4.aging and periodontium.. dr.manisha

AGE
CHANGES IN THE
PERIODONTIUM
PRESENTED BY:
DR. MANISHA DEOL
M.D.S. 1ST YEAR
DEPT. OF PERIODONTOLOGY&
ORAL IMPLANTOLOGY
GUIDED BY:
DR. TANVI OHRI
SENIOR LECTURER
DEPT. OF PERIODONTOLOGY &
ORAL IMPLANTOLOGY

CONTENTS
 Introduction
 Definitions & General aspects of Aging
 Aging and vasculature
 Aging and gingival epithelium
 Aging and gingival connective tissue
 Aging and periodontal ligament
 Aging and cementum
 Aging and alveolar bone
 Aging and oral mucosa

 Aging and bacterial plaque
 Aging and progression of periodontal disease
 Aging and masticatory efficiency
 Aging and nutrition
 Aging and tooth-periodontium relationships
 Aging and immune response
 Aging and wound healing
 Aging and the cumulative effects of oral cavity
 Treatment of aging patient
 Aging and response to treatment
 Aging and prognosis
 Conclusion
 References

INTRODUCTION
 Diseases of the Periodontium occurs in the
childhood, adolescence and early adulthood, but
the prevalence of periodontal diseases and tissue
destruction increases with age.
 Many tissue changes occur with aging, some of
which may affect the diseases of the periodontium.
 It is a well known fact that the percentage of
edentulousness in man increases with age. There
is no doubt that caries and periodontal disease are
important etiological factors in tooth loss.

 Geriatric Dentistry Or
Gerodontics is the delivery of
dental care to older adults involving
the diagnosis, prevention, and
treatment of problems associated
with normal aging and age-related
diseases as part of an
interdisciplinary team with other
health care professionals.

 Aging is a slowing of natural
function, a disintegration of the
balanced control and organization
that characterize the young adult.
 It is a process of physiologic and
morphologic disintegration, as
distinguished from infancy,
childhood, and adolescence, which
are typified by processes of
integration and coordination.
-Carranza

Aging is a progressive impairment of
function resulting in loss of adaptive
response to stress and in increasing
risk of age-related diseases and
disabilities.
---Dr. O.P. Sharma

 Senescence includes changes in the adult
organism that occur with time. such changes may
be:
 Intrinsic and chronologically related
or
Extrinsic and attributable to the environment.
 Unfortunately the distinction between the
physiologic time-related and the environmental
pathologic changes are often unclear.
 (Grant j.perio 1972)

THEORIES
 The basic concept of aging is loss of the organism’s
adaptability with time.
 Various mechanisms and theories of aging have
been proposed:
1. Immune theory (immunological failure)
2. Free radical theory
3. Cell aging theory
4. Somatic mutation theory
5. Error theory
6. Neuroendocrine theory.

 The most convincing theory has been put forward
by Thomas Kirkwood.
 This is the DISPOSABLE SOMA THEORY which
proposes that ageing results from the body’s
inability to repair random environmental damage.
 As a result, random defects occur in somatic cells
and the additive effects of these results in
senescence and death.

 Arteriosclerosis i.e. a reduction in luminal volume is
a frequent finding in aging humans.
(Bernick et al.,1969;Grant and Bernick 1970,1972;
Bradley 1972)
 It may be seen in large vessels with muscular
elements in the vessel wall, vessels in the alveolar
bone and vessels in the periodontal ligament.

 The relative ischemia that arteriosclerosis may
produce in periodontal tissues because of the
reduction in blood flow has been hypothesized as
predisposing these tissues to disease or provoking
other changes such as fibrosis, loss of cellularity,
and focal calcification.
 It may also reduce bone metabolism and may be
correlated with slower or altered wound healing.

Alveolar artery
with
arteriosclerosis:
Intimal thickening
with cellular and
fibrous proliferation

.
 The reduced arterial flow may be related to
changes that have been observed elsewhere in the
body and in experimental animals.
 For instance, the loss of ground substance may
be a result of the reduced supply of oxygen
associated with diminished arterial flow.
 Also, basement membranes have been reported to
be thicker in old persons and markedly distinct from
the surrounding ground substance.

PERIODONTIUM:
The periodontium, also called
"the attachment apparatus" or
"the supporting tissues of the
teeth", constitutes a
developmental, biologic, and
functional unit which undergoes
certain changes with age and is,
in addition, subjected to
morphologic changes related to
functional alterations and
alterations in the oral
environment.
Source:Jan Lindhe 4th edition

* EFFECTS OF AGING ON
THE
PERIODONTIUM
GINGIVAL EPITHELIUM
GINGIVAL CONNECTIVE TISSUE
PERIODONTAL LIGAMENT
CEMENTUM
ALVEOLAR BONE
BACTERIAL PLAQUE
IMMUNE RESPONSE

The gingiva is that part of the
masticatory mucosa which covers the
alveolar process and surrounds the
cervical portion of the teeth.
Source:Jan Lindhe

1. Thinning of gingival epithelium ( Shklar 1966) or
no change in width have been reported to occur
with age.
2. Diminished keratinization of gingival epithelium (
Papic & Glickman 1950)in both men and women.
In menopausal patients the gingiva is less
keratinized than in patients of comparable age with
active menstrual cycles.
 The significance of these findings could mean an
increase in epithelial permeability to bacterial
antigens, a decreased resistance to functional
trauma or both. If so, such changes might influence
long-term periodontal outcomes.

3. Conflicting results have been published regarding
the shape of retepegs.
 Shklar(1966) reported a flattening of rete-pegs,
where as Wentz. et al.(1952) found that the height
of the epithelial ridges increased with age.

 In a 3-dimensional study on the morphology of the
epithelium connective tissue interface, Loe &
Karring (1972) demonstrated that younger
individuals show mainly connective tissue ridges
whereas in older individuals connective tissue
papillae predominate.
 The change from ridges to papillae involves the
formation of epithelial cross-ridges with increasing
age.

4. Altered cell density
 With aging, the oral epithelium shows an increase
in cell density and in the mitotic activity of the oral
epithelium.
 Moreover, an increased mitotic activity may have
been induced by increased inflammatory response
during aging. (Tonna et al. 1972)

EFFECT OF AGE ON PERIODONTIUM; JCP
1984, 11: 281-294
 Results from some studies have indicated that the
mitotic activity increases with increasing age.
 However, Ryan et al, (1974) found a constant
mitotic activity.
 Whereas results from other studies indicated a
decrease in the mitotic activity with age (Sharav &
Massler 1967).

THE EFFECT OF AGE ON PROLIFERATING CELL NUCLEAR
ANTIGEN EXPRESSION IN ORAL GINGIVAL EPITHELIUM OF
HEALTHY AND INFLAMED HUMAN GINGIVA,
J PERIODONTOL 2000; 71: 1567-1574.
 Proliferating cell nuclear antigen (PCNA) is a nuclear
protein associated with the cell cycle.
 Its cell concentration is directly correlated with the
proliferative state of the cell, increasing through G1,
peaking at the G1/S phase interface, decreasing
through G2 and reaching low levels in M-phase and
interphase.
 The aims of this study were to investigate the
localization of PCNA expression in oral gingival
epithelium and to define age-related changes as to
PCNA-proliferative index in inflamed as well as healthy
gingiva.
 It was found that PCNA expression in inflamed gingiva is
higher in older subjects.

5. The effect of aging on the location of the junctional
epithelium has been the subject of much
speculation.
 Some reports show migration of the junctional
epithelium from its position in healthy individuals
(i.e., on enamel) to a more apical position on the
root surface with accompanying gingival recession.
 However, in other animal studies, no apical
migration has been noted.

6. Reduced or unchanged amount of stippling.
7. Aging also brings an increased prevalence of
gingival recession.
 This finding appears to be largely due to the
cumulative environmental effects of vigorous tooth
brushing and due
to the inflammatory
periodontal disease.

8. With continuing gingival recession, the width of
the attached gingiva would be expected to
decrease with age, but the opposite appears to be
true.
 The consensus is that gingival recession is not an
inevitable physiologic process of aging but is
explained by cumulative effects of inflammation or
trauma on the periodontium.
 So, the migration of the junctional epithelium to the
root surface could be caused by the tooth erupting
through the gingiva in an attempt to maintain
occlusal contact with its opposing tooth (passive
eruption) as a result of tooth surface loss from
attrition.

THE INCREASE IN THE WIDTH OF
ATTACHED GINGIVA WITH AGE
 Ainamo & Loe (1966) found that the width of
attached gingiva was the same in young adults with
the gingival margin on enamel as in older patients
whose gingival margin after retraction was located
on the cementum.
 This finding was at that time suggested to be a
result of an apical migration with age of the
mucogingival junction.
 According to another hypothesis (Pietrokowski &
Massler 1967), the mucogingival junction forms the
border line between the genetically determined
basal bone of the jaws and the alveolar processes,
the growth of which is induced by the developing
teeth.

 The finding that the distance between the mandibular
mucogingival junction and the lower border of the
mandible does not change with age seems to out-rule
the possibility that the mucogingival junction would shift
apically (Ainamo & Loe1966), and supports the view of
Pietrokowski & Massler (1967) of a predetermined
borderline between basal and alveolar bone. The same
distance is greater in males than in females.
 Location of the mucogingival junction is stable, the
increase in the anatomical width of the attached gingiva
must be the result of a continuous shift through adult life
of the cementoenamel junction.
 It thus seems that the teeth of adult humans, are
subjected to a continuous eruption (Ainamo & Talari
1975).
 It is the cementoenamel junction which shifts coronally
and not the mucogingival junction and lower border of
the mandible shifting apically.

 According to Murphy (1959) an eruption of the teeth
during adult human life is necessary to compensate
for the progressive wear of the occlusal surfaces
and incisal edges.
 The genetically predetermined compensatory
eruption of the teeth of adult humans thus — in the
absence of concurrent retraction of the periodontal
attachment seems to result in an increased width of
attached gingiva with advancing age.

AGING
V/S
GINGIVAL CONNECTIVE TISSUE

 One prominent feature of aging is the appearance
of wrinkles in the skin.
 According to Kanungo (1980) this is due mainly to
the loss of subcutaneous fat.
 Since the gingiva lacks a submucosa, the
implication is that the gingiva retains, at least
visually, its youth permanently.
 However, like other tissues, the connective tissue of
the gingiva cannot avoid the aging process.

QUALITATIVE AND QUANTITATIVE CHANGES
ASSOCIATED WITH INCREASING AGE ARE:
1. Number of (connective tissue) cellular elements
decreases (Wentz et al 1952, Klingsberg &
Butcher 1960, Ryan et al 1974).
2. Increased intercellular substances.
3. Wentz et al (1952) found that the irregular, finely
textured pre-pubertal connective tissue shows a
gradual transition with age to a denser, coarsely
textured tissue in the higher age groups
connective tissue.

4. Collagen changes:
 Rate of collagen synthesis is decreased (Claycomb
et al 1967).
 Rate of maturation of the synthesized collagen
changes with age. There is increased rate of
conversion of salt-soluble to salt-insoluble collagen
i.e. a reduction in the amount of soluble collagen.
 Increase in the thickness of collagen fibrils.
 Increased tensile and mechanical strength.
 An increase in thermal contraction.
 A decrease in water content.
 An increased resistance to proteolytic enzymes.
 Increased denaturing temperature.

 Some of these changes may be related to the loss
of acid mucopolysaccharide and water as well as to
increased cross-linkages.
 These results indicate increased collagen
stabilization caused by changes in the
macromolecular conformation.
 Not surprisingly, greater collagen content has been
found in the gingiva of older animals despite a
lower rate of collagen synthesis decreasing with
age.

AGING
V/S
PERIODONTAL LIGAMENT

The periodontal ligament is the soft, richly
vascular and cellular connective tissue which
surrounds the roots of the teeth and joins the root
cementum with socket wall.
Source:Jan Lindhe

1. Most investigators agree that, in man, the
periodontal ligament of young individuals is well
organized and regularly structured.
 With increasing age, the fiber and cellular
contents decrease and the structure of the
ligament becomes more and more irregular
(Grant & Bernick 1972, Levy et al, 1972, Gargiulo
& Grant 1973, Severson et al, 1978).

2. Principal fibres:
 Thickened with age.
 Bundles of PDL fibres are wavy and broad.
 Inter-fibrillal areas are reduced in size.
 Well organized but less distinct since they contain
fewer reticular or argyrophillic fibers.
 Staining characteristics are altered. Young collagen
takes up silver nitrate readily (argyrophilia) where
as old collagen takes up the stain only slightly.

YOUNG
OLD
Fibers
thick in
old,
sharpeys
fibers
easily
seen in
young,

3. Decreased number of cell density: fibroblasts,
cementoblasts and osteoblasts are seen.
4. Results of autoradiographic studies reveal that the
mitotic activity of the cells decreases with age.
5. Furthermore, Stahl & Tonna (1977) found an
overall reduction in organic matrix production
with advancing age.
6. In addition. Levy et al, (1972) demonstrated a loss
of acid mucopolysaccharides in the periodontal
ligament with increasing age.

Thick principal fibers,
reduced cellularity,
spaces between fiber
bundles are reduced in
size,
cementum is also thick

Fewer osteoblasts and
cementoblasts are seen
bordering bone and tooth,
lessened cellularity of
fibers also evident,
bone margin is irregular.

7. PDL shows degenerative hyaline changes.
 At times, cells within lacunae are demonstrable.
 These are characteristic of fibrocartilage and
indicate a chondroid degeneration, probably a
sequel to injury.
 Both the hyalinization and the chondroid
degeneration may be:
1. Casually related to or an accompaniment of a
reduced vascular supply. i.e. increases in
arteriosclerotic changes.
2. a response to injury
3. an undetermined effect of aging

Hyaline and
chondroid
degeneration:
(a)Cartilage like
cells

8. Calcified bodies are common in the PDL of aging
humans.
 Two types are of calcospheroid bodies are found, small
rounded calcospherites and larger irregular shaped
calcifications.
 The calcospherites appear to be formed in relation to
fiber bundles.
 They coalesce to form the larger rounded or irregularly
shaped bodies.
 Occasionally they increase in number and appear to
calcify a complete fibre bundle, producing an ankylosis.

(b) Larger irregularly
shaped calcified bodies
(a)Small calcospherites

Sometimes
calcospheroid bodies
are so numerous that
entire fiber bundle
becomes calcified,
linking the tooth to
bone.

9. Epithelial rests in the PDL show altered forms of
aggregation.
 Rest aggregates tend to contain
more cells with both proliferative
and degenerative morphology.
 The aggregates are frequently
encircled by a thickened basement
membrane.
 Rather than being situated near
the root surface (as in young
persons), these epithelial rests are
found irregularly located in the PDL,
near the tooth, midway between the
tooth and bone, and near bone.
 Whereas some rests may degenerate,
others may become calcified.

Calcification of
epithelial rest

EFFECT OF AGE ON PERIODONTIUM, JCP
1984, 11: 281-294
 Aging fibroblasts synthesize a different type of
collagen. Such a phenomenon has been described
by Mayne et al. (1976) for aging chondrocytes.
Normally, chondrocytes in in-vitro cultures
synthesize type II collagen, but when they are
growing old, type I collagen is synthesized.
 There are an increased number of elastic fibers
(Haitn & Baumgartel 1968) and a decrease in the
number of epithelial rests (Reeve & Wentz 1962).

WIDTH OF THE PERIODONTAL LIGAMENT
SPACE WITH AGE
Conflicting results have been reported for changes in the
width of periodontal ligament in relation to age in human
and animal models.
 Due to the great variability in their autopsy material, both
between age groups and between individuals of the
same age group, Severson et al, (1978) could not make
any definite statements.
 Klein (1928) and , Jozat (1933) concluded that the width
increases with age.
 On the contrary, a decrease with age was reported in
mice ( Ionna et al. 1972), in monkeys (Ive et al. 1980)
and in man (Coolidge 1937, Gotze 1965).

Although true variation might exist, this finding
probably reflects the functional status of the teeth in
the studies because the width of the space will
decrease if the tooth is unopposed (hypofunction)
or will increase with excessive occlusal loading.
These conflicting results may be explained as
follows:
 If with increasing age, less teeth are present, the
forces acting on the remaining teeth may increase.
This could explain an increasing width of the
periodontal ligament space with age.
 On the other hand, it has also been noted that the
masticatory forces decrease with age (Ilelkimo et al,
1977, Herring 1977). This could explain a decrease
in the periodontal ligament space with age.

 In conclusion, it may be hypothesized that if no
teeth are lost, the periodontal width probably
decreases with increasing age.
 Besides having found a decreasing width of the
periodontal ligament space with age, Ive et al.
(1980) also noted that both the width of the socket
and the width of the cementum increased with age.
 They suggested that, as the socket remodels and
increases in size with age, cementum is deposited
at a relatively greater rate than the bone, causing a
decrease in the periodontal ligament space.

The cementum is a specialized mineralized
tissue covering the root surfaces and,
occasionally, small portions of the crown of
the teeth.
Source:Jan Lindhe

1. With age, the cementum increases in width.
 The total width of cementum at age 76 is three
times that at age 11.
 This increase may be 5 to 10 times with increasing
age.
 This finding is not surprising
because cementum deposition
continues after tooth eruption and
occurs throughout the life of man.

Mid-root area
of tooth
showing thick
layers of
cementum(c)
as a result of
continuous
apposition

 The increase in width is greater apically and
lingually.
 Greater cemental apposition
in the apical region is a
response to passive eruption.
 The laminar deposition
results in a broad zone of
cementum clothing the root.

2. Indications exist that cemental deposition slows
in old age.
3. An older root surface is less highly populated
with fiber bundles than a younger root surface.

4. Although remodeling of cementum does not
normally take place, local resorption at the
cementum surface followed by cementum
apposition is often observed.
 Weinmann (1951) reported that, in a study of
human teeth, areas of post and active resorption
increased with age.
 Resorption and apposition of cementum may also
be responsible for the finding of an increased
irregularity of the cemental surface with age as
has been noted in humans (Grant & Bernick 1972,
Severson et al. 1978).

5. Seen microscopically, only the surface layer of
cementocytes appears viable. All other lacunae
appear empty.
6. Spurring of cementum is sometimes the result of
the fusion of calcospheroid near cementum or of
the calcification of epithelial rest aggregates.

7. In general, cementum is acellular except at the root
apices and in the furcation areas of multi-rooted
teeth. With increasing age, the process of
cementum formation becomes essentially
acellular.
8. Attachment of cementum to dentin may be
weakened with increasing age.
9. Frequent cemental tears seen in specimens of
aging humans may be related to the age changes
in the ground substance of cementum, to reduced
vascularity, or to thickened and less extensible
ligament fibers embedded in the cementum.

The alveolar process is defined as the parts of the
maxilla and the mandible that form and support the
sockets of the teeth.
Source:Jan Lindhe

1. The alveolar bone has a darkly stained margin,
which may be interpreted as an aging
characteristic of bone.20
2. Physiologic migration:
 Little evidence of continued bone apposition is
present in senescence.
 In view of this, physiologic tooth migration may be
slowed or even halted in old age.20
3. Topographic labelling with H-proline
autoradiography is reduced in the periodontal
bone of aging mice.20

4. More irregular periodontal surface of bone.
5. It has been noted that, with increasing age, the
periodontal surfaces of the alveolar bone become
jagged and that collagen fibers insert less regularly
in bone (Severson et al 1978, Ive et al 1980).49

Margin of
alveolar
bone
proper (b)
is darkly
stained and
is jagged

6. Reduction in bone height with aging (senile
atrophy).
 Vertical (inter-occlusal) dimension and arch
continuity are usually maintained into old age, since
wear is compensated for by bone apposition on
distal surfaces and at the fundus of the sockets.
 Continuous apposition of cementum at the apex
also helps to compensate for such wear.
 If continuous apposition of bone is slowed or even
halted, such compensation for attrition doesn’t
occur.
 Together with atrophy of musculature, a decreased
vertical facial height may result (closed bite).

7. Bone undergoes osteoporosis with aging.
 Although age is a risk factor for the bone mass
reductions in osteoporosis, it is not causative and
therefore should be distinguished from physiologic
aging processes.
 Osteoporosis has been reported particularly in the
alveolar bone of postmenopausal women, but the
decrease in the trabeculation of alveolar bone
sometimes seen radiographically is more often
related to loss of function (extraction of an opposing
tooth).

8. Overriding the diverse observations of bony changes
with age is the important finding that the healing rate of
bone in extraction sockets appears to be unaffected
by increasing age.
 So , the success of osseointegrated dental implants,
which relies on intact bone healing responses, does not
appear to be age related.
 However, balancing this view is the recent observation
that bone graft preparations (decalcified freeze-dried
bone) from donors more than 50 years old possessed
significantly less osteogenic potential than graft
material from younger donors.
 The possible significance of this phenomenon on normal
healing responses needs to be investigated.
(Schwartz Z, et.al, 1998)

9. Bone is rarefied (Loss of bone mineral density).
10. Trabeculae are reduced in numbers.
11. Cortical plates are thinned.
12. Vascularity is decreased.
13. Increased susceptibility to fractures.
14. Water content of bone is reduced.

15. Collagen fibers are thickened.
16. Bone formation is decreased.
17. There is reduction in metabolism.
18. Resorptions on endosteal surfaces is relatively
greater than the slight apposition that occur on the
periosteal surface, thus total bone mass become
reduced with age.

1984, 11: 281-29449
 The width of the cribiform in plate may decrease
with age, as has been found in monkeys (Levy et
al, 1972). However, this phenomenon could not be
confirmed in humans due to large individual
variations (Severson et al, 1978).
 A decreasing width of the interdental alveolar
septum has been noted in rats and monkeys. This
may be a result of interproximal wear of the teeth at
the contact areas (Belting etal, 1953, Levy et al,
1972).
 With age, the alveolar bone in the rat, hamster and
monkey is transformed from an immature
trabeculated bone to a dense, lamellated bone
(Klingsberg & Butcher 1960, Grant et al, 1973).

 In man, too, an increase in the number of interstitial
lamellae has been found (Severson et al. 1978).
 Results from auto-radiographic studies in rats and
mice suggest that the proliferative activity of the
cells in the osteogenic layer at the surface of the
cribiform plate is low compared to the cells of the
epithelium and connective tissue (Stahl et al, 1969,
Tonna 1973).
 On the basis of autopsy material, Severson et al,
(1978) concluded that, also in man, the number of
cells in this osteogenic layer decreases with age.

 The keratinization potential of the hard palate
epithelium does not change with age. An increased
keratinization of lip and cheek mucosa with age has
been reported. This might, however, be related to
smoking.2
 Changes in other areas of the oral mucosa include
atrophy of the epithelium and connective tissue with
loss of elasticity, decrease in protein-bound
hexoses and mucoproteins, which may reduce
resilience and increase susceptibility to trauma;
increase in mast cells.1

 Elastoid degeneration is reported in the collagen
fibers of the alveolar mucosa.20
 Atrophy of the papillae of the tongue, with the
filiform papillae more severely affected; decrease in
the number of taste buds in the circumvallate
papillae, nodular varicose enlargement of veins on
the ventral surface of the tongue; and increase in
the sebaceous glands in the lip and cheek.1
 Arteriosclerotic vessels have been described.20

 Regressive changes in the salivary glands with
retention cyst formation and associated xerostomia
have been identified with aging.
 Decrease in salivary flow and in the amount of
ptyalin has been described as the causes of
inadequate lubrication of food during mastication
and poor starch digestion.
 Fatty degeneration of the parotid gland occurs in
aged experimental animals. There appears to be a
reduction in the number of secretory units with age,
as well as an increase in the amount of fibrous
tissue.1

THICKNESS OF PALATAL MASTICATORY MUCOSA
ASSOCIATED WITH AGE;
JOP 2001; 72: 1407-141244
 The mean thickness of palatal mucosa ranged from
2 to 3.7mm. The younger age group had
significantly thinner mucosa (mean 2.8 +/- 0.3mm)
than the older age group (mean 3.1 +/- 0.3mm).
 Females had thinner mucosa than the males in the
same age group, but the difference was not
statistically significant.
 Overall, the thickness of palatal mucosa increased
from the canine to second molar areas and in sites
furthest from the gingival margin toward the mid-
palate (with the exception of the first molar area,
where significantly decreased thickness was
observed).

1. Dentogingival plaque accumulation has been
suggested to increase with age.
 This might be explained by the increase in hard
tissue surface area as a result of gingival
recession and the surface characteristics of the
exposed root surface as a substrate for plaque
formation compared with enamel.
 Other studies have shown no difference in plaque
quantity with age.
 This contradiction might reflect the different age
ranges of experimental groups as variable
degrees of gingival recession and root surface
exposure.

2. Composition of the plaque in relation to age-
plaque of adolescents contains lower levels of
calcium and phosphorus than the plaque of
adults. This phenomenon might be explained by a
difference in calcium and phosphorus levels in the
saliva.
3. For SUPRA-GINGIVAL PLAQUE, no real
qualitative differences have been shown for plaque
composition.

4. For SUBGINGIVAL PLAQUE:
 one study has shown similar subgingival flora to a
normal flora,
 whereas another study reported increased numbers of
enteric rods and pseudomonas in older adults.
 Mombelli suggests caution in the interpretation of this
finding because of increased oral carriage of these
species among older adults.
 It has been speculated that a shift occurs in the
importance of certain periodontal pathogens with age,
specifically including an increased role for
Porphyromonas gingivalis and a decreased role for
Actinobacillus actinomycetemcomitans.
 However, differentiating true age effects from the
changes in ecological determinants for periodontal
bacteria will be difficult.

1984, 11: 281-29449
 Various biochemical and microbiological changes
occur in dental plaque with increasing age .
 Plaque from young patients contain more viable
microbes per mg than plaque from the elderly.
 There is an increase in Spirochete and Bacteroids
melaninogenicus with age.
 The number of streptococci fall in plaque with
increasing age. Levan hydrolase activity is
markedly lower than in the young. This difference is
may be related to differences in number of
streptococci.

 Softer diets, reduced oral cavity and an increased
incidence of xerostomia in elderly may also
contribute to gross accumulation of deposits.
 Certain enzymatic and immunological differences
are apparent in the plaque from elderly patients.
 The concentration of immune factors (IgA, IgM, and
C3, lactoferrin, lysozyme and lactoperoxidase) is
reported to be higher in plaque obtained from older
people.

AGING
V/S
PROGRESSION OF
PERIODONTAL DISEASE

 The phrase "getting long in the tooth" expresses a
widespread belief that age is inevitably associated
with an increased loss of connective tissue
attachment.
 However, this observation might equally well reflect
a cumulative exposure to a number of potentially
destructive processes.
 These exposures might include plaque associated
periodontitis, chronic mechanical trauma from tooth
brushing, and iatrogenic damage from unfavorable
restorative dentistry or repeated scaling and root
planing.
 The effects of these exposures act in one direction
only (i.e., increased loss of attachment).

 In an attempt to differentiate the effects of age from
these other processes, several studies have been
designed to eliminate confounding issues and address
more clearly the question of age as a risk factor for
periodontitis.
 A risk factor is defined as an exposure or factor that
increases the probability that the disease (periodontitis)
will occur.
 The conclusions from these studies are strikingly
consistent and show that the effect of age is either
nonexistent or provides a small and clinically
insignificant increased risk of loss of periodontal
support.
 In addition, the recent reports of a genetic basis for
susceptibility to severe forms of periodontitis underline
the overriding importance of plaque, smoking, and
susceptibility in explaining most of the variation in
periodontal disease severity between individuals.

AGING
V/S
MASTICATORY EFFICIENCY2

 Slight atrophy of the buccal musculature has been
described as a physiologic feature of aging.
 However, reduction in masticatory efficiency in
aged individuals is more likely to be the result of
unreplaced missing teeth, loose teeth, poorly fitting
dentures or an unwillingness to wear dentures.
 Reduced masticatory efficiency leads to poor
chewing habits and the possibility of associated
digestive disturbances.

 Aged persons select carbohydrates and food requiring
less chewing effort when masticatory efficiency is
impaired.
 Avitaminosis is relatively common in aged persons, but
the extent to which it results from impaired masticatory
efficiency has not been established.
 The vitamin requirements of older persons may be
increase because of their dietary habits.
 Long-standing calcium deficiency has been considered
by some to be a causative factor in senile osteoporosis.
 The advisability of increased calcium intake in aged
individuals is doubtful, but a diet high in protein and
vitamins and comparatively low in carbohydrates and fat
may be beneficial.

AGING
V/S
TOOTH PERIODONTIUM
RELATIONSHIPS2

ATTRITION
 There is loss of tooth substance due to attrition.
 There is reduction in cuspal height and inclination
due to wear.
 Bone loss results in an increase
in crown/root ratio
 Tooth wear tends to modify
increase in crown/root ratio.

 The rate of attrition may be coordinated with other
age changes such as continuous tooth eruption and
gingival recession.
 As the tooth erupts, cementum is usually deposited
in the apical region of the root.
 The reduction in bone height that occurs with aging
is not necessarily related to occlusal wear.
 If bone support is reduced, the clinical crown tends
to become disproportionately long and exerts
excessive leverage on the bone.
 By reducing the clinical crown length, attrition
appears to preserve the balance between the tooth
and its bony support.

PHYSIOLOGICAL MESIAL DRIFTING
 Wear of teeth also occurs on the proximal surfaces,
accompanied by mesial migration of teeth.
 Proximal wear reduces the antero-posterior length
of the dental arch by approximately 0.5cm by age
40.
 Antero-posterior narrowing from proximal wear is
greater in teeth that taper toward the cervical
aspect, such as the incisors.
 Progressive proximal wear and attrition results in a
reduced maxillary mandibular overjet in the molar
area and an edge to edge bite anteriorly.

 Differences between young and older individuals can be
demonstrated for T and B cells, cytokines, and natural
killer cells but not for polymorphonuclear cells and
macrophage activity.
 McArthur concludes, “Measurement of indicators of
immune and inflammatory competency suggested that,
within the parameters tested, there was no evidence for
age-related changes in host defenses correlating with
periodontitis in an elderly (65 to 75 years) group of
individuals, with and without disease.”
 In summary, although many contradictions exist, a
survey of the literature demonstrates that some age
related changes are evident in the periodontium and
host response.

EFFECT OF AGING ON IMMUNOCOMPETENT AND
INFLAMMATORY CELLS;
PERIO 2000; VOL 16, 1998, 53-7945

 Rate of healing of wounds decreased with
increasing age probably connected to a slower
restitution of the microvascular system.
 In response to treatment of periodontitis, older
patients generally have all the needed cellular and
molecular mechanisms to ensure healing and
repair, but these mechanisms may be slower and
somewhat lower than those in young patients.

1984, 11: 281-29449
 In a study on wound healing in man after
gingivectomy, no correlation could be found
between the healing response and age (Stahl et al.
1968).
 However, Holm-Pedersen & Loe (1971)
demonstrated that the rate of wound healing of
standardized biopsies of the vestibular gingiva in
subjects with a healthy periodontium was
somewhat more rapid in young as compared to old
individuals.
 Furthermore, the gingival tissues never regenerated
completely in the older age group.

AGING
V/S
THE CUMULATIVE EFFECTS OF
ORAL DISEASE2

 With time chronic diseases can produce many oral
changes, and it is difficult to determine how much
physiologic aging contributes to the total picture.
 Some believe that gingival recession, attrition and
reduction in bone height in the aged results more
from disease and factors in the oral environment
than from physiologic aging.
 Although recession, attrition and bone loss
commonly occur with the age, they are not present
in all patients, and vary considerably In the same
age group.
 An aged individual with marked attrition may
present relatively little bone loss.
 Marked attrition may also be produced in young
and middle aged adults by bruxing and clenching
habits.

 Increased alveolar bone loss in the aged has been
related to less efficient oral hygiene.
 Bone loss, pathologic migration of the teeth, and
loss of the vertical dimension in the aged may be
the results of periodontal disease and failure to
replace missing teeth.
 Leukoplakia of the oral mucosa and staining of the
teeth are common in aged individuals who are
inveterate smokers.
 Wearing artificial dentures for years without
rebasing, with a resultant reduction in vertical
dimension, is a common cause of angular cheilosis
in the aged.1

 Plaque accumulation starts as soon as teeth erupt.
 However, the experimental gingivitis model has
shown that inflammation develops more rapidly in
older individuals than in children.
 This may occur in part because areas of recession
in older individuals may result in increased plaque
accumulation; it may also be due to a reduced
immune response with aging.

GOAL OF PERIODONTAL THERAPY IN OLDER
ADULTS35
 Regardless of age, the overall objective of
periodontal therapy is to preserve a functional
dentition by preventing the progression of
periodontal diseases.
 But this will require high standards of self-
performed plaque control, which unfortunately may
not always be possible for each individual patient.43

PERIODONTAL THERAPY49
 Periodontal treatment is always directed towards
plaque control.
 Patients are instructed and motivated to eliminate
plaque as much as possible.
 If periodontium is inflamed and only shallow
pathological pockets are present then plaque
control in conjunction with removal of supra- and
subgingival deposits is generally sufficient to obtain
a healthy periodontium.

 With daily plaque removal by the patient
him/herself, the periodontium will remain healthy.
 In patients with inflammation of the periodontal
tissues and deep pathological pocketing, the
treatment will also consist of plaque elimination and
removal of supra- and subgingival deposits.
 For the complete elimination of subgingival
deposits, 2 different treatment procedures are
available:

1. Professional removal of subgingival deposits by
means of scaling and root planing during a flap
procedure.
2. Changing subgingival into supragingival deposits
by means of a gingivectomy or an apically
positioned flap procedure, where after the patient
him/herself can remove the originally subgingival
deposits.

 Complex cellular interactions that occur in
association with the healing of advanced
regenerative periodontal surgical operations
involving bone grafts, GTR, and bioactive agents,
older patients cannot be expected to have as
favorable treatment outcomes as young once.
 Thus clinicians may decide to use simpler
approaches to treat advanced periodontal lesions in
older patients.
 Nonsurgical procedures are favored.

AGING
V/S
RESPONSE TO TREATMENT OF
THE PERIODONTIUM

 The successful treatment of periodontitis requires
both meticulous home-care plaque controls by the
patient and meticulous supragingival and
subgingival debridement by the therapist.
 Unfortunately, only a few studies have directly
compared such an approach among patients of
different age groups.
 The few studies that have done so clearly
demonstrate that despite the histologic changes in
the periodontium with aging, no differences in
response to nonsurgical or surgical treatment have
been shown for periodontitis.
 However, if plaque control is not ideal, continued
loss of attachment is inevitable.

 Aging might affect other aspects of managing the
periodontal diseases, such as the risk of root
caries, and the resulting difficulties should not be
underestimated.
 Interestingly, a recent study has identified greater
compliance with supportive maintenance among
older individuals than younger patients.

The prognosis is a prediction of the
probable course, duration, and
outcome of a disease based on a
general knowledge of pathogenesis of
the disease and the presence of risk
factors for the disease.
--Carranza

 It is generally believed that in patients with the
same amount of periodontal disease, the rule holds:
the older the patient, the better the prognosis in
terms of no recurrence of the disease (Goldman &
Cohen 1973, Schluger et al, 1977).
 This belief is based mainly on the reasoning that
the resistance to periodontal breakdown must be
higher in older individuals, since the process of
periodontal destruction takes much less time in
younger individuals.
 This line of reasoning has far-reaching implications,
since a younger patient with severe periodontal
disease would not only be more susceptible to
recurrence of breakdown but, in addition, the teeth
have to serve for another 40-50 years.

 For the older patient, different rules apply.
 The patient has demonstrated to be, to some extent
resistant to periodontal disease and the older the
patient, the fewer arc the years remaining for the
functioning of the teeth.
 In other words, in spite of age changes in the
periodontal tissues and retarded wound healing
periodontal treatment including surgical elimination
of pathologically deepened pockets has a
favorable prognosis in old patients since they do
not represent individuals who are highly susceptible
to periodontal disease.

 Periodontal tissues are programmed to provide
healthy support for the dentition for the life of the
patient.
 Periodontal disease increases in prevalence and
severity with increasing age.
 The increase may be caused by the cumulative
effect of the number of bursts of periodontal
destruction, deterioration in plaque removal
efficiency, or an increase in the number of teeth
retained in old age and therefore affected by
plaque-induced disease.
 Although there are concerns that older patients
have increased susceptibility to periodontal
disease, role of age in disease progression is
minimal.

 With appropriate dental therapy, and maintenance
of low plaque levels, clinicians can assure older
patients that they can keep a functioning dentition
even though there may be a slightly lower
resistance to bacterial induced periodontal
inflammation and higher levels of putative perio-
pathogens present.

 Glickman’s Clinical Periodontology, 5th edition by Fermin A. Carranza and
Jr. Dr. Odont
 Glickman’s Clinical Periodontology, 7th edition by Fermin A. Carranza and
Jr. Dr. Odont
 Clinical Periodontology, 8th edition by Newman and Carranza.
 Carranza’s Clinical Periodontology, 9th edition by Newman, Takei,
Klokkevold and Carranza.
 Essentials of Periodontology and Periodontics, 2nd edition, by Shantipriya
Reddy
 Essentials of Periodontology and Periodontics, 3rd edition, by Shantipriya
Reddy
 Clinical Periodontolgy and Implant Dentistry, 5th edition, by Jan Lindhe
 Clinical Periodontolgy and Implant Dentistry, 4th edition, by Jan Lindhe

 Periodontal Therapy, 6th edition, By Henry M. Goldman, D.Walter
Cohen
 The Periodontic Syllabus, 5th edition, by R.Vernino, Jonathan
Gray, Elizabeth Hughes
 Periodontics, 6th edition, by B.M.Eley, M.Soory, J.D.Manson
 Periodontics, 5th edition, by B.M.Eley and J.D.Manson
 Outline of Periodontics, 4th edition, by J.D.Manson and B.M.Eley
 Fundamentals of Periodontics by Thomas G. Wilson and
Kenneth S. Kornman
 Critical Decisions in Periodontology, 4th edition, by Hall
 Contemporary Periodontics, by Robert J. Genco, Henry M.
Goldman, D.Walter Cohen.
 Periodontology and Periodontics: Modern Theory and Practice,
1st edition, by Sigurd P. Ramfjord and Major M. Ash.
 Periodontics, 5th edition, by Daniel A. Grant, Irving B. Stern,
Frank G. Everett

 Periodontics, A Synopsis, by W M M Jenkins and C J Allan
 Current Concepts in periodontics, 1st edition, by B.R.R. Varma,
R.P.Nayak
 Textbook of Periodontology, 2nd edition, by Gruraja Rao
 Manual of Clinical Periodontics, Howard L. Ward and Marvin Simring
 Color Atlas of Dental Medicine, Periodontology, 2nd edition, by Klaus H. &
Edith M. Rateitschak, Herbert F. Wolf, Thomas M. Hassell
 Drugs, diseases and the Periodontium, by Robin A. Seymour, Peter A.
Heasman, Ian D.M.Macgregor
 Clinical Periodontology for Dental Hygienist, by Perry and Carranza.
 Foundations of Periodontics for the Dental Hygienist, 3rd edition, by Jill S.
Nield Gehrig, Donald E. William
 Orban’s Oral Histology and Embryology, 13th edition, by G.S.Kumar
 Oral Anatomy, Histology and Embryology, 4th edition, by B.K.B.Berkovitz,
G.R.Holland and B.J.Moxham

 Oral Development and Histology, 3rd edition, by James
K.Avery
 Tencate’s Oral histology, 7th edition, by Antonio Nanci
 Oral Histology-Inheritance and Development, 2nd edition,
by D. Vincent Prowenza and Werner Seibel
 Textbook of Periodontology and Oral Implantology, by
Dilip G Nayak, Ashita Uppoor and Mahesh C.P..
 A Guide to Elderly Care by Dr. O.P. Sharma
 Aging in human attached gingival epithelium, Journal of
Dental Research, Volume 53, No.1, Pages 74-76.
 Alveolar bone loss and Aging: A model for the study in
mice, J Periodontol 2005; 76: 1966-1971
 Casual factors in shortening tooth series with age, the
Journal of Dental Research, Vol 17, No.1, Pages 1-13.

 The effect of age on proliferating cell nuclear antigen expression in oral
gingival epithelium of healthy and inflamed human gingiva, J Periodontol
2000; 71: 1567-1574.
 Aging and the periodontal and peri-implant microbiota, Perio 2000; vol
16, 1998: pages 44-52.
 Treatment of periodontal disease in older adults, perio 2000, Vol 16,
1998; 106-112.
 Thickness of palatal masticatory mucosa associated with age, J
Periodontol 2001; 72: 1407-1412
 Effect of aging on immunocompetent and inflammatory cells, Perio 2000;
Vol 16, 1998, 53-79.
 The potential for increase in the periodontal diseases of the aged
population, J Periodontol, December 1983, Vol 54, No.12, 721-730.
 Age changes and Sex differences in the clinically healthy ginigva, JOP,
pg 13-24, by Frank M.Wentz, Alexis W.Maler and Balint Orban
 Effect of aging on functional changes of periodontal tissue cells, Ann
Periodontol 1998; 3: 350-369.
 Effect of age on periodontium, JCP 1984, 11: 281-294.

4.aging and periodontium.. dr.manisha

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to 4.aging and periodontium.. dr.manisha

Similar to 4.aging and periodontium.. dr.manisha (20)

Recently uploaded

Recently uploaded (20)

4.aging and periodontium.. dr.manisha