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Age changes in oral tissues

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Age changes in oral tissues

  5. 5. Introduction • Aging is the accumulation of changes over time. • Aging in humans is a multidimensional process. • Like any tissue in human body, dental tissues also undergo changes from the time of development as the age advances
  6. 6. GROWTH Growth is increase in size. DEVELOPMENT Development is progress towards maturity. MATURATION The stabilization of the adult stage brought about by the growth and development TODD
  7. 7. Definition • According to Comfort (1956) Aging is defined as biologic process that causes increased susceptibility to disease.
  8. 8. • According to Athens & Papas Defined as the sum of all morphologic & functional alterations that occur in an organism and lead to functional impairment which decline the ability to survive stress • According to Carranza Aging is defined as a process of morphological and physiological disintegration as distinguished from infant, childhood and adolescence which are typified by processes of integration and coordination
  9. 9. GERONTOLOGY According to Pederson & Loe : Is the study of aging in all its aspects biologic,physiologic,sociologic & psychologic.
  10. 10. GERIATRIC DENTISTRY • “ Geriatric Dentistry is the branch of dentistry that emphasizes dental care for the elderly population and focuses upon patients with chronic physiological, physical and/ psychological changes or morbid conditions/ diseases “
  11. 11. IMMUNOSENESCENCE • Declined function of the immune system with advanced age resulting in increased susceptibility of elderly individuals to microbial infections • is mainly due to the host immune response toward the micro-organisms and their products than the organism
  12. 12. • In 2000, Franceschi et al. coined the term “INFLAMMAGING” in order to refer to a low grade pro-inflammatory status appearing during the aging process.
  13. 13. CAUSES OF AGING • Aging is the end result of various biological processes :  Genetic causes : Where information for the initiation & maintainace of cellular functions are encoded  Cellular causes : Where integrity of somatic cells is maintained  Organ & Organ System Level : Where physiologic functions are performed  Coordination Level:  Physiologic functions are controlled & assembled into complex function
  14. 14. MOLECULAR LEVELS MOLECULE DAMAGE DNA Mutations, epimutations, base modifications, strand breaks RNA Base modifications, miscoding PROTEIN Amino acid modifications, miss incorporation, miss folding, aggregation Carbohydrates, lipids, and molecular conjugates Advanced glycation end- products (AGE), lipofuscin
  15. 15. SENESCENCE SIGNALS • p53 • p16 • p21 • pRB • INSULIN GROWTH FACTOR-1
  16. 16. THEORIES OF AGING • MEDVEDEV Listed 300 theories that have been offered in an attempt to answer this but nothing conclusive comes. • The abundance of theories indicate the multitude of interpretations possible on aging.
  17. 17. 1)Wear And Tear Theory 2) Mathematical Theory 3) Cellular Interaction Theory 4) Collagen Theory 5) Waste Product Theory 6) Endocrine Theory 7) Calcium Theory 8) Somatic Mutation 9) Autoimmune Theory 10)Circulatory Deficiencies Theory
  18. 18. WEAR AND TEAR THEORY • Wear and tear theory postulates that the organism wears out with age. • Each cells contains some specific amounts of vital substances such as enzymes and once these substances are used up these are not replaced. • This leads to death of the cells and finally death of organism
  19. 19. • Cellular interaction theory is based on the dependence of every part of the body on every other part. • Eg. All the endocrine glands are dependent on each other for proper functioning. • Individual cells in any organ are dependent on their neighboring cells. • Any alteration between these will lead to aging of individual. Cellular interaction theory
  20. 20. Collagen theory • Collagen theory postulates that collagen fibers form continuously at a slow rate and the collagen is eliminated slowly . • As there is more and more formation of collagen fibers they lead to chocking of the cells of tissue. • Thus hampering the functions of tissue and finally leads to cell death.
  21. 21. Waste Product theory Metabolic waste products are not continuously excreted from the cells and intercellular fluids. With the time this leads to altered functions and ultimately organism is poisoned and finally leading to its death
  22. 22. Endocrine functions slowly decrease and cell metabolism is slowly affected adversely ENDOCRINE THEORY
  23. 23. Calcium theory Aging is caused by defect in calcium metabolism. According to Selye when large doses of Vitamin D and parathyroid hormone were administered in rats, it resulted in mineralization of many soft tissues. Such changes resembled the changes seen in aged tissue. Injury to the tissue results in calcification (Caliciphyloxis) rendering the tissue non functional
  24. 24. Somatic Mutation theory Somatic cells of the body develops spontaneous mutation. As more and more cells mutate, an appreciable number of cells eventually becomes mutants. Almost all the cell movements are deleterious and eventually the organ becomes inefficient. SOMATIC MUTATION THEORY
  25. 25. Autoimmune Theory • Autoimmune reaction develop when some of the cells of the body synthesize proteins that differ immunologically from other bodily proteins. • These altered proteins cause anaphylactic reaction and immune reaction in the body. • Further lymphocytes from elder patient have impaired proliferated capacity when stimulated. • Thus immune system may be compromised in elderly
  26. 26. Circulatory Deficiency theory Circulatory deficiency result in deficient oxidation of cells, resulting in cell death and further replacement by collagen with increase in collagen deposition more capillaries are choked off resulting in more anoxia.
  27. 27. Free radical theory Introduced by R.Gerschman,1954 • Free radical is a molecule that has one free electron… • Free radical activity is required to produce energy, maintain immunity, nerve transmission…. • But free radicals also attack cell membranes producing metabolic waste products – LIPOFUSCHINS. • Lipofuschins interfere with the ability of the cells to repair and reproduce themselves FREE RADICAL THEORY
  28. 28. The Telomerase Theory • Monumental progress in aging research • States that Cells undergo finite number of replications & The chromosomes shorten a bit with each cell division until some critical point is reached • At that point cell become dormant & dies • These end point are called telomere. • Thereby aging
  29. 29. FACTORS AFFECTING AGING GENETIC 1.MUTATIONS: Several mutations reduces life span 2. SPECIES SPECIFIC LIFE SPAN :-Each species is characterized by its own pattern of aging & maximum life span 3. HYBRID VIGOR :- Out breeding enchancement -The effect of genetic constitution on longevity is perhaps best exemplified where hybrid vigor is demonstrated
  30. 30. 4. SEX :- In humans/animals, female lives longer. 5. PARENTALAGE :- Like father like son. 6. PREMATURE AGING SYNDROME :- Single gene changes results in premature senscence in humans e.g. progeria, cockayne’s syndrome, werner’s syndrome
  31. 31. Environmental factors 1. PHYSICAL AND CHEMICAL :- Pollution, radiations, working atmosphere etc 2. BIOLOGICAL FACTORS :- Nutrition, general health etc 3. PATHOGENS AND PARASITES :- They influence the rate of human development low income group 4. SOCIOECONOMIC CONDITIONS :- Bad housing, stresses etc
  32. 32. General affects *Tissue desiccation *Altered cell permeability *Decreased elasticity *Diminished reparative capacity
  33. 33. • Thus Age related changes do not occur uniformly in individuals, but they are under the influence of genetic and environmental factors.
  34. 34. AGE CHANGES IN ORAL TISSUES TISSUE CHANGES FUNCTIONAL CHANGES 1. Teeth 2. Periodontium -Bone - Periodontal ligament -cementum 3.oral mucous membrane 1.Salivary 2.Taste 3. Deglutition 4.Oral motor function 5. TMJ
  35. 35. ENAMEL Tissue Changes Macroscopic • Dark In Colour • Attrition, Abrasion , Erosion • Longitudinal Cracks • Brittle • Decay resistant
  36. 36. ATTRITION “It is defined as loss of tooth structure resulting from direct functional forces between contacting teeth”
  37. 37. A)Proximal surface attrition (Proximal surface faceting) - Caries susceptible , ↓ cleansibility , - Drifting Decreased arch length • B) Occluding surface attrition (occlusal wear) • -Loss of Vertical dimension of tooth • Loss of Vertical dimension of face + cheek biting + lip biting • -Overclosure of mandible during functional movements, caries prone , TMJ problems
  38. 38. ABRASION Abrasion is defined as loss of tooth structure resulting from direct functional forces between the teeth and external objects.
  39. 39. EROSION • Loss of tooth structure resulting from chemico- mechanical act in the absence of specific micro- organisms • Also termed Abfraction .
  40. 40. LONGITUDINAL CRACKS Excessive tensile strength at the tooth
  41. 41. • Microscopic • Enamel rods are reduced in number • Perikymata(Perikymata an external manifestations of striae of retzius & Imbrication Lines) decreases. NEWLY ERUPTED AGED ENAMEL
  42. 42. Chemical Changes  Levels of N2 & FLOURINE’ therefore,inorganic matrix. Enamel near the surface become DARKER & DECAY RESISTANT There is reduced PERMEABILITY & enamel becomes BRITLLE.
  43. 43. AGE CHANGES IN DENTIN • Dentin is laid down through out life.. • Dentinal age changes are – Changes in physical properties -Vitality Of dentine -Reparative Dentin -Dead Tract - Sclerotic Dentin -Thickness of dentine -Secondary dentine -Aspartic Acid Racemization
  44. 44. Changes In Physical Properties • Dentine becomes dark with age • Density & mineralization increases with age Vitality Of Dentine • Decreases due to decrease in odontoblastic activity Thickness Of Dentine • Increases with age
  45. 45. REPARATIVE DENTIN • Also called as Irregular Dentin/ Tertiary Dentin/ Irritation Dentin • Localised close to the irritated zone of the tooth. • Histopathologically : dentinal tubules lesser in number, irregular, tortuous . • Radiologically : decreased size of pulp chambers and root canals
  46. 46. DEAD TRACTS • Empty tubules filled with air, where odontoblast have degenerated. • In ground sections, they entrap air ,so appear black in transmitted light and white in reflected light. • Decreased sensitivity in these areas. • Probably the initial step to form sclerotic dentin
  47. 47. SCLEROTIC DENTINE Sclerosis is the result of occlusion of the dentinal tubules by a mineral substance with a refractive index similar to that of the rest of the dentine Increases with age
  48. 48. Sclerotic dentine
  49. 49. Aspartic Acid Racemization • Racemization is a natural process which will eventually convert optically active compounds into a racemic mixture. • L-Amino acids → D-Amino acids • The aspartic acid in human tooth enamel shows increasing racemization with age.
  50. 50. • Rate constant = 8.29x10⁻⁴yr⁻ⁱ • This rate constant suggests that in any protein with a long in vivo lifetime, D-aspartic acid will accumulate with age
  51. 51. AGE CHANGES IN THE PULP • The age-related changes of the dental pulp are difficult to separate from physiologic defensive changes • Size and Morphology • Compromised circulation and innervations • Fat droplet deposition • Odontoblastic vacuolization • Reticular atrophy • Pulpal fibrosis • Hyaline degeneration,and • Calcifications.
  52. 52. SIZE AND MORPHOLOGY • ↓ in pulp size • Less prominent pulp horns • More fibrous tissue with mature collagen • Reduction in cellular components • Reduced ground substances
  55. 55. CALCIFICATIONS Pulp calcifications
  57. 57. PULP STONES AGE INCIDENCE (ORBAN,S) a) 10-30 Yr 66% b) 30-50 Yr 80% c) > 50 Yr 90%
  58. 58. Calcific Metamorphosis
  59. 59. • GINGIVA (Epithelium) • Thinning and decreased keratinization of gingival epithelium • Increased width of attached gingiva • An increase in epithelium permeability to bacterial antigens • Decrease resistance to trauma • Reduced stippling • Flattening of rete pegs, altered density. • Gingival recession AGE CHANGES IN THE PERIODONTIUM
  60. 60. Gingival Connective Tissue • More dense and coarse connective tissue. • Quantitative & Qualitative changes in collagen: *↑ in tensile strength of collagen fibrils *↑ in thermal contraction *↓ in extensibility *↓in ratio of ground substance to collagen *↓ in amount of soluble collagen *↓ in collagen turnover *↓ in water content * ↑ resistance to proteolytic enzyme
  61. 61. PERIODONTAL LIGAMENT • Greater number of elastic fibres • ↓ vascularity • ↓mitotic figures • ↓ number of fibrous tissue • ↑ & ↓ width of PDL space • ↑Pocket depth • ↓Chemotaxy, motility and proliferation rate of periodontal ligament cells. • Attachment of PDL fibres to cemental spikes .
  62. 62. ALVEOLAR BONE • ↑ osteoporosis • ↓ vascularity • Alveolar socket appear jagged and uneven • Fewer fibres attached to Bone and Cementum • Marrow space have fatty infiltration • Bone loss • Increase in distance between crest of a alveolar bone and CEJ - 2.81mm
  63. 63. • Recent observations with bone graft preparations from donors more than 50years showed less osteogenic potential when compared with younger age group.
  64. 64. • Rate of formation diminishes with age- scalloped IRREGULAR SURFACE • A thickening of cementum at the apex may obstruct the canal (HYPERCEMENTOSIS). •  in cemental width(5-10 times). •  in width is greater APICALLY & LINGUALLY CEMENTUM
  65. 65. • Acellular Cementum with increasing age. • Calcified bodies called CEMENTICLES are found in PDL in older individual. • Cemental Spikes : Due to scalloping of cementum PDL fibres appears to be attched to the scalloped peaks. EXCEMENTOSIS As cementum thickens with age it envelops these masses(CEMENTICLES) & called as EXCEMENTOSIS
  66. 66. • Thinning • Loses elasticity and becomes atrophic • Smooth Gingiva • Increased keratinization of lip mucosa • Increase in number of mast cells. • Progressive loss of sensitivity due to fibrosis • Flattening of rete ridges • Less moist • Fordyces granules increase in number. AGE CHANGES IN ORAL MUCOUS MEMBRANE
  67. 67. • Stratum Corneum- Decreased keratinization →Smooth mucosal surface • Stratum Spinosum – Reduction Of Thickness → Frequent Ulcerations • Basal Layer- Hyperactivity Of Melanocytes → Dark Pigmentation • Submucosal Membrane → Reduction Of Elastic Fiber
  68. 68. Age Changes In Tongue • Dorsum surface shows loss of filiform papilla • Foliate papillae more prominent. • Fissures increase • Dryness of the mouth • The ventral surface of the tongue shows the presence of nodular varicose enlargement also known as caviar tongue • Loss of tastebuds with age
  69. 69. Caviar tongue
  70. 70. • The thickness of epithelium of lingual mucosa decreased with aging • Acinar atrophy of lingual gland increased with aging, especially quickly in females. • The atrophy of the acinus from- -40 years old in Blandin-nuhn gland -30 in von Ebner gland. • Lingual muscles Decrease in muscle fiber diameter with aging is also observed
  71. 71. AGE CHANGES IN SALIVARY GLANDS Age Changes are - Acinar Atrophy, - Ductal Dilatation, - Fatty infilteration, - Fibrosis, -Peri Acinar Callus -Inflammatory Infiltration -Oncocytes • Submandibular gland – 40% loss of acinar cells • Parotid gland - 30% loss of acinar cells • Minor labial glands - 45% loss of acinar cells formation
  72. 72. Some of the ductal and acinar cells transform into non functional cells called ONCOCYTES. • These cells have swollen appearance eosinophilic granular cytoplasm and pyknotic nucleus. Protein plugs are found more frequently in ducts of older salivary glands. These ducts have a tendency to calcify.
  73. 73. ONCOCYTES
  74. 74. Salivary flow • It is generally believed that salivary flow decreases with age But This reduction in flow is more as a consequence of xerogenic medication taken by an older individual rather than due to the physiologic process of aging
  75. 75. Change in Composition •↑ Phosphorous and calcium content • No change in potassium •↓Sodium •↓Chloride and protein concentration •↓Viscosity of saliva
  76. 76. AT BIRTH • Mouth of full term foetus is sterile • After birth it acquires from mother and from the environment • Consists: streptococcal staphylococcal species Lactobacilli Bacillus, Neisseria and Yeasts. • Mainly Streptococcus salivarius with Staphylococcus albus. ORAL MICROBIAL CHANGES
  77. 77. At Infancy And Early Childhood • ↑microorganisms . • The eruption of deciduous teeth provides a new attachment surface and turns Streptococcus sanguis and mutans as regular inhabitants of oral cavity. • Anaerobes are few in number due to absence of deep gingival crevice. • Actinomyces , Lactobacilli are found regularly
  78. 78. Adoloscence • Max increase in the microbes • Mainly because of the varied tooth morphology Adulthood • Complex microflora • As the teeth are lost the available sites for microbial colonisation decreases and several species diminish. • Edentulous persons harbour few Spirochetes or Bacteroides. • S.sanguis & mutans disappear
  79. 79. Immune Factors • IgA • IgM • C3 specific immune factors • Nonspecific immune factors such as lactoferrin, lysozyme and lactoperoxidase were higher in plaque of older age group
  80. 80. Changes In Oral Motor Function SPEECH MASTICATION DEGLUTITION • TISSUES INVOLVED ARE :-upper lip, lower lip , jaws, tongue, floor of oral cavity, soft palate etc.
  81. 81. SPEECH Speech production is most resistant to aging but that does not mean there are no age related changes in speech. • You can very well perceive differences when person of old age speaks but these are largely related to LARYNGEAL rather than oral events. • The main identifying feature of older speech is an increase in the fundamental frequencies OTHER SPEECH CHANGES MAY OCCUR DUE TO: • EDENTULOUS PATIENT(partial or complete) • ILL FITTING PROSTHESIS.
  82. 82. MASTICATION AND DEGLUTITION ↓Masticatory activity ↓Biting Force (16%) People chew slowly as they get older Older adults are capable of fewer swallows in a 10 second period of time than younger adults Even healthy older persons open their mouth less wide and chew with less power which is thought to be related to loss of muscle bulk with age and which is worsened in edentulous persons
  83. 83. Age changes in jaw bones
  84. 84. Changes In Palate • Changes in the dimensions • Configuration • Surface pattern of the hard palate • Loss of concavity • Flat palate with the loss of the teeth.
  85. 85. • The presence of teeth was associated with the height of the alveolar ridge, which decreased from 7.3 +/- 4.4 mm in specimens with intact teeth to 4.7 +/- 4.1 mm in specimens without teeth (P = 0.020). • Less prominent Palatine rugae • Soft palate becomes smaller in size.
  86. 86. Changes in Maxilla & Mandible • Maxilla resorbs in UPWARD & INWARD direction • Mandible DOWNWARD & OUTWARD so as to become progressively wider thereby leading to class-III relation
  87. 87. Longer the maxilla is edentulous, smaller the denture bearing area • Incisive foramen becomes closer to the residual ridge
  88. 88. Residual Ridge Resorption Consequences of Residual Ridge Resorption # Apparent loss of sulcus width and depth #Displacement of muscle attachment closer to crest of the residual ridge # Loss of vertical dimension of occlusion # Reduction of the lower face height #Anterior rotation of mandible #Increase in relative prognathism #Changes in interalveolar ridge relation #Morphological changes in alveolar bone such as sharp ,shiny uneven residual ridge
  89. 89. AGE CHANGES IN FORAMENS • With the resorption of the alveolar process the mental foramen lies at or near the level of the upper border of ramus. • Denture wearers might face problems due to application of pressure on the mental nerve
  90. 90. AGE CHANGES IN GENIAL TUBERCLES • The genial tubercles project above the upper border of the mandible in the symphyseal region. • These sharp prominence make wearing of the lower denture painful
  91. 91. AGE CHANGES IN TMJ • With increasing age the joint tends to lose its ability to withstand degenerative changes and shows progressive change comparable to those seen in osteoarthrosis.
  92. 92. • Articular disc – May show islands of cartilage and nodules of calcification Joint space – Encroachment of large villi of the synovial membrane into the joint cavities after the age of 50
  93. 93. AGE CHANGES IN MAXILLARY SINUS • Infants & Children – Higher Than The Nasal Floor • Adolescence – Level With The Nasal Floor • Adults – Lower Than The Nasal Floor • Old Age – Level With The Nasal Floor
  94. 94. AGING AND FORENSICS • The techniques used to estimate age by means of teeth include Gustafson's technique Incremental lines of Retzius Perikymata Prenatal and postnatal line formation Racemization of collagen in dentin Cemental incremental lines and Translucency of dentin.
  95. 95. Gustafson used six dental changes connected with aging namely Attrition, Apical Migration Of Periodontal Ligament, Deposition Of Secondary Dentin, Cemental Opposition, Root Resorption And Transparency Of The Root Dentin
  96. 96. PROGEROID SYNDROME • Progeroid syndromes (PS) are a group of rare genetic disorders that mimic physiological aging, making affected individuals appear to be older than they are
  97. 97. • Werners Syndrome • Rothmund –Thomson Syndrome • Blooms Syndrome • Hutchinson Gilford Progeria Syndrome • Cockaynes Syndrome • Restrictive Dermopathy • Xeroderma Pigmentosum • Trichothiodystrophy
  103. 103. To conclude…
  104. 104. REFERENCES • Jose.M: Essentials Of Oral Biology, CBS • Nanci. A: Ten Cates Oral Histology, 8th Ed, Elsevier • Kumar. G S : Orban’s Oral Histology & Embryology, 13th Ed , Elsevier • Berkovitz. B K B: Oral Anatomy , Histology And Embryology,3rd Ed, Mosby • Gerlad Shklar ;The Affect Of Aging Upon Oral Mucosa • Robbins General Pathology Kumar /Cotran
  105. 105. • 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
  106. 106. • Patricia Masters Helfman* And Jeffrey L. BADAT “Aspartic Acid Racemization In Tooth Enamel From Living Humans” 1975 • Age related changes of the dental pulp complex and their relationship to systemic aging. (oral surgery oral medicine oral pathology,December 1991,721- 745) • Dorrit W.Nitzan, et al : The effect of aging on tooth morphology : A study on impacted teeth. Oral Surg Oral Med Oral Pathol. 61 : 54-60 : 1986.
  107. 107. Bullets 1. Bodies seen in reduced inflammation 2. Osteodentine – a type of reparative dentine ..consists entrapped odontoblasts or fibroblasts with fewer dentinal tubules resembling bone. 3. Compensatory curves in aging 4. Clinical crown and anatomic crown 5. Proteins expressed in rep dentine 6. Sclerotic dentine and dead tracts 7. Enzymes in bone remodelling –acid phosphatase and alk.phosphatase, pyroposphatase 8. Cell rests of malazzez degenerate??? 9. Reason for formation of rep dentine 10. Y der is an increase in mast cell population 11. Y der is decrease in bone mass density 12. Y resorption is more in mandible 13. Tmj 14. Diff between pri ,sec & rep dentine 15. Age changes r damaging or protective?? 16. List age changes which r damaging 17. Age changes in pdl