Your SlideShare is downloading. ×
Age changes in periodontium
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Age changes in periodontium

906

Published on

Published in: Technology, Health & Medicine
0 Comments
3 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
906
On Slideshare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
59
Comments
0
Likes
3
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. 1
  • 2. SEMINAR ON AGE CHANGES IN PERIODONTIUM Presented by Dr. Vartika Srivastava Pg I yr 2
  • 3. CONTENT  Age Related Changes In;  Epithelium  Connective Tissue  Periodontal Ligament  Cementum  Alveolar Bone  Bacterial Plaque  Gingival Recession  Immune Response  Introduction  Factors Influencing Aging  Theories of Aging  The Aging Periodontium;  Intrinsic Changes  Stochastic Changes  Physiologic Changes  Functional Changes  Clinical Changes 3
  • 4.  Treatment Of Aged Patients  Wound Healing In The Aged  Prognosis  Conclusion 4
  • 5. INTRODUCTION 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. Comfort (1956) defined aging as a biological process that causes increased susceptibility to disease. With age, there are physiologic and structural alternations in almost all organ systems. 5
  • 6. Gottlieb & Orban – Believed that with age, gingival recession and alveolar bone resorption occur and termed it as Senile Atrophy. Aging in individuals is affected to a great extent by genetic factors, diet, social conditions and occurrences of age related diseases, such as atherosclerosis, diabetes, and osteoarthritis. Aging induced alterations in cells are an important component of aging of the organism.6
  • 7. Tencate – Stated that studies on the age changes in the periodontium are on the whole, fairly inconclusive. The World Conference on Periodontology in 1966 reviewed only the few reports in the literature which dealt with the apical downgrowth of attachment epithelium, the width of periodontal ligament and isolated changes in the gingiva. 7
  • 8. Society has long held the belief that tooth loss is an inevitable consequence of aging.  The success of both increased health awareness and preventive dentistry have led to decreasing tooth loss for all age groups. Thus it is important not only to review aging effects in isolation but also from the prospective of their clinical significance to the disease process and their possible effect on the treatment outcomes.8
  • 9. CELLULAR AGING 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. 9
  • 10. REPLICATIVE SENESCENCE: The concept that cells have a limited capacity for replication was developed from a simple experimental model for aging. Normal human fibroblasts, when placed in tissue culture, have limited division potential. Cells from children undergo more rounds of replication than cells from older people. After a fixed number of divisions, all cells become arrested in a terminally non-dividing state, known as Cellular Senescence. Many changes in gene expression occur during cellular aging. 10
  • 11. 11
  • 12. Structural And Biochemical Changes With Cellular Aging A number of cell functions decline progressively with age and there are morphologic alterations in aging cells. 12
  • 13. 13 Oxidative phosphorylati on 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. Irregular and abnormally lobed nuclei , 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 non- enzymatic glycosylation which are capable of cross linking adjacent proteins.
  • 14. 14
  • 15. 15
  • 16. 16
  • 17. Polyamines are polycations that interact with negatively charged molecules such as DNA, RNA and proteins. They play multiple roles in cell growth, survival and proliferation. Changes in polyamine levels have been associated with aging and diseases. Their levels decline continuously with age . 17
  • 18. 18
  • 19. FACTORS INFLUENCING AGING Aging is due to complex interaction of hereditary and epigenetic factors with environmental factors. 19 Genetic factors Environmental factors
  • 20. 20 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.
  • 21. Genes That Influence The Aging Process 21 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. Decreased signalling 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.
  • 22. BIOLOGIC THEORIES OF AGING Redundanci es Somatic Theory Genetically Programme d Senescence Disposable Soma Theory Error Theory Autoimmun e Theory 22 Genetic Theories
  • 23. 23 Non -Genetic Theories Immunologic Theory Free Radical Theory Metabolic Rate Or Wear And Tear Theory Acidification Theory Neuroendocri ne Theory Collagen Theory
  • 24. 24
  • 25. SOCIOLOGICAL THEORIES OF AGING: 25 Role Theory Disengage -ment Theory Activity Theory Continuity Theory Political Economy Theory
  • 26. 26 Genetic Theories
  • 27. ERROR THEORY : First formulated by Orgel . He postulated that the bio-chemical and physiologic changes seen during aging were the result of mutations or errors in regulatory molecules (particularly enzymes) within the cells. The errors accumulated until a bio-chemical catastrophe was inevitable. 27
  • 28.  The failure to document random change was one of the many indicators that random change was not producing aging or put another way, that aging might be different from accumulating disease.  The concept that aging may be the result of programmed change is supported by the experiment; Individual cells, when removed from their hosts and grown in tissue culture or when serially transplanted into young host animals, will propagate themselves for a finite number of divisions.28
  • 29.  The memory of the past divisions is contained in the cell nucleus; If nuclei from old and young cells are transplanted into the opposite cytoplasm the product cells will live as long as the nucleus would have originally done.  It has recently been reported that if young and old cells are fused together the old nucleus will actively inhibit the DNA synthesis in the young cell. This implies that the old cell is actively preventing cell division, rather than having randomly lost needed information for cell division.29
  • 30. Somatic Mutation Theory If the spontaneous mutations occur in the germ line cells , it may also occur in the somatic cells which in turn lead to alterations in the cell and the tissue functions leading to decline in the functional capacities & aging. 30
  • 31.  Redundancies: Loss of unique , non repeated, genetic information from the genome. Genetically Programmed Senescence: It is the extension of an development process. 31
  • 32. Disposal 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. 32
  • 33. 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. 33
  • 34. Autoimmune Theory Autoimmune reaction developed when some of the cells of the body synthesize proteins that differ immunologically from other bodily proteins. Altered proteins cause anaphylactic and immune reaction in the body . Lymphocytes from older patient have impaired proliferated capacity when stimulated by mitogens . 34
  • 35. 35
  • 36. 36 Non Genetic Theories
  • 37. Immunologic Theory: This theory 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 . 37
  • 38. Free Radical Theory: The free radical theory proposed by Harman in 1956, emphases the importance of the mechanism of oxygen use by the cell. Short lived, highly reactive chemicals produced during normal metabolic reactions which combines with essential molecules , causing damage to DNA or the other structures, contribute to aging . 38
  • 39. 39
  • 40. 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. 40
  • 41. Acidification Theory Aging results from the accumulation of acid waste products. These products are not completely excreted from the body which leads to cellular malfunction. 41
  • 42. Collagen Theory Collagen fibers forms at a slow rate The more formation of collagen fibers leads to choking of the cell tissue. It hampers the function of tissues and finally cause cell death. 42
  • 43. 43
  • 44. Neuroendocrine Theory First proposed by Professor Vladimir Dilman and Ward Dean. System is complicated network of bio chemicals that governs the release of hormones which are altered by hypothalamus. 44
  • 45. 45
  • 46. 46 Sociological Theories
  • 47. 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 issues in role theory as applied to the older people. Losses of roles exclude older people from significant social participation and revalue their contribution. 47
  • 48. 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. 48
  • 49. ACTIVITY THEORY: Supports the maintenance of regular actions, roles (formal or informal) and solitary as well as social pursuits for a satisfactory old age. (Havighurst 1963) 49
  • 50. 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. 50
  • 51. 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. 51
  • 52. THE AGING PERIODONTIUM Normal aging of the periodontium is a result of cellular aging. The aging process does not affect every tissue in the same way. 52
  • 53. Intrinsic Changes Stochasti c Changes Function al changes Physiolo gic Changes Clinical changes 53
  • 54. Intrinsic Changes In epithelium a progenitor population of cells (stem cells)is situated in the basal layer , provides new cells. These cells of the basal layer are the least differentiated cells of the oral epithelium. 54
  • 55. 55
  • 56. This differentiated cell or epithelial cell can no longer divide. There is constant source of renewal. 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. 56
  • 57. By the action of gerontogene or replicative senescence (Hayflick’s limit and telomere shortening), the number of progenitor cells decreases. Hayflick, an American microbiologist , observed that fetal cells(i.e fibroblasts)displayed a consistently greater growth potential (app. 50 cumulative population doublings)than those derived from adult tissues(20-30 cumulative population doublings). 57
  • 58. Stochastic Changes These changes occurring within cells also affect tissue; for example , glycosylation and cross linking produce morphologic and physiologic changes. Structures become stiffer ,with loss of elasticity and increased mineralization. 58
  • 59. Somatic mutations lead to decreased protein synthesis and structurally altered protein. Free radicals contribute to accumulation of waste in the cell. 59
  • 60. Physiologic Changes In the periodontal ligament , a decrease in the number of collagen fibres , leads to a reduction or loss in tissue elasticity. With aging ,the alveolar bone shows a decrease in bone density and increase in bone resorption. 60
  • 61. 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. There is reduction in healing capacity and rate. 61
  • 62. Clinical Changes Gingival recession and reductions in bone height. Attrition is a compensatory change that acts as a stabilizer between loss of bony support and excessive leveraging from occusal forces imposed on the teeth. A reduction in “overjet” of the teeth is seen ,manifesting as an increase in edge to edge contact of the anterior teeth. 62
  • 63. 63
  • 64. 64
  • 65. REFERENCES ROBBINS GENERAL PATHOLOGY KUMAR /COTRAN POLYAMINES IN AGING AND DISEASE ;AGING AUG 2011 VOL 3 NO,8 AGING –PROGRAMMED CHANGE DCNA, GERIATRIC DENTISTRY 1989;33 19-22. EFFECT OF AGE ON PERIODONTIUM U VAN DER VELDEN J CLIN PERIODONT 1984; 11:281-294. PERIODONTICS GRANT 6TH EDITION CARRANZA’S CLINICAL PERIODONTOLOGY 9TH and 10th EDITION 65
  • 66. SEMINAR ON AGE CHANGES IN PERIODONTIUM PART -II Presented by Dr. Vartika Srivastava PG I yr66
  • 67. CONTENT 67  Age Related Changes In;  Epithelium  Connective Tissue  Periodontal Ligament  Cementum  Alveolar Bone  Bacterial Plaque  Gingival Recession  Immune Response  Treatment Of Aged Patients  Wound Healing In The Aged  Prognosis  Conclusion
  • 68. CHANGES IN EPITHELIUM: Thinning and decreased keratinization of the gingival epithelium which leads to , an increase in permeability to bacterial antigens and decreased resistance to functional trauma or both.(Shklar 1961). But the study conducted by Zarb et al 1998 found no differences in the gingival epithelium of both humans and dogs . 68
  • 69. 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) 69
  • 70. 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 ) . 70
  • 71. CHANGES IN CONNECTIVE TISSUE 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. 71
  • 72. 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 . 72
  • 73. CHANGES IN PROPERTIES OF COLLAGEN 73 Increase in tensile strength of collagen fibrils Decrease in extensibility Increase in thermal contraction Decrease in ratio of ground substance to collagen Decrease in amount of soluble collagen Decrease in collagen turnover Decrease in water content Increase resistance to proteolytic enzyme
  • 74. CHANGES IN GROUND SUBSTANCE: A decrease in the chondroitin sulphate to hyaluronic acid ratio has been noted with advancing age (Milch RA 1966). Location of junctional epithelium has been subject of much speculation. 74
  • 75. 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. Apical migration of the junctional epithelium can occur in the absence of plaque and inflammatory cells. (Skilleni 1930, Rushton 1951, Beersten et al 1982 ) 75
  • 76.  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, Klingsberg and Butcher 1960) 76
  • 77. CHANGES IN PERIODONTAL LIGAMENT: 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. 77
  • 78. Fibers are interrupted by larger interstitial spaces in older groups. These ranged from small circular areas of 0.05mm to 0.15mm in diameter to large, oblong areas of more than 1mm. these interruption resulted in irregularly spaced areas of dense fiber concentration separated by regions without suspensory fiber attachment The fiber and cellular contents decrease. Fewer fibroblasts, osteoblasts and cementoblasts can be seen. 78
  • 79. Increased fuchsinophila was evident, indicating increased concentration of neutral carbohydrates. Calcified bodies are common in the periodontal ligament of elderly humans. Two types of calcospheroid like bodies are demonstrable: 79 Larger, irregularly shaped calcification Small rounded calcospherite s
  • 80. They appear to form in relation to fiber bundles. They coalesce to from the larger round or irregularly shaped bodies. Occasionally they increase in number and appear to calcify a complete fiber bundle producing an ankylosis. Calcospherites have been described by Gottlieb to the inductive activity of epithelial rests, and their degeneration. 80
  • 81.  Barnfield and Bartieri attributed them to inflammation. Insofar as inflammation is concerned, globular calcospherites were found in areas free of inflammation.  The calcospherites may be ascribed to “age changes” gain support from the observation of similar calcifications in the pulps of aging humans (Bernick 1967) and other organs (Smith JV 1971). 81
  • 82. Epithelial rests in the periodontal ligament show alter forms of aggregation. Rests aggregates tend to contain more cells with both proliferative and degenerative morphology. The PDL has been reported to increase and decrease in with age. Van der Velden explains this discrepancy on the basis of the number of remaining teeth. 82
  • 83. Width Of The Periodontal Ligament Space  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. 83
  • 84.  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. 84
  • 85. CEMENTUM: 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) 85
  • 86. 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 . 86
  • 87. 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) 87
  • 88. 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. 88
  • 89. 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. 89
  • 90. 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 90
  • 91. During cementum formation collagen fibres are embedded within the cementum. The course of the embedded fiber differ in various layers of the cementum depending on the direction of the forces acting on the tooth at the moment of cementum formation (Gustafsson and Persson 1957). Indications exist that cemental deposition shows in old age. Cementocytes exhibit the lowest proliferative capacity. With increasing age the process of cementum formation becomes essentially acellular. 91
  • 92. Aging and Gingival Recession: 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 has age advances a gradual physiological recession of the gingiva occurs concomitantly with an apical migration of the epithelium. 92
  • 93. 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. 93
  • 94.  In contrast results from studies by Manson 1963; Anne Roth and Fricsson 1967; 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 no gingival recessions are present it has been noted that gingival width increases with age . 94
  • 95. 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 (Loe et al 1978).  Recession of the gingival has also been found after extrusion of teeth (Batenhorst et al 1974). 95
  • 96. It may be concluded that, with regard to migration insufficient evidence is available for a physiological apical migration of the junctional epithelium due to aging. It seems probable that periodontal destruction will occur only by mechanical trauma in the presence of plaque and consequent inflammation of the periodontium. 96
  • 97. CHANGES IN ALVEOLAR BONE:  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. 97
  • 98. 98 Experimental animals show: Decreased width of cribriform plate with age. Decrease width of interdental alveolar septum may be a result of interproximal wear of the teeth at the contact area Transformation from immature trabeculated bone to a dense lammellated bone.
  • 99. Proliferative activity of the cells in the osteogenic layer at the surface of the cribriform plate is low compare to cells in epithelium and connective tissue. Decreased trabeculation is often seen which may be related to diminished functional stimulation because of tooth loss or to the presence of osteoporotic changes. 99
  • 100. Severson et al (1978 )studied the age related changes in adult human periodontal ligament. 100 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 attachment
  • 101. 101 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. Areas of intermittent deposition of woven bone were seen throughout the entire socket wall in older specimens; which contrasts with the localization of such areas in young adults at the distal wall of the socket and in the coronal and apical regions of the mesial walls
  • 102. EFFECTS ON PLAQUE  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. 102
  • 103.  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. 103
  • 104.  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) 104
  • 105.  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 105
  • 106. 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. 106
  • 107.  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) 107
  • 108. Effect of Age on Development of Gingivitis: Fransson C, Berglundh T & Lindhe J conducted a experimental gingivitis study to study the response of the marginal gingival to plaque formation in one group of young subjects, 20-25 years of age and in one group of older subjects aged 65-80 years.  The data collected demonstrated that: Old subjects, during a 3 weeks period of oral hygiene abstention formed similar amounts of plaque as the young subjects, but developed more gingivitis than young subjects. 108
  • 109. The clinical gingivitis assessments, the gingival fluid measurements and morphometric determination made in the biopsy samples documented, that the gingival lesion formed in the old individual was more pronounced and contained more inflammatory cells than the corresponding lesion in the young subject samples. 109
  • 110. These findings in all respect correlated the data previously reported by Holm-Pedersen et al (1975) from a trial in humans, who studied the influence of age on the response of gingival tissue to denovo dental plaque in different groups of young and older subjects who reported that the gingival of older subjects responded earlier and more pronounced to plaque accumulation than younger subjects. 110
  • 111. Lesion of young subject had a larger density of lymphocyte but a smaller volume of plasma cells than the infiltrative connective tissue of old subjects. Page and Schroeder et al (1975) reported similar differences in cellular composition of the gingival lesion in a study of young and old monkeys. 111
  • 112. Berglundh and Lindhe (1993) from an experiment in the beagle dog model also confirmed these findings. Studies in man and experimental animals have documented that the periodontal tissue undergo change with age. Such age related qualitative and quantitative alterations occur in intra and extra cellular component of the epithelium and the connective tissue of both gingival, periodontal ligament, root cementum and bone. 112
  • 113. The findings by the Amsterdam group Velden et al 1985, Abbas et al 1986, and Winkel et al 1987 failed to identify age as a factor of importance in response of gingival to denovo plaque formation. The divergent findings in the two groups of studies main part explained by differences in the design of trials performed and in subject samples examined. 113
  • 114. Results from epidemiological investigations show that as soon as the permanent dentition is viable in nearly all instances plaque and gingivitis are present. Yet, the prevalence of periodontal breakdown prior to age of 20 is rather low. Hence in most individuals, plaque may be present for years before gingivitis progress to periodontitis. It may be wondered whether the plaque change with age and/or the response of the periodontium undergoes a change. 114
  • 115. Treatment Of Aging Patient: Hansen GC 1973 conducted a study to determine if certain clinical changes in the oral cavity or more highly correlated with chronologic age (reflected length of exposure to various etiologic agents) with an estimate of biologic age (reflecting length of exposure to various etiologic agents and intrinsic host changes with age). 115
  • 116. He concluded that gingival recession, loss of gingival attachment and the number of total remaining teeth are significantly correlated with both chronological and estimated biologic age of the measured oral variables, gingival recession and loss of gingival attachment were found to be significantly more highly correlated with an estimate of biologic age than chronologic age 116
  • 117. 117 Treatment options fall into 3 modalities Minimum intervention –OHI, fillings and extractions Multiple extractions and dentures More extensive periodontal treatment.
  • 118. SURGERY? Age does not contraindicate periodontal surgery. However, 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. 118
  • 119. 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. 119
  • 120. 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. 120
  • 121. 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) 121
  • 122.  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) 122
  • 123. IMPLANTS IN AGED? Three questions have been posed in relation to the prosthodontic treatment of geriatric patients in the context of osseointegration( Zarb 1994) Can Osseo integrated implants be prescribed for elderly patients? Can successful osseointegration Be maintained as patients age? Can the principles of osseointegration be reconciled with different prosthodontic techniques to facilitate treatment accessibility to geriatric patients?123
  • 124. The author 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 . 124
  • 125. WOUND HEALING: Studies in man and animals have shown that the rate wound healing is more rapid in the young. Du Nouy 1916, Howes & Harvey 1939 found that the rate of healing of skin wound decreased with increasing age.  Holm-Pederson and Zederfeldt 1971, Sussman 1973 reported tensile strength development of skin incision wounds seemed to be retarded in older animals. This was attributed to slower restitution of the microvascular system and an altered fibroblastic function. 125
  • 126. Lindhe, Sockransky, Nyman, Haffajee, Westfelt 1985 studied the effect of age healing of the periodontal tissues following treatment. There data indicated that younger individual taken as group heal after treatment as well as an perhaps even better than older subject. 126
  • 127. The concept that younger individual with moderate to advance periodontal disease has a worse prognosis than in older individuals with similar level of disease (Amsterdam 1974) is probably less related to the healing capacity of this individual than the risk of re-infection over a longer lifespan. 127
  • 128. Abbas 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. 128
  • 129. PROGNOSIS 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). 129
  • 130. CONCLUSION 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 . 130
  • 131. 131
  • 132. REFERENCES 132 ROBBINS GENERAL PATHOLOGY KUMAR /COTRAN POLYAMINES IN AGING AND DISEASE ;AGING AUG 2011 VOL 3 NO,8 AGING –PROGRAMMED CHANGE DCNA, GERIATRIC DENTISTRY 1989;33 19-22. EFFECT OF AGE ON PERIODONTIUM U VAN DER VELDEN J CLIN PERIODONT 1984; 11:281-294. PERIODONTICS GRANT 6TH EDITION CARRANZA’S CLINICAL PERIODONTOLOGY 9TH and 10th EDITION
  • 133. A histologic study of age changes in the adult human periodontal joint Severson etal j periodontol 1978;49:169-200. Factors Influencing Periodontal Therapy For Geriatric Patient Green et al DCNA 1989;33:91-99. Effect of age on healing following periodontal therapy Lindhe et al j clin periodontol 1985;12:774-787. The Effect Of Age On Pcna Expression In The Oral Gingival Epithelium Of Healthy And Inflamed Human Gingiva Nazliel Et al J Periodontol 2000;71:1567-1574. The Elderly At Risk For Periodontitis & Systemic Disease E Persson Etal DCNA 2005;49:279-292. Effect of age on the development of gingivitis :clinical, microbiological and histological findings Fransson C et al J CliN Periodontonl 1996;23:379-385 13 3

×