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Aging and perio

Influence of Aging on Peridontium and general body structure, Treatment Modalities

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Aging and perio

  1. 1. AGING AND PERIODONTIUM Aging: Is a slowing of natural function, a disintegration of the balanced control and organization that characterize the young adult. 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 1994). The historically accepted chronologic land mark of old age is 65 years. Categories of ageing: 1. Functionally dependent elderly (with illness or impairment) 2. Frail and institutionalized elderly 3. Young old (65-70years, healthy and vigorous) 4. Old (75-85years) 5. Old old (85years and older) 1
  2. 2. Demographics: 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 periodontal disease. 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. Stochastic theories: These theories suggest that aging events occur randomly and accumulate with time. These theories include 2
  3. 3. 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
  4. 4. 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 membrane. 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
  5. 5. 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: 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 until death. Common neurons in the high brain centers act as pacemakers that regulate the biological clock during 5
  6. 6. 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 thymus gland. 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 of immunodefeciencies. Immune system begins to decline when the following effects occur: 6
  7. 7. 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 contribution. Role theorist saw cessation of paid work as an enormous loss for older people, who were made to take compulsory retirement. 7
  8. 8. 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 and women 8
  9. 9. 2. Personality influences life satisfaction regardless of role activity. 5. Political economy theory: Townsend (1981)proposes that people experience and status in later life is the direct consequence of political and economic policies. He gives the following example, Older people are forced into a structured dependence as a result of compulsory retirement, thus having to live on a much reduced income. EFFECTS OF AGING: Age changes occur in most systems of the body. 1. SKIN :  Dehydration.  Senile freckles.  Keratoses epithelium.  Thermosensitive.  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 proliferation.  Dry mucous membrane and decreased.  Thinner sweat gland output. 9
  10. 10. 2. HAIR:  Brittle.  Less abundant.  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. 3. EYES:  Enopthalmos.  Presbyopia.  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 lacrimal apparatus.  Corneal flattening and loss of luster.  Fading or irregular pigmentation of iris.  scleral thickening and rigidity, yellowing due to fat deposits.  Impaired color vision due to deterioration of retinal cones. 10
  11. 11.  Decreased reabsorption of intra ocular fluid predisposing to glaucoma. 4. EARS AND HEARING:  Atropy of nerve cells in basal coil of cochlea and organ of corti.  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 cartilages.  Lung rigidity and decreased number and size of alveoli.  respiratory muscle degeneration or atrophy.  Decreased inspiratory or expiratory muscle strength. 11
  12. 12.  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 years.  Heart valve thickening, causing incomplete closure (systolic murmer).  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 flutter.  ECG changes; increased PR, QRS and QT intervals, decreased amplitude of QRS complex.  Heart rate takes longer to return to normal after exercise. 12
  13. 13. 7. GASTROINTESTINAL SYSTEM: Nutrition:  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. Liver changes:  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.  Constipation.  Overall decreased gastric activity. 13
  14. 14.  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 intake.  Decreased renal blood flow leads to water retention and difficulty in removing waste products and drugs.  Nocturnal polyurea.  Prostatic hypertrophy.  Increased renal threshold of sugar excretion. 9. MALE REPRODUCTIVE SYSTEM:  Decreased testosterone production, resulting in decreased libido as well as atrophy and softening of testes.  69% reduction in sperms production between ages 60 and 80. 14
  15. 15.  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.  Shrinking uterus.  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 temperature.  Increased pain threshold. 12. IMMUNE SYSTEM: Blood:  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. 15
  16. 16.  Decreased antibody response, resulting in greater susceptibility to infection.  Tonsillar atrophy.  Lymphadenopathy.  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 haematocrit. 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: 1. GINGIVA: 16
  17. 17.  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 epithelium.  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 denaturing temperature. 3. Periodontal ligament: 17
  18. 18.  Greater number of elastic fibres.  Decrease in vascularity.  Decrease in mitotic activity.  Decrease in the number of collgen fibres and mucopolysaccharides.  Decrease number of fibroblasts and more irregular structure.  Decrease organic matrix production and epithelial cell rests.  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 mucoplysacharids. 4. Alveolar bone:  Osteoporosis.  Decrease in vascularity. 18
  19. 19.  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.  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. 5. Cementum:  Cementum deposition appears to be continuous throught life.  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- junction. 19
  20. 20.  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 aging humans.  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 streptococci. 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, 20
  21. 21. 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 Actinobaccilus actinomycitocomitans. 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 gingival recession. 21
  22. 22. 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. 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 surfaces. 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 fitting dentures. 22
  23. 23. 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 age groups. 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 with aging. 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. 23
  24. 24. SOCIAL AND MENTAL EXAMINATION OF AGING INDIVIDUALS: Elderly patients attitude toward therapy have a significant impact on the success or failure of periodontal therapy. Freedman has described three commonly encountered behavior types. Overdependent: demanding, urgent and repetitious Pseudocooperative: comes on times, pays for service, is friendly and listen to instructions, but some how never carries them out. 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 natural teeth. CONCLUSION: 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. 24
  25. 25. 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 periodontal care. 25