are induced to undergo differentiation & become
odontoblasts (under influence of IEE of HERS)
• these cells undergo dentinogenesis & begin to secrete
predentin
• when root dentin formation is completed, the entire HERS will
disintegrates & become epithelial rests of Malassez

61. outer cells of dental
papilla differentiate into
odontoblasts &
apposition of dentin in
root area
when root dentin
formation is completed,
the entire HERS will
disintegrates & become
epithelial rests of
Malassez

62. CEMENTUM & PULP FORMATION
• Cementogenesis (apposition of cementum) occurs after
HERS disintegrates
• induction of dental sac / follicle cells to differentiate into
cementoblasts
• cementoblasts produce cementum matrix (cementoid)
• many cementoblasts become entrapped by cementum matrix
& become mature cementocytes
• as cementum matrix surrounding the cementocytes
becomes calcified or matured → cementum
• central cells of dental papilla → pulp

63. *after HERS
disintegration, dental sac
cells differentiate into
cementoblasts
*cementoblasts produce
cementum matrix
*cementoblasts
entrapped in cementum
matrix & become
cementocytes

64. PERIODONTAL LIGAMENT &
ALVEOLAR BONE DEVELOPMENT
• as crown & root develop, surrounding supporting tissues of tooth are
also developing
• mesenchyme from dental sac / follicle begins to form periodontal
ligament (PDL) adjacent to newly formed cementum
• ends of these fibres insert into outer portion of cementum &
surrounding alveolar bone to support tooth
• mesenchyme of dental sac also begins to mineralize to form tooth
sockets surrounding the PDL

65. PRIMARY TOOTH ERUPTION & SHEDDING
• eruption of primary tooth involves active vertical movement of tooth
• after enamel apposition ceases in crown area, layers of enamel organ
are compressed, forming reduced enamel epithelium (REE)
*enamel organ → REE
• REE fuses with oral epithelium in oral cavity
• REE produce enzymes that cause disintegration of area of fused
tissues, creating a tunnel for tooth movement & eruption into oral cavity
• tissue disintegration causes an inflammatory response known as
“teething” which accompanied by tenderness & edema of local tissues

66. • as tooth erupts, coronal fused tissues detached from the crown, leaving cervical
portion still attached to neck of tooth
• this fused tissue that remain near CEJ after tooth erupts, serves as initial
junctional epithelium (JE) & later replaced by definitive JE as root is formed
• primary tooth is then exfoliated, as permanent tooth erupts lingual to it
• the process of primary tooth loss involves :
→ resorption of alveolar bone bw the two teeth (by osteoclasts)
→odontoclasts resorb primary tooth's root dentin, cementum & small portions of
enamel crown

67. PERMANENT TOOTH ERUPTION
• permanent tooth erupt in a position lingual to roots of
shedding primary tooth
• eruption process = primary tooth
• permanent tooth starts to erupt before primary tooth is fully
shed

68. A. before eruption process begins
- REE covers newly formed
enamel
B. REE fused with oral epithelium
C. disintegration of fused tissue,
leaving a tunnel for tooth
movement & eruption
D. as tooth erupts, coronal fused
tissues detached from the crown,
leaving cervical portion still
attached to neck of tooth

69. COMMON DENTAL DISTURBANCES
Initiation stage :
Hypodontia
*absence of single or multiple teeth
*perm.max.lateral incisor, 3rd molar, mand.2nd premolar
*result from endocrine dysfuntion, systemic disease, excess
radiation
*may be a/w syndrome of ectodermal dysplasia

70. Supernumerary / hyperdontia
*development of one or extra teeth
*extra teeth are initiated from dental lamina
*commonly found → bw maxillary central incisors,
distal to 3rd molars & premolar region
*may cause crowding, failure of normal eruption & disrupt
occlusion

71. HYPODONTIA

72. HYPODONTIA

73. SUPERNUMERARY

74. SUPERNUMERARY

75. ECTODERMAL DYSPLASIA
• hereditary
• abnormal development of ectodermal structure
• affected persons have abnormalities of teeth, skin, hair, nails, eyes,
facial stucture & glands (because these are derived from ectoderm
struscture)
• child resemble “little old men”
• clinical features :
*skin - smooth, dry
*hair - fine, scanty
*sweat glands - partial / total absence → hyperthermia
*teeth - anodontia / hypodontia, retard eruption, malformations

76. ECTODERMAL DYSPLASIA

77. ECTODERMAL DYSPLASIA

78. ECTODERMAL DYSPLASIA

79. Bud stage :
Micro / macrodontia
*abnormally small or large teeth
*cause → abnormal proliferation may cause tooth to be larger or
smaller than normal
*commonly affects perm.Max.lateral incisor & 3rd molars
*complete micro / macrodontia rarely occurs & can be due to
dysfunction of pituitary gland

80. MICRO / MACRODONTIA

81. Cap stage :
Dens in dente (dens invaginatus)
*enamel organ invaginates into dental papilla
*a.k.a “tooth within a tooth”
*commonly affects perm.max.lateral incisor ;
***due to external forces applied on lateral incisor tooth bud by developing central incisor or
canine which develops earlier
*may have deep lingual pit in area of invagination - may lead to pulp exposure
+ pathology → may need endodontic therapy
*r/g → tooth within a tooth

82. DENS IN DENTE

83. DENS IN DENTE

84. Germination
*single tooth germ tries to divide into two tooth germs (unsuccessful
division)
*large single-rooted tooth with one pulp cavity
*exhibits “twinning” in crown area
*appearance of splitting / cleft in the incisal surface, resembling 2 crowns
*number of teeth in dentition is normal
*usually occurs in anterior teeth (primary / permanent dentition)
*problem in appearance & spacing

85. GERMINATION

86. GERMINATION

87. Fusion
*union of 2 adjacent tooth germs, possibly due to pressure in the area
*large tooth with 2 pulp cavities
*lack amount of tooth in dentition
*fusion occurs only in crown area, but it can involve both crown & root
*common → anterior teeth
*problems in appearance & spacing

88. FUSION

89. Dens evaginatus (extra cusps)
*presence of extra cusp in a form of tubercle
**tubercle usually contain pulp tissue
*arise from occlusal or lingual surface of tooth
*a.k.a Talon cusp (anterior teeth) or Leong’s premolar (premolars)
*causes → trauma, pressure, metabolic disease that affects enamel
organ forming the crown area

90. TUBERCLES

91. Apposition & maturation stages :
Enamel dysplasia
*faulty development of enamel due to interference of ameloblasts activities
**small gp ameloblasts (-trauma, infection) → local enamel dysplasia
**large number ameloblasts (-traumatic birth, systemic infections, nutritional deficiencies,
fluorosis) → systemic dysplasia
*enamel → pitting, opaque-yellow-brownish discolouration
*types :
→ enamel hypoplasia (↓volume enamel matrix)
→ enamel hypocalcification (↓maturation enamel matrix)
→ amelogenesis imperfecta

92. ENAMEL DYSPLASIA

93. AMELOGENESIS IMPERFECTA
• hereditary, positive family history
• 2 major types :
→hypoplastic
→hypomineralization / hypomaturation
• affect primary & permanent dentitions
• most of enamel on all teeth is involved

94. Hypoplastic type :
• ↓ volume enamel matrix, normal mineralization
• enamel - thin & hard
• generalized pitting, grooving of enamel

95. Hypomineralization / hypomaturation type :
• enamel matrix volume is normal, ↓ mineralization
• enamel - normal thickness, but soft & porous
• mottled, opaque, yellow-brownish appearance
• rapidly lost by abrasion, attrition exposing the dentin

96. AMELOGENESIS IMPERFECTA

97. MOLAR-INCISOR HYPOMINERALIZATION (MIH)
• mineralization / maturation of enamel matrix is affected
• enamel - normal thickness, but soft & porous
• cause → disturbance in ameloblasts activity which
disturbs the amelogenesis
• enamel is opaque, yellow-brownish appearance
• enamel easily breakdown, more prone to caries
• localized - affect several teeth (usu.molar & incisor)

98. MIH

99. Cementum formation stage :
Concrescence
*union of root structure of 2 or more teeth by cementum
*common - permanent max.molars
*teeth involved are originally separate but join because of
excessive cementum deposition
*causes - traumatic injury or crowding of teeth in area
during apposition & maturation stage of tooth development
*problems during extraction & endodontic treatment

100. CONCRESCENCE

101. CONCRESCENCE

102. Root formation stage :
Enamel pearl
*causes : displacement of ameloblasts to root area, causing enamel
to be abnormally formed on cemental root surface
*small, spherical enamel projections on root surface, especially at
CEJ or in furcation area on molars
*they may have a tiny dentin & pulp core - appear radiopaque on
radiographs
*it may be confused with a calculus deposit upon exploration of root
surface - but cannot be removed

103. Dilaceration
*distorted root or crown angulation
*results from distortion of HERS due to injury or pressure
*can cause problem during extraction & endodontic therapy

104. Taurodontism
*bull like tooth
*pulp chamber has greater apico-occlusal height than in
normal teeth, with no constriction at level of CEJ
*result in chamber extend apically, beyond neck of tooth
*affects multirooted tooth
*cause → failure of HERS to invaginate at proper horizontal
level

105. Accessory roots
*may be due to trauma, pressure or metabolic disease that
affects HERS
*can affect any tooth, but commonly in permanent 3rd molar
*problems in extraction & endodontic therapy

106. ENAMEL PEARL

107. ENAMEL PEARL

108. DILACERATION

109. DILACERATION

110. DILACERATION

111. ACCESSORY ROOTS

112. ACCESSORY ROOTS

113. Dentin formation stage :
Dentinogenesis Imperfecta
*type I, II, III
***type I - a/w Osteogenesis Imperfecta
***type II - only teeth affected
*genetic
*affect - primary & permanent dentition
*teeth have normal contour with opalescent, translucent apperance
*↓dentin hardness causing rapid attrition of teeth following enamel loss
*r/g → blunt roots with partial / total obliteration pulp chamber & root canal by
dentin
*HPE → dentinal tubules -↓number, wide, irregular
→√ areas of atubular / abnormal dentin that may partly / totally obliterates
pulp chamber & root canal

114. DENTINOGENESIS IMPERFECTA

115. DENTINOGENESIS IMPERFECTA

116. Eruption stage :
Odontogenic cysts
*Dentigerous (follicular) cyst) → forms by accumulation of fluid
bw REE & crown of unerupted / impacted tooth
*can displaced teeth, jaw fracture & pain
*needs to removed competely surgically
*Eruption cyst → erupting tooth
*bluish, fluctuant, vesicle-like lesion on erupting tooth
*will disintegrates as the tooth erupt
*no tx is needed

117. DENTIGEROUS CYST

118. ERUPTION CYST

119. OTHER ABNORMALITIES
• delay eruption
• natal / neonatal teeth
• fluorosis
• tetracycline staining

120. DELAYED TOOTH ERUPTION
LOCAL FACTORS
• Physical obstruction - supernumerary, scar tissue, tumor
• Gingival hyperplasia (↑density CT) - hereditary, drugs
• Traumatic injuries - unerupted, delayed eruption, displacement of
tooth germ, dilaceration
• Cystic transformation - NV deciduous tooth may induce cystic
transformation of underlying permanent tooth

121. • Ankylosis - fusion of root dentin to alveolar bone
(delayed exfoliation of deciduous tooth → delayed
tooth eruption)
• Arch length deficiency - space loss → crowding
impactions

122. SYSTEMIC FACTORS
• Genetic disorder - Apert syndrome, cleidocranial
dysostosis, Gardner syndrome
• Endocrine disorder - delayed eruption & shedding of tooth -
eg : hypthyroid, cretinism, pituitary dwarfism
• Preterm birth - born less than 37 weeks, ↓ birth weight -
retarded dental growth
• Anemia - growth impairment
• Malnutrition

123. DELAYED TOOTH ERUPTION

124. DELAYED TOOTH ERUPTION

125. FLUOROSIS
• ingestion of excess fluoride during period of tooth formation
• severity depends on amount fluoride ingested, duration &
timing of exposure
• generalized mottled appearance of teeth ; yellow-brownish-
black discoloration
• enamel → hypomineralization of subsurface enamel or
hypoplastic pitting
• can affect primary & permanent dentition

126. FLUOROSIS

127. NATAL & NEONATAL TEETH
• natal teeth = teeth present at birth
• neonatal teeth = teeth erupted within 1st mth of life (day 1-30)
• can be supernumerary or primary mandibular incisors
• problems :
→mobility
→ulceration of tongue
→difficulty in breastfeeding

128. NATAL & NEONATAL TEETH

129. TETRACYCLINE STAINING
• systemic tetracycline therapy of pregnant women during
fetal period of prenatal development
• may result in permanent tetracycline staining in primary
teeth that are developing at that time
• intrinsic yellow-brown staining of teeth
• antibiotic bound to dentin & because the transparency of
enamel, the stain is visible
• can also affect permanent teeth if drug is given during their
development

130. TETRACYCLINE STAINING

131. TERIMA KASIH
Disediakan oleh :
Dr. Norazreen Abdul Jalil
Pegawai Pergigian Yang Menjaga (PPYM)
Jabatan Pergigian Pediatrik
Hospital Melaka