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CONTENTS
INTRODUCTION
Increased life
expectancy and greater health expectations may lead to changes in demand
From older
individuals for periodontal treatment .Therefore, an understanding of the
impact of aging on the periodontium is critical. This topic first reviews the
literature concerning the fundamental aspects of aging on the periodontium,
then examines the broader aspects of aging and the possible effects on
treatment outcomes.
THE AGING
PERIODONTIUM
Normal aging of the periodontium is a
result of cellular aging .In general cellular aging is the basis for the
intrinsic changes seen in oral tissues over time. The aging process does not
effect every tissue in the same way. For example, muscle tissue and nerve
tissue undergo minimal renewal,whereas epithelial tissue, which is one of the
primary components of the periodontium, always renews itself.
INTRINSIC
CHANGES
In epithelium, a
progenitor population of cells (stem cells), situated in the basal layers are
the least differentiated cells of the oral epithelium. A small subpopulation of
these cells produce basal cells and retains proliferative potential of the
tissue. A larger sub population of these cells produces cells available for
subsequent maturation .This maturing population of cells continually undergoes
a process of differentiation on maturation.
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. As the progenitor cells wear
out and die, there were fewer and fewer of these cells to renew the dead ones
.This effect is characteristic of the age related changes and the biologic
changes that occur with aging.
STOCHASTIC
CHANGES
Stochastic changes
occurring within the cells also effect tissues, for eg. glycosylation and cross
linking produces morphological and physiological changes. Structures become
stiffer with a loss of elasticity and increased mineralization
(fossilation).With a loss of regenerated power, structures become less soluble
and more thermally stable. Somatic mutation leads to decreased protein
synthesis and structurally altered proteins. Free radicals contribute to the
accumulation of toxic waste in the cells.All these changes produce a decline in
the physiologic process of tissue.
PHYSIOLOGIC CHANGES
In the periodontal
ligament,decrease in the number of collagen fibres leads to a reduction or loss
in tissue elasticity.A decrease in vascularity results in decreased production
of mucopolysacharides.All these types of changes are seen in the alveolar
bone.With ageing, the alveolar bone show a decrease in bone density and
increase in bone resorption,a decrease in vascularity also occurs.In contrast
however cementum shows cemental thickness.
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 .These changes also affect the immune system and affect healing capacity
and rate.Inflammation when present,develops more rapidly and more
severely.Individuals are highly susceptible to viral and fungal infections
because of abnormalities in T cell function.
CLINICAL
CHANGES
Compensatory changes
occur as a result of aging or disease. These changes affect the tooth or
periodontium that presents the clinical condition.Gingival recession and
reductions in bone height are common conditions.
EFFECTS
OF AGING ON THE PERIODONTIUM
GINGIVAL
EPITHELIUM
Thinning
and keratinisation of the gingival epithelium have been reported with age .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.Other reported changes with aging include the flattening of rate pegs
and altered cell density
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 to a more apical position in the root
surfaces,with accompanying gingival recession.In other animal studies however
no apical migration has been noted .With continuing gingival recession ,the
width of the attached gingival would be expected to decrease with age, but the
opposite appears to be true
Alternatively the
migration of the junctional epithelium to the root surface could be caused by
the tooth erupting through the gingival in an attempt to maintain occlusal
contact with its opposing tooth as a result of tooth loss from attrition. 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.
GINGIVAL
CONNECTIVE TISSUES
Increasing age results in coarse and denser
gingival connective tissues .Qualitative and quantitative changes to collagen
include an increased rate of conversion of soluble to insoluble collagen,
increased mechanical strength and increased denaturing temperature. These
resulted indicate collagen stabilization caused by changes in the
macromolecular conformation .
Periodontal
ligament
Changes include
decreased number of fibroblasts and a more irregular structure paralleling the
change sin the gingival connective tissues. Other findings include decreased
organic matrix production and epithelial cell rests and increased amount of
elastic fibres.Conflicting results have been reported for changes in the width
of periodontal ligament in human and animal models. This findings probably
reflects the functional status of teeth in the studies, because the width of
space will decrease if the tooth is unopposed, or well increase with excessive
occlusal loading .Both scenarios might be anticipated
As a result of tooth
loss in this population.
Cementum
An increase in
cemental width is a common finding; this increase may be 5-10 times with
increasing age
This finding is not
surprise because deposition continues after tooth eruption. The increase in
width is greater apically and lingually.Although cementum has limited capacity
for remodelling ,an accumulation of resorption bays explain the findings of
increasing surface irregularity.
Alveolar
bone
Reports of
morphologic change sin alveolar bone mirror age related change sin other bony
sites.Specific to periodontium are findings of a more irregular periodontal
surface of bone and less irregular insertion of collagen fibers .Over riding
the diverse observations of bony changes with age is the important finding that
the healing of bone in extraction sockets appears to be unaffected by
increasing age. Indeed ,the success of osseo integrated dental implants ,which
rely on intact bone healing responses, does not appear to be age related.
However, balancing this view is the observation thatbone graft preparations
from donors more than 50 years old possessed significantly less osteogenic
potential than graft material from younger ones.
Bacterial
plaque
Dento gingival
plaque accumulation has been suggested to increase with age .This might be
explained by the increase in the hard tissue surface area resulting from
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 the plaque quantity with age. This contradiction may
reflect the different age ranges of experimental groups with variable degrees
of root surfaces exposure and gingival recessions .For supragingival plaque, no
real qualitative differences have been shown for plaque composition.
For subgingival
flora to a normal flora ,where as another study reported enteric rods and
pseudomonas in older individuals. it has been speculated that a shift occurs in
the importance of certain pathogens with age ,specifically including an
increased role for porphyromonas gingivalis and a decreased role for A.a.
However
differentiating true age effects from the changes in ecologic determinants for
periodontal bacteria will be difficult
IMMUNE
RESPONSE
Research advances in
the study of the effects of aging on immune response have altered the
understanding of this phenomenon .Age has been recognized as having much less
effect in altering the host response rather than previously thought.
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
Mr. Arthur concludes
‘Measurement of indications of immune
and inflammatory competency suggested that, within parameters tested, there was
no evidence for age related changes in host defenses correlating with
periodontitis in an elderly group of individuals with and without disease
In summary, although
many contradictions exist, a survey of literature demonstrates that some age
related changes are evident in the periodontium and host responses
EFFECTS
OF AGING ON PROGRESSON OF PERIODONTAL DISEASE
In
classic experiment study, subjects were rendered plaque and inflammation free
through frequent professional cleaning .Once this was achieved the
subjects abstained from oral hygiene measures for periods of 3 weeks to
allow gingivitis to develop.In this experimental model, a comparison of
developing gingivitis between young and older individuals demonstrated a
greater inflammatory response in older subjects, both in humans and dogs.In the
older age group (65 to 80 years), the findings included a greater size of
infiltrated
connective
tissue, increased gingival crevicular fluid flow, and increased gingival index.Other
studies have not demonstrated differences between subjects; this may be related
to smaller differences between the ages of the younger and older experimental
groups.
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 plaqueassociated 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.
Indeed, in comparison
with the odds ratio of 20.52 for poor oral hygiene status and periodontitis,
the odds ratio for age was only 1.24.Therefore age has been suggested to be not
a true risk factor but a background or an associated factor for
periodontitis.28 In addition, the recent reports of a genetic basis for
susceptibility to severe formsof periodontitis underline the overriding importance
of plaque, smoking, and susceptibility in explaining most of the variation in
periodontal disease severity between individuals.
EFFECTS
OF AGING ON THE RESPONSE TO
TREATMENT
OF THE PERIODONTIUM
The successful treatment of
periodontitis requires both meticulous home-care plaque control by the patient
and meticulous supragingival and subgingival debridement by the therapist.
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.
A purely biologic or
physiologic review indicates that the effects of aging on the structure of the
periodontium,function of the immune response, and nature of either
supragingival or subgingival plaque have a negligible impact on an individual's
experience of periodontal diseases.
Aging
might affect other aspects of managing the periodontal diseases , and the
resulting difficulties should not be underestimated.
References
1. CARRANZA'S CLINICAL PERIODONTOLOGY-10TH
EDITION;- Michael G. Newman , Henry H. Takei,
Fermin A. Carranza,
2. CLINICAL PERIODONTOLOGY AND IMPLANT
DENTISTRY-Fifth Edition;- Jan Lindhe ,Niklaus P. Lang, Thorkild
Karring
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