effects of aging on periodontium

3. CONTENTS:
INTRODUCTION
FACTORS INFLUENCING AGING
AGE RELATED CHANGES IN
EPITHELIUM
CONNECTIVE TISSUE
PERIODONTAL LIGAMENT
CEMENTUM
ALVEOLAR BONE
BACTERIAL PLAQUE
GINGIVAL RECESSION
IMMUNE RESPONSE

4. TREATMENT OF AGED PATIENTS
WOUND HEALING IN THE AGED
PROGNOSIS
CONCLUSION

5. Shakespeare described the seven
ages of man and observed that the “last
scene ……….. is second childishness
& is mere oblivion, sans teeth, sans eye,
sans taste, sans everything. This
perception becomes less true with each
advance of the calendar.

6. 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

7. 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.

8. A number of cell functions decline progressively
with age and there are morphologic alterations in aging
cells.
 Oxidative phosphorylation 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.

9. Nuclei irregular and abnormally lobed , 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 nonenzymatic glycosylation which are capable of
cross linking adjacent proteins.

10. 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.

11.  Decreased signaling 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.

12. Aging is due to complex interaction of
hereditary and epigenetic factors with
environmental factors.
GENETIC FACTORS
GENETIC FACTORS
Genetic Factors :
 Mutations
 Sex
 Parental age.
 Premature aging syndromes

13. 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.

14. BIOLOGIC THEORIES OF AGING
A) Genetic theories:
Error theory
Somatic theory
Redundancies
Genetically programmed senescence
Disposable soma theory
B) Non -genetic theories
Immunologic theory
Free radical theory
Cross linking theory
Metabolic rate or wear and tear theory

15. ERROR THEORY :Aging is related to progressive
accumulation of metabolic errors in macromolecules.
This theory is more applicable for those cells which
don't divide after they become differentiated
SOMATIC MUTATIONS THEORIES : if the
spontaneous mutations occur in the germ line cells , it
may also occurs in the somatic cells which in turn lead
to alterations in the cells and the tissues functions
leading to decline in the functional capacities & aging.

16. Redundancies: loss of unique , non
repeated, genetic information from the genome
Genetically programmed senescence: is the
extension of an development process

17. NON GENETIC THEORIES:
Immunologic theories :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

18. Free radical theory: short lived, highly reactive
chemicals produced during normal metabolic reactions
which combines with essential molecules , causing
damage to DNA or the other structures, which in
turn contribute to aging
Cross linking theory: caused by molecules becoming
irreversibly immobilized due to cross linking of
substances which play an important role in cell
function.
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.

19.  Thinning and decreased keratinization of the
gingival epithelium (Shklar 1961).
which leads to,
An increase in permeability to bacterial
antigens
Decreased resistance to functional trauma or
both.
But the study conducted by Zarb etal 1998
found no differences in the gingival epithelium
of both humans and dogs

20.  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)

21. 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 ) .

22. 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.

23. 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 .

24. Increase in tensile strength of collagen fibrils
Decrease in extensibility
Increase in thermal contraction
Decrease in ratio of ground substance to
collagen

25. Decrease in amount of soluble collagen
Decrease in collagen turnover
Decrease in water content
Increase resistance to proteolytic enzymes

26. A decrease in the
chondroitin sulphate to hyaluronic acid
ratio has been noted with advancing
age (Milch RA 1966).

27. Location of junctional epithelium has been
subject of much speculation.
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

28. Apical migration of the junctional
epithelium can occur in the absence of plaque
and inflammatory cells. Rushton 1951
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,

29. 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.

30. The interfibrillar areas are reduced in
size.
Fibers are interrupted by larger
interstitial spaces.
The fiber and cellular content decreases.
 Decrease in number of fibroblasts,
osteoblasts and cementoblasts .

31. Number of Calcified bodies in the periodontal
ligament increases .
Two types
Small rounded calcospherites
Larger, irregularly shaped calcification
They appear to form in relation to fibre
bundles. Occasionally they increase in number and
appear to calcify a complete fibre bundle
producing an ankylosis.

32. Calcospherites have been ascribed by
Gottlieb to the inductive activity of
epithelial rests, and their degeneration.
Barnfield and Bartieri attributed them
to inflammation. But, globular
calcospherites were found in areas free of
inflammation.

33. 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.

34. 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.

35.  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)

36. 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 .

37. 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)

38.  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.

39.  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.

40. 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

41. 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 as
age advances a gradual physiological recession of
the gingiva occurs concomitantly with an apical
migration of the epithelium.

42. 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.

43. In contrast results from studies by
Ericsson & 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 there is no gingival recession
the gingival width increases with age.

44. 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 . Recession of
the gingiva has also been found after extrusion
of teeth . It should be mentioned that during
extrusion, inflammation of the tissue developed.

46.  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.

47. Severson et al 1978 studied the age related changes in
adult human periodontal ligament. They found:
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 attachments

48. The width of cribriform plate may decrease
with age.
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.

49. 1) 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.

50. 2) 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.

51. 3) 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)

52. 4) 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

53. 5) 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

54. 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)

56.  Loss of tooth substance due to attrition
 Reduction in cusp height and
inclination due to wear
 Bone loss results in increase in
crown/root ratio

57.  Wear on proximal surfaces results in
physiological mesial drifting
Reduced maxillary/mandibular molar
overjet and an edge to edge bite
anteriorly

58. AGE ALONE SHOULD NOT
DIMINISH AN INDIVIDUAL’S RIGHT
TO CARE.
Treatment options for elderly patient
depends upon factors such as their attitudes
and expectations, previous treatment, medical
complications, and other factors.

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

60. SURGERY?
Age does not contraindicate periodontal
surgery. However, recent 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.

61. 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.

62. 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.

63. 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)

64. 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)

65. SPLINTING
Mobile teeth with no active periodontal disease
may remain functional and in a stable position for
many years.
Splinting should not be undertaken lightly
because it often encourages plaque accumulation and
inhibits its removal.
However, splinting is indicated when the
mobility of a tooth is increasing, or is so great that
exfoliation is threatened, or when it causes
discomfort.

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

67. The authors 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 , the level of risk

68. Studies in man and animals have shown
that the rate wound healing is more rapid in the
young.
Lindhe, 1985 studied the effect of age
healing of the periodontal tissues following
treatment. The data indicated that younger
individual taken as group heal after treatment
as well as an perhaps even better than older
subject.

69. 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).
Van der valden 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.

70. 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 .