The document discusses various age-related changes that occur in oral tissues. It describes changes at the macroscopic, microscopic, and cellular levels in tissues like enamel, dentin, pulp, cementum, periodontal ligament, alveolar bone, gingiva and salivary glands. With increasing age, the oral tissues show signs of wear and tear like cracks, discoloration and loss of elasticity. There are also changes in vascularity, cellularity and thickness of various tissues. The rate of tissue turnover reduces with aging affecting the structure and function of oral tissues.

1. `
AGE
CHANGES IN
ORAL TISSUES
SHRAVYA.M

2. CONTENTS
 INTRODUCTION
 DEFINITIONS
 CAUSES OF AGING
 THEORIES OF AGING
 FACTORS AFFECTING AGING
 AGE CHANGES IN ORAL TISSUES
 MACROSCOPIC AGE CHANGES
-ATTRITION -CRACKS
-ABRASION -ABFRACTION
-EROSION -COLOUR CHANGE

3.  MICROSCOPIC AGE CHANGES
-AGE CHANGES IN ENAMEL
-AGE CHANGES IN DENTIN
-AGE CHANGES IN PULP
-AGE CHANGES IN CEMENTUM
-AGE CHANGES IN PDL
 FUNCTIONAL AGE CHANGES
 AGE CHANGES IN SALIVARY GLANDS
 AGE CHANGES IN TASTE ( TONGUE)
 AGE CHANGES IN PALATE
 AGE CHANGES ON ORAL MOTOR PERFORMANCES
 AGE CHANGES IN TMJ

4.  AGE CHANGES IN MAXILLA & MANDIBLE
 RESIDUAL RIDGE RESORPTION
 AGING & FORENSICS
 IMMUNOSENESCENCE
 PROGEROID SYNDROMES
 REFERENCES

5. Introduction
• Aging is the accumulation of changes over time.
• Aging in humans is a multidimensional process.
• Like any tissue in human body, dental tissues also
undergo changes from the time of development as
the age advances

6. GROWTH
Growth is increase in size.
DEVELOPMENT
Development is progress towards maturity.
MATURATION
The stabilization of the adult stage brought about by the
growth and development
TODD

7. Definition
• According to Comfort (1956)
Aging is defined as biologic process that causes
increased susceptibility to disease.

8. • According to Athens & Papas
Defined as the sum of all morphologic & functional
alterations that occur in an organism and lead to
functional impairment which decline the ability to
survive stress
• According to Carranza
Aging 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

9. GERONTOLOGY
According to Pederson & Loe :
Is the study of aging in all its aspects
biologic,physiologic,sociologic &
psychologic.

10. GERIATRIC DENTISTRY
• “ Geriatric Dentistry is the
branch of dentistry that
emphasizes dental care for
the elderly population and
focuses upon patients with
chronic physiological,
physical and/ psychological
changes or morbid
conditions/ diseases “

11. IMMUNOSENESCENCE
• Declined function of the immune system with advanced
age resulting in increased susceptibility of elderly
individuals to microbial infections
• is mainly due to the host immune response toward the
micro-organisms and their products than the organism

12. • In 2000, Franceschi et al. coined the term
“INFLAMMAGING” in order to refer
to a low grade pro-inflammatory status
appearing during the aging process.

13. CAUSES OF AGING
• Aging is the end result of various biological processes :
 Genetic causes :
Where information for the initiation & maintainace of cellular
functions are encoded
 Cellular causes :
Where integrity of somatic cells is maintained
 Organ & Organ System Level :
Where physiologic functions are performed
 Coordination Level:
 Physiologic functions are controlled & assembled into complex
function

14. MOLECULAR LEVELS
MOLECULE DAMAGE
DNA Mutations, epimutations, base
modifications, strand breaks
RNA Base modifications, miscoding
PROTEIN Amino acid modifications, miss
incorporation, miss folding,
aggregation
Carbohydrates, lipids, and
molecular conjugates
Advanced glycation end-
products (AGE), lipofuscin

15. SENESCENCE SIGNALS
• p53
• p16
• p21
• pRB
• INSULIN GROWTH FACTOR-1

16. THEORIES OF AGING
• MEDVEDEV Listed 300 theories that have been
offered in an attempt to answer this but nothing
conclusive comes.
• The abundance of theories indicate the multitude of
interpretations possible on aging.

17. 1)Wear And Tear Theory
2) Mathematical Theory
3) Cellular Interaction Theory
4) Collagen Theory
5) Waste Product Theory
6) Endocrine Theory
7) Calcium Theory
8) Somatic Mutation
9) Autoimmune Theory
10)Circulatory Deficiencies Theory

18. WEAR AND TEAR THEORY
• Wear and tear theory
postulates that the
organism wears out with
age.
• Each cells contains
some specific amounts
of vital substances such
as enzymes and once
these substances are
used up these are not
replaced.
• This leads to death of
the cells and finally
death of organism

19. • Cellular interaction theory is based on the
dependence of every part of the body on every
other part.
• Eg. All the endocrine glands are dependent on
each other for proper functioning.
• Individual cells in any organ are dependent on
their neighboring cells.
• Any alteration between these will lead to aging of
individual.
Cellular interaction theory

20. Collagen theory
• Collagen theory postulates that
collagen fibers form continuously at a
slow rate and the collagen is eliminated
slowly .
• As there is more and more formation
of collagen fibers they lead to chocking
of the cells of tissue.
• Thus hampering the functions of tissue
and finally leads to cell death.

21. Waste Product theory
Metabolic waste products
are not continuously
excreted from the cells and
intercellular fluids.
With the time this leads to
altered functions and
ultimately organism is
poisoned and finally
leading to its death

22. Endocrine
functions slowly
decrease and
cell metabolism
is slowly
affected
adversely
ENDOCRINE
THEORY

23. Calcium theory
Aging is caused by defect in
calcium metabolism.
According to Selye when
large doses of Vitamin D
and parathyroid hormone
were administered in rats, it
resulted in mineralization of
many soft tissues.
Such changes resembled the
changes seen in aged tissue.
Injury to the tissue results in
calcification
(Caliciphyloxis) rendering
the tissue non functional

24. Somatic Mutation theory
Somatic cells of the body develops
spontaneous mutation.
As more and more cells mutate, an
appreciable number of cells eventually
becomes mutants.
Almost all the cell movements are
deleterious and eventually the organ
becomes inefficient.
SOMATIC MUTATION THEORY

25. Autoimmune Theory
• Autoimmune reaction develop when
some of the cells of the body synthesize
proteins that differ immunologically
from other bodily proteins.
• These altered proteins cause anaphylactic
reaction and immune reaction in the
body.
• Further lymphocytes from elder patient
have impaired proliferated capacity when
stimulated.
• Thus immune system may be
compromised in elderly

26. Circulatory Deficiency theory
Circulatory deficiency result
in deficient oxidation of
cells, resulting in cell death
and further replacement by
collagen with increase in
collagen deposition more
capillaries are choked off
resulting in more anoxia.

27. Free radical theory
Introduced by R.Gerschman,1954
• Free radical is a molecule that has one free electron…
• Free radical activity is required to produce energy,
maintain immunity, nerve transmission….
• But free radicals also attack cell membranes producing
metabolic waste products – LIPOFUSCHINS.
• Lipofuschins interfere with the ability of the cells to
repair and reproduce themselves
FREE RADICAL THEORY

28. The Telomerase Theory
• Monumental progress in aging research
• States that Cells undergo finite number of replications
& The chromosomes shorten a bit with each cell division
until some critical point is reached
• At that point cell become dormant & dies
• These end point are called telomere.
• Thereby aging

30. FACTORS AFFECTING AGING
GENETIC
1.MUTATIONS: Several mutations reduces life span
2. SPECIES SPECIFIC LIFE SPAN :-Each species is
characterized by its own pattern of aging & maximum life
span
3. HYBRID VIGOR :- Out breeding enchancement
-The effect of genetic constitution on longevity is perhaps
best exemplified where hybrid vigor is demonstrated

31. 4. SEX :- In humans/animals, female lives longer.
5. PARENTALAGE :- Like father like son.
6. PREMATURE AGING SYNDROME :- Single gene
changes results in premature senscence in humans
e.g. progeria, cockayne’s syndrome, werner’s syndrome

32. Environmental factors
1. PHYSICAL AND CHEMICAL :- Pollution, radiations,
working atmosphere etc
2. BIOLOGICAL FACTORS :- Nutrition, general health etc
3. PATHOGENS AND PARASITES :- They influence the
rate of human development low income group
4. SOCIOECONOMIC CONDITIONS :- Bad housing,
stresses etc

33. General affects
*Tissue desiccation *Altered cell permeability
*Decreased elasticity *Diminished reparative capacity

34. •
Thus Age related changes do not occur
uniformly in individuals, but they are under the
influence of genetic and environmental
factors.

35. AGE CHANGES IN ORAL
TISSUES
TISSUE CHANGES
FUNCTIONAL CHANGES
1. Teeth
2. Periodontium
-Bone
- Periodontal ligament
-cementum
3.oral mucous membrane
1.Salivary
2.Taste
3. Deglutition
4.Oral motor function
5. TMJ

36. ENAMEL
Tissue Changes
Macroscopic
• Dark In Colour
• Attrition, Abrasion , Erosion
• Longitudinal Cracks
• Brittle
• Decay resistant

37. ATTRITION
“It is defined as loss of tooth structure resulting from direct
functional forces between contacting teeth”

38. A)Proximal surface attrition (Proximal surface faceting)
- Caries susceptible , ↓ cleansibility ,
- Drifting Decreased arch length
• B) Occluding surface attrition (occlusal wear)
• -Loss of Vertical dimension of tooth
• Loss of Vertical dimension of face + cheek biting + lip biting
• -Overclosure of mandible during functional movements, caries
prone , TMJ problems

39. ABRASION
Abrasion is defined as loss of tooth structure resulting
from direct functional forces between the teeth and
external objects.

40. EROSION
• Loss of tooth structure
resulting from chemico-
mechanical act in the
absence of specific micro-
organisms
• Also termed Abfraction .

41. LONGITUDINAL CRACKS
Excessive tensile strength at the tooth

42. • Microscopic
• Enamel rods are
reduced in number
• Perikymata(Perikymata
an external
manifestations of striae
of retzius &
Imbrication Lines)
decreases.
NEWLY ERUPTED
AGED ENAMEL

43. Chemical Changes
 Levels of N2 & FLOURINE’ therefore,inorganic matrix.
Enamel near the surface become DARKER & DECAY
RESISTANT
There is reduced PERMEABILITY & enamel becomes
BRITLLE.

45. AGE CHANGES IN DENTIN
• Dentin is laid down through out life..
• Dentinal age changes are – Changes in physical properties
-Vitality Of dentine
-Reparative Dentin
-Dead Tract
- Sclerotic Dentin
-Thickness of dentine
-Secondary dentine
-Aspartic Acid Racemization

46. Changes In Physical Properties
• Dentine becomes dark with age
• Density & mineralization increases with age
Vitality Of Dentine
• Decreases due to decrease in odontoblastic activity
Thickness Of Dentine
• Increases with age

47. REPARATIVE DENTIN
• Also called as Irregular Dentin/ Tertiary Dentin/
Irritation Dentin
• Localised close to the irritated zone of the tooth.
• Histopathologically : dentinal tubules lesser in
number, irregular, tortuous .
• Radiologically : decreased size of pulp chambers
and root canals

48. DEAD TRACTS
• Empty tubules filled with air, where odontoblast have
degenerated.
• In ground sections, they entrap air ,so appear black in
transmitted light and white in reflected light.
• Decreased sensitivity in these areas.
• Probably the initial step to form sclerotic dentin

49. SCLEROTIC
DENTINE
Sclerosis is the result
of occlusion of the
dentinal tubules by a
mineral substance
with a refractive
index similar to that
of the rest of the
dentine
Increases with age

50. Sclerotic dentine

51. Aspartic Acid Racemization
• Racemization is a natural process which will
eventually convert optically active compounds
into a racemic mixture.
• L-Amino acids → D-Amino acids
• The aspartic acid in human tooth enamel
shows increasing racemization with age.

52. • Rate constant = 8.29x10⁻⁴yr⁻ⁱ
• This rate constant suggests that in any protein
with a long in vivo lifetime, D-aspartic acid
will accumulate with age

53. AGE CHANGES IN THE PULP
• The age-related changes of the dental pulp are difficult to separate from
physiologic defensive changes
• Size and Morphology
• Compromised circulation and innervations
• Fat droplet deposition
• Odontoblastic vacuolization
• Reticular atrophy
• Pulpal fibrosis
• Hyaline degeneration,and
• Calcifications.

54. SIZE AND MORPHOLOGY
• ↓ in pulp size
• Less prominent pulp horns
• More fibrous tissue with mature collagen
• Reduction in cellular components
• Reduced ground substances

57. ODONTOBLASTIC VACUOLIZATION

58. PULPAL FIBROSIS

59. CALCIFICATIONS
Pulp calcifications

60. HYALINIZATION
OF
INJURED CELL
VASCULAR
DAMAGE
FIBROSIS

62. PULP STONES
AGE INCIDENCE
(ORBAN,S)
a) 10-30 Yr 66%
b) 30-50 Yr 80%
c) > 50 Yr 90%

67. Calcific Metamorphosis

68. • GINGIVA
(Epithelium)
• Thinning and decreased keratinization of gingival epithelium
• Increased width of attached gingiva
• An increase in epithelium permeability to bacterial antigens
• Decrease resistance to trauma
• Reduced stippling
• Flattening of rete pegs, altered density.
• Gingival recession
AGE CHANGES IN THE
PERIODONTIUM

69. Gingival Connective Tissue
• More dense and coarse connective tissue.
• Quantitative & Qualitative changes in collagen:
*↑ in tensile strength of collagen fibrils
*↑ in thermal contraction
*↓ in extensibility
*↓in ratio of ground substance to collagen
*↓ in amount of soluble collagen
*↓ in collagen turnover
*↓ in water content
* ↑ resistance to proteolytic enzyme

70. PERIODONTAL LIGAMENT
• Greater number of elastic fibres
• ↓ vascularity
• ↓mitotic figures
• ↓ number of fibrous tissue
• ↑ & ↓ width of PDL space
• ↑Pocket depth
• ↓Chemotaxy, motility and proliferation rate of
periodontal ligament cells.
• Attachment of PDL fibres to cemental spikes .

71. ALVEOLAR BONE
• ↑ osteoporosis
• ↓ vascularity
• Alveolar socket appear jagged and uneven
• Fewer fibres attached to Bone and Cementum
• Marrow space have fatty infiltration
• Bone loss
• Increase in distance between crest of a alveolar bone and CEJ -
2.81mm

72. • Recent observations with
bone graft preparations
from donors more than
50years showed less
osteogenic potential
when compared with
younger age group.

73. • Rate of formation diminishes with age-
scalloped IRREGULAR SURFACE
• A thickening of cementum at the apex
may obstruct the canal
(HYPERCEMENTOSIS).
•  in cemental width(5-10 times).
•  in width is greater APICALLY &
LINGUALLY
CEMENTUM

74. • Acellular Cementum with increasing age.
• Calcified bodies called CEMENTICLES are found in PDL in
older individual.
• Cemental Spikes : Due to scalloping of cementum PDL fibres
appears to be attched to the scalloped peaks.
EXCEMENTOSIS
As cementum thickens with age it envelops these
masses(CEMENTICLES) & called as EXCEMENTOSIS

75. • Thinning
• Loses elasticity and becomes atrophic
• Smooth Gingiva
• Increased keratinization of lip mucosa
• Increase in number of mast cells.
• Progressive loss of sensitivity due to fibrosis
• Flattening of rete ridges
• Less moist
• Fordyces granules increase in number.
AGE CHANGES IN ORAL
MUCOUS MEMBRANE

76. • Stratum Corneum- Decreased keratinization →Smooth mucosal
surface
• Stratum Spinosum – Reduction Of Thickness → Frequent
Ulcerations
• Basal Layer- Hyperactivity Of Melanocytes → Dark
Pigmentation
• Submucosal Membrane → Reduction Of Elastic Fiber

77. Age Changes In Tongue
• Dorsum surface shows loss of filiform papilla
• Foliate papillae more prominent.
• Fissures increase
• Dryness of the mouth
• The ventral surface of the tongue shows the presence of
nodular varicose enlargement also known as caviar
tongue
• Loss of tastebuds with age

78. Caviar tongue

79. • The thickness of epithelium of lingual mucosa decreased with aging
• Acinar atrophy of lingual gland increased with aging, especially
quickly in females.
• The atrophy of the acinus from-
-40 years old in Blandin-nuhn gland
-30 in von Ebner gland.
• Lingual muscles Decrease in muscle fiber diameter with aging is also
observed

80. AGE CHANGES IN SALIVARY
GLANDS
Age Changes are
- Acinar Atrophy,
- Ductal Dilatation,
- Fatty infilteration,
- Fibrosis,
-Peri Acinar Callus
-Inflammatory Infiltration
-Oncocytes
• Submandibular gland – 40% loss of acinar cells
• Parotid gland - 30% loss of acinar cells
• Minor labial glands - 45% loss of acinar cells
formation

81. Some of the ductal and acinar cells transform into non
functional cells called ONCOCYTES. •
These cells have swollen appearance eosinophilic
granular cytoplasm and pyknotic nucleus.
Protein plugs are found more frequently in ducts of
older salivary glands. These ducts have a tendency to
calcify.

82. ONCOCYTES

84. Salivary flow
• It is generally believed that salivary flow decreases
with age
But
This reduction in flow is more as a consequence of
xerogenic medication taken by an older individual
rather than due to the physiologic process of aging

85. Change in Composition
•↑ Phosphorous and calcium content
• No change in potassium
•↓Sodium
•↓Chloride and protein
concentration
•↓Viscosity of saliva

86. AT BIRTH
• Mouth of full term foetus is sterile
• After birth it acquires from mother and from the
environment
• Consists: streptococcal
staphylococcal species
Lactobacilli
Bacillus, Neisseria and Yeasts.
• Mainly Streptococcus salivarius with
Staphylococcus albus.
ORAL MICROBIAL CHANGES

87. At Infancy And Early Childhood
• ↑microorganisms .
• The eruption of deciduous teeth provides a new attachment
surface and turns Streptococcus sanguis and mutans as regular
inhabitants of oral cavity.
• Anaerobes are few in number due to absence of deep gingival
crevice.
• Actinomyces , Lactobacilli are found regularly

88. Adoloscence
• Max increase in the microbes
• Mainly because of the varied tooth morphology
Adulthood
• Complex microflora
• As the teeth are lost the available sites for microbial
colonisation decreases and several species diminish.
• Edentulous persons harbour few Spirochetes or Bacteroides.
• S.sanguis & mutans disappear

89. Immune Factors
• IgA
• IgM
• C3 specific immune factors
• Nonspecific immune factors such as
lactoferrin, lysozyme and lactoperoxidase were
higher in plaque of older age group

90. Changes In Oral Motor Function
SPEECH MASTICATION DEGLUTITION
• TISSUES INVOLVED ARE :-upper lip, lower
lip , jaws, tongue, floor of oral cavity, soft
palate etc.

91. SPEECH
Speech production is most resistant to aging but that
does not mean there are no age related changes in
speech.
• You can very well perceive differences when person of
old age speaks but these are largely related to
LARYNGEAL rather than oral events.
• The main identifying feature of older speech is an
increase in the fundamental frequencies
OTHER SPEECH CHANGES MAY OCCUR DUE TO:
• EDENTULOUS PATIENT(partial or complete)
• ILL FITTING PROSTHESIS.

92. MASTICATION AND DEGLUTITION
↓Masticatory activity
↓Biting Force (16%)
People chew slowly as they get older
Older adults are capable of fewer swallows in a 10 second period
of time than younger adults
Even healthy older persons open their mouth less wide and chew
with less power which is thought to be related to loss of
muscle bulk with age and which is worsened in edentulous
persons

93. Age changes in jaw bones

94. Changes In Palate
• Changes in the dimensions
• Configuration
• Surface pattern of the hard
palate
• Loss of concavity
• Flat palate with the loss of
the teeth.

95. • The presence of teeth was associated with the height of
the alveolar ridge, which decreased from 7.3 +/- 4.4
mm in specimens with intact teeth to 4.7 +/- 4.1 mm in
specimens without teeth (P = 0.020).
• Less prominent Palatine rugae
• Soft palate becomes smaller in size.

96. Changes in Maxilla & Mandible
• Maxilla resorbs in UPWARD &
INWARD direction
• Mandible DOWNWARD &
OUTWARD so as to become
progressively wider thereby leading
to class-III relation

97. Longer the maxilla is edentulous,
smaller the denture bearing area
• Incisive foramen becomes
closer to the residual ridge

99. Residual Ridge Resorption
Consequences of Residual Ridge Resorption
# Apparent loss of sulcus width and depth
#Displacement of muscle attachment closer to crest of the residual ridge
# Loss of vertical dimension of occlusion
# Reduction of the lower face height
#Anterior rotation of mandible
#Increase in relative prognathism
#Changes in interalveolar ridge relation
#Morphological changes in alveolar bone such as sharp ,shiny uneven
residual ridge

100. AGE CHANGES IN FORAMENS
• With the resorption of the alveolar process the mental foramen
lies at or near the level of the upper border of ramus.
• Denture wearers might face problems due to application of
pressure on the mental nerve

101. AGE CHANGES IN GENIAL TUBERCLES
• The genial tubercles project above the upper
border of the mandible in the symphyseal
region.
• These sharp prominence make wearing of the
lower denture painful

102. AGE CHANGES IN TMJ
• With increasing age the joint tends to lose its ability
to withstand degenerative changes and shows
progressive change comparable to those seen in
osteoarthrosis.

103. • Articular disc – May show islands of cartilage and
nodules of calcification Joint space – Encroachment
of large villi of the synovial membrane into the joint
cavities after the age of 50

104. AGE CHANGES IN MAXILLARY SINUS
• Infants & Children – Higher Than The Nasal Floor
• Adolescence – Level With The Nasal Floor
• Adults – Lower Than The Nasal Floor
• Old Age – Level With The Nasal Floor

105. AGING AND FORENSICS
• The techniques used to estimate age by means of
teeth include
Gustafson's technique
Incremental lines of Retzius
Perikymata
Prenatal and postnatal line formation
Racemization of collagen in dentin
Cemental incremental lines and
Translucency of dentin.

106. Gustafson used six dental changes connected with aging
namely
Attrition,
Apical Migration Of Periodontal Ligament,
Deposition Of Secondary Dentin,
Cemental Opposition,
Root Resorption And
Transparency Of The Root Dentin

107. PROGEROID SYNDROME
• Progeroid syndromes (PS) are a group of rare
genetic disorders that mimic physiological
aging, making affected individuals appear to
be older than they are

108. • Werners Syndrome
• Rothmund –Thomson Syndrome
• Blooms Syndrome
• Hutchinson Gilford Progeria Syndrome
• Cockaynes Syndrome
• Restrictive Dermopathy
• Xeroderma Pigmentosum
• Trichothiodystrophy

109. WERNERS SYNDRROME

110. BLOOMS SYNDROME

111. COCKAYNES SYNDROME

112. ROTHMUND THOMSON
SYNDROME

113. HUTCHINSON GILFORD PROGERIA
SYNDROME

115. To conclude…

116. REFERENCES
• Jose.M: Essentials Of Oral Biology, CBS
• Nanci. A: Ten Cates Oral Histology, 8th Ed, Elsevier
• Kumar. G S : Orban’s Oral Histology & Embryology, 13th Ed ,
Elsevier
• Berkovitz. B K B: Oral Anatomy , Histology And
Embryology,3rd Ed, Mosby
• Gerlad Shklar ;The Affect Of Aging Upon Oral Mucosa
• Robbins General Pathology Kumar /Cotran

117. • Polyamines In Aging And Disease ;Aging Aug 2011 Vol 3
No,8
• Aging –Programmed Change Dcna, Geriatric Dentistry
1989;33 19-22.
• Effect Of Age On Periodontium U Van Der Velden J Clin
Periodont 1984; 11:281-294.
• Periodontics Grant 6th Edition Carranza’s Clinical
Periodontology 9th And 10th Edition

118. • Patricia Masters Helfman* And Jeffrey L. BADAT “Aspartic
Acid Racemization In Tooth Enamel From Living Humans”
1975
• Age related changes of the dental pulp complex and their
relationship to systemic aging. (oral surgery oral medicine
oral pathology,December 1991,721- 745)
• Dorrit W.Nitzan, et al : The effect of aging on tooth
morphology : A study on impacted teeth. Oral Surg Oral Med
Oral Pathol. 61 : 54-60 : 1986.

120. Bullets
1. Bodies seen in reduced inflammation
2. Osteodentine – a type of reparative dentine ..consists entrapped odontoblasts or fibroblasts with
fewer dentinal tubules resembling bone.
3. Compensatory curves in aging
4. Clinical crown and anatomic crown
5. Proteins expressed in rep dentine
6. Sclerotic dentine and dead tracts
7. Enzymes in bone remodelling –acid phosphatase and alk.phosphatase, pyroposphatase
8. Cell rests of malazzez degenerate???
9. Reason for formation of rep dentine
10. Y der is an increase in mast cell population
11. Y der is decrease in bone mass density
12. Y resorption is more in mandible
13. Tmj
14. Diff between pri ,sec & rep dentine
15. Age changes r damaging or protective??
16. List age changes which r damaging
17. Age changes in pdl