Age Changes in Enamel, Dentin and Pulp

Presented by:-
Harpreet Kaur
 Ageing is defined as a process of morphological
and physiological disintegration as distinguished
from infant, childhood and adolescence which
are typified by processes of integration and
coordination.
Carranza.
The completely formed teeth and the periodontium should remain intact and fully
functional without disease for a lifetime.
MACROSCOPIC
-Becomes darker
-Attrition, Abrasion, Erosion
-Longitudinal cracks
MICROSCOPIC
- Decreased - enamel rod ends
- perikymata
- permeability to fluids
- Increase in nitrogen and fluorine
• Increased resistance to decay
MACROSCOPIC CHANGES
 Becomes darker with age.
 Associated with changes in

the organic portion of
enamel, presumably near
the surface.
Attrition Abrasion
Erosion
 Physiologic
wear of the occlusal surfaces and
proximal contact points as a result of mastication.
 Evidencedby a loss of vertical dimension of the
crown and by flattening of the proximal contour.
Causes
 Masticatory stress
 Para-functional habits
Stage I- Wear of enamel at cusps and incisal edges
without exposure of dentin.
Stage II Wear of enamel and exposure of dentin on incisal
edges and isolated area over individual cusps.
Stage III Wear of enamel forming a broad strip on incisal
edges and the confluence of two are more areas of wear
over adjacent cusps.
Stage IV Wear of enamel and dentin on incisors to form a
plateau on the teeth to form a central area of dentin
surrounded by a peripheral rim of enamel.
 Pathological wearing away of tooth through
abnormal mechanical processes.
e.g.- abrasive dentifrice
- occupational
- improper flossing
 Loss of tooth substance by a chemical process
that does not involve known bacterial action.
 Lingual erosion
e.g. -chronic vomiting
-acidic carbonated
beverages
 Labial erosion
 May be developmental in origin.
 Although their numbers do not increase with

age , they become more obvious.
•Thinning of enamel at the level
of cementoenamel junction.
• Thickening at the incisal edge

(maximum facial-palatal width)
due to wear with advancing age.
•These phenomena results in an

overall decrease in the height of
the tooth’s crown.
MICROSCOPIC CHANGES
 Transverse wave like grooves which lie parallel to each
other and also to cemento -enamel junction.
 The surfaces of unerupted and recently erupted teeth are
covered completely with pronounced rod ends and
perikymata.
 Advancing age shows generalized loss of rod ends and
slower flattening of perikymata which are eventually lost.
 More rapid loss of structure
Facial and lingual surfaces
Anterior teeth
Due to acquisition of ions from oral fluids.
Crystal size increases
Reduction in pore size within the substance of enamel.
Decrease in permeability and water content

Continuous deposition of
fluoride and nitrogen on
enamel surface
Increase in fluoride
concentration of enamel
Hardness and Elastic
modulus of enamel
Increased resistance to increases .
decay
Increases the brittleness of
teeth and decreases
permeability.
Cracks
 Two major changes in
dentin:
 Formation of secondary
dentin.
 Sclerosing or obturation of
the dentinal tubules.
A- dead tract
B- sclerotic dentin
 Secondary dentin forms after the complete
formation of the tooth.
Types:
 Physiologicsecondary dentin, which forms

with normal stimulus,
 Reparative secondary dentin, which forms
with traumatic or abnormal stimulus.
Regular Irregular
Cause: mild stimuli (slow attrition, Cause: severe stimuli, severe
slowly progressing caries) attrition, erosion, deep caries.
Site of formation: entire pulpal Site of formation: localized (eg

surface (thicker on pulp roof
pulp horn)
and floor)
Tubules: wavy course, decrease in Tubules: wavy and twisted course,

number decrease in number or atubular
Clinically:
The increase of the dentin Clinically:
thickness and the closure of the Functions as a barrier for
pulp horns make it much less against caries.
possible to expose the pulp
chamber during preparation.
Primary D
Secondary D
Reparative
Replaced by the
migration of
Degenerate undifferentiated Dentin
cells from cell rich
zone
Odontoblasts
are cut Reactionary/
Extensive
abrasion , Live
Regenerated
Erosion odontoblasts
,caries and Odontoblasts Dentin
Operative are cut
process
 Odontoblastic cell processes in the
dentinal tubules are degenerated,
leaving behind empty, air-filled
tubules referred to as “dead tracts”.
 Appear black in transmitted light
and white in reflected light.
 Probably the initial step to form
sclerotic dentin.
 Demonstrate decreased sensitivity.
 Physiological change or
pathological change (caries,
attrition, deep fillings, ) in
primary or secondary dentin.
 More highly mineralized,

harder and denser than normal
dentin
 Seen first near the root apex

in a middle aged person.
 Spreads upwards from the

apex with advancing age.
 This is one of the criteria used

in forensic odontology to
assess the age of an individual
Young dentin Adult dentin Sclerotic dentin
Appears light in transmitted light and dark in
reflected light
Age related Sensitivity changes
Secondary dentin grows inwardly into the pulp chamber

decreasing the chamber’s size .
Tubular lumen becomes obturated by peritubular dentin.

By age 80, almost all dentinal tubules are fully occluded.
Decrease in sensation to hot and cold stimuli.

 Reduction in the size and volume of the pulp as
a result of a continuous deposition of dentin.
 Decrease in the number of cells and apparent

increased fibrosis with time, may not be from
continued formation of collagen but may be
due to the persistence of connective tissue
sheath in an increasingly narrow pulp space.
 Cellular composition of the pulp is modified.
 Fibroblasts and Odontoblasts show

degeneration with decrease in size and
decrease in the number of cell organelles.
 Ultrastructural studies reveal an increase in

vacuole numbers and gradual degenerative
changes leading to the absence of cells.
Changes in vascular distribution:
• There is a narrowing of the circumference of
the blood vessels.
• Atherosclerotic changes are seen in small

arteries in the root pulp of aging teeth.
• Intimal layer of the vessel is thickened

resulting in a small lumen.
Changes in nerve distribution:
• Degeneration and loss of pulpal nerve fibres
may affect transmission from pulpal structures,
resulting in increased thresholds to pain
stimuli.
• Myelin sheath changes and terminal axon

remolding due to age related axon injury could
be sources of abnormal pain in the oral region.
 These are nodular, calcified masses appearing in either or both
the coronal or root portions of the pulp organ.
 True -Made of dentin and lined by odontoblasts ,found close to

root apex
 False -Formed from degenerating cells which mineralize, usually

found in the pulp chamber
Free -Stone not related to pulp
space wall, surrounded by soft
tissue.
Adherent -Stone attached to wall

of pulp space, not fully enclosed
by dentin.
Embedded -Stone enclosed within

canal wall.
 Fibrodentine -Material produced by fibroblast-
like cells against dentin prior to differentiation
of a new generation of odontoblast-like cells.
 Dystrophiccalcification -Inappropriate
biomineralization of the pulp in the absence of
mineral imbalance.
 Root caries, a pathologic process, occur
with greater frequency in older adults
than in any other age groups.
 Xerostomia, a common symptom in older

adults, along with cementum loss,
gingival recession, poor oral hygiene,
high plaque, and periodontal disease
increase risk for root caries.
 Asyptomatic but if left untreated, root

caries can progress into pulpal infection
resulting in local infection of surrounding
bone and gingival tissue.
 Formation of a permanent tooth
generally completes in three
years after its eruption into the
oral cavity but this doesnot
apply to maturation of apex.
 Remodeling/deposition of the
cementum occuring at the apex
is an aging process.
 This probably occurs to
compensate for the attrited
enamel, or due to physiological
mesial migration of teeth, or as
a response to occlusal forces.
 As a sequelae to depostion, there is an increase in
the overall distance from the root apex to the
apical constriction of the root canal.
 Working length of a tooth is relatively shorter
from the radiographic apex for an aged tooth than
it is for a young adult.
 Diameter of the apical foramen does not change
with age.
 D. Arola, R.K. Reprogel carried out a study to evaluate effects
of aging on the mechanical behavior of human dentin and
concluded :
 The maximum flexure strength and energy to fracture dentin
decreases with age.
 The mean flexural strength of dentin beams from the youngest

patients (17) exceeded 140MPa, whereas dentin beams from
the oldest patients exhibited a mean strength of less than
80MPa.
 There is a reduction in the fatigue strength of dentin and

becomes more brittle with age.
 Theold dentin was less tolerant to damage than
young dentin.
 Microcracks were more prevalent in young dentin
and provided evidence of an increased ability to
withstand fatigue damage.
 Based on differences in the stiffness history and
microcrack density, aging appears to result in an
increase in both the rate of damage initiation and
propagation in dentin.
 Although the dentinal thickness may aid in pulpal
protection, the pulp itself decreases in its
reparative capabilities with age.
 The pulpal blood flow declines due to a decrease

in the number of blood vessels, and an increase in
calcified tissues in pulp.
 MRI findings suggest a decline in pulp signal

intensity.
 Pulpstones, benign masses of mineralization
within the pulp chamber, occur in approximately
6–7% of normal pulp in older adults.
 Theresults of these physiologic changes along

with dentinal thickness decrease pulpal resiliency
and its ability to sense insult.
 Orbans textbook of oral histology and embryology 12
th edition.
 Pathways of pulp by Stephen Cohen : 9th edition.
 Normal Aging of Teeth Gregory An, Biology of Aging.
 Effects of aging on the mechanical behavior of human
dentin D. Arola, R.K. Reprogel. Biomaterials 26 (2005)
4051–4061
 Age-related transparent root dentin: mineral
concentration, crystallite size, and mechanical properties.
J.H. Kinneya,, R.K. Nallab, J.A. Poplec, T.M. Breunigd,
R.O. Ritchieb
 Sex- and Age-related Differences in Primary and
Secondary Dentin Formation. U. Zilberman, P. Smith
 Pulp stones: a review R. Goga1, N. P. Chandler2 & A. O.
Oginni3. International Endodontic Journal, 41, 457–468,
2008

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Presented by:-

 Associated with changes in

 Although their numbers do not increase with

• Thickening at the incisal edge

•These phenomena results in an

Crystal size increases

Reduction in pore size within the substance of enamel.

Decrease in permeability and water content

 Physiologicsecondary dentin, which forms

Site of formation: entire pulpal Site of formation: localized (eg

Tubules: wavy course, decrease in Tubules: wavy and twisted course,

 More highly mineralized,

 Seen first near the root apex

 Spreads upwards from the

 This is one of the criteria used

Secondary dentin grows inwardly into the pulp chamber

Tubular lumen becomes obturated by peritubular dentin.

Decrease in sensation to hot and cold stimuli.

 Decrease in the number of cells and apparent

 Fibroblasts and Odontoblasts show

 Ultrastructural studies reveal an increase in

• Atherosclerotic changes are seen in small

• Intimal layer of the vessel is thickened

• Myelin sheath changes and terminal axon

 True -Made of dentin and lined by odontoblasts ,found close to

 False -Formed from degenerating cells which mineralize, usually

Adherent -Stone attached to wall

Embedded -Stone enclosed within

 Xerostomia, a common symptom in older

 Asyptomatic but if left untreated, root

 The mean flexural strength of dentin beams from the youngest

 There is a reduction in the fatigue strength of dentin and

 The pulpal blood flow declines due to a decrease

 MRI findings suggest a decline in pulp signal

 Theresults of these physiologic changes along

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