1. Presented by :
Piyush Verma
Mds 2 nd year
Department of Pedodontics
and preventive dentistry
27 – 09 - 2012
1

2. Contents
 Introduction
 Eruption
 Pre eruptive tooth movement
 Eruptive tooth movement
 Theories of tooth eruption
 Post eruptive tooth movement
 Shedding of teeth
 Pattern of shedding
 Tooth resorption and repair
 Conclusion
 References
2

3. Introduction
 The timely initiation and eruption of teeth into the
oral cavity is very important for healthy dentition .
It is the process by which tooth moves within the
Jaw bone comes into the oral cavity and comes up to
the occlusal contact and maintains its clinical position.
3

4. Eruption
Eruption refers to the axial or occlusal movement of the
tooth from its developmental position within the jaw to
its functional position in the occlusal plane.
 Physiological tooth movements consists of the
following:
Pre eruptive tooth movement
Eruptive tooth movement
Post eruptive tooth movement
4

5. 5
Primary dentition: - 2
to 6 years of age
Permanent dentition:
> 12 years
DIPHYODONT

6. Phases of tooth eruption
 Preeruptive phase: made by the deciduous and permanent tooth
germs within tissues of the jaw before they begin to erupt.
 Eruptive phase: Starts with initiation of root formation and
made by teeth to move from its position within bone of the jaw
to its functional position in occlusion. Has an intraosseous and
extraosseous compartments.
 Posteruptive phase: Takes place after the teeth are functioning
to maintain the position of the erupted tooth in occlusion while
the jaws are continuing to grow and compensate for occlusal
and proximal tooth wear.
6

7. Made by the deciduous and permanent tooth germs within tissues
of the jaw before they begin to erupt.
tooth germs grow rapidly
crowded
relieved by lengthening of jaws
deciduous second molar tooth germs move backward
anterior tooth germ moves forward
Pre eruptive tooth movement
7

8. Permanent anterior tooth germs
develop lingual to the primary
anterior teeth and later as
primary teeth erupt, the
permanent crowns lie at the
apical 3rd of primary roots.
Premolars tooth germs are
finally positioned between the
divergent roots of deciduous
molars.
8

9. Histologic features
 Remodeling of the bony wall of crypt by selective
deposition and resorption of bone by osteoblasts and
osteoclasts.
 Normal skeletal morphogenesis might be involved in
determining tooth position
9

10. Eruptive tooth movement
 The axial or occlusal movement of the tooth from its
developmental position within the jaw to its final functional
position in the occlusal plane.
 The actual eruption of the tooth when it breaks through the
gum is only one stage of eruption.
10

11. Histology
 Degeneration of connective tissues
immediately overlying the erupting teeth.
 Eruption pathway – altered tissue area
overlying the teeth.
 Macrophages destroy cells and fibers by
secreting hydrolytic enzymes.
 Gubernacular cord: The connective tissue
overlying a successional tooth that connects
with the lamina propria of the oral mucosa by
means of a strand of fibrous connective tissue
that contains remnants of dental lamina
11

12. 12
 Gubernacular canal: Holes
noted in a dry skull noted
lingual to primary teeth in
jaws that represent openings
of gubernacular cord .

13. 13

14. • As the tooth moves occlusally it creates space underneath the tooth to
accommodate root formation
• Fibroblasts around the root apex form collagen that attach to the newly formed
cementum
• Bone trabeculae fill in the space left behind as the tooth erupts in the pattern of a
ladder which gets denser as the tooth erupts
• After tooth reaches functional occlusion periodontal fibers attach to the apical
cementum and extend into the adjacent alveolar bone
14

15. Stages of tooth eruption
Essentials of Oral Histology and Embryology. James Avery, 2nd edition 15

16. The rate of tooth eruption depends on the type of
movement
16
• 1 to 10
µm/dayINTRAOOSEOUS
PHASE
• 75 μm/day
EXTRAOSSEOUS
PHASE

17. are those movements made by the tooth after it has reached its functional position in
the occlusal plane.
They may be divided in three categories:
Post Eruptive Tooth Movements
17
Accomodation for
growth
Compensation for
occlusal wear
Accomodation for
interproximal wear

18.  ACCOMMODATION FOR GROWTH - Mostly
occurs between 14 and 18 years by formation of new
bone at the alveolar crest and base of socket to keep
pace with increasing height of jaws.
 COMPENSATION FOR OCCLUSAL WEAR -
Compensation primarily occurs by continuous
deposition of cementum around the apex of the tooth.
However, this deposition occurs only after tooth
moves.
 ACCOMMODATION FOR INTERPROXIMAL
WEAR - Compensated by mesial or approximal drift.
18

19. FACTORS CONTROLLING MESIAL DRIFT:
(a) Contraction of the transseptal fibers: As the proximal tooth
surfaces of adjacent teeth become worn from functional tooth
movement, the transseptal fibers of the periodontal ligament
become shorter (due to contraction) and thereby maintain tooth
contact .
(b) Adaptability of bone tissue: The side of pressure on PDL fibers
causes bone resorption, whereas pull on the fibers causes bone
apposition. Therefore, as the contact areas of the crowns
wear, the teeth tend to move mesially, thereby maintaining the
contact.
19

20. (c) Anterior compartment of occlusal force: An anteriorly
directed force is generated when teeth are clenched, due
to the mesial inclination of most teeth and the forward-
directed force generated from inter-cuspal forces.
Eliminating opposing teeth results in elimination of
biting forces, causing a slowing down of the mesial
migration
(d) Pressure from soft tissues: Buccal mucosa and tongue
push teeth mesially
20

21. Theories of resorption
 Root formation ( tomes 1872 )
 Bone remodeling ( brash 1928 )
 Dental follicle ( marks and cahill 1984)
 Periodontal ligament ( thomas 1967 )
 Hydrostatic pressure ( sutton and graze 1985 )
 Pulpal pressure ( v . Korff 1935 )
 Cellular theory ( eidmann 1923)
 Molecular theory ( marks et al )
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22.  Active eruption
 Passive eruption
 Genetic factors
 Local factors ( steggerda and hill 1942)
22

23. Root Formation :
 Root formation would appear to be the obvious cause of tooth
eruption since it causes an overall increase in the length of the
tooth along with the crown moving occlusally.
 Clinical observation, experimental studies and histologic
analysis argue strongly against such a conclusion as rootless
teeth do erupt
 some teeth erupt more than the total length of the roots and the
teeth still erupt after completion of root formation.
23

24. Bone remodeling
The growth pattern of the maxilla and the mandible moves teeth
by selective deposition and resorption of bone.
Major proof is when a tooth is removed without disturbing its
follicle tooth germ, an eruptive pathway still forms within bone
as osteoclasts widen the gubernacular canal.
 If the dental follicle is also removed no eruption path develops.
 It establishes absolute requirement for a dental follicle to
achieve bony remodeling and tooth eruption.
24

25. Dental Follicle
 Studies have shown that the reduced dental epithelium
initiates a cascade of intercellular signals that recruit
osteoclasts to the follicle.
 By providing a signal and chemoattractant for
osteoclasts, it is possible that the dental follicle can initiate
bone remodeling which goes with tooth eruption. Teeth
eruption is delayed or absent in and human diseases that
cause a defect in osteoclast differentiation.
25

26.  Experiments done by Cahill & Marks says that viable dental
follicle is required for the eruption.
 Further studies by them has shown that tooth eruption is a
series of metabolic events in alveolar bone characterized by
bone resorption and formation on opposite sides of the
dental follicle and the tooth does not contribute to this
process.
26

27. Periodontal ligament
 Available evidences strongly indicate that the force for eruptive
tooth movement lies in PDL.
 the PDL and dental follicle from where it forms are implicated
in the process of tooth eruption linked to contractility of
fibroblasts.
 PDL fibroblasts are able to provide a force sufficient to move
the tooth and certainly the proper structural elements exist to
translate such force into eruptive tooth movement.
27

28. Cellular and molecular basis of tooth eruption
Cellular basis
prior to onset of eruption
influx of mononuclear cells into coronal
portion of dental follicle
cellular events
influx of mononuclear cells
28

29. Required for formation of osteoclasts
Resorb bone for the eruption pathway
Dental follicle is interposed between the alveolar bone and tooth
, it is an ideal location to regulate the cellular events of eruption
and receive signals from the tooth.
29

30. Molecular basis
 Eruption molecules
the molecules that initiate eruption , their localization and the
regulation of the cellular events of eruption all must fit within the
context that each tooth erupts independently
Determination of the molecules that may be required for eruption
began with the isolation of –
 EGF (epidermal growth factor )
 TGF α (transforming growth factor )
 Colony stimulating factor 1
30

31.  TGF α , EGF ↑ in incisor eruption
 colony stimulating ↑ in molar eruption
factor 1
31

32.  Nakchbandi IA et al (june 2000)
 experiments in vivo have established that tooth eruption fails in
the absence of parathyroid hormone (PTH)-related protein
(PTHrP) action in the microenvironment of the tooth because
of the failure of osteoclastic bone resorption on the coronal
tooth surface to form an eruption pathway.
32

33. Localization of eruption molecules:
 Studies have demonstrated that the eruption genes and their
products are localized primarily in either the dental follicle or
stellate reticulum.
 The tissue required for eruption , the dental follicle produces
the majority of the potential eruption molecules.
 The remainder of the molecules reside in the stellate reticulum
adjacent to the dental follicle.
E.g IL – 1 – resides in dental follicle
DF -95 resides in stellate reticulum
33

34.  Pulp theory
 It suggests that the tooth is moved lingually by the pressure
from the pulp the explosive effect of pulpal bulge is produced
by the osmotic pressure of the briskly proliferating and
differentiating mesenchymal cells.
 Alveolar bone deposition
 Deposition of bone beneath the tooth during eruption is
unlikely to be the cause rather than consequence of the tooth
erupting.
34

35.  The classic experimental model for studying eruption
is the rat’s incisor , where continuous eruption occurs
without any additional bone being formed at the base
of tooth.
 However, it is quite likely that bone growth is partly
responsible for the pre eruptive phase during which
growth of the entire alveolus and remodeling around
the tooth crypt helps to move it into place for the
eruptive phase.
35

36.  Active eruption
bodily movement of tooth from its site
of development to its functional position in the oral
cavity.
 Passive eruption
Apparent lengthening of the crown due to
loss of attachment or recession of gingiva.
36

37.  Genetic and environmental factors
The environment, prenatal and maternal factors, social
factors, climate etc. may influence the timing of tooth eruption
but the determinants of this timing are still thought to be more
genetic than environmental.
Lewis and Garn (1960) and Garn et al. (1965) theorized that tooth
formation is genetically determined and in an analysis of
monozygotic twin pairings found strong correlations of tooth
formation
37

38.  Local factors
Local alterations frequently form a physical barrier to normal
tooth eruption. In the gingiva, fibromatous or hyperplastic
alterations may hamper the eruption of the underlying tooth .
In the bone, supernumeraries, odontogenous or non-
odontogenous tumours, cysts or cleft anomalies may interfere
with proper eruption.
38

39.  Tooth eruption in children with growth deficit.
Barberia Leache E et al
found that children whose delayed growth is accompanied by a
low genetic height or growth hormone deficit presented
retardation in dentition and retardation in bone age.
 J Int Assoc Dent Child. 1988 Dec;19(2):29-35
39

40. Shedding of teeth
 Physiologic process resulting in the complete elimination of the
deciduous dentition.
Pattern of shedding
Result of progressive resorption of roots of deciduous teeth and
its supporting tissues.
Pressure generated by the erupting permanent tooth guides the
pattern of deciduous tooth resorption.
Initially , pressure is against the root surface of the deciduous
tooth and resorption occurs on the lingual surface.
40

41.  Later these developing tooth germs occupy a position directly
apical to the deciduous tooth.
 In mandibular incisors the apical positioning of the tooth germs
does not occur and permanent tooth erupts lingually.
41

42. Resorption of deciduous molars
 Resorption of the roots of deciduous molars first begin on their
inner surfaces because the early developing bicuspids are found
between them.
 With continued growth of the jaws and occlusal movement of
the deciduous molars, the successional tooth germs lie apical to
the deciduous molars.
 When the bicuspids begin to erupt , resorption of the deciduous
molars is again initiated and continues until the roots are
completely lost and the tooth is shed.
42

43.  Resorption occurs on the surface of cementum and dentine .
 Resorption involves a loss of the organic as well as the mineral
constituent of the matrix .
 during resorption the process of disorganization relative to the
mineral and the organic components occurs more or less
concomitantly.
 Resorption of cementum and dentine of deciduous teeth is
characterized by the presence of osteoclasts.
43

44.  Root resorption seems to be initiated and regulated by the
stellate reticulum and dental follicle of the underlying
permanent tooth via the secretion of stimulatory molecules i. e.
cytokines and transcription factors .
 The primary root resorption process is regulated in a manner
similar to the bone remodeling , involving the same receptor
ligand system known as RANK/ RANKL
( receptor activator of nuclear factor – kappa B / RANK ligand)
44

45. PRIMARY ROOT RESORPTION WITH
PERMANENT SUCCESSOR
 The pressure of erupting tooth is believed to play a contributory
role in setting of resorption but the presence of permanent
successor is not a prerequisite for this process to occur.
 Root resorption of primary teeth starts at the site of root that is
closest to the permanent successor. E.g in anterior teeth
completed crown of permanent successor is found lingual to
apical third of root of primary predecessor:
Resorption of lingual surface of apical third of primary tooth
root.
Resorption of labial surface.
Resorption proceeds horizontally in incisal direction until
primary tooth sheds & permanent tooth erupts.
45

46. PRIMARY ROOT RESORPTION WITHOUT
PERMANENT SUCCESSOR
 The root is protected from resorption by presence of
narrow PDL cell layers which are composed of:
Collagen fibers
Fibroblasts
Cementoblasts
 Degradation of PDL precede root resorption & removal of
collagen fibers of PDL is considered main step in initiation
of this process.
 As face grows & muscles of mastication enlarge, forces that
are applied on the deciduous teeth become heavier than
primary tooth periodontal ligament can withstand.
46

47. Histology of shedding
 Odontoclasts are resorbing cells derived from monocyte –
macrophage lineage.
 Giant multinuclear cells with 4 – 20 nuclei.
 Resorption occurs at the ruffled border which greatly increases
the surface area of the odontoclast in contact with bone.
 Found on surfaces of the roots in relation to advancing
permanent tooth.
 Single rooted teeth shed before root resorption is completed.
Distribution of odontoclasts during tooth resorption
47

48.  Odontoclasts are not found in pulp chamber of these teeth.
 In molars , the roots are completely resorbed and crown is
partially resorbed.
 Odontoblasts layer is replaced by odontoclasts.
 Sometimes all the dentine is removed and the vascular tissue is
seen beneath the translucent cap of enamel.
48

49. 5 months
At birth 1 year
2 years 3.5 years 4.5 years
Shedding of mandibular incisor
Figure Source: Dr. Sandra Meyers 49

50. Tooth resorption and repair
 Resorption is not a continuous process but have also periods of
repair.
 Resorption predominates repair.
 Repair is achieved by cells resembling cementoblasts.
 Final repair tissue resembles cellular cementum but is less
mineralized.
50

51. Mechanism of resorption and shedding
 Pressure from the erupting successional tooth and appearance
of odontoclasts at the site of pressure.
 Membrane of ruffled borders act as proton pump → adding
hydrogen ions to extracellular region → acidification →
mineral dissolution.
 Increased forces of mastication with increase in jaw size
leading to trauma to PDL → degeneration of PDL
51

52.  Resorb bone for the eruption pathway
 Dental follicle is interposed between the alveolar bone
and tooth , it is an ideal location to regulate the
cellular events of eruption and receive signals from the
tooth
52

53. 7 years-functional occlusion attained
but root apex is still not fully formed
15 years – incisal wear
Figure Source: Dr. Sandra Meyers
53

54. Sequence and chronology of tooth eruption
Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf
54

55.  According to Hillson (1996), eruption times can be
broken into three phases:
 Phase One includes the emergence of permanent first
molars and incisors (5 to 8 years of age);
 Phase Two consists of the emergence of the
canines, premolars, and second molars (9.5 to 12.5
years);
 Phase Three consists of the emergence of the third
molars (late teens to early twenties)
55

56. Chronology of Human Permanent Dentition
56

57. The six/four rule for primary tooth emergence
Four teeth emerge for each 6 months of age
1. 6 months: 4 teeth (lower centrals & upper centrals)
2. 12 months: 8 teeth (1. + upper laterals & lower laterals)
3. 18 months: 12 teeth (2. + upper 1st molars & lower 1st molars)
4. 24 months: 16 teeth (3. + upper canines & lower canines)
5. 30 months: 20 teeth (4. + lower 2nd molars & upper 2nd molars)
1. By 5 months in utero, all crowns started calcification
2. By 1 year old, all crowns completed formation
3. By 2.5 years, all primary teeth erupted
4. By 4 years old, all primary teeth completed root formation
57

58. The rules of “Fours” for permanent tooth
development (3rd molars not included)
At birth, four 1st molars have initiated calcification
At 4 years of age, all crowns have initiated calcification
At 8 years, all crowns are completed
At 12 years, all crowns emerge
At 16 years, all roots are complete
58

59. Rules of “sixes” in dental development
6 weeks old in utero: beginning of dental development
6 months old: emergence of the first primary tooth
6 years old: emergence of first permanent tooth
59

60. Problems of Primary Tooth Eruption
Natal and Neonatal Teeth
60

61.  Eruption cyst
- follicular enlargement occurring just before eruption.
- blue-black color due to presence of blood
- no specific treatment if uninfected
61

62. Submerged primary teeth
62

63.  Failure of eruption of first and second permanent molars
Camila Palma et al
CONCLUSIONS
 1. In this series, the failure of eruption of permanent molars was the
consequence of impactions and primary retentions.
 2. Unfavorable prognosis is associated with advanced age and with molars
in the last stages of root formation.
 3. Root dilaceration is a major factor limiting eruption and an indicator of
poor prognosis.
 4. The degree of non-eruption and the inclination axis are not key factors in
prognosis.
 5. Posterior dento-alveolar discrepancy is associated with impaction of
second molars.
 J Clin Pediatr Dent 27(3): 239-246, 2003
63

64.  Congenital hypothyroidism/ Cretinism
- due to hypo function of thyroid gland
- primary tooth eruption is delayed till 2
years.
- large head, protruding tongue
- as soon as it is detected, treated with
thyroxin.
64

65.  (Rushton, 1937; Jensen and Kreiborg, 1990,1993
 The defects seen in the dentitions of patients affected with
Cleidocranial dysplasia have been thought to arise from a
disruption in the bone remodeling process. In addition to an
increased density in the maxilla and mandible, multiple
supernumerary teeth are present that show a marked delay or
arrest in eruption
65

66.  Impaction
due to failure in eruption
mechanism
maxillary canine, 3rd molars
– commonest form
66

67.  (Sauk, 1988; Gorlin et al., 1990; Jones, 1997).
 Eruption failure and delayed eruption are conditions
that do not naturally involve ankylosis and are
associated with craniofacial
dysostosis, hypothyroidism, hypopituitarism, and
several genetic and medical syndromes.
67

68.  Ectopic eruption
describes a path of eruption that
causes root resorption of a
portion or all of the adjacent
primary teeth.
mandibular lateral incisor –
commonest
maxillary 1st molar and canine.
68

69. 69

70. Conclusion
 For the clinicians to treat dental problems knowledge
of proper eruption and shedding time is very
important .
 A variety of developmental defects that are evident
after eruption and shedding of the primary and
permanent teeth can be related to local and systemic
factors.
70

71. References
Textbook of oral histology by Ten cate,7 th edition; 268
– 289
Orban‘s textbook of oral histology and embryology –
(10 th edition); 372 - 386
Textbook of oral development and histology by James
Avery 3. rd. edition : 92-105.
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72. Thank you
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