This document summarizes age-related changes to the periodontium. It discusses how aging affects tissues like the epithelium, connective tissue, periodontal ligament, cementum and alveolar bone at the cellular level through intrinsic changes like decreased cell renewal and stochastic changes due to mutations. It also reviews theories of aging and describes functional, physiologic and clinical changes that occur with age like gingival recession and bone loss. The document provides an overview of considerations for treating aged patients and the effects of aging on wound healing and prognosis.

1. 1

2. SEMINAR ON
AGE CHANGES
IN PERIODONTIUM
Presented by
Dr. Vartika Srivastava
Pg I yr
2

3. CONTENT
 Age Related Changes
In;
 Epithelium
 Connective Tissue
 Periodontal Ligament
 Cementum
 Alveolar Bone
 Bacterial Plaque
 Gingival Recession
 Immune Response
 Introduction
 Factors Influencing
Aging
 Theories of Aging
 The Aging
Periodontium;
 Intrinsic Changes
 Stochastic Changes
 Physiologic
Changes
 Functional Changes
 Clinical Changes
3

4.  Treatment Of Aged Patients
 Wound Healing In The Aged
 Prognosis
 Conclusion
4

5. INTRODUCTION
The aging process may be defined as the sum of all
morphologic and functional alterations that occur in
an organism and lead to function impairment, which
decreases the ability to survive stress.
Comfort (1956) defined aging as a biological process
that causes increased susceptibility to disease.
With age, there are physiologic and structural
alternations in almost all organ systems.
5

6. Gottlieb & Orban – Believed that with age, gingival
recession and alveolar bone resorption occur and
termed it as Senile Atrophy.
Aging in individuals is affected to a great extent by
genetic factors, diet, social conditions and
occurrences of age related diseases, such as
atherosclerosis, diabetes, and osteoarthritis.
Aging induced alterations in cells are an important
component of aging of the organism.6

7. Tencate – Stated that studies on the age changes
in the periodontium are on the whole, fairly
inconclusive.
The World Conference on Periodontology in 1966
reviewed only the few reports in the literature
which dealt with the apical downgrowth of
attachment epithelium, the width of periodontal
ligament and isolated changes in the gingiva.
7

8. Society has long held the belief that tooth loss is
an inevitable consequence of aging.
 The success of both increased health awareness
and preventive dentistry have led to decreasing
tooth loss for all age groups.
Thus it is important not only to review aging
effects in isolation but also from the prospective
of their clinical significance to the disease
process and their possible effect on the
treatment outcomes.8

9. CELLULAR AGING
Cellular aging is progressive decline in the
proliferative capacity and life span of cells and the
effects of continuous exposure to exogenous
influences that result in the progressive
accumulation of cellular and molecular damage.
9

10. REPLICATIVE SENESCENCE:
The concept that cells have a limited capacity for replication
was developed from a simple experimental model for
aging.
Normal human fibroblasts, when placed in tissue culture,
have limited division potential.
Cells from children undergo more rounds of replication
than cells from older people.
After a fixed number of divisions, all cells become arrested
in a terminally non-dividing state, known as Cellular
Senescence.
Many changes in gene expression occur during cellular
aging.
10

11. 11

12. Structural And Biochemical Changes With
Cellular Aging
A number of cell functions decline progressively
with age and there are morphologic alterations in
aging cells.
12

13. 13
Oxidative
phosphorylati
on by
mitochondria
is reduced; as
is synthesis
of nucleic
acids and
structural and
enzymatic
proteins, cell
receptors,
and
transcription
factors.
Cells have a
decreased
capacity for
uptake of
nutrients and
for repair of
chromosomal
damage.
Irregular and
abnormally
lobed nuclei ,
pleomorphic
vacuolated
mitochondria,
decreased
endoplasmic
reticulum,
and distorted
Golgi
apparatus.
Accumulation
of the
pigment
lipofuscin, is
a tell tale
sign of
oxidative
damage.
Accumulation
of advanced
glycation end
product, due
to non-
enzymatic
glycosylation
which are
capable of
cross linking
adjacent
proteins.

14. 14

15. 15

16. 16

17. Polyamines are polycations that interact with negatively
charged molecules such as DNA, RNA and proteins.
They play multiple roles in cell growth, survival and
proliferation.
Changes in polyamine levels have been associated with
aging and diseases.
Their levels decline continuously with age .
17

18. 18

19. FACTORS INFLUENCING AGING
Aging is due to complex interaction of hereditary and
epigenetic factors with environmental factors.
19
Genetic
factors Environmental
factors

20. 20
Environmental Factors:
 Physical and chemical
components of the
environment, such as
radiation may affect aging.
 Biologic factors such as
nutrition.
 Pathogens and parasites .
 Socioeconomic factors, such
as bad housing, poor
working conditions, or the
stresses of life, are
commonly believed to
accelerate the aging process.

21. Genes That Influence The Aging Process
21
Studies in drosophila, C. elegans and mice are
leading to the discovery of genes that influence
the aging process. One interesting set of genes
involves the insulin/insulin growth factor-1
pathway.
Decreased signalling through the IGF-1
receptor as a result of decreased caloric intake,
or mutations in the receptor, resulted in
prolonged life span in C. elegans .
Analyses of humans with premature aging are
also establishing the fundamental concept that
aging is not a random process but is regulated
by specific genes, receptors and signals.

22. BIOLOGIC THEORIES OF AGING
Redundanci
es
Somatic
Theory
Genetically
Programme
d
Senescence
Disposable
Soma
Theory
Error Theory
Autoimmun
e Theory
22
Genetic Theories

23. 23
Non -Genetic
Theories
Immunologic
Theory
Free Radical
Theory
Metabolic
Rate Or
Wear And
Tear Theory
Acidification
Theory
Neuroendocri
ne Theory
Collagen
Theory

24. 24

25. SOCIOLOGICAL THEORIES OF AGING:
25
Role
Theory
Disengage
-ment
Theory
Activity
Theory
Continuity
Theory
Political
Economy
Theory

26. 26
Genetic
Theories

27. ERROR THEORY :
First formulated by Orgel .
He postulated that the bio-chemical and physiologic changes
seen during aging were the result of mutations or errors in
regulatory molecules (particularly enzymes) within the cells.
The errors accumulated until a bio-chemical catastrophe was
inevitable.
27

28.  The failure to document random change was one of the
many indicators that random change was not producing
aging or put another way, that aging might be different
from accumulating disease.
 The concept that aging may be the result of programmed
change is supported by the experiment;
Individual cells, when removed from their hosts
and grown in tissue culture or when serially transplanted
into young host animals, will propagate themselves for a
finite number of divisions.28

29.  The memory of the past divisions is contained in the cell
nucleus;
If nuclei from old and young cells are transplanted
into the opposite cytoplasm the product cells will live as
long as the nucleus would have originally done.
 It has recently been reported that if young and old cells
are fused together the old nucleus will actively inhibit the
DNA synthesis in the young cell.
This implies that the old cell is actively preventing cell
division, rather than having randomly lost needed
information for cell division.29

30. Somatic Mutation Theory
If the spontaneous mutations occur in the germ
line cells , it may also occur in the somatic cells
which in turn lead to alterations in the cell and the
tissue functions leading to decline in the functional
capacities & aging.
30

31.  Redundancies:
Loss of unique , non repeated, genetic information from
the genome.
Genetically Programmed Senescence:
It is the extension of an development process.
31

32. Disposal Soma Theory
The disposable soma theory lends support to the
idea that aging results from the destruction caused
by molecules in the normal course of living,
including the havoc caused by oxygen free radicals,
and Cerami's glycolysation theory.
32

33. Cerami (1986) postulated that glucose and other
non-reducing sugars react with proteins overtime
in a non-enzymatic reaction to produce substances
which cross-link with proteins.
The accumulation of these altered proteins might
account for conditions associated with aging.
33

34. Autoimmune Theory
Autoimmune reaction developed when some of the cells
of the body synthesize proteins that differ
immunologically from other bodily proteins.
Altered proteins cause anaphylactic and immune
reaction in the body .
Lymphocytes from older patient have impaired
proliferated capacity when stimulated by mitogens .
34

35. 35

36. 36
Non Genetic
Theories

37. Immunologic Theory:
This theory will not be able to distinguish normal
molecules from the abnormal ones, thus the
abnormal cells may proliferate and autoimmune
reaction may takes place & aging may result due
the long term, minor histoincompatibility reactions
in the cell populations .
37

38. Free Radical Theory:
The free radical theory proposed by Harman in
1956, emphases the importance of the mechanism
of oxygen use by the cell.
Short lived, highly reactive chemicals produced
during normal metabolic reactions which combines
with essential molecules , causing damage to DNA
or the other structures, contribute to aging .
38

39. 39

40. Metabolic –Rate Or Wear And Tear Theory:
More the metabolic rate more will be the wear and
tear of the organism and shorter is the life span.
40

41. Acidification Theory
Aging results from the accumulation of acid
waste products.
These products are not completely excreted from
the body which leads to cellular malfunction.
41

42. Collagen Theory
Collagen fibers forms at a slow rate
The more formation of collagen fibers leads to
choking of the cell tissue.
It hampers the function of tissues and finally
cause cell death.
42

43. 43

44. Neuroendocrine Theory
First proposed by Professor Vladimir Dilman
and Ward Dean.
System is complicated network of bio chemicals
that governs the release of hormones which are
altered by hypothalamus.
44

45. 45

46. 46
Sociological
Theories

47. ROLE THEORY
When considering the role of older people in our
society , we might examine the regard in which
they are esteemed.
 Rosow (1985) identifies the major issues in role
theory as applied to the older people. Losses of
roles exclude older people from significant social
participation and revalue their contribution.
47

48. DISENGAGEMENT THEORY
Cumming and Henry (1961) stated that aging is
inevitable, mutual withdrawl or disengagement,
resulting in decreased interaction between the
aging person and others in the social system he
belongs to. The theory was seen as universal and
applicable to older people.
48

49. ACTIVITY THEORY:
Supports the maintenance of regular actions,
roles (formal or informal) and solitary as well as
social pursuits for a satisfactory old age.
(Havighurst 1963)
49

50. CONTINUITY THEORY:
The continuity theory proposed by Neugarten
(1968) focused on relationship between life
satisfaction and activity as an expression of
enduring the personality traits.
50

51. POLITICAL ECONOMY THEORY
Townsend (1981)proposes that people
experience and status in later life is the direct
consequence of political and economic policies.
He gives the following example,
Older people are forced into a structured
dependence as a result of compulsory retirement,
thus having to live on a much reduced income.
51

52. THE AGING PERIODONTIUM
Normal aging of the periodontium is a result of
cellular aging.
The aging process does not affect every tissue in
the same way.
52

53. Intrinsic
Changes
Stochasti
c
Changes
Function
al
changes
Physiolo
gic
Changes
Clinical
changes
53

54. Intrinsic Changes
In epithelium a progenitor population of cells
(stem cells)is situated in the basal layer ,
provides new cells.
These cells of the basal layer are the least
differentiated cells of the oral epithelium.
54

55. 55

56. This differentiated cell or epithelial cell can no
longer divide.
There is constant source of renewal.
In the aging process , cell renewal takes place at
a slower rate and with fewer cells ,so the effect
is to slow down the regenerative processes.
56

57. By the action of gerontogene or replicative
senescence (Hayflick’s limit and telomere
shortening), the number of progenitor cells
decreases.
Hayflick, an American microbiologist , observed
that fetal cells(i.e fibroblasts)displayed a
consistently greater growth potential (app. 50
cumulative population doublings)than those
derived from adult tissues(20-30 cumulative
population doublings).
57

58. Stochastic Changes
These changes occurring within cells also affect
tissue; for example , glycosylation and cross
linking produce morphologic and physiologic
changes.
Structures become stiffer ,with loss of elasticity
and increased mineralization.
58

59. Somatic mutations lead to decreased protein
synthesis and structurally altered protein.
Free radicals contribute to accumulation of waste
in the cell.
59

60. Physiologic Changes
In the periodontal ligament , a decrease in the
number of collagen fibres , leads to a reduction
or loss in tissue elasticity.
With aging ,the alveolar bone shows a decrease
in bone density and increase in bone resorption.
60

61. Functional Changes
With aging , the cells of the oral epithelium and
periodontal ligament have reduced mitotic
activity and all cells experience a reduction in
metabolic rate.
There is reduction in healing capacity and rate.
61

62. Clinical Changes
Gingival recession and reductions in bone height.
Attrition is a compensatory change that acts as a stabilizer
between loss of bony support and excessive leveraging
from occusal forces imposed on the teeth.
A reduction in “overjet” of the teeth is seen ,manifesting as
an increase in edge to edge contact of the anterior teeth.
62

63. 63

64. 64

65. REFERENCES
ROBBINS GENERAL PATHOLOGY KUMAR /COTRAN
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
65

66. SEMINAR ON
AGE CHANGES IN
PERIODONTIUM
PART -II
Presented by
Dr. Vartika Srivastava
PG I yr66

67. CONTENT
67
 Age Related Changes In;
 Epithelium
 Connective Tissue
 Periodontal Ligament
 Cementum
 Alveolar Bone
 Bacterial Plaque
 Gingival Recession
 Immune Response
 Treatment Of Aged
Patients
 Wound Healing In The
Aged
 Prognosis
 Conclusion

68. CHANGES IN EPITHELIUM:
Thinning and decreased keratinization of the gingival
epithelium which leads to , an increase in permeability
to bacterial antigens and decreased resistance to
functional trauma or both.(Shklar 1961).
But the study conducted by Zarb et al 1998 found no
differences in the gingival epithelium of both humans
and dogs .
68

69. Flattening of the rete pegs (Shklar 1966)
Height of epithelial ridges increases with age
(Wentz 1952 )
Connective ridges is prominent in younger
individual where as connective papilla is
predominant in elders ( Loe & Karring 1972)
Increased cell density (Shklar 1966)
69

70. There is uncertainty about mitotic activity of the
epithelial cells with some reporting an increase with
age (Toto etal 1975) , constant rate (Ryan etal 1974)
and Karring and Loe (1973) indicate decrease in
activity,
These may be related to level of inflammation present
in this tissue prior to harvesting (Van der valden 1984
) .
70

71. CHANGES IN CONNECTIVE TISSUE
Number of gingival vessels increased with age
while the percentage of vessels exhibiting active
blood flow decreased
Red blood cell velocity showed no statistically
significant change with age, although a trend
toward decrease with age is observed.
71

72. Peripheral oxygen saturation was lower in old
compared to young and middle aged (Jacob et al
1990)
Age related increase in blood pressure was also
expected and not involved in the changes of the
gingival microcirculation .
72

73. CHANGES IN PROPERTIES OF COLLAGEN
73
Increase in tensile strength of collagen fibrils
Decrease in extensibility
Increase in thermal contraction
Decrease in ratio of ground substance to
collagen
Decrease in amount of soluble collagen
Decrease in collagen turnover
Decrease in water content
Increase resistance to proteolytic enzyme

74. CHANGES IN GROUND SUBSTANCE:
A decrease in the chondroitin sulphate to
hyaluronic acid ratio has been noted with
advancing age (Milch RA 1966).
Location of junctional epithelium has been
subject of much speculation.
74

75. In healthy periodontium, the apical termination of
the junctional epithelium is located at CEJ, just
coronal to the connective tissue fiber attachment .
With periodontitis, these dentogingival fibres are
broken down and junctional epithelium migrates
apically along the root surface.
Apical migration of the junctional epithelium can
occur in the absence of plaque and inflammatory
cells. (Skilleni 1930, Rushton 1951, Beersten et al
1982 )
75

76.  Found no relation between presence of gingivitis and
extent of apical migration of the junctional epithelium.
They did find a relation between the age of the
experimental animals and the extent of apical
migration.( Belting et al 1953, Klingsberg and Butcher
1960)
76

77. CHANGES IN PERIODONTAL LIGAMENT:
With increase in age the well organized bundle
are broad and wavy and the structure of the
ligament becomes more and more irregular.
The principal fibers of PDL become thicker and
cellularity is lessened.
77

78. Fibers are interrupted by larger interstitial spaces in
older groups. These ranged from small circular areas of
0.05mm to 0.15mm in diameter to large, oblong areas
of more than 1mm. these interruption resulted in
irregularly spaced areas of dense fiber concentration
separated by regions without suspensory fiber
attachment
The fiber and cellular contents decrease. Fewer
fibroblasts, osteoblasts and cementoblasts can be seen.
78

79. Increased fuchsinophila was evident, indicating
increased concentration of neutral carbohydrates.
Calcified bodies are common in the periodontal ligament
of elderly humans.
Two types of calcospheroid like bodies are demonstrable:
79
Larger,
irregularly
shaped
calcification
Small
rounded
calcospherite
s

80. They appear to form in relation to fiber bundles.
They coalesce to from the larger round or
irregularly shaped bodies.
Occasionally they increase in number and
appear to calcify a complete fiber bundle
producing an ankylosis.
Calcospherites have been described by Gottlieb
to the inductive activity of epithelial rests, and
their degeneration.
80

81.  Barnfield and Bartieri attributed them to inflammation.
Insofar as inflammation is concerned, globular
calcospherites were found in areas free of inflammation.
 The calcospherites may be ascribed to “age changes” gain
support from the observation of similar calcifications in
the pulps of aging humans (Bernick 1967) and other
organs (Smith JV 1971).
81

82. Epithelial rests in the periodontal ligament show alter
forms of aggregation. Rests aggregates tend to
contain more cells with both proliferative and
degenerative morphology.
The PDL has been reported to increase and decrease in
with age. Van der Velden explains this discrepancy on
the basis of the number of remaining teeth.
82

83. Width Of The Periodontal Ligament Space
 It is well known that the width of the periodontal
ligament space of nonfunctioning teeth is narrower
than that of functioning teeth (Klein 1928, Kronfeld
1931).
 If, with increasing age, less teeth are present, the force
acting on the remaining teeth may increase and an
increasing width of the periodontal ligament space with
age.
83

84.  On the other hand, it has also been noted that
the masticatory forces decrease with age
(Helkins etal 1977, Herring 1977). This could
explain decrease in the periodontal ligament
space with age.
84

85. CEMENTUM:
Cementum formation is a continuous process which
occurs throughout the life of man and animal (Gottlieb
1943). Hence, with age, the cementum increases in
width .
 Cementoblasts were few in number or lacking.
Sharpey’s fibres is present in cementum but not in
bone. (Zander 1958)
85

86. There is a tendency towards greater cementum apposition
in the apical region of the tooth in response to passive
eruption.
According to Ive et al (1980), passive eruption and
migration of teeth involves reattachment of fibers
between the cementum and the PDL for which increased
cemental deposition is required .
86

87. Cementum undergoes only minor remodeling. Although
remodeling of cementum does not normally take place,
local resorption at the cementum surface followed by
cementum apposition .
The susceptibility to resorption and the number of
resorption areas increase with age . (Henery 1951)
87

88. Increased formation leads to lack of nutrition to
Cementocytes hence they degenerate and empty lacunae
are found in the deep layers of cementum.
Cemental deposition slows in old age. Cementocytes
exhibit the lowest proliferative capacity.
With increasing age the process of cementum formation
becomes essentially acellular.
88

89. Cemental tears are frequently found and it may
be that attachment of cementum to dentin is
weakened with age or that the increase fibrosis
and increased strength of principal fibres and
decreased extensibility of collagen make the
cementum of older persons to injury.
89

90. Spurring of cementum is sometimes seen as the result
of the fusion of calcospheroid bodies near cementum or
of the calcification of epithelial rest aggregates.
Composition also changes , content of fluoride and
magnesium.
Due to gingival recession the cervical cementum is
exposed which may be lost leading to sensitivity
90

91. During cementum formation collagen fibres are embedded
within the cementum. The course of the embedded fiber
differ in various layers of the cementum depending on the
direction of the forces acting on the tooth at the moment
of cementum formation (Gustafsson and Persson 1957).
Indications exist that cemental deposition shows in old
age. Cementocytes exhibit the lowest proliferative
capacity. With increasing age the process of cementum
formation becomes essentially acellular.
91

92. Aging and Gingival Recession:
It has been determined through studies that with
age physiological apical migration of the
epithelium can occur.
 This hypothesis also fits with the continuous
passive eruption theory by Gottlieb and Orban
1936. It is postulated that has age advances a
gradual physiological recession of the gingiva
occurs concomitantly with an apical migration of
the epithelium.
92

93. The recession of the gingiva is the result of
occlusal migration of teeth compensating for
occlusal wear and a stable location of the
gingival margin. In other words the gingiva
cannot keep even pace with the migrating teeth
and consequently recession takes place.
93

94.  In contrast results from studies by Manson 1963; Anne
Roth and Fricsson 1967; Loe 1967 indicate that occlusal
movement of teeth does not imply an apical migration of
junctional epithelium. If the periodontium remains
healthy.
 As far as the location of mucogingival junction is
concerned, no changes with advancing age have been
observed. Furthermore, if no gingival recessions are
present it has been noted that gingival width increases
with age .
94

95. The phenomenon that in general the degree of
recession increases with age is well known. However,
this is not necessarily the result of aging since
mechanical trauma e.g. tooth brushing can cause
recession (Loe et al 1978).
 Recession of the gingival has also been found after
extrusion of teeth (Batenhorst et al 1974).
95

96. It may be concluded that, with regard to
migration insufficient evidence is available for a
physiological apical migration of the junctional
epithelium due to aging. It seems probable that
periodontal destruction will occur only by
mechanical trauma in the presence of plaque
and consequent inflammation of the
periodontium.
96

97. CHANGES IN ALVEOLAR BONE:
 Attrition of tooth substance on occlusal and incisal
surfaces and at the contact points is well recognized
changes of aging.
 Vertical (inter occlusal) dimension and arch continuity
are usually maintained into old age, since wear is
compensated by bone apposition on distal surfaces
and at the fundus of sockets and continuous
apposition of cementum at the apex.
97

98. 98
Experimental animals show:
Decreased width of cribriform plate with age.
Decrease width of interdental alveolar septum may be a
result of interproximal wear of the teeth at the contact
area
Transformation from immature trabeculated bone to a
dense lammellated bone.

99. Proliferative activity of the cells in the osteogenic
layer at the surface of the cribriform plate is low
compare to cells in epithelium and connective tissue.
Decreased trabeculation is often seen which may be
related to diminished functional stimulation because
of tooth loss or to the presence of osteoporotic
changes.
99

100. Severson et al (1978 )studied the age related changes in
adult human periodontal ligament.
100
The bone surface of the PDL was often irregular in outline
in contrast to that in young adults
Jagged in appearance with spicules of both lamellar and
non lamellar bone typically projecting into bundles of
suspensory fibers.
In histologic sections fibers interrupted by large
interstitial spaces appeared to lack either osseous or
cemental attachment

101. 101
The number of cells in the osteogenic layer have been found to
decrease with age.
Osteoporosis is seen commonly in post menopausal women but in
the presence of good plaque control there is no evidence that it
predisposes to loss of periodontal attachment and alveolar bone.
Areas of intermittent deposition of woven bone were seen
throughout the entire socket wall in older specimens; which
contrasts with the localization of such areas in young adults at the
distal wall of the socket and in the coronal and apical regions of
the mesial walls

102. EFFECTS ON PLAQUE
 Inorganic composition of plaque;
Kleinberg et al (1971) showed that plaque contains
higher levels of calcium and phosphorus. This
might be due to increase in the calcium and
phosphorus levels in saliva.
102

103.  Bacterial composition
Socransky et al (1963) reported the
prevalence of spirochetes increases with age and
fall in number of streptococci. Plaque of young
patients contains more viable microorganisms per
mg than plaque from elderly persons
Greater plaque accumulation in older age group
may be possibly due to more recession of gingiva
in the older age group or due to physiologic age
change in salivary composition and flow rate.
103

104.  Enzymatic change
Levan hydrolase activity is lower in the plaque
in the older age group this may be due to low level
of streptococci in plaque of older individuals.
(Holm-Pedersen 1980)
104

105.  Immune factors
IgA, IgM and C3 specific immune factors and
nonspecific immune factors such as lactoferrin,
lysozyme and lactoperoxidase were higher in plaque of
older age group
105

106. Response of the periodontal tissue
Gaumer et al (1976) using experimental
gingivitis model in young individual with a healthy
periodontium showed that with plaque
accumulation peripheral blood leukocytes become
sensitive to lipopolysaccharide but this
sensitization is not seen in elderly.
106

107.  Amount of gingival exudate and tendency towards
gingival bleeding was increased. (Holm-Pedersen 1980)
This could be due to decrease in immune response with
age, but recent studies have shown that the
susceptibility to disease is more important determinant
than age for the rate of development of periodontal
inflammation. (Holm-Pedersen 1980)
107

108. Effect of Age on Development of Gingivitis:
Fransson C, Berglundh T & Lindhe J conducted a
experimental gingivitis study to study the response of
the marginal gingival to plaque formation in one group
of young subjects, 20-25 years of age and in one group
of older subjects aged 65-80 years.
 The data collected demonstrated that:
Old subjects, during a 3 weeks period of oral hygiene
abstention formed similar amounts of plaque as the young
subjects, but developed more gingivitis than young
subjects.
108

109. The clinical gingivitis assessments, the gingival
fluid measurements and morphometric
determination made in the biopsy samples
documented, that the gingival lesion formed in
the old individual was more pronounced and
contained more inflammatory cells than the
corresponding lesion in the young subject
samples.
109

110. These findings in all respect correlated the data
previously reported by Holm-Pedersen et al
(1975) from a trial in humans, who studied the
influence of age on the response of gingival
tissue to denovo dental plaque in different
groups of young and older subjects who
reported that the gingival of older subjects
responded earlier and more pronounced to
plaque accumulation than younger subjects.
110

111. Lesion of young subject had a larger density of
lymphocyte but a smaller volume of plasma cells
than the infiltrative connective tissue of old
subjects.
Page and Schroeder et al (1975) reported similar
differences in cellular composition of the
gingival lesion in a study of young and old
monkeys.
111

112. Berglundh and Lindhe (1993) from an experiment in the
beagle dog model also confirmed these findings.
Studies in man and experimental animals have
documented that the periodontal tissue undergo change
with age. Such age related qualitative and quantitative
alterations occur in intra and extra cellular component
of the epithelium and the connective tissue of both
gingival, periodontal ligament, root cementum and
bone.
112

113. The findings by the Amsterdam group Velden et
al 1985, Abbas et al 1986, and Winkel et al
1987 failed to identify age as a factor of
importance in response of gingival to denovo
plaque formation.
The divergent findings in the two groups of
studies main part explained by differences in
the design of trials performed and in subject
samples examined.
113

114. Results from epidemiological investigations show that as
soon as the permanent dentition is viable in nearly all
instances plaque and gingivitis are present. Yet, the
prevalence of periodontal breakdown prior to age of 20 is
rather low. Hence in most individuals, plaque may be
present for years before gingivitis progress to
periodontitis.
It may be wondered whether the plaque change with age
and/or the response of the periodontium undergoes a
change.
114

115. Treatment Of Aging Patient:
Hansen GC 1973 conducted a study to determine
if certain clinical changes in the oral cavity or
more highly correlated with chronologic age
(reflected length of exposure to various etiologic
agents) with an estimate of biologic age
(reflecting length of exposure to various
etiologic agents and intrinsic host changes with
age).
115

116. He concluded that gingival recession, loss of gingival
attachment and the number of total remaining teeth are
significantly correlated with both chronological and
estimated biologic age of the measured oral variables,
gingival recession and loss of gingival attachment were
found to be significantly more highly correlated with an
estimate of biologic age than chronologic age
116

117. 117
Treatment options fall into 3 modalities
Minimum intervention –OHI, fillings
and extractions
Multiple extractions and dentures
More extensive periodontal
treatment.

118. SURGERY?
Age does not contraindicate periodontal
surgery. However, longitudinal studies (Mc Hugh
1983 ) have shown that in patients with
moderately advanced periodontal disease, where
adequate plaque control was achieved, there was
no significant difference between sites treated
surgically and those treated non-surgically by OHI,
scaling and root planing.
118

119. Although surgery produced a greater reduction
in depth of severe pockets, both treatment
modalities were capable of arresting periodontal
destruction. Thus, for most elderly patients,
especially those with medical complications of
inadequate home care, a non-surgical approach is
advisable.
119

120. Gingivectomy , flap surgery and root
amputation are probably the most useful surgical
techniques for the older patient. These procedures
facilitate visual and mechanical access to the root
surface for cleaning by the patient or by the
clinician.
120

121. RESPONSE TO SURGERY
Factors include the rate of healing, and the strength of
the healed tissues.
This may be a reflection of altered fibroblastic function
and slower revascularization in the elderly.
However, it appears that age is not a clinically significant
factor with regard to healing of the periodontal tissues.
Healing after gingivectomy is not affected by age. (Stahl
1968)
121

122.  The amount of periodontal breakdown, and hence
susceptibility to periodontal disease, is of greater
importance in determining healing following
periodontal surgery than age.( Van der Velden 1982)
Surgery performed on any patient with poor oral
hygiene may constitute 'over-treatment' and may result
in even greater damage being done to the periodontium.
(Lindhe 1977)
122

123. IMPLANTS IN AGED?
Three questions have been posed in relation to
the prosthodontic treatment of geriatric patients in
the context of osseointegration( Zarb 1994)
Can Osseo integrated implants be prescribed for
elderly patients?
Can successful osseointegration Be maintained
as patients age?
Can the principles of osseointegration be
reconciled with different prosthodontic
techniques to facilitate treatment accessibility to
geriatric patients?123

124. The author concluded that Osseo integrated implants
can be maintained regardless of age but further studies
are required to establish the long term success .
Supportive Periodontal Treatment :
Once in 3-6 months depending on the standard of oral
hygiene .
124

125. WOUND HEALING:
Studies in man and animals have shown that the rate
wound healing is more rapid in the young. Du Nouy
1916, Howes & Harvey 1939 found that the rate of
healing of skin wound decreased with increasing age.
 Holm-Pederson and Zederfeldt 1971, Sussman 1973
reported tensile strength development of skin incision
wounds seemed to be retarded in older animals. This was
attributed to slower restitution of the microvascular
system and an altered fibroblastic function.
125

126. Lindhe, Sockransky, Nyman, Haffajee, Westfelt 1985
studied the effect of age healing of the periodontal
tissues following treatment. There data indicated that
younger individual taken as group heal after treatment
as well as an perhaps even better than older subject.
126

127. The concept that younger individual with moderate
to advance periodontal disease has a worse
prognosis than in older individuals with similar
level of disease (Amsterdam 1974) is probably less
related to the healing capacity of this individual
than the risk of re-infection over a longer lifespan.
127

128. Abbas et al 1984 concluded that “the time span
for wound healing is longer in patients who are
more susceptible to periodontal disease (younger)
than in those who are less susceptible”. They
noticed that sites with more loss of attachments
had slow rate of wound healing.
128

129. PROGNOSIS
Patients with same amount of periodontal
destruction , the rule holds “older the patient, the
better the prognosis in terms of no recurrence of the
disease (Goldman 1973).
129

130. CONCLUSION
Old age is inevitable but need not be debilitating.
Aging dental patients have particular oral and
general health conditions that dentists should be
familiar with detecting ,consulting &treating . Medical
diseases and conditions that occur more often with age
may require modification to periodontal preventive tools
as well as for the planning and treatment phases of
periodontal care .
130

131. 131

132. REFERENCES
132
ROBBINS GENERAL PATHOLOGY KUMAR /COTRAN
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

133. A histologic study of age changes in the adult human periodontal
joint Severson etal j periodontol 1978;49:169-200.
Factors Influencing Periodontal Therapy For Geriatric Patient
Green et al DCNA 1989;33:91-99.
Effect of age on healing following periodontal therapy Lindhe et
al j clin periodontol 1985;12:774-787.
The Effect Of Age On Pcna Expression In The Oral Gingival
Epithelium Of Healthy And Inflamed Human Gingiva Nazliel Et al
J Periodontol 2000;71:1567-1574.
The Elderly At Risk For Periodontitis & Systemic Disease E Persson
Etal DCNA 2005;49:279-292.
Effect of age on the development of gingivitis :clinical,
microbiological and histological findings Fransson C et al J CliN
Periodontonl 1996;23:379-385
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