Age changes in dental tissues bhavan

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Age changes in dental tissues bhavan

  1. 1. CONTENTS  Introduction  Definition  Theories of aging  Factors affecting aging  Macroscopic age changes - Attrition  Definition  Types  Clinical features  Treatment - Abrasion  Definition  Causes  Signs and Symptoms  Treatment - Erosion  Definition  Types  Action of erosion  Clinical features  Treatment  Microscopic age changes - Age changes in Enamel - Age changes in dentin  Dentinal sclerosis  Secondary dentin  Tertiary dentin  Dead tracts  Decreased cellular components - Age changes in pulp  Decreased cellular components  Decrease in number of nerve and B.V.  Pulposis  Dystropic mineralization  Denticles  Decrease in number and thickness of collagen fibres.  Age changes in cementum, periodontal ligament  Clinical considerations  References  Conclusion
  2. 2. INTRODUCTION : The science of gerodontology is receiving more attention as life span of individual increases. Like any tissue in human body, dental tissues also undergo changes from the time of development as the age advances. Dental tissues are continuously being subjected to variety of insults, like physical, chemical and thermal etc, which may contribute for the changes in them. However not all the changes that occur can be related etiologically or pathologically and only can be attributed to the general aging process of the individual. The changes may result from a combination of causes including aging process. Age changes can merely effect esthetics and may cause problems like sensitivity, mechanical problems or at later stages can cause pathological changes in underlying pulpal tissues. Most important fact is that aging itself is not a disease. Aging of human tissue is genetically controlled. It has often sand in a jest that “living to ripe old age involves selection of proper parents but unfortunately this is not in hand of an individual”. DEFINITION : According to Comfort (1956) Aging is defined as biologic process that causes increased susceptibility to disease. Aging is also defined as the sum of all morphologic and functional alterations that occur in an organism and lead to functional impairment, which decrease the ability to survive stress. THEORIES OF AGING : Numerous models have been proposed to explain the mechanism of aging. The abundance of theories indicate the multitude of interpretations possible on aging. Many theories presume that a single mechanism is
  3. 3. responsible for all the characteristic of changes seen with aging. Most focus on the derangements that occurs and ignore the possibility that aging may be the result of several independent events involving genetic and environmental insults. Most commonly considered theories are :- 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 theory 9) Autoimmune theory 10)Circulatory deficiencies theory 1) 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. Cells from older patients have decreased capacity to repair deoxyribonucleic acid. This leads to death of the cells and finally death of organism. 2) Mathematical theory: Postulated in empirical mortality curve fits into a formulated equation. 3) Cellular Interaction Theory : 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
  4. 4. on their neighboring cells. Any alteration between these will lead to aging of individual. 4) Collagen Theory : Collagen theory postulates that collagen fibers form continuously at a slow rate and the collagen is eliminated slowly or not at all. 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. 5) Waste Product Theory : Waste product theory postulates that 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. 6) Endocrine Theory : This theory states that endocrine functions slowly decrease and cell metabolism is slowly affected adversely. 7) Calcium Theory : Calcium theory suggests that ageing 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. 8) Somatic Mutation theory : It is postulated in somatic mutation theory that somatic cells of the body develops spontaneous mutation. As more and more cells mutate, an appreciable
  5. 5. number of cells eventually becomes mutants. Almost all the cell movements are deleterious and eventually the organ becomes inefficient. 9) Autoimmune Theory : Autoimmuno theory suggest that 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 by mitogens. Thus immune system may be compromise d in elderly. 10) Circulatory Deficiencies : 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. Changes can also occur in the endothelial cells of capillary, leading to breakdown in the part of FACTORS AFFECTING AGING : Aging, in essence, reflects a complex interaction of hereditary and epigenetic factors with environmental factors.  Genetic factors  Environmental factors Genetic Factors : Evidence that genetic factors play a role in aging is substantial. The principal evidence that aging, as expressed by life span, is genetically determined derives from the following kind of observations. 1) Mutations : several mutations reduce the life span. It is unclear whether life shortening mutations occur in specific longevity genes or the anomalies they produce are fundamentally inconsistent with maintenance of viability.
  6. 6. 2) Species – Specific Life Spans : Each species is characterized by its own pattern of aging and maximum life span. Differences in life span of members of various animal groups argue strongly in favour of a species specific genetic basis for longevity. 3) Hybrid vigor : The effect of genetic construction on longevity is best exemplified by those experiments in which hybrid vigor has been demonstrated, increased longevity seen in hybrids. 4) Sex : In humans, male is shorter lived than the female. Leaving aside social factors such as smoking, it has been hypothesized that if genes carried on the sex chromosomes indicate life span then genes on the x- chromosome may decrease vulnerability to degenerative diseases. 5) Parental Age : Persons whose parents live to an older age have a greater life expectancy than persons whose parents die young. 6) Premature aging syndromes : Single genes changes result in premature senescence in humans Egs. Progeria, Werner’s syndrome, Cockayne’s syndrome. Environmental Factors : Four categories of environmental factors influence rate of aging. 1) Physical and chemical components have been implicated as causing differential rates of aging. Some investigators have claimed that environmental pollutants, radiation affect aging. 2) Biologic factors : Such as nutrition as a probable cause of differential aging is also been considered. 3) Pathogens and parasites have been implicated in influencing the rate of human development and aging, particularly in low income in tropical countries. Although they are important determinants of life expectancy, there is no evidence that they influence the aging process. 4) Socioeconomic factors : Such as poor living conditions, stress of life are believed to accelerate aging process.
  7. 7. Age changes can be further divided into : A) Macroscopic age changes B) Microscopic age changes A) Macroscopic Age Changes includes ; a) Attrition b) Abrasion c) Erosion B) Microscopic age changes includes ; a) Age changes in enamel b) Age changes in dentin c) Age changes in pulp d) Age changes in cementum e) Age changes in periodontium A) MACROSCOPIC AGE CHANGES : Attrition : Definition : “It is defined as loss of tooth structure resulting from direct functional forces between contacting teeth”. Any contacting tooth surface is subjected to attrition beginning from its eruption till it comes in contact to reciprocatory tooth surface. Attrition is continuous, age depending process and above all, it is physiologic process. Attrition affects : Occlusal Surfaces : 1) Occlusal surfaces resulting in the flattening of inclined planes and facet formation. 2) Proximal contact areas : It leads to flat proximal areas and in some cases concave proximal surfaces.
  8. 8. Types : A) Proximal surface attrition (Proximal surface faceting) B) Occluding surface attrition (occlusal wear) A) Proximal Surface Attrition : Definition : It occurs from loss of surface tooth structure and flattening and widening of proximal contact area. Results of Proximal Attrition : 1) Proximal surface area is increased in dimension and this area is more susceptible to decay. 2) Decrease in dimension of surrounding embrasures, which will affect cleansability. 3) Mesio distal dimensions are decreased resulting in drifting. 4) Further due to this drifting there is decrease in dental arch length. All of these above will result in difficulty in plaque control and than leads to periodontitis. B) Occlusal Surface Attrition (Occlusal Wear) : Definition : It is loss, flattening, faceting and reverse cusping of occluding surfaces. Affects or Results of Occlusal Wearing : 1) Loss of Vertical Dimensions of Tooth : A) Loss occurring in short time B) Loss occurring in greater time A) Loss Occurring in Short Time : If loss of vertical dimension occurs in short time and is severe than there will be no chance for the alveolar bone to erupt occlusally to compensate for
  9. 9. vertical tooth loss.  This will result in loss of vertical dimension of face.  This will result in overclosure of mandible during functional movements  cause strain in stomatognathic system. B) Loss Occurring in Longer Period : When loss of vertical dimension occurs for longer period i.e. 10-15 years. Then alveolar bone can grow occlusally  Thus bringing teeth to their occlusal position. Further there is no loss of vertical dimension of face. But there is loss of vertical dimensions of tooth. 2) Deficient Masticatory Capabilities : Deficient masticatory capabilities can also result from occlusal wear. Blunting of cusps  Compells patient to apply more forces of mastication to crush the food for proper swallowing  These forces strains the muscles and teeth, periodontium and joints. 3) Cheek Biting (Cotton Roll Cheeks) : Cheek biting also occurs as a result of occlusal wearing. Occlusal wear will lead to flattening of cuspal elements  Vertical overlap between working inclined planes is lost. This will result in cheek bite, lip bite or even tongue bite. Gingival irritation can also occur due to food impaction and closeness of occlusal table to gingiva. 4) Decay : Can also result from attrition as there is loss of enamel as a result dentin is exposed and thus dentin is more susceptible to decay. Attrition will lead to reverse cusps which will lead to reverse cusps which will lead to dentin exposure and this dentin is more susceptible to decay.
  10. 10. 5) Tooth Sensitivity : Tooth sensitivity can also occur from occlusal wear. Attrition  Excessive force  Dentin exposure  Pulpal exposure Apical Strangulation  tearing of PDL Microcracks 6) TMJ Problems : Attrition  Excessive force  TMJ problems  Strain on stomatognathic system. Treatment : Treatment of attrition depends upon several factors i.e. a) Whether it is related to one tooth. b) Whether it is related to whole arch c) Whether there is less tooth loss d) Whether there is loss of entire crown Following is the sequence of treatment of attrition : - 1) Pulpally exposed teeth : Pulpally involved teeth should undergo endodontic therapy or they may be extracted. Depending upon these future role in stomatognathic system and restorability. 2) Parafunctional habits : Parafunctional habits such as bruxism should be treated with ‘occlusal splints’. 3) Myofunctional habits : TMJ problems and other Myofunctional problems should be diagnosed and proper treatment should be given. Sometimes ‘occlusal splints’ are helpful in treating such problems. 4) Occlusal equilibration : Occlusal equilibration is done  If there is little loss of tooth stricture.  If remaining tooth structure can be reshaped to effect mandibular movements. Occlusal equilibration includes selective grinding of tooth surfaces, rounding and smoothing of occlusal table. One should create adequate overlap between working inclines.
  11. 11. 5) Protection of exposed dentinal areas : Exposed dentinal areas should be protected and actual carious lesion should be removed and obliterated. Protection : can be provided by using fluorides solution. Obliteration : Is obtained by proper restoration. During this periodontium should be examined and any pathology should be treated. 6) Restorative Procedure : Restorative procedure can now be done. Attrited tooth structure is under high stress. Therefore only metallic crowns should be used to replace them. Restorations are needed in following situations : A) When there is excessive loss of vertical dimension and is effecting stomato-gnathic system. B) There is extensive loss of tooth structure either localized or generalized. C) Decay or any other lesion which is super imposed on attrition. D) Tooth is cracked or endo-treated. E) When there is greater loss of tooth structure proximally which is not capable of maintaining proper state of periodontium. F) Reshaping of tooth structure is not capable of creating physiologic mandibular movements. Most commonly restorative materials are used to reduce vertical dimensions. They should be used very cautiously and carefully in the following sequence. A) Verify and reverify necessity of restorative material : Be sure that alveolar bone does not grow occlusally with the same pace that attrition occurs. If bone grows at the same pace then occlusal level of the tooth is maintained and any building up of such rest in will impinge the free way space and thus resulting in bruxism or other parafunctional habits. B) Estimate of loss vertical dimension : Estimate of vertical dimension must be made that how much vertical dimension is lost. Firstly we take the estimate of vertical dimension as it is done in case of dentures i.e. from Nasion to Gnathion.
  12. 12. Then measure vertical dimension, when patient brings his teeth together. Difference of these two is calculated – (minus) free way space (2-3 mm) should give us the estimate for how much the height of crown is needed. C) Estimate of additional vertical dimension : Estimate of how much additional vertical dimension can be accommodated by stomato-gnathic system. - If attrition occurred over a long period (15 years) then with the time there is permanent physiological change which cannot be disturbed. - If there is decreased in vertical dimension for more than 2 mm then temporary restoration or removable occlusal splint is used because one can go for addition or removal of material. Composite temporary restorations are most commonly used. Then gradually additions are done to increase vertical dimensions. But before adding the restorative material one should again verify that entire stomato-gnathic system is tolerating the previous addition of vertical dimension and is ready for one more addition. These additions are continued unless there are symptoms of intolerance. When these symptoms appears then there the dimension is further decreased until symptoms disappears. D) Permanent restoration . Permanent restoration is done in a cast alloy. 1. Fully adjustable articulator. 2. Hinge axis determination 3. Stereographic tracing 4. Facebow records are must for these cases. 5. These permanent restorations are firstly given temporarily for some time. Patients who have undergone treatment in this way should undergo periodic occlusal equilibration. OTHER CASES :
  13. 13. A) When there is no need to increase in vertical dimension and in such cases one should also give cast metal restorations to preserve the remaining tooth structure and integrity of surrounding tissues. B) Cases with carious lesions or defects superimposed attrition and the lesion is small and there is greater amount of remaining tooth structure then amalgam and gold restorations can be given. But when the carious or defects are greater then cast metal restoration is given again occlusal equilibration is done. ABRASION : Definition : “Abrasion is defined as loss of tooth structure resulting from direct functional forces between the teeth and external objects. Or from frictional forces between contacting teeth in presence of abrasive medium”. Abrasion can affect one or more teeth as entire dentition. Any surface can be affected but most commonly affected areas are cervical areas. Causes for Cervical abrasion : 1) Faulty brushing technique : Most common cause of abrasion is faulty brushing technique i.e. Horizontal brushing technique. Excessive forces, time during brushing also causes cervical abrasions. 2) Oral hygiene products : Oral hygiene products are also responsible for abrasions. Eg. Hardness of bristles, Amount of dentifrice used, Grip of tooth brush. Powders are 5 times abrasive than tooth pastes. 3) Ill fitting clasps of RPD are also responsible of cervical abrasions. 4) Tooth picks and interproximal brushing. Enamel is not easily abraded. Dentin is 25 times faster abraded then enamel Cementum is abraded 35 times faster than enamel
  14. 14. Abrasion can stimulate formation of secondary dentin, sometimes abrasion rate is greater than the secondary dentin formation and this can result in direct or indirect involvement of pulp. TOOTH BRUSH ABRASION : Most common abrasion is tooth brush abrasion, which occurs cervically. Mostly on facial prominent teeth i.e. canine and premolar. It occurs usually on left side of light handed individuals and right side of left sided individuals. Tooth brush abrasion usually depends upon : - a) Direction of brushing strokes eg. Horizontal direction. b) Size of abrasive particle : Larger size and irregular size of abrasive particles will cause more abrasion. c) Percentage of abrasive : More the percentage of abrasive more will be the abrasion. d) Type of abrasives : Silica abrasives are much more abrasive than phosphate and carbonate. e) Bristles : Diameter of bristles : More the dia more the abrasion. Type of bristles : Natural bristles are more abrasive than synthetic ones. f) Forces used during brushing : More forces more abrasion. g) Type of tooth tissue abraded Least enamel Enamel is not easily abraded. Dentin is 25 times faster abraded then enamel Cementum is abraded 35 times faster than enamel SIGNS AND SYMPTOMS : A) Defects : 1) Notch / V shaped defects : Where oblique occlusal and cervical walls intercet at a certain depth with no axial wall. 2) C-shaped defects : Where defect is C-shaped with rounded floor.
  15. 15. 3) Undercut concave : Where oblique occlusal and cervical wall intersect. Each other with axial wall in between them. 4) Divergent box : Where definite axial wall is present with divergent occlusal and cervical walls. B) Cervical lesions generally have 6. Sharpely defined margins. 7. Hard smooth surfaces 8. Burnished appearance C) They may also exhibit scratches. D) Hypersensitivity also occurs with appearing and disappearing intervals. Depths : Abrasion lesion may be of varying depths : 1) Shallow (S) : 0.1 to 0.5 mm in depth. 2) Deep (D) : 0.5 mm but no pulpal exposure. 3) Exposed : Exposed pulp Other Habits : Many other habits can also cause abrasion such as : - 1) Chewing tobacco – Causes generalized abrasion. 2) Forcing tooth picks. 3) Interdental stimulates 4) Solid plaque control, measures can cause interdental abrasion 5) Cutting sewing thread with incisor teeth 6) Pulling nails with incisor teeth. 7) PICA Syndrome : Habit of chewing clay also leads to certain pattern of abrasion. Iatrogenic Tooth Abrasion : This is caused by 9. Porcelain teeth opposing natural teeth.
  16. 16. 10.Rough occluding surface of restoration can also lead to abrasion. TREATMENT : Treatment should be carried in following sequence. 1) Diagnosis of Cause : First step is to diagnose the proper cause of abrasion. If there is no proper diagnosis and we give the restoration it will abrade after some time or opposing natural tooth can abrade or teeth could move. 2) After knowing the cause then correct iatrogenic factors or cause : Then remove iatrogenic cause of abrasion and if required break the habits. If success occurs then go for restorative procedure and if there is no success then go for further treatment. 3) If habits cannot be broken : Then in some cases restorative treatment can bypass the effect of habit. But most important thing is to stop the habit totally as it will help in proper functioning of stomatognathic system. 4) Evaluation of abraded tooth surface : A) when there is no need to restore abraded surface a) Lesion in Dentin : If lesion is shallow, multiple and not exceeding 0.5 mm within the dentin there is no need to restore them. b) Enamel and cementum : If lesion involves enamel or cementum only there is no need to restore them. c) If lesion is not restored then the edges or margins of the lesion are made smooth so that there is no accumulation of plaque and also it looks quite aesthetic and tooth surface is then treated with fluorides. B) Need to restore abraded tooth surface : When lesion is wedge shaped and is 0.5 mm into dentin then the lesion should be restored. 5) Desensitizing of dentin: Before restoration of tooth surface it is very important to desensitize dentinal surface. This may take several visits.
  17. 17. If tooth is restored in single visit then tooth may remain sensitive to thermal changes forever. Desensitizing : Is particularly done by application of fluorides. 8-30% stannous fluoride for 4-8 minutes or with Ionophoresis : in this galvanic energy is supplied to the tooth in presence of electrolyte which drives fluoride ions deep into dentin. 6) Restorative Treatment : A) When anterior tooth or facial surface of posterior tooth is affected then restoration is done with direct tooth colored materials. In most of the cases no restorative procedure is required because there is direct physicochemical adhesion between tooth and colored materials. B) Posterior teeth: If there is need of cavity preparation it should not be done as it will impinge pulpal tissue and root canal system due to this tooth becomes sensitive forever. One should always use physico-chemically adhering tooth and colored materials. Although this is not so durable but it is more safer than the metal crowns. Therefore such lesions are treated again and again. EROSION : Definition : Loss of tooth structure resulting from chemico-mechanical act in the absence of specific micro-organisms. Erosion is one of the most predominant oral pathologic change and 18% adult population was effected according to one study. Etiology : There is no particular etiology for erosion till now. It is caused by multiple factors, following are most common causative agents. a) Ingested acids b) Salivary citrates c) Secreted acids
  18. 18. d) Mechanical abrasion e) Microbial metabolic products f) Acid fumes g) Excessive tensile stresses at tooth clinical cervix h) Refused acids i) Salivary flow A) Ingested Acids : Ingested acids can lead to an erosion. These acids are (a) citric acid (Lemon or citrus fruits) especially in large amount can produce erosion. (b) Other acids found in Deodizers, can lead to erosive process. B) Salivary citrates : Some authors said that salivary citrates help or produce erosion but others has disproved this fact. C) Salivary flow : Patient with decreased salivary flow and buffering capacity are more prone to erosive lesion. D) Secreted acids : Acids exists in gingival cervice due to occlusal trauma (Bruxism). This acidic crevicular fluid is responsible for crevicular erosion. Although this acidic GCF cannot be fully responsible for erosive lesion, it can act as a ppting factor. E) Acid fumes : Environmental acidic fumes has been correlated to number of erosive lesions in certain populations. F) Refused acids : As a result of frequent regurgitation (forced or non forced) stomach hydrochloric acid can hit the teeth at specific location and causes erosion. (Lingual surface of upper teeth especially molars and premolars). G) Mechanical abrasion : Can act as a contributing factor. H) Chelating microbial metabolic products : Most common product which can cause erosion is pyrophosphate. It could be one of the contributing factors.
  19. 19. I) Excessive tensile strength at the tooth clinical cervix : Excessive tensile strength can also lead to erosion. As when excessive forces are applied on tooth structure, at tooth cervix. There is thin enamel present in this area. These forces will lead to separation of enamel prisms and the underlying dentin.  These can easily peel off or develops cracks.  Then there is penetration of acids and this will lead to erosion. This is most commonly seen in facial surfaces. Erosion can be Intrinsic or Extrinsic : I. Intrinsic Erosion : Intrinsic erosion is seen in the following situations : - A) Gastric Acid Contact : Gastric acid contact to the teeth during recurrent vomiting, regurgitation can lead to erosion.  This is particularly seen in psychosomatic disorders. Eg. Nervous vomiting, self induced anarexia, nervousbulimia etc. or somatic disorders like – pregnancy, peptic ulcers, gastric dysfunction constipation, duodenal ulcers.  This type of intrinsic erosion is most commonly seen on lingual surfaces of anterior teeth especially maxillary. Because accumulation of vomitus on dorsum of tongue first reaches this area. B) Disease due to lack of oxygen as faulty metabolism : Diseases due to lack of oxygen or faulty metabolism results in excessive formation of acid sodium phosphate, acid calcium phosphate from labial and buccal mucous glands. Mostly seen on labial surface of anterior teeth. C) Acids from periodontal tissue II. Extrinsic Erosion : Extrinsic erosion is most commonly caused from ; A) Acids battery factories. B) Chlorinated swimming pools C) Low pH medications like – Iron tonics
  20. 20. D) Aspirin E) Hydrochloric acid placements. F) Most commonly caused and damaging acidic ducts are 11.Fruit rich diets 12.Lemon 13.Vinegar 14.Phosphoric acid in fruit juices 15.Ascorbic acid / citric acid added to variety of drinks Citrate ions binds with calcium in enamel and dentin forming soluble calcium citrate. G) Drug fasting : Also during fasting one use to drink acidic drinks and this combination of acidic drinks and reduced salivary flow are responsible for increased rate of erosion. Lesions Location : Lesions because of acidic diet and medicines are seen on facial surface of anterior teeth. Fruits – Anterior teeth Fruit juices – Premolar and molar Cervical surfaces are more prone as they are close to gingiva and less cleansable.  Prolonged contact of acid to tooth surfaces leads to erosion. Eg. When beverage is swished inside the oral cavity this leads to depression of pH in oral cavity for longer period of time and lead to erosion. Action : How Erosion is Produced : In erosion mineral dissolved from enamel particularly depends upon following thing. 16.pH 17.Buffering effect
  21. 21. 18.Amount of calcium, phosphate, and fluoride present in the drink. When there is drop in pH, solubility of enamel apatite increases. At pH 3 solubility is 75 g/L which increases sharply to 400 g/L at pH of 2.5. But when pH is 4 it is possible to counteract the enamel dissolution by adding calcium phosphate to the drink. Below this pH as solubility of enamel increases very much then even additional CaPO4 will not help more. Ability of acid solution to dissolve enamel apatite depends upon : For how long it on maintain pH at lower level and prevent itself from dissolution by saliva or dissolution by the apatite and this property of drink is of a buffering effect. Higher the buffering effect greater will be the apatite dissolved. Role of Saliva : Saliva plays very important role in reducing the erosive effects by following mechanisms. 1) Dilution and clearance of erosive agent from oral cavity. 2) Neutralization and buffering of dietary acids. 3) Formation of pellicle layer on surface of enamel which protects it from demineralization. Clinical Features : 1) Lesion surface is glazed. 2) Erosion usually does not effect occluding surfaces. Except in advanced lesions. 3) Erosion rate is same for enamel, dentin, cementum and sometimes for restorative material. 4) P.D. reacts by both healthy and unhealthy reactions. 5) Adjacent periodontium and gingiva are almost healthy. 6) Carious lesion do not occur on the tooth surfaces attacked by erosion.
  22. 22. It is noted that loss of tooth structure by lesion is just 1 µ/day and formation of reparative / sec dentin 1.5 – 4 µ/day. So there are very rare or no chances of pulpal exposure. Treatment Modalities : Although the exact cause for erosion is not known, complete analysis of diet, occlusion, habits, chronic vomiting and environmental factors should be performed for patients exhibiting these lesions. Every attempt should be made to correlate the presence of the lesions to possible causes. After this initial correlation, try to eliminate the causes. The patient should be informed that this may not be the cause, but it is the most probable one. He should be told that the treatment to be pursued is mainly symptomatic, and that corrective therapy will, by no means, stop the disease. He should also be told that the process could recur, not only affecting tooth structures, but the restorative material, as well. Preoperative study models or photographs should be taken and kept for future references. This is to evaluate the progress of the lesion, if no restoration is the treatment modality, and to see the extent of recurrence, if a restoration is the treatment modality. There should not be any rush to attempt restorative modalities, except in extremely symptomatic or disfiguring lesions. It is preferable to observe the rate of the lesion's progress and, according to this observation, choose the most appropriate restorative procedure, or decide if treatment is even indicated at all. The rest of the treatment is exactly as described for abrasion and attrition, except that, if possible, metallic restorations should be the material of choice if restorations are indicated. Metallic restorations have proven to be more resistant to the erosion process than non-metallic ones. Tooth-colored materials capable of chemico-
  23. 23. physical bonding to tooth structure can also be used with minimum or no tooth preparation, with the assumption that the restoration may require periodic replacement. The use of these materials is especially indicated when the erosive lesion is extremely deep, badly disfiguring, or when it is expected that the underlying pulp-dentin organ is undergoing advanced degeneration. Again, all this should be done with the understanding that the lesion might progress around these restorations and even involve them.
  24. 24. MICROSCOPIC AGE CHANGES : Age changes in the structure or internal age changes. Age Changes in Enamel : Enamel is a highly mineralized tissue that forms a protective covering of variable thickness over the entire surface of the crown. Because of its high content of mineral salts and their crystalline arrangement, enamel is the hardest calcified tissue in the human body, whose function is to form a resistant covering of the teeth rendering them suitable for mastication. The most apparent age change in enamel is wear that occurs over the surface either as attrition, abrasion or erosion. In addition to the gross changes that occur due to wear, enamel surface itself undergo post-eruptive alterations in structure at the microscopic level. These result from environmental influences and occur with a regularity that can be related to age. The surfaces of unerupted and recently erupted teeth are covered completely with pronounced rod ends and perikymata. At the points of highest contour of the surfaces these structures soon begin to disappear. This is followed by a generalized loss of the rod ends and a much slower flattening of the perikymata. Finally, the perikymata disappear completely. The rate at which structure is lost depends on the location of the surface of the tooth and on the location of the tooth in the mouth. Facial and lingual surfaces lose their structure much more rapidly than do proximal surfaces, and anterior teeth lose their structure more rapidly than do posterior teeth. Perikymata an external manifestations of striae of retzius. They are transverse grooves that run over the enamel. Age changes within the enamel proper have been difficult to assess microscopically. The fact that alterations do occur has been demonstrated by chemical analysis, but the changes are not well understood. For example, the total amount of organic matrix is said by some to increase, by others to remain
  25. 25. unchanged, and by still others to decrease. Localised increases of certain elements such as nitrogen and fluorine, however, have been found in the superficial enamel layers of older teeth. This suggests a continuous uptake, probably from the oral environment, during aging. As a result of age changes in the inorganic portion of enamel, presumably near the surface, the teeth may become darker, and their resistance to decay may be increased. Suggestive of an aging change is the greatly reduced permeability of older teeth to fluids. There is insufficient evidence to show that enamel becomes harder with age. AGE CHANGES IN DENTIN AND PULP : Age changes that occur in pulp and dentin are : a) Decrease in cellular components b) Dentinal sclerosis c) Decrease in number and quality of blood vessels and nerves d) Reduction in size and volume of the pulp owing to - Secondary dentin formation - Reparative dentin formation e) Increase in number and thickness of collage fibres. f) Increase in pulp stones and dystrophic mineralization. Age Changes in Dentin : Age changes that occurs in dentin include : - A. Dentinal sclerosis B. Formation of secondary dentin C. Formation of tertiary dentin D. Dead tracts E. Decrease in cellular components A. DENTINAL SCLEROSIS : Dentinal sclerosis is associated with ; - Ageing - Dental caries - Abrasion, Attrition, Erosion
  26. 26. - Certain rays Dentinal Sclerosis Due to Ageing : I. Primary dentinal tubules are affected by ageing. There is increase in peritubular dentin (dentin that immediately surrounds dentinal tubes). Increase in deposition of appetite crystals. The dentinal tubules are ultimately occluded resulting in formation of condition called “Sclerosis of Dentin”. Sclerosis occurs in apical third of root with ageing. Odontoblasts lining sclerotic dentin becomes reduced in number and then disappears. According to Miles (1972) these are due to cell-mediated age changes. Absence of tubules causes transparent appearance of dentin. II. Sclerosis of dentin also occurs with dental caries Dental caries tries to elicit the reaction within primary dentinal tubules, which tends to slow down the progress of the disease. Pulp defends itself quite effectively because of this response. As a response to this decay, dentinal tubules of primary dentin gradually becomes mineralized provided that odontoblasts remain vital. This process of sclerotic dentin forms the vital line of defence of pulp against dental caries. Bradford (1960) : Noted that where dead tracts forms instead of sclerotic dentin caries spread more rapidly towards the pulp. Thus rapid carious penetration occurs more in younger teeth, then older teeth as in older teeth caries spread along dentino enamel junction. III. Dentinal sclerosis because of abrasion, attrition and erosion. Sclerosis of dentin can also occurs in response to certain irritations like. 1) Attrition 2) Abrasion
  27. 27. 3) Erosion 1) Sclerosis due to Attrition : • Sclerosis due to attrition is permeable to dies this is due to opening of some dentinal tubules. • Sclerosis in attrition occurs because of 2 particular patterns. i. Continuous growth of intratubular dentin. ii. Intratubular crystal deposition. Mendis and Daroling (1979) found that pretubular dentin thickness is increased by only 20% by attrition. Lumina of tubules was filled by large crystals. 2) Sclerosis due to erosion : Erosion Definition Loss of tooth structure resulting from chemico-mechanical act in the absence of specific micro-organisms. So under erosion mineral are deposited within the tubules leading to sclerosis. IV. Certain drugs leading to dentinal sclerosis : • Calcium hydroxide • Corticosteroids, when placed after cavity preparation leads to dentin sclerosis. • Some remineralization also occurs when sedative dressing such as zinc oxide eugenol are placed in carious cavities. B. DEAD TRACTS : In ground section of normal human dentin, odontoblastic processes disintegrate and empty tubules are filled with air and appear black. In transmitted light these are called 'Dead tracts'.
  28. 28. Loss of odontoblastic processes may also occur in teeth containing vital pulp as a result of caries, attrition, abrasion, erosion and cavity preparation. These degeneration of odontoblastic processes is often observed in the area of narrow pulpal horns because of crowding of odontoblasts, when reparative dentin seals the dentinal tubules at these pulpal end, tubules are filled with fluid and gaseous substances. Dentin areas characterized by degenerated odontoblastic processes becomes dead tracts. These areas appears to greater extend in older teeth. Dead tracts are probably initial step in formation of sclerotic dentin. C) Formation of Secondary Dentin : Secondary dentin is the dentin which develops after root formation is completed. It was one thought that secondary dentin is formed as a result of functional stimuli, but it has been found in unerupted teeth also. Thus secondary dentin represents the continuous but much slower, deposition of dentin by odontoblasts.  Secondary dentin contains fewer tubules than primary dentin and there is usually a bend in the tubules where primary and secondary tubules meet.  This continuous deposition of dentin which reduces the volume of the pulp takes place throughout the life.  Mineral to organic material ratio as same as primary dentin.  As age advances, tubule becomes less regular and more waxy thus indicating changes occurring in odontoblasts (as a result of ionic exchange from the saliva).  Secondary dentin occurs in the absence of inflammation.  Secondary dentin formation increases when tooth is worn by chewing, which leads to dentin exposure. Pattern :  Of secondary dentin deposition varies in different groups of teeth.
  29. 29.  In molars secondary dentin is deposited mainly on the floor of pulp chamber, with less deposition on occlusal and lateral walls. Upper Anterior Teeth :  Greatest deposition occurs on lingual wall of pulp chamber as result of masticating forces with less deposition at incisal edges.  At age of 71, old patients pulp canals becomes almost obliterated.  Thus pulp chamber shrinks in occluso radicular direction than mesio- distally. Care must be taken during cavity preparation and one should avoid cutting recessional lines of the pulp.  Thus young patients going for the full crown are at higher risk of involving dental pulp by mechanical procedures than older patients because of recession of pulp horns. D. REPARATIVE DENTIN (TERTIARY DENTIN, IRREGULAR DENTIN, IRRITATION DENTIN) Reparative dentin is formed by replacement odontoblasts (secondary odontoblasts) in response to moderate level irritation. The secondary odontoblasts are irritated by - Attrition - Abrasion - Erosion - Trauma - Moderate rate dentinal caries - Some operative procedures. • This dentin is more amorphous, less tubular and slightly less regular than primary dentin. • Exposure of the dentin to oral environment leads to an increase in mineral content of dentin. However the mineral content of
  30. 30. reparative dentin is uneven (Tronstad). Hypomineralized as well as hypermineralized zones are present. • If odontoblasts are injured as a result of dental caries or operative procedures, some odontoblasts may die and dentin formed is less regular. This is called as reparative dentin. 1) Reparative Dentin Under Caries : Reparative dentin formed under caries is much more regular than that formed under restoration. • Odontoblasts here are arranged in orderly, palisaded fashion. • When pulp is functioning properly, then pulp maintains an amount of dentin between itself and advancing process of decay which is at least equal to the quantity of primary dentin lost because of disease process. • If there is RAMPANT caries then reparative dentin is decayed as readily as primary dentin. • Inflammatory cells mainly macrophages, lymphocytes are found in pulp, primarily under the reparative dentin . 2) Reparative Dentin Under Restorations : • Reparative dentin under restorations is much more amorphous and irregular than reparative dentin found in other conditions. • Reparative dentin is also softer than primary dentin in same tooth (Cox 1980). Rate of formation : • Daily rate of reparative dentin formation after operative procedures varies with time. In monkey teeth : Dentin has been reported to form at the rate of 2.9 µm to 4.0 µm (Fisher 1970). In humans daily average :
  31. 31. Reparative dentin formation has been reported to be ;  2.8 µm for deciduous (Goto 1972).  1.5 µm for permanent (Starley et al 1966). Quality of Reparative Dentin : Formed after operative procedures depends upon the depth of the cavity. In deep cavities there may be a lag period in onset of new predentin followed by elaboration of huge amounts under the rest dentinal tubules. Odontoblastic pattern is altered in this region, regular, palliated arrangement is changed instead of collmnual appearance typical in coronal portion of uninflammed pulp. Odontoblasts are flattened like fibroblasts and are induced in number. Odontoblastic layer is sometimes 2 cells in depth. It is like most of the odontoblasts have died and are replaced by other pulp cells. Pulp under the region of cut dentinal tubules is implanted with chronic inflammatory cells. 3) Reparative Dentin In root Canals : Reparative dentin is formed in root canals that are ; 19.Chronically inflamed. 20.Periodontally involved. In both of these cases root canals are very narrow and almost obliterated. However the complete obliteration is rarely seen. There is always some viable tissue present in the canals. Certain factors we interfere with formation of reparative dentin. A. Local factors : • Sequel pulpal inflammation. • Operative manipulations • Ionizing radiation
  32. 32. B. Systemic factors • Neonatal • Fluorosis • Deficiency of Vitamin A • Deficiency of Vitamin C • Deficiency of Vitamin D C) Hormones Progesia (Pituitary sensitivity) E) Decreased In Cellular Components : Odontoblasts : Undergo degeneration with advancing age. More vacuoles are present in older odontoblasts. Gradually odontoblasts disappear over some or all areas of pulp. AGE CHANGES IN PULP : 1. Decrease in cellular components. 2. Decrease in number and quality of blood vessels and nerves. 3. Pulposis (Atrophy) 4. Dystrophic mineralization 5. Denticles 6. Decrease in number and thickness of collagen fibers. 1) Decrease in Cellular Components : A) Fibroblasts B) Odontoblasts A) Fibroblasts : With the age there is decrease in number of cells of pulp because of reduced circulation.
  33. 33. • Most of intracellular organelles of older fibroblasts such as rough surface endoplasmic reticulum (rER) and mitochondria are smaller. • Golgi complex is rarely found. • There is also decrease in number of regeneraable cells. • With increasing in maturity fibroblasts shows decrease oxygen uptake. • But aging does not result in alteration of enzyme of catabolic cycles. B) Odontoblasts : Undergo degeneration with advancing age. More vacuoles are present in older odontoblasts. Gradually odontoblasts disappear over some or all areas of pulp. 2. Decrease in number and quality of blood vessels and nerves : A. Blood Vessels : Aging has adverse effect on number and quality of blood vessels supplying dental pulp. a) Blood vessels undergoes arteriosclerotic changes resulting in decreased blood supply to the cells of coronal portion of pulp. b) When we compare the blood vessels of pulp in younger individuals and an older individual. The pulpal arterioles from younger teeth typically consisted of endothelial layers abutting directly on a thin elastic membrane. Whereas in older individuals pulp there was hyperplasia of intima, resulting in narrowing of vessel lumen. In some older individuals there was also the hyperplasia of elastic fibres. c) Blood vessel supplying the coronal pulp tissue were extensive and numerous in younger individuals. These blood vessels decrease in number in older individuals.
  34. 34. B) Nerves : There is reduction in number of nerve branches in coronal pulpal portion of aged pulp because of progressive mineralization of radicular nerve sheath and nerve itself (Bernick 1967). Under caries the pulp nerve fibres become coarsened and irregular and asgyrophilic varicosities are formed. 3) ATROPHY PULPOSIS : An atrophied pulp is that which has become smaller through some physiologic of pathologic process. a) Atrophy of the pulp normally occurs with the advancing age. - As the age increases there is increase in the amount of collagen fibers in the pulp due to decrease in the number of cells. So this prominence of fibres bundles in pulp are due to presence of connective tissue sheaths in a narrow pulp chamber. - In addition to decrease in ratio of ground substance to collagen, aged pulps also exhibited an increase in resistance to proteolytic enzymes and this decreases collagen solubility, water content and chemical toxicity. - This above process is a normal process, thus it is even seen in young persons as there is increase collagen fibres, mineralization in pulp. Thus even younger individuals may encounter this. b) Atrophy from Caries and Operative Procedures : Atrophy can also result from caries and operative procedures under such conditions there is decrease in size and total number of cells. - Pulp underlying larger areas of reparative dentin appears to be more atrophic, having fewer cell and more collagen fibers. • The remaining cells appear shrunken. • Pulp seems to be “burned out” under such cases. • There is increase in dystrophic mineralization scattered throughout both the coronal and radicular pulp.
  35. 35. • Mineralization is found in the walls of blood vessels and permanent sheaths. c) Atrophy From Periodontal Disease : Atrophy of pulp is found frequently in the individuals with advanced periodontal disease. • Cells are smaller in size • Fewer in number. As a result of impairment of nutritional supply. 4) DYSTROPHIC MINERALIZATION : Dystrophic mineralization is found in varying amounts and degrees in most of pulps. In some pulps where there is no caries or operative intervention, the coronal portions are free from mineralization. However in those teeth, the apical portion of pulp, especially in region of collagen fibers contains scattered mineralization. Ground substance alteration occurs in the dental pulp because of ageing and result sin decreased reactivity of less soluble macromolecules. Such changes can lead to dystrophic mineralization. Electron microscopy has shown beginning of mineralization in collagen fibrils occurs long before the mineralization can be seen in light microscope. a) Mineralization : Normally mineralization takes place in preformed organic matrix. But Appleton and Williams described small-smooth surface spherical clusters either closely packed around collagen fibres, or in the form of intercellular deposits in fibroblasts. The crystals were plate like or needle like and diffused and varied in different sizes. Now once the nucleus is deposited further mineralization takes place by secretion. The exact reason of the mineralization of pulp fibrils is unknown. But the changes that helps in mineralization of pulp fibrils seem to occur in
  36. 36. mucopolysaccharide content of sheaths around fibrils. It is believed that these mucopolysaccharides becomes sulfated and these sulfated mucopolysaccharides are involved in attrition mechanisms for mineralization but other factors are also involved. Mineralization is rarely seen in mylar sheaths of nerves. Older fibrotic pulps attracts mineral salts more rapidly. A mineralized pulp when extirpated, feel wooden and hard. b) Dystrophic Mineralization due to cases and Periodontal diseases : Dystrophic mineralization also occurs due to caries and periodontal disease. In teeth with caries and periodontal disease there is significant increase in coronal dystrophic mineralization. c) Teeth with Chronically Inflamed Pulp : Mineralization in the region of previous contains dystrophic liquefaction and necrosis. SEM studies of chronically inflamed pulp shows the presence of pathologic mineralization. Both cells and fibres are involved mineralizing process. Cells : Surface of cells become smooth and folded. Cells degenerate, resulting in hollow interior various cells included are fibroblasts, odontoblasts, endothelial cells and inflammatory cells. Fibres : Fibres shows braded appearance initially and the later mineralized fibres coalesce to form larger masses. Mineralization (Flesh 1964) : Some authors say that inhibitors of mineralization such as polyphosphates and diphosphonates are removed resulting in mineralization. Finally grantorm indicated that alkaline phosphatase in odontoblasts may function as calcium pyrophosphates there by stimulating Ca2+ uptake in pulps.
  37. 37. In teeth with periodontal disease dystrophic mineralization occurs both in coronal and radicular portions of the pulps. 5) DENTICLES : Larger mineralization are called denticles. 21.These are larger mineralized bodies which sometimes results from fusion of smaller ones. 22.Denticles can become extremely large, at times almost obliterating the pulp chamber of the root canal. Classification : These can be classified I. According to structure II. According to size III. According to location I. According to Structure : According to structure denticles can be ; A) True denticles B) False denticles The difference is between morphology and not chemical. A) True Denticle : Is made up of dentin and is lined by odontoblasts. Generally they are found in apical portion of pulp. B) False denticles : Are formed from degenerating cells of pulp that tend to mineralize These mineralizing cells coalesce. Then layer upon layer of mineral salts are laid down. II. According to Size : According to size they are ; A) Fine mineralization B) Diffused mineralization (Fibrillar mineralization)
  38. 38. Former are found more frequently in root canals but may also be present in the coronal portion of pulp. III. According to Location : According to location these can be A) Embedded or interstitial denticles. B) Adherent denticles C) Free denticles A. Embedded Denticles : These are formed originally in the pulp. Dentin matrix is deposited and mineralization occurs. As more and more dentin is elaborated, the denticles may be completely embedded. Embedded denticles are found mostly in apical portions of the root. They are of clinical importance during endodontic therapy because they can be dislodged during instrumentation and may block the apex of the tooth, thus causing difficulties in further treatment and thus blockage of apical third of root canal may be attributed mistakenly to the packing of debris. When large denticle are present they may interfere with extirpation of entire pulp or removal of coronal portion of pulp. B. Adherent Denticles : Are those which are attached to the dentin but are not completely embedded in it. C. Free Denticles :  Free denticles as those which are found lying free in pulp.  They are present in large percentage of teeth and so prevalent that almost all the pulps have some mineralization within them.  They are present in young as well as old people.  There is a tendency of more and more denticles to be deposited with age.
  39. 39. Denticles are even found in teeth in vitro and in teeth which have not yet erupted and in deciduous as well as permanent teeth. Incidence of denticles is greater in females than males. They are not always detected in radiographs unless they are fairly large. 6) Increase in Number and Thickness of Collagen Fibres (Fibrosis) : Fibrosis means proliferation of fibrous connective tissue. This process results namely in the formation of scar tissue to replace normal tissue lost through injury or infection. In uninflamed pulps, collagen fibres are infrequent or absent in coronal portions of posterior teeth that are free of caries and are not operated on. In anterior teeth the quantity of coronal collagen is significantly greater. In apical third of root canal there is more collagenous pulp. Histology : Histologically older pulps shows greater number of argyrophilic reticular fibres as compared to young pulps. This increase is due to reduction in the volume of pulp by continuous deposition of secondary dentin. In younger individuals the distribution of collagen fibers in the ground substance is sparse, as compared to older individuals where there is increase in number of collagen fibrils. Fibrosis in Coronal Portion of Pulp Increases under : 23.Caries 24.Abrasion 25.Attrition 26.Operative procedure In chronically inflamed pulps, fibrosis is markedly increased and blood vessels become prominent and dilated. Clinical Correlations of Induced Pulp Aging :
  40. 40. Pulps of all the teeth are subjected to caries, attrition, abrasion, erosion, operative procedures such as crown cutting, cavity preparation results in the changes such as – decrease in number of cells, increase in number of collagen fibers, dystrophic mineralization. Volume of these pulps have been reduced by formation of reparative dentin. In regions where chronic inflammation has been present, the lumina of root canals also have been narrowed. In general aged tissue cannot defend itself as well against injury as young tissue. For example, when youngster fractures a limb, he usually becomes quickly and within short period of time be is functioning normally. However fracture in older individual is more serious and recovery is not rapid. Complications may arise more rapidly. Pain may persist in older individuals for longer time. Thus aging of dental pulp by dental procedures should be avoided in order to avoid impairment of defence capacity of the pulp. Greater the injury to the pulp greater will be the aging of the pulp. i.e. more formation of secondary dentin. Artifacts : Some of the artifacts can occur because of poor fixation or errors in processing of tissues. These artifacts are ; 27.Reticular atrophy 28.Vacuolization of odontoblastic layer 29.Blister formation 30.Fatty degeneration AGE CHANGES IN CEMENTUM : Cementum : Definition :
  41. 41. • Cementum is calcified mesenchymal tissue that forms the outer covering of the anatomic root. • It begins at the cervical portion of the tooth at cemento enamel junction and continues to the apex. It functions as a medium for the attachment of collage fibers that bind the tooth to the surrounding structure. Acellular Cementum : Acellular cementum is first to be formed and covers approximately cervical 3rd and half of the root. This cementum is formed before the tooth reaches the occlusal plane and its thickness ranges from 30-230 µm. Sharpey’s fibres make up the most structure of acellular cementum. Staging fibres size, number and distribution increases with function. Cellular Cementum : Cellular cementum is formed after the tooth reaches the occlusal plane. This cementum contains cells, cementocytes. Thickness of Cementum : Deposition of cementum is a continuous process. Cementum deposition is most rapid in apical region. Thickness of cementum on coronal half of the root varies from 16-60 µm. It attains greater thickness of 150-200 µm in the apical areas and areas of bifurcation and trifurcation. It is thicker in mesial surface than distal surfaces because of functional stimulation from mesial drift over time. Average thickness of cementum at age of 20 is about 95 µm which increase at the age 60 upto 215 µm. Hypercementosis :
  42. 42. Hypercementosis is abnormal thickness of cementum. It may affect all the teeth of dentition or a single tooth or even effects only a part of tooth. Most commonly seen in apical third of the root. If the overgrowth improves the functional qualities of cementum is known as cementum hypertrophy. In localized hypertrophy prong like extensions are formed. This condition is formed in teeth path are exposed to greater stresses. Prong like extensions provides a larger surface area for attaching fibers, thus finer anchorage of tooth to surrounding alveolar bone is assessed. Etiology : Etiology of hypercementosis varies : • Spike like extensions generally results from excessive tension from orthodontic appliances or from occlusal forces. • Teeth with missing antagonists show hypercementosis as an effort to keep pace with excessive tooth eruption. • Hypercementosis of entire dentition may occur in patient with pagets disease. AGE CHANGES IN PERIODONTAL LIGAMENT : In periodontal ligament aging results in a) Increased number of elastic fibres b) Decrease in vascularity c) Decrease in Mitotic activity d) Decrease in Fibroplasia e) Decrease in Number of collagen fibers f) Decrease in Mucopolysaccharides g) Increase in arteriosclerotic changes h) There is both increase and decrease in the width of periodontal ligament.
  43. 43. - Decrease in width may be due to lower functional demand owing to the decrease in strength of masticatory musculature. - Increase can be due to availability of fewer teeth to support the entire functional load. - Decrease in width can also result from continuous deposition of cementum and bone. REFERENCES: 1.Age related changes of the dental pulp complex and their relationship to systemic aging. (oral surgery oral medicine oral pathology,December 1991,721- 745) 2.The effect of ageing on tooth morphology:a study on impacted teeth 3. 0ral rehabilitation of bulimic patient(a case report) (quintessence international,vol32,no 6,2001,469-475) CONCLUSION : Aging is a natural process which can neither be accelerated nor can be stopped but age changes can be reduced sufficiently so that person can maintain healthy teeth for life time. If people take care of their teeth one can assure that most of teeth can outlive them. At the end I would like to say that "aging is going to effect each and every individual on earth except for those who leave the earth before time".
  44. 44. REFERENCES : 1. 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. 2. Donald R. Morse : Age related changes of the dental pulp complex and their relationship to systemic aging. Oral Surg Oral Med Oral Pathol. 72 (6) : 721-744. 3. Age related changes in blood capillary endothelium of human dental pulp : An ultrastructural study. International Endodontic Journal. 36 : 395-403 : 2003. 4. Athena S. Papas, Linda C. Niessen, Howard H. Chauncey : Geriatric Dentistry. 5. Poul Holm, Pedersen, Harrald Loe : Geriatric Dentistry. 6. Ian Barner, Angus Walls : Gerodontology. 7. Bhaskar S.N. Orbans Oral histology and Embryology. 8. Marzauk : Principles and practice of operative dentistry.
  45. 45. DEPARTMENT OF CONSERVATIVE DENTISTRY ANDDEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICSENDODONTICS COLLEGE OF DENTAL SCIENCESCOLLEGE OF DENTAL SCIENCES DAVANGERE.DAVANGERE. SEMINAR ONSEMINAR ON AGE CHANGES IN DENTAL TISSUES Presented by : DrDr. BHAWANPREET SINGHBHAWANPREET SINGH

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