AGING AND PERIODONTIUM
Is a slowing of natural function, a disintegration
of the balanced control and organization that characterize the
Is the process by which a person grows old, irrespective
of the time required. It includes the complex interaction of
biologic, psychologic, and sociologic process over time.
Is an energy process beginning at conception that is
directed by endowments and impelled by perceived
phenomenologic events, which sustain the process until the
biologic mechanism ceases to function (Ebersole and hess
The historically accepted chronologic land mark of old
age is 65 years.
Categories of ageing:
1. Functionally dependent elderly (with illness or
2. Frail and institutionalized elderly
3. Young old (65-70years, healthy and vigorous)
4. Old (75-85years)
5. Old old (85years and older)
The elderly population has increased in an explosive
fashion. In 1900, three million people were considered aged.
Currently the number is 23 million or 11.3%of u.s.population.
It is estimated that by 2030, 67 million persons or 20%of the
population will be 65 years of age or older.
The A.D.A. has reported an increase in the number of
elderly patients seeking restorative and preventive care, yet
older people use fewer dental services than younger adults.
70 % of elderly persons require some dental treatment; yet
only 25%-40% perceive this need, and only 20% -35%
actually seek treatment. Socioeconomic status seems to play a
role, as do functional dependence and poorer health status.
95%of dentulous individuals older than 65 years have
Theories of aging:
Biologic theories of aging:
These theories constitute the cellular aging process which
results in mechanical failure of non-replaceable parts in organ
systems, and morphological problems of the cell development
that gives organs size, shape and structure.
These theories suggest that aging events occur randomly
and accumulate with time. These theories include
1. Gene theory
2. Disposable soma theory
3. Free radical theory and
4. Connective tissue theory.
1. Gene theory: (kyriazis, 1994) supporters of this theory
believe that we have a pool of advantageous and
disadvantageous at birth. Natural selection protects
individuals from harmful effects of disadvantageous genes
prior to reproduction, but once this has taken place
disadvantageous genes cause deleterious effects almost
without control, causing aging, disease and death.
2. Disposable 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.
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. It is thought that proteins
undergo this process leading to cataract formation.
3. Free radical theory:
The free radical theory proposed by Harman in
1956, emphases the importance of the mechanism of oxygen
use by the cell. Free radicals are the charged molecules that
are produced during normal cell metabolism. They are also
powerful oxidants and can destroy cellular components,
particularly the lipids and proteins that make up the cellular
The greatest source of free radicals is the metabolism of
oxygen, which produces the superoxide radical o2. Within the
cell, metallic ions, enzymes and cellular materials combine
with oxygen to form free radicals and compounds. In arterial
walls, oxygen interacts with lipoproteins (substance in
arterial wall), forming free radical. This plays an important
part in pathogenesis of atherosclerosis (kyriazis1994).
Free radical activity is also introduced in to the body
from the environment; the best known source is air pollution.
Other environmental sources thought to cause harmful
cumulative breakdown effects in cells are oxidation of petrol
in car engines, by-products in the plastic industry, drying
linseed oil paints and atmospheric ozone.
4. Cross link OR Connective tissue theory:
The cross-link theory is based on internal and external
behavior of collagen, elastin and ground substances in cells
and tissues. With age collagen develops an increased number
of cross-links. Aging collagen becomes increasingly
insoluble, chemically stable and progressively rigid.
Elastin is the connective tissue mirrors collagen
behavior and is equally prone to cross linkage. Skin that was
smooth, firm and soft becomes drier, saggy and less elastic
DNA also is capable of cross linkage. (Hayflick1987).
Non- stochastic theories consider aging to be predetermined.
These theories include;
1. Neuroendocrinal control theory and
2. Immune theory.
1. Neuro endocrine control theory:
The neuro endocrine control theory focuses on aging as
part of the life span programme regulated by neuro hormonal
signals that begin at the time of fertilization and continue
Common neurons in the high brain centers act as
pacemakers that regulate the biological clock during
development and aging. Aging is manifested in slowing down
or activity imbalance of pacemaker neurons in the
hypothalamus that connect with the pituitary gland. The
pituitary gland is considered to be in direct control of thyroid,
adrenals and gonads. With increasing age, some signal
efficiency of the pituitary-hypothalamas connection is lost or
changed, resulting in the decreased function and an increase
in pathology of most organ and tissue systems.
2. Immunology theory:
Control of immunity is shared by the humoral (B-cell)
and cellular (T-cell) systems. In brief, the humoral system
provides protection for the body against bacterial and viral
infections. Cellular immunity delays hypersensitivity, causes
rejection of foreign tissue cells and organ graft, and provides
protection against tumour formation through the activity of
Autoimmune and immunodefecient diseases in older
adults illustrates the impact of immunological theory on
aging. Amyloidosis, Cancer and Adult-onset diabetes mellitus
have been considered diseases of aging that occur as a result
Immune system begins to decline when the following effects
1. Thymic atrophy and possibly a decrease of thymic
hormone (thymosine) in blood.
2. A significant increase in plasma cell activity.
3. Circulating lymphocytes with an abnormal number of
chromosomes are increased.
ΙΙ.SOCIOLOGICAL THEORIES OF AGING:
The sociological theories include;
1. Role theory.
2. Disengagement theory.
3. Activity theory.
4. Continuty theory
5. Political economy theory.
1. 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 sisces in role theory
as applied to the older people. Losses of roles exclude older
people from significant social participation and revalue their
Role theorist saw cessation of paid work as an enormous
loss for older people, who were made to take compulsory
2. 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.
3. Activity theory:(Havighurst 1963)
Supports the maintenance of regular actions, roles
(formal or informal) and solitary as well as social pursuits for
a satisfactory old age.
The theory is idealistic in the sense that activity may
eventually be limited for some older people by the onset of ill
health and chronic disease.
4. 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. The ideas
important to this perceptive remain fundamental to beliefs
about the aging individual.
1. In normal aging, personality remains constant in men
2. Personality influences life satisfaction regardless of role
5. Political economy theory:
Townsend (1981)proposes that people experience and
status in later life is the direct consequence of political and
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.
EFFECTS OF AGING:
Age changes occur in most systems of the body.
1. SKIN :
Facial lines resulting from subcutaneous fat loss.
Decreased skin elasticity, because of this number
of wrinkles increases with age.
Brown spots due to localized melanocyte
Dry mucous membrane and decreased.
Thinner sweat gland output.
Decreased pigment causing gray or white hair.
Thinning as the number of melanocytes declines.
Pubic hair loss resulting from hormonal changes.
Facial hair increases in post menopausal women and
decreases in men.
Baggy and wrinkled eyelids due to decreased elasticity,
with eyes sitting deeper in the sockets.
Thinner and yellow conjunctiva.
Decreased tear production due to loss of fatty tissue in
Corneal flattening and loss of luster.
Fading or irregular pigmentation of iris.
scleral thickening and rigidity, yellowing due to fat
Impaired color vision due to deterioration of retinal
Decreased reabsorption of intra ocular fluid
predisposing to glaucoma.
4. EARS AND HEARING:
Atropy of nerve cells in basal coil of cochlea and organ
Inability to distinguish high-pitched consonants.
Tinnitis and impairment of sound localization are
increasingly frequent with old age.
Loss of auditory acuity.
5. RESPIRATORY SYSTEM:
Decreased sense of smell.
Nose enlargement from continued cartilage growth.
General atrophy of tonsils.
Tracheal deviation due to changes in aging spine.
Increased anteroposterior chest diameter as a result of
altered calcium metabolism and calcification of costal
Lung rigidity and decreased number and size of
respiratory muscle degeneration or atrophy.
Decreased inspiratory or expiratory muscle strength.
Poor ventilation of basal areas resulting in decreased
surface area for gas exchange and reduced partial
pressure of oxygen.
30% reduction in respiratory fluids, heightening the
risk of pulmonary infections.
6. CARDIOVASCULAR SYSTEM:
Slightly smaller heart size.
Loss of cardiac contractile strength efficiency.
30-35%diminished cardiac out put by the age of 70
Heart valve thickening, causing incomplete closure
5.25%decrease in left ventricular wall thickness
between ages 30and 80.
6.35%decrease in coronary artery blood flow between
ages 20 and 60.
Fibrous tissue infiltration of the sinoatrial node and
internodal atrial tracts causing atrial fibrillations and
ECG changes; increased PR, QRS and QT intervals,
decreased amplitude of QRS complex.
Heart rate takes longer to return to normal after
7. GASTROINTESTINAL SYSTEM:
Decreased salivary flow and decreased sense of taste.
Diminished absorption of calcium and vitamin b1 and
b12, due to reduced pepsin and Hcl secretion.
Decreased intestinal motility and peristalisis of colon.
Decreased gag reflex.
Decreased gastro intestinal secretions, affecting
digestion and absorption.
Decreased motility, bowel wall and anal sphincter tone,
and abdominal wall strength.
Decrease in weight.
Decreased regenerative capacity.
Decreased blood flow.
Decreased glycogen content.
Decreased bile secretion.
Impaired cholesterol metabolism.
Decline in haepatic enzymes involved in oxidation and
reduction, causing less efficient metabolism of drugs
and detoxification of substances.
Gas accumulation due to hypotonic musculature.
Overall decreased gastric activity.
Hypochlorhydria- common at the age of 80 years, with
decreased absorption of calcium and vitamin C.
8. RENAL SYSTEM:
Decline in GFR.
53% reduction in renal blood flow secondary to reduced
cardiac output and atherosclerotic changes.
Decrease in size and number of functioning nephrons.
Reduction in bladder size capacity.
Weakening of bladder muscles, causing incomplete
emptying and chronic urine retention.
Diminished kidney size.
Decreased ability to respond to variations in sodium
Decreased renal blood flow leads to water retention and
difficulty in removing waste products and drugs.
Increased renal threshold of sugar excretion.
9. MALE REPRODUCTIVE SYSTEM:
Decreased testosterone production, resulting in
decreased libido as well as atrophy and softening of
69% reduction in sperms production between ages 60
Decreased volume and viscosity of seminal fluid.
10. FEMALE REPRODUCTIVE SYSTEM:
Declining estrogen and progesterone levels (about age
of 50 years) cause; cessation of ovulation, atrophy,
thickening and decreased size ovaries.
Loss of pubic hair and flattening of labia majora.
Vaginal atrophy, thin and dry mucous lining.
Nipple flattening and decrease in size.
11. NEUROLOGIC SYSTEM:
Degenerative changes in neurons of central and
peripheral nervous system.
Slower nerve transmission.
20% neuron loss in cerebral cortex.
Hypothalamus less effective at regulatory body
Increased pain threshold.
12. IMMUNE SYSTEM:
Increased RBC count and Hb% owing to reduced activity
of bone marrow, and increased fragility of cells.
Anaemias are common.
Loss of ability to recognize and destroy mutant cells.
Decreased antibody response, resulting in greater
susceptibility to infection.
Lymphnode and spleen size slightly decreased.
Some active blood forming bone marrow replaced by
fatty bone marrow.
Decreased vitamin b12 absorption results in reduced
erythrocyte mass and decreased haemoglobin and
13. ENDOCRINE SYSTEM:
Decreased ability to tolerate stress.
Blood glucose concentration increases and remains
elevated than younger adult.
Decreased levels of estrogen and increasing levels of
follicle stimulating during menopause, causing coronary
thrombosis and osteoporosis.
Decreased progesterone production.
50% decline in serum aldosterone levels.
25% decrease in cortisol secretion rate.
AGE RELATED CHANGES IN THE GINGIVA AND
OTHER AREAS OF ORAL MUCOSA:
Reduced or unchanged amount of splinting.
Thinning and decrease in keratinization.
Increased width of attached gingival.
Increase in epithelial permeability to bacterial antigens.
Decreased resistance to functional trauma.
Oral epithelium becomes thinner with age.
An increase or no change in mitotic index of gingival
The keratinization potential of hard palate epithelium
does not change with age.
An increased keratinization of lip and cheek mucosa.
Atrophy of connective tissue with loss of elasticity.
Decrease in the number of protein bound hexoses and
mucoproteins and increase in the number of mast cells.
The cellular component of connective tissue also
decreases with age.
Decreased oxygen consumption.
2. Gingival connective tissue:
Coarser and denser gingival connective tissue.
Qualitative and quantitative changes to collagen-include
increase rate of conversion of soluble to insoluble
collagen, increased mechanical strength, increased
3. Periodontal ligament:
Greater number of elastic fibres.
Decrease in vascularity.
Decrease in mitotic activity.
Decrease in the number of collgen fibres and
Decrease number of fibroblasts and more irregular
Decrease organic matrix production and epithelial cell
Increase in arteriosclerotic changes.
Both in increase and decrease in the width of the
ligament has been described with aging.
Unopposed tooth-hypofunction and masticatory forces
decrease with age, which may contribute to reduction in
the width of the periodontal ligament.
Increase in width may be due to the availability of fewer
teeth to support the entire functional load.
A decrease in the width may also result from
encroachment on the ligament by continuous deposition
of cementum and bone.
A reduction in organic matrix productionand loss of acid
4. Alveolar bone:
Decrease in vascularity.
Decrease in metabolic rate.
Decrease healing capacity.
Increase in the intestinal lamellae.
Decrease in the number of cells in the osteogenic layer
of cribriform plate.
With increasing age the periodontal surface of alveolar
bone become jagged or irregular.
Collagen fibres show a less regular insertion to the
Bone density decreases by around 20% between ages of
45 and 90.
The peak adult bone mass is attained at 35 years,
subsequently bone mass decreases with age.
Cementum deposition appears to be continuous throught
Increase in width is most marked (5-10 times) in the
apical and lingual regeion of the tooth.
A slight increase in the remodeling of cementum also
occurs with age and is charectrised by areas of
resorption and apposition, which may account for
increased irregularity observed on the cemental surfaces
of older teeth.
Cementum deposition is less near cemento-enamel-
Average thickness of 95 μm at age 20 and 215 µm at age
60 has been reported at almost three times increase.
Cemental tears are frequently seen in specimens of
The total width of cementum at age 76 is three times
that at age 11.
6. Effects on plaque:
Plaque increases with age, because of increases in hard
tissue surface area as a result of gingival recession and
surface characteristics of the exposed root surfaces.
Calcium and phosphorus levels increase with age.
Plaque from young patients contains more viable
microorganisms per milligram than plaque from the elderly.
The number of spirochetes is reported to increase in plaque
with increase age. Conversely there is a fall in the number of
In early stages of plaque accumulation there are
significantly fewer bacteria in the elderly patient. This
phenomenon may caused by physiological changes in saliva.
An increase incidence of xerostomia in the elderly may also
contribute to gross accumulation of deposits. Certain enzyme
and immunological differences are apparent in plaque from
elderly patients. Levan hydrolase activity is markedly lower
than in young. The concentration of immune factors (IgA,
IgM, C3, Lactoferrin, Lysozyme and Lactoperoxidase) is
reported to be higher in plaque obtained from older people.
For supra gingival plaque no real qualitative differences
have been shown for plaque composition. For sub gingival
plaque there is increase in number of enteric rods and
pseudomonas in older patients.
There is slight shift in the microorganisms in plaque
with increase in age, they are increase role of
Porphyromonalis gingivalis and decrease in role of
7. Tooth-periodontal Relationships:
The most obvious change in the teeth with aging is a
loss of tooth substance caused by attrition. Attrition is
defined as the physiologic wearing of a tooth as a result of
tooth contact, as in mastication. The degree of attrition is
influenced by musculature, consistency of the food, tooth
hardness, occupational factors, and habits such as grinding
(bruxism) and clenching.
The rate of attrition may be coordinated with other
aging related changes such as continuous tooth eruption and
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
Wear of teeth also occurs on the proximal surfaces,
accompanied by mesial migration of the teeth. Proximal wear
reduces the anteroposterior length of dental arch by
approximately 0.5cm by age 40years.
Abrasion is the pathologic wearing of tooth substance
through some abnormal mechanical process. This describes
the condition in which tooth substance is lost by frictional
effects other than those associated with mastication. It is most
marked in cervical regions of crown on buccal and labial
8. Masticatory Efficiency:
Slight atrophy of buccal musculature has been described
as the 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
Reduced masticatory efficiency leads to poor chewing
habits and the possibility of associated digestive disturbances.
Aged persons select foods requiring less chewing effort when
masticatory efficiency is impaired. A diet high in fiber,
vitamins and comparatively low in fat is beneficial for older
9. Aging and The cumulative effects of oral disease:
Changes such as gingival recession, attrition and
reduction in bone height in the elderly results from the
disease and factors in the oral environment and not from
physiologic aging. The experimental gingivitis models have
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 favour plaque
accumulation and partly from decreased immune response
Inflammation develops more rapidly and wound healing
proceeds more slowly in old than young with the same
susceptibility to periodontal disease.
Rapidly destructive form of periodontal disease occurs
in younger patients and is usually associated with deficient
leukocyte function. Elderly individuals have a slowly
progressive form of the disease that does not result from
impaired leuckocyte function or host defence mechanism.
SOCIAL AND MENTAL EXAMINATION OF AGING
Elderly patients attitude toward therapy have a
significant impact on the success or failure of periodontal
therapy. Freedman has described three commonly encountered
Overdependent: demanding, urgent and repetitious
Pseudocooperative: comes on times, pays for service, is
friendly and listen to instructions, but some how never carries
Perfectionist: makes unrealistic demands with veiled threats,
interprets his or her own symptoms, and adjusts own dentures,
makes suggestions about the diagnosis or treatment plan, and
try to eat with dentures with him or she could not eat with
Geriatric population is expanding, and their needs for
periodontal services are becoming specialized. The variety of
intraoral, medical, social, mental, and physical problems
encountered provide unlimited challenges to the clinicians. If
the needs of the geriatric patient are to be met, clinicians
must be willing to care for each individual with patience. The
mouth must be viewed as a reflection of the systemic
condition, and treatment is approached accordingly.
Dental practioners of the 21st
century should be
comfortable providing comprehensive periodontal care for
aging population. Aging dental patients have particular oral
and general health conditions that dentists should be familiar
with detecting, consulting, and treating.
Medical diseases and conditions that occur more often
with age may require modification to periodontal preventive
tools as well as the planning and treatment phases of