As teeth age, several changes occur in the major tissues: - Enamel becomes darker, develops cracks, and increases in mineral content, making it more resistant to decay. Dentin also increases in mineral content, forming secondary dentin and occluding dentinal tubules. This decreases pulp size and sensitivity. The pulp exhibits decreased cellularity, vascularity, and reparative ability with age. These anatomical and physiological changes are natural aging processes that can impact dental treatment for older patients.

1. Age Changes in Enamel,
Dentin and Pulp

2. • 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.

3. Major Tissues of the Tooth
The completely formed teeth and the periodontium should remain intact and
fully functional without disease for a lifetime.

4. Age changes in Enamel
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

5. MACROSCOPIC CHANGES

6. COLOUR
• Becomes darker with
age.
• Associated with changes
in the organic portion of
enamel, presumably near
the surface.

7. ATTRITION ,ABRASION AND EROSION
Attrition Abrasion
Erosion

8. ATTRITION
• Physiologic wear of the occlusal surfaces and
proximal contact points as a result of
mastication.
• Evidenced by a loss of vertical dimension of
the crown and by flattening of the proximal
contour.
Causes
• Masticatory stress
• Para-functional habits

9. Stages of Attrition
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

10. ABRASION
• Pathological wearing away of tooth
through abnormal mechanical processes.
e.g.- abrasive dentifrice
- occupational
- improper flossing

11. EROSION
• Loss of tooth substance by a chemical
process that does not involve known
bacterial action.
• Lingual erosion
e.g. -chronic vomiting
-acidic carbonated
beverages

12. LONGITUDINAL CRACKS
• May be developmental in origin.
• Although their numbers do not increase
with age , they become more obvious.

13. Site-specific thickness of
enamel
•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

14. MICROSCOPIC CHANGES

15. PERIKYMATA
• 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

17. PERMEABILITY TO FLUIDS AND
WATER CONTENT
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

18. Continuous deposition
of fluoride and nitrogen
on enamel surface
Increase in fluoride
concentration of
enamel
Increased resistance to
decay
Hardness and Elastic
modulus of enamel
increases .
Increases the brittleness of
teeth and decreases
permeability.
Cracks

19. Age changes in Dentin
• Two major changes in
dentin:
• Formation of secondary
dentin.
• Sclerosing or obturation
of the dentinal tubules. A- dead tract
B- sclerotic dentin

20. Secondary dentin
• Secondary dentin forms after the
complete formation of the tooth.
Types:
• Physiologic secondary dentin, which forms
with normal stimulus,
• Reparative secondary dentin, which forms
with traumatic or abnormal stimulus.

21. Types of secondary dentin
Regular
Cause: mild stimuli (slow attrition,
slowly progressing caries)
Site of formation: entire pulpal
surface (thicker on pulp roof
and floor)
Tubules: wavy course, decrease
in number
Clinically:
The increase of the dentin
thickness and the closure of
the pulp horns make it much
less possible to expose the
pulp chamber during
preparation.
Irregular
Cause: severe stimuli, severe
attrition, erosion, deep
caries.
Site of formation: localized (eg
pulp horn)
Tubules: wavy and twisted
course, decrease in number
or atubular
Clinically:
Functions as a barrier for
against caries.

22. Physiologic regular secondary dentin
Secondary D
Primary D

23. Odontoblas
ts are cut
Degenerate
Replaced by the
migration of
undifferentiated
cells from cell
rich zone
Odontoblasts
are cut
Live
odontoblast
s
Reparative
Dentin
Reactionar
y/Regenera
ted
Dentin
Extensiv
e
abrasion
,
Erosion
,caries
REPARATIVE /REACTIONARY DENTIN

24. DEAD TRACTS
• 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

25. TRANSLUCENT OR SCLEROTIC DENTIN
• 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
Young dentin Adult dentin Sclerotic denti

26. Sclerotic dentin
Appears light in transmitted light and dark
in reflected light

28. Decrease in sensation to hot and cold stimuli.
Tubular lumen becomes obturated by peritubular dentin.
By age 80, almost all dentinal tubules are fully occluded.
Secondary dentin grows inwardly into the pulp chamber
decreasing the chamber’s size .
Age related Sensitivity changes

29. Age changes in the pulp
• 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.

30. • 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

31. 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.

32. 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.

33. Pulp stones
• 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

34. 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.

36. • Fibrodentine -Material produced by
fibroblast-like cells against dentin prior to
differentiation of a new generation of
odontoblast-like cells.
• Dystrophic calcification -Inappropriate
biomineralization of the pulp in the
absence of mineral imbalance.

37. Root Caries: An Epidemic of Aging Teeth
• 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

38. ENDODONTIC CONSIDERATIONS
• 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

39. • 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.

40. • 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.

41. • The old 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.

42. Summary
• 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.

43. • Pulp stones, benign masses of
mineralization within the pulp chamber,
occur in approximately 6–7% of normal pulp
in older adults.
• The results of these physiologic changes
along with dentinal thickness decrease
pulpal resiliency and its ability to sense
insult.

44. REFERENCES
• 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

45. • 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