CONTENTS Introduction Definition Theories of aging Factors affecting aging Macroscopic age changes - Attrition Definition Types Clinical

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 !"! #ulposis Dystropic minerali$ation Denticles Decrease in number and thic%ness of collagen fibres! Age changes in cementum& periodontal ligament Clinical considerations 'eferences Conclusion

INTRODUCTION : The science of gerodontology is receiving more attention as life span of individual increases! (i%e any tissue in human body& dental tissues also undergo changes from the time of development as the age advances! Dental tissues are continuously being sub)ected to variety of insults& li%e physical& chemical and thermal etc& *hich may contribute for the changes in them! +o*ever 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 li%e 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 )est 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& *hich decrease the ability to survive stress! THEORIES OF A IN :

.umerous models have been proposed to e/plain the mechanism of aging! The abundance of theories indicate the multitude of interpretations possible on aging! Many theories presume that a single mechanism is

responsible for all the characteristic of changes seen *ith 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 012 3ear and tear theory 42 Mathematical theory 52 Cellular interaction theory 62 Collagen theory 72 3aste product theory 82 Endocrine theory 92 Calcium theory :2 Somatic mutation theory ;2 Autoimmune theory 1<2Circulatory deficiencies theory 1) !"#r #nd T"#r T$"or% : 3ear and tear theory postulates that the organism *ears out *ith age! Each cells contains some specific amounts of vital substances such as en$ymes and once these substances are used up these are not replaced! Cells from older patients have decreased capacity to repair deo/yribonucleic acid! This leads to death of the cells and finally death of organism! &) '#t$"m#tic#( t$"or%: #ostulated in empirical mortality curve fits into a formulated e=uation! )) C"((*(#r Int"r#ction T$"or% : 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 bet*een these *ill lead to aging of individual! +) Co((#g"n T$"or% : Collagen theory postulates that collagen fibers form continuously at a slo* rate and the collagen is eliminated slo*ly or not at all! As there is more and more formation of collagen fibers they lead to choc%ing of the cells of tissue! Thus hampering the functions of tissue and finally leads to cell death! 5) !#,t" -rod*ct T$"or% : 3aste product theory postulates that metabolic *aste products are not continuously e/creted from the cells and intercellular fluids! 3ith the time this leads to altered functions and ultimately organism is poisoned and finally leading to its death! 6) Endocrin" T$"or% : This theory states that endocrine functions slo*ly decrease and cell metabolism is slo*ly affected adversely! .) C#(ci*m T$"or% : Calcium theory suggests that ageing is caused by defect in calcium metabolism! According to Selye *hen large doses of "itamin D and parathyroid hormone *ere administered in rats& it resulted in minerali$ation of many soft tissues! Such changes resembled the changes seen in aged tissue! In)ury to the tissue results in calcification >Caliciphylo/is2 rendering the tissue non functional! /) Som#tic '*t#tion t$"or% : It is postulated in somatic mutation theory that 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! 9) A*toimm*n" T$"or% : Autoimmuno theory suggest that autoimmune reaction develop *hen some of the cells of the body synthesi$e 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 *hen stimulated by mitogens! Thus immune system may be compromise d in elderly! 10) Circ*(#tor% D"fici"nci", : Circulatory deficiency result in deficient o/idation of cells& resulting in cell death and further replacement by collagen *ith increase in collagen deposition more capillaries are cho%ed off resulting in more ano/ia! Changes can also occur in the endothelial cells of capillary& leading to brea%do*n in the part of FACTORS AFFECTIN A IN :

Aging& in essence& reflects a comple/ interaction of hereditary and epigenetic factors *ith environmental factors! ?enetic factors Environmental factors "n"tic F#ctor, : Evidence that genetic factors play a role in aging is substantial! The principal evidence that aging& as e/pressed by life span& is genetically determined derives from the follo*ing %ind of observations! 12 Mutations 0 several mutations reduce the life span! It is unclear *hether life shortening mutations occur in specific longevity genes or the anomalies they produce are fundamentally inconsistent *ith maintenance of viability!

42 Species @ Specific (ife Spans 0 Each species is characteri$ed by its o*n pattern of aging and ma/imum life span! Differences in life span of members of various animal groups argue strongly in favour of a species specific genetic basis for longevity! 52 +ybrid vigor 0 The effect of genetic construction on longevity is best e/emplified by those e/periments in *hich hybrid vigor has been demonstrated& increased longevity seen in hybrids! 62 Se/ 0 In humans& male is shorter lived than the female! (eaving aside social factors such as smo%ing& it has been hypothesi$ed that if genes carried on the se/ chromosomes indicate life span then genes on the /chromosome may decrease vulnerability to degenerative diseases! 72 #arental Age 0 #ersons *hose parents live to an older age have a greater life e/pectancy than persons *hose parents die young! 82 #remature aging syndromes 0 Single genes changes result in premature senescence in humans Egs! #rogeria& 3ernerAs syndrome& Coc%ayneAs syndrome! En1ironm"nt#( F#ctor, : Four categories of environmental factors influence rate of aging! 12 #hysical and chemical components have been implicated as causing differential rates of aging! 42 Some investigators have claimed that environmental pollutants& radiation affect aging! iologic factors 0 Such as nutrition as a probable cause of differential aging is also been considered! 52 #athogens and parasites have been implicated in influencing the rate of human development and aging& particularly in lo* income in tropical countries! Although they are important determinants of life e/pectancy& there is no evidence that they influence the aging process! 62 Socioeconomic factors 0 Such as poor living conditions& stress of life are believed to accelerate aging process!

Age changes can be further divided into 0 A2 Macroscopic age changes 2 Microscopic age changes A2 Macroscopic Age Changes includes B a2 Attrition b2 Abrasion c2 Erosion 2 Microscopic age changes includes B a2 Age changes in enamel b2 Age changes in dentin c2 Age changes in pulp d2 Age changes in cementum e2 Age changes in periodontium A2 MAC'CSCC#IC A?E C+A.?ES 0 Attrition 0 Definition 0 ,It is defined as loss of tooth structure resulting from direct functional forces bet*een contacting teeth-! Any contacting tooth surface is sub)ected 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 #ff"ct, : Occ(*,#( S*rf#c", : 12 Ccclusal surfaces resulting in the flattening of inclined planes and facet formation! 42 #ro/imal contact areas 0 It leads to flat pro/imal areas and in some cases concave pro/imal surfaces!

Types 0 A2 #ro/imal surface attrition >#ro/imal surface faceting2 2 Cccluding surface attrition >occlusal *ear2 A) -ro2im#( S*rf#c" Attrition : Definition 0 It occurs from loss of surface tooth structure and flattening and *idening of pro/imal contact area! 'esults of #ro/imal Attrition 0 12 #ro/imal surface area is increased in dimension and this area is more susceptible to decay! 42 Decrease in dimension of surrounding embrasures& *hich *ill affect cleansability! 52 Mesio distal dimensions are decreased resulting in drifting! 62 Further due to this drifting there is decrease in dental arch length! All of these above *ill result in difficulty in pla=ue control and than leads to periodontitis! 3) Occ(*,#( S*rf#c" Attrition (Occ(*,#( !"#r) : Definition 0 It is loss& flattening& faceting and reverse cusping of occluding surfaces! Affects or 'esults of Ccclusal 3earing 0 12 (oss of "ertical Dimensions of Tooth 0 A2 (oss occurring in short time 2 (oss occurring in greater time A) 4o,, Occ*rring in S$ort Tim" : If loss of vertical dimension occurs in short time and is severe than there *ill be no chance for the alveolar bone to erupt occlusally to compensate for

vertical tooth loss! This *ill result in loss of vertical dimension of face! This *ill result in overclosure of mandible during functional movements cause strain in stomatognathic system! 3) 4o,, Occ*rring in 4ong"r -"riod : 3hen loss of vertical dimension occurs for longer period i!e! 1<-17 years! Then alveolar bone can gro* occlusally Thus bringing teeth to their occlusal position! Further there is no loss of vertical dimension of face! there is loss of vertical dimensions of tooth! &) D"fici"nt '#,tic#tor% C#5#6i(iti", : Deficient masticatory capabilities can also result from occlusal *ear! lunting of cusps Compells patient to apply more forces of mastication to crush the food for proper s*allo*ing These forces strains the muscles and teeth& periodontium and )oints! 52 Chee% iting >Cotton 'oll Chee%s2 0 Chee% biting also occurs as a result of occlusal *earing! Ccclusal *ear *ill lead to flattening of cuspal elements "ertical overlap bet*een *or%ing inclined planes is lost! This *ill result in chee% bite& lip bite or even tongue bite! ?ingival irritation can also occur due to food impaction and closeness of occlusal table to gingiva! 62 Decay 0 Can also result from attrition as there is loss of enamel as a result dentin is e/posed and thus dentin is more susceptible to decay! Attrition *ill lead to reverse cusps *hich *ill lead to reverse cusps *hich *ill lead to dentin e/posure and this dentin is more susceptible to decay! ut

72 Tooth Sensitivity 0 Tooth sensitivity can also occur from occlusal *ear! Attrition E/cessive force Dentin e/posure #ulpal e/posure Apical Strangulation tearing of #D( Microcrac%s 82 TMD #roblems 0 Attrition E/cessive force TMD problems Strain on stomatognathic system! Tr"#tm"nt : Treatment of attrition depends upon several factors i!e! a2 3hether it is related to one tooth! b2 3hether it is related to *hole arch c2 3hether there is less tooth loss d2 3hether there is loss of entire cro*n Follo*ing is the se=uence of treatment of attrition 0 12 #ulpally e/posed teeth 0 #ulpally involved teeth should undergo endodontic therapy or they may be e/tracted! Depending upon these future role in stomatognathic system and restorability! 42 #arafunctional habits 0 #arafunctional habits such as bru/ism should be treated *ith Eocclusal splintsA! 52 Myofunctional habits 0 TMD problems and other Myofunctional problems should be diagnosed and proper treatment should be given! Sometimes Eocclusal splintsA are helpful in treating such problems! 62 Ccclusal e=uilibration 0 Ccclusal e=uilibration is done If there is little loss of tooth stricture! If remaining tooth structure can be reshaped to effect mandibular movements! Ccclusal e=uilibration includes selective grinding of tooth surfaces& rounding and smoothing of occlusal table! Cne should create ade=uate overlap bet*een *or%ing inclines!

72 #rotection of e/posed dentinal areas 0 E/posed dentinal areas should be protected and actual carious lesion should be removed and obliterated! #rotection 0 can be provided by using fluorides solution! Cbliteration 0 Is obtained by proper restoration! During this periodontium should be e/amined and any pathology should be treated! 82 'estorative #rocedure 0 'estorative procedure can no* be done! Attrited tooth structure is under high stress! Therefore only metallic cro*ns should be used to replace them! R",tor#tion, #r" n""d"d in fo((o7ing ,it*#tion, : A2 3hen there is e/cessive loss of vertical dimension and is effecting stomato-gnathic system! 2 There is e/tensive loss of tooth structure either locali$ed or generali$ed! C2 Decay or any other lesion *hich is super imposed on attrition! D2 Tooth is crac%ed or endo-treated! E2 3hen there is greater loss of tooth structure pro/imally *hich is not capable of maintaining proper state of periodontium! F2 'eshaping 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 follo*ing se=uence! A2 "erify and reverify necessity of restorative material 0 e sure that alveolar bone does not gro* occlusally *ith the same pace that attrition occurs! If bone gro*s at the same pace then occlusal level of the tooth is maintained and any building up of such rest in *ill impinge the free *ay space and thus resulting in bru/ism or other parafunctional habits! 2 Estimate of loss vertical dimension 0 Estimate of vertical dimension must be made that ho* much vertical dimension is lost! Firstly *e ta%e the estimate of vertical dimension as it is done in case of dentures i!e! from .asion to ?nathion!

Then measure vertical dimension& *hen patient brings his teeth together! Difference of these t*o is calculated @ >minus2 free *ay space >4-5 mm2 should give us the estimate for ho* much the height of cro*n is needed! C2 Estimate of additional vertical dimension 0 Estimate of ho* much additional vertical dimension can be accommodated by stomato-gnathic system! - If attrition occurred over a long period >17 years2 then *ith the time there is permanent physiological change *hich cannot be disturbed! - If there is decreased in vertical dimension for more than 4 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! ut 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! 3hen these symptoms appears then there the dimension is further decreased until symptoms disappears! D2 #ermanent restoration ! #ermanent restoration is done in a cast alloy! 1! Fully ad)ustable articulator! 4! +inge a/is determination 5! Stereographic tracing 6! Facebo* records are must for these cases! 7! These permanent restorations are firstly given temporarily for some time! #atients *ho have undergone treatment in this *ay should undergo periodic occlusal e=uilibration! CT+E' CASES 0

A2 3hen 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! 2 Cases *ith 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! ut *hen the carious or defects are greater then cast metal restoration is given again occlusal e=uilibration is done! A3RASION : D"finition : ,Abrasion is defined as loss of tooth structure resulting from direct functional forces bet*een the teeth and e/ternal ob)ects! Cr from frictional forces bet*een 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! C#*,", for C"r1ic#( #6r#,ion : 12 Faulty brushing techni=ue 0 Most common cause of abrasion is faulty brushing techni=ue i!e! +ori$ontal brushing techni=ue! E/cessive forces& time during brushing also causes cervical abrasions! 42 Cral hygiene products 0 Cral hygiene products are also responsible for abrasions! Eg! +ardness of bristles& Amount of dentifrice used& ?rip of tooth brush! #o*ders are 7 times abrasive than tooth pastes! 52 62 Ill fitting clasps of '#D are also responsible of cervical abrasions! Tooth pic%s and interpro/imal brushing! Enamel is not easily abraded! Dentin is 47 times faster abraded then enamel Cementum is abraded 57 times faster than enamel

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 3RUSH A3RASION : Most common abrasion is tooth brush abrasion& *hich 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 0 a2 Direction of brushing stro%es eg! +ori$ontal direction! b2 Si$e of abrasive particle 0 (arger si$e and irregular si$e of abrasive particles *ill cause more abrasion! c2 #ercentage of abrasive 0 More the percentage of abrasive more *ill be the abrasion! d2 Type of abrasives 0 Silica abrasives are much more abrasive than phosphate and carbonate! e2 ristles 0 Diameter of bristles 0 More the dia more the abrasion! Type of bristles 0 .atural bristles are more abrasive than synthetic ones! f2 Forces used during brushing 0 More forces more abrasion! g2 Type of tooth tissue abraded (east enamel Enamel is not "#,i(% abraded! Dentin is &5 times faster abraded then enamel Cementum is abraded )5 times faster than enamel SI NS AND S8'-TO'S : A) D"f"ct, : 12 .otch F " shaped defects 0 3here obli=ue occlusal and cervical *alls intercet at a certain depth *ith no a/ial *all! 42 C-shaped defects 0 3here defect is C-shaped *ith rounded floor!

52 Gndercut concave 0 3here obli=ue occlusal and cervical *all intersect! Each other *ith a/ial *all in bet*een them! 62 Divergent bo/ 0 3here definite a/ial *all is present *ith divergent occlusal and cervical *alls! 3) C"r1ic#( (",ion, g"n"r#((% $#1" 8! Sharpely defined margins! 9! +ard smooth surfaces :! urnished appearance C) T$"% m#% #(,o "2$i6it ,cr#tc$",9 D) H%5"r,"n,iti1it% also occurs *ith appearing and disappearing intervals! D"5t$, : Abrasion lesion may be of varying depths 0 12 Shallo* >S2 0 <!1 to <!7 mm in depth! 42 Deep >D2 0 <!7 mm but no pulpal e/posure! 52 E/posed 0 E/posed pulp Ot$"r H#6it, : Many other habits can also cause abrasion such as 0 12 Che*ing tobacco @ Causes generali$ed abrasion! 42 Forcing tooth pic%s! 52 Interdental stimulates 62 Solid pla=ue control& measures can cause interdental abrasion 72 Cutting se*ing thread *ith incisor teeth 82 #ulling nails *ith incisor teeth! 92 #ICA Syndrome 0 +abit of che*ing clay also leads to certain pattern of abrasion! I#trog"nic Toot$ A6r#,ion : This is caused by ;! #orcelain teeth opposing natural teeth!

1<! 'ough occluding surface of restoration can also lead to abrasion! TREAT'ENT : Treatment should be carried in follo*ing se=uence! 12 Diagnosis of Cause 0 First step is to diagnose the proper cause of abrasion! If there is no proper diagnosis and *e give the restoration it *ill abrade after some time or opposing natural tooth can abrade or teeth could move! 42 After %no*ing the cause then correct iatrogenic factors or cause 0 Then remove iatrogenic cause of abrasion and if re=uired brea% the habits! If success occurs then go for restorative procedure and if there is no success then go for further treatment! 52 If habits cannot be bro%en 0 Then in some cases restorative treatment can bypass the effect of habit! ut most important thing is to stop the habit totally as it *ill help in proper functioning of stomatognathic system! 62 Evaluation of abraded tooth surface 0 A2 *hen there is no need to restore abraded surface a2 (esion in Dentin 0 If lesion is shallo*& multiple and not e/ceeding <!7 mm *ithin the dentin there is no need to restore them! b2 Enamel and cementum 0 If lesion involves enamel or cementum only there is no need to restore them! c2 If lesion is not restored then the edges or margins of the lesion are made smooth so that there is no accumulation of pla=ue and also it loo%s =uite aesthetic and tooth surface is then treated *ith fluorides! 2 .eed to restore abraded tooth surface 0 3hen lesion is *edge shaped and is <!7 mm into dentin then the lesion should be restored! 72 Desensiti$ing of dentin0 efore restoration of tooth surface it is very important to desensiti$e dentinal surface! This may ta%e several visits!

If tooth is restored in single visit then tooth may remain sensitive to thermal changes forever! Desensiti$ing 0 Is particularly done by application of fluorides! :-5<H stannous fluoride for 6-: minutes or *ith Ionophoresis 0 in this galvanic energy is supplied to the tooth in presence of electrolyte *hich drives fluoride ions deep into dentin! 82 'estorative Treatment 0 A2 3hen anterior tooth or facial surface of posterior tooth is affected then restoration is done *ith direct tooth colored materials! In most of the cases no restorative procedure is re=uired because there is direct physicochemical adhesion bet*een tooth and colored materials! 2 #osterior teeth0 If there is need of cavity preparation it should not be done as it *ill impinge pulpal tissue and root canal system due to this tooth becomes sensitive forever! Cne should al*ays use physico-chemically adhering tooth and colored materials! Although this is not so durable but it is more safer than the metal cro*ns! Therefore such lesions are treated again and again! EROSION : D"finition 0 (oss 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 1:H adult population *as effected according to one study! Etio(og% : There is no particular etiology for erosion till no*! It is caused by multiple factors& follo*ing are most common causative agents! a2 Ingested acids b2 Salivary citrates c2 Secreted acids

d2 Mechanical abrasion e2 Microbial metabolic products f2 Acid fumes g2 E/cessive tensile stresses at tooth clinical cervi/ h2 'efused acids i2 Salivary flo* A2 Ingested Acids 0 Ingested acids can lead to an erosion! These acids are >a2 citric acid >(emon or citrus fruits2 especially in large amount can produce erosion! >b2 Cther acids found in Deodi$ers& can lead to erosive process! 2 Salivary citrates 0 Some authors said that salivary citrates help or produce erosion but others has disproved this fact! C2 Salivary flo* 0 #atient *ith decreased salivary flo* and buffering capacity are more prone to erosive lesion! D2 Secreted acids 0 Acids e/ists in gingival cervice due to occlusal trauma > ru/ism2! This acidic crevicular fluid is responsible for crevicular erosion! Although this acidic ?CF cannot be fully responsible for erosive lesion& it can act as a ppting factor! E2 Acid fumes 0 Environmental acidic fumes has been correlated to number of erosive lesions in certain populations! F2 'efused acids 0 As a result of fre=uent regurgitation >forced or non forced2 stomach hydrochloric acid can hit the teeth at specific location and causes erosion! >(ingual surface of upper teeth especially molars and premolars2! ?2 Mechanical abrasion 0 Can act as a contributing factor! +2 Chelating microbial metabolic products 0 Most common product *hich can cause erosion is pyrophosphate! It could be one of the contributing factors!

I2 E/cessive tensile strength at the tooth clinical cervi/ 0 E/cessive tensile strength can also lead to erosion! As *hen e/cessive forces are applied on tooth structure& at tooth cervi/! There is thin enamel present in this area! These forces *ill lead to separation of enamel prisms and the underlying dentin! These can easily peel off or develops crac%s! Then there is penetration of acids and this *ill lead to erosion! This is most commonly seen in facial surfaces! Ero,ion c#n 6" Intrin,ic or E2trin,ic : I9 Intrin,ic Ero,ion : Intrinsic erosion is seen in the follo*ing situations 0 A2 ?astric Acid Contact 0 ?astric acid contact to the teeth during recurrent vomiting& regurgitation can lead to erosion! This is particularly seen in psychosomatic disorders! Eg! .ervous vomiting& self induced anare/ia& nervousbulimia etc! or somatic disorders li%e @ pregnancy& peptic ulcers& gastric dysfunction constipation& duodenal ulcers! This type of intrinsic erosion is most commonly seen on lingual surfaces of anterior teeth especially ma/illary! ecause accumulation of vomitus on dorsum of tongue first reaches this area! 2 Disease due to lac% of o/ygen as faulty metabolism 0 Diseases due to lac% of o/ygen or faulty metabolism results in e/cessive formation of acid sodium phosphate& acid calcium phosphate from labial and buccal mucous glands! Mostly seen on labial surface of anterior teeth! C2 Acids from periodontal tissue II9 E2trin,ic Ero,ion 0 E/trinsic erosion is most commonly caused from B A2 Acids battery factories! 2 Chlorinated s*imming pools C2 (o* p+ medications li%e @ Iron tonics

D2 Aspirin E2 +ydrochloric acid placements! F2 Most commonly caused and damaging acidic ducts are 11! Fruit rich diets 14! (emon 15! "inegar 16! #hosphoric acid in fruit )uices 17! Ascorbic acid F citric acid added to variety of drin%s Citrate ions binds *ith calcium in enamel and dentin forming soluble calcium citrate! ?2 Drug fasting 0 Also during fasting one use to drin% acidic drin%s and this combination of acidic drin%s and reduced salivary flo* are responsible for increased rate of erosion! 4",ion, 4oc#tion : (esions because of acidic diet and medicines are seen on facial surface of anterior teeth! Fruits @ Anterior teeth Fruit )uices @ #remolar and molar Cervical surfaces are more prone as they are close to gingiva and less cleansable! #rolonged contact of acid to tooth surfaces leads to erosion! Eg! 3hen beverage is s*ished inside the oral cavity this leads to depression of p+ in oral cavity for longer period of time and lead to erosion! Action : Ho7 Ero,ion i, -rod*c"d : In erosion mineral dissolved from enamel particularly depends upon follo*ing thing! 18! p+ 19! uffering effect

1:! Amount of calcium& phosphate& and fluoride present in the drin%! 3hen there is drop in p+& solubility of enamel apatite increases! At p+ 5 solubility is 97 gF( *hich increases sharply to 6<< gF( at p+ of 4!7! ut *hen p+ is 6 it is possible to counteract the enamel dissolution by adding calcium phosphate to the drin%! elo* this p+ as solubility of enamel increases very much then even additional Ca#C6 *ill not help more! Ability of acid solution to dissolve enamel apatite depends upon 0 For ho* long it on maintain p+ at lo*er level and prevent itself from dissolution by saliva or dissolution by the apatite and this property of drin% is of a buffering effect! dissolved! Ro(" of S#(i1# : Saliva plays very important role in reducing the erosive effects by follo*ing mechanisms! 12 Dilution and clearance of erosive agent from oral cavity! 42 .eutrali$ation and buffering of dietary acids! 52 Formation of pellicle layer on surface of enamel *hich protects it from deminerali$ation! C(inic#( F"#t*r", : 12 (esion surface is gla$ed! 42 Erosion usually does not effect occluding surfaces! E/cept in advanced lesions! 52 Erosion rate is same for enamel& dentin& cementum and sometimes for restorative material! 62 #!D! reacts by both healthy and unhealthy reactions! 72 Ad)acent periodontium and gingiva are almost healthy! 82 Carious lesion do not occur on the tooth surfaces attac%ed by erosion! +igher the buffering effect greater *ill be the apatite

It is noted that loss of tooth structure by lesion is )ust 1 Fday and formation of reparative F sec dentin 1!7 @ 6 Fday! So there are very rare or no chances of pulpal e/posure! Tr"#tm"nt 'od#(iti", : Although the e/act cause for erosion is not %no*n& complete analysis of diet& occlusion& habits& chronic vomiting and environmental factors should be performed for patients e/hibiting 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! +e should be told that the treatment to be pursued is mainly symptomatic& and that corrective therapy *ill& by no means& stop the disease! +e should also be told that the process could recur& not only affecting tooth structures& but the restorative material& as *ell! #reoperative study models or photographs should be ta%en and %ept for future references! This is to evaluate the progress of the lesion& if no restoration is the treatment modality& and to see the e/tent of recurrence& if a restoration is the treatment modality! There should not be any rush to attempt restorative modalities& e/cept in e/tremely symptomatic or disfiguring lesions! It is preferable to observe the rate of the lesionIs 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 e/actly as described for abrasion and attrition& e/cept 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-

physical bonding to tooth structure can also be used *ith minimum or no tooth preparation& *ith the assumption that the restoration may re=uire periodic replacement! The use of these materials is especially indicated *hen the erosive lesion is e/tremely deep& badly disfiguring& or *hen it is e/pected that the underlying pulp-dentin organ is undergoing advanced degeneration! Again& all this should be done *ith the understanding that the lesion might progress around these restorations and even involve them!

'ICROSCO-IC A E CHAN ES : Age changes in the structure or internal age changes! Ag" C$#ng", in En#m"( : Enamel is a highly minerali$ed tissue that forms a protective covering of variable thic%ness over the entire surface of the cro*n! ecause of its high content of mineral salts and their crystalline arrangement& enamel is the hardest calcified tissue in the human body& *hose function is to form a resistant covering of the teeth rendering them suitable for mastication! The most apparent age change in enamel is *ear that occurs over the surface either as attrition& abrasion or erosion! In addition to the gross changes that occur due to *ear& enamel surface itself undergo post-eruptive alterations in structure at the microscopic level! These result from environmental influences and occur *ith a regularity that can be related to age! The surfaces of unerupted and recently erupted teeth are covered completely *ith pronounced rod ends and peri%ymata! At the points of highest contour of the surfaces these structures soon begin to disappear! This is follo*ed by a generali$ed loss of the rod ends and a much slo*er flattening of the peri%ymata! Finally& the peri%ymata disappear completely! The rate at *hich structure is lost depends on the location of the surface of the tooth and on the location of the tooth in the mouth! Facial and lingual surfaces lose their structure much more rapidly than do pro/imal surfaces& and anterior teeth lose their structure more rapidly than do posterior teeth! #eri%ymata an e/ternal manifestations of striae of ret$ius! They are transverse grooves that run over the enamel! Age changes *ithin 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 *ell understood! For e/ample& the total amount of organic matri/ is said by some to increase& by others to remain

unchanged& and by still others to decrease! (ocalised increases of certain elements such as nitrogen and fluorine& ho*ever& have been found in the superficial enamel layers of older teeth! This suggests a continuous upta%e& 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 dar%er& 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 sho* that enamel becomes harder *ith age! A E CHAN ES IN DENTIN AND -U4- : Age changes that occur in pulp and dentin are 0 a2 Decrease in cellular components b2 Dentinal sclerosis c2 Decrease in number and =uality of blood vessels and nerves d2 'eduction in si$e and volume of the pulp o*ing to - Secondary dentin formation - 'eparative dentin formation e2 Increase in number and thic%ness of collage fibres! f2 Increase in pulp stones and dystrophic minerali$ation! Ag" C$#ng", in D"ntin : Age changes that occurs in dentin include 0 A! Dentinal sclerosis ! Formation of secondary dentin C! Formation of tertiary dentin D! Dead tracts E! Decrease in cellular components A9 DENTINA4 SC4EROSIS : Dentinal sclerosis is associated *ith B - Ageing - Dental caries - Abrasion& Attrition& Erosion

- Certain rays D"ntin#( Sc("ro,i, D*" to Ag"ing : I9 -rim#r% d"ntin#( t*6*(", #r" #ff"ct"d 6% #g"ing9 There is increase in peritubular dentin >dentin that immediately surrounds dentinal tubes2! 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 *ith ageing! Cdontoblasts lining sclerotic dentin becomes reduced in number and then disappears! According to Miles >1;942 these are due to cell-mediated age changes! Absence of tubules causes transparent appearance of dentin! II9 Sc("ro,i, of d"ntin #(,o occ*r, 7it$ d"nt#( c#ri", Dental caries tries to elicit the reaction *ithin primary dentinal tubules& *hich tends to slo* do*n the progress of the disease! #ulp defends itself =uite effectively because of this response! As a response to this decay& dentinal tubules of primary dentin gradually becomes minerali$ed provided that odontoblasts remain vital! This process of sclerotic dentin forms the vital line of defence of pulp against dental caries! radford >1;8<2 0 .oted that *here dead tracts forms instead of sclerotic dentin caries spread more rapidly to*ards the pulp! Thus rapid carious penetration occurs more in younger teeth& then older teeth as in older teeth caries spread along dentino enamel )unction! III9 D"ntin#( ,c("ro,i, 6"c#*," of #6r#,ion: #ttrition #nd "ro,ion9 Sclerosis of dentin can also occurs in response to certain irritations li%e! 12 Attrition 42 Abrasion

52 Erosion 1) Sc("ro,i, d*" 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 4 particular patterns! i! ii! Continuous gro*th of intratubular dentin! Intratubular crystal deposition!

Mendis and Daroling >1;9;2 found that pretubular dentin thic%ness is increased by only 4<H by attrition! (umina of tubules *as filled by large crystals! &) Sc("ro,i, d*" to "ro,ion : Ero,ion D"finition (oss of tooth structure resulting from chemico-mechanical act in the absence of specific micro-organisms! So under erosion mineral are deposited *ithin the tubules leading to sclerosis! I;9 C"rt#in dr*g, ("#ding to d"ntin#( ,c("ro,i, : Calcium hydro/ide Corticosteroids& *hen placed after cavity preparation leads to dentin sclerosis! Some reminerali$ation also occurs *hen sedative dressing such as $inc o/ide eugenol are placed in carious cavities! 39 DEAD TRACTS : In ground section of normal human dentin& odontoblastic processes disintegrate and empty tubules are filled *ith air and appear blac%! transmitted light these are called IDead tractsI! In

(oss 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 narro* pulpal horns because of cro*ding of odontoblasts& *hen reparative dentin seals the dentinal tubules at these pulpal end& tubules are filled *ith fluid and gaseous substances! Dentin areas characteri$ed by degenerated odontoblastic processes becomes dead tracts! These areas appears to greater e/tend in older teeth! Dead tracts are probably initial step in formation of sclerotic dentin! C) Form#tion of S"cond#r% D"ntin : Secondary dentin is the dentin *hich develops after root formation is completed! It *as one thought that secondary dentin is formed as a result of functional stimuli& but it has been found in unerupted teeth also! dentin by odontoblasts! Secondary dentin contains fe*er tubules than primary dentin and there is usually a bend in the tubules *here primary and secondary tubules meet! This continuous deposition of dentin *hich reduces the volume of the pulp ta%es place throughout the life! Mineral to organic material ratio as same as primary dentin! As age advances& tubule becomes less regular and more *a/y thus indicating changes occurring in odontoblasts >as a result of ionic e/change from the saliva2! Secondary dentin occurs in the absence of inflammation! Secondary dentin formation increases *hen tooth is *orn by che*ing& *hich leads to dentin e/posure! -#tt"rn 0 Cf secondary dentin deposition varies in different groups of teeth! Thus secondary dentin represents the continuous but much slo*er& deposition of

 In molars secondary dentin is deposited mainly on the floor of pulp chamber& *ith less deposition on occlusal and lateral *alls! U55"r Ant"rior T""t$ : ?reatest deposition occurs on lingual *all of pulp chamber as result of masticating forces *ith less deposition at incisal edges! At age of 91& old patients pulp canals becomes almost obliterated! Thus pulp chamber shrin%s in occluso radicular direction than mesiodistally! Care must be ta%en during cavity preparation and one should avoid cutting recessional lines of the pulp! Thus young patients going for the full cro*n are at higher ris% of involving dental pulp by mechanical procedures than older patients because of recession of pulp horns! D9 RE-ARATI;E DENTIN (TERTIAR8 DENTIN: IRRE U4AR DENTIN: IRRITATION DENTIN) 'eparative dentin is formed by replacement odontoblasts >secondary odontoblasts2 in response to moderate level irritation! 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! E/posure of the dentin to oral environment leads to an increase in mineral content of dentin! +o*ever the mineral content of The secondary

reparative dentin is uneven >Tronstad2! +ypominerali$ed as *ell as hyperminerali$ed $ones are present! If odontoblasts are in)ured as a result of dental caries or operative procedures& some odontoblasts may die and dentin formed is less regular! This is called as reparative dentin. 1) R"5#r#ti1" D"ntin Und"r C#ri", : 'eparative dentin formed under caries is much more regular than that formed under restoration! Cdontoblasts here are arranged in orderly& palisaded fashion! 3hen pulp is functioning properly& then pulp maintains an amount of dentin bet*een itself and advancing process of decay *hich is at least e=ual to the =uantity of primary dentin lost because of disease process! If there is 'AM#A.T caries then reparative dentin is decayed as readily as primary dentin! Inflammatory cells mainly macrophages& lymphocytes are found in pulp& primarily under the reparative dentin ! &) R"5#r#ti1" D"ntin Und"r R",tor#tion, : 'eparative dentin under restorations is much more amorphous and irregular than reparative dentin found in other conditions! 'eparative dentin is also softer than primary dentin in same tooth >Co/ 1;:<2! R#t" of form#tion : Daily rate of reparative dentin formation after operative procedures varies *ith time! In mon<"% t""t$ 0 Dentin has been reported to form at the rate of 4!; Jm to 6!< Jm >Fisher 1;9<2! In $*m#n, d#i(% #1"r#g" :

'eparative dentin formation has been reported to be B 4!: Jm for deciduous >?oto 1;942! 1!7 Jm for permanent >Starley et al 1;882!

=*#(it% of R"5#r#ti1" D"ntin : Formed after operative procedures depends upon the depth of the cavity! In deep cavities there may be a lag period in onset of ne* predentin follo*ed by elaboration of huge amounts under the rest dentinal tubules! Cdontoblastic pattern is altered in this region& regular& palliated arrangement is changed instead of collmnual appearance typical in coronal portion of uninflammed pulp! Cdontoblasts are flattened li%e fibroblasts and are induced in number! Cdontoblastic layer is sometimes 4 cells in depth! It is li%e most of the odontoblasts have died and are replaced by other pulp cells! #ulp under the region of cut dentinal tubules is implanted *ith chronic inflammatory cells! )) R"5#r#ti1" D"ntin In root C#n#(, : 'eparative dentin is formed in root canals that are B 1;! Chronically inflamed! 4<! #eriodontally involved! In both of these cases root canals are very narro* and almost obliterated! +o*ever the complete obliteration is rarely seen! There is al*ays some viable tissue present in the canals! C"rt#in f#ctor, 7" int"rf"r" 7it$ form#tion of r"5#r#ti1" d"ntin9 A9 4oc#( f#ctor, : Se=uel pulpal inflammation! Cperative manipulations Ioni$ing radiation

39 S%,t"mic f#ctor, .eonatal Fluorosis Deficiency of "itamin A Deficiency of "itamin C Deficiency of "itamin D C) Hormon", #rogesia >#ituitary sensitivity2 E) D"cr"#,"d In C"((*(#r Com5on"nt, : Odonto6(#,t, : Gndergo degeneration *ith advancing age! More vacuoles are present in older odontoblasts! ?radually odontoblasts disappear over some or all areas of pulp!

A E CHAN ES IN -U4- : 1! Decrease in cellular components! 4! Decrease in number and =uality of blood vessels and nerves! 5! #ulposis >Atrophy2 6! Dystrophic minerali$ation 7! Denticles 8! Decrease in number and thic%ness of collagen fibers! 1) D"cr"#," in C"((*(#r Com5on"nt, : A2 Fibroblasts 2 Cdontoblasts A) Fi6ro6(#,t, : 3ith the age there is decrease in number of cells of pulp because of reduced circulation!

 Most of intracellular organelles of older fibroblasts such as rough surface endoplasmic reticulum >rE'2 and mitochondria are smaller! ?olgi comple/ is rarely found! There is also decrease in number of regeneraable cells! 3ith increasing in maturity fibroblasts sho*s decrease o/ygen upta%e! ut aging does not result in alteration of en$yme of catabolic cycles! 3) Odonto6(#,t, 0 Gndergo degeneration *ith advancing age! More vacuoles are present in older odontoblasts! ?radually odontoblasts disappear over some or all areas of pulp! &9 D"cr"#," in n*m6"r #nd >*#(it% of 6(ood 1",,"(, #nd n"r1", : A9 3(ood ;",,"(, : Aging has adverse effect on number and =uality of blood vessels supplying dental pulp! a2 lood vessels undergoes arteriosclerotic changes resulting in decreased blood supply to the cells of coronal portion of pulp! b2 3hen *e 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! 3hereas in older individuals pulp there *as hyperplasia of intima& resulting in narro*ing of vessel lumen! In some older individuals there *as also the hyperplasia of elastic fibres! c2 lood vessel supplying the coronal pulp tissue *ere e/tensive and numerous in younger individuals! number in older individuals! These blood vessels decrease in

3) N"r1", : There is reduction in number of nerve branches in coronal pulpal portion of aged pulp because of progressive minerali$ation of radicular nerve sheath and nerve itself > ernic% 1;892! Gnder caries the pulp nerve fibres become coarsened and irregular and asgyrophilic varicosities are formed! )) ATRO-H8 -U4-OSIS : An atrophied pulp is that *hich has become smaller through some physiologic of pathologic process! a2 Atro5$% of t$" 5*(5 normally occurs *ith the advancing age! As the age increases there is increase in the amount of collagen fibers in the pulp due to decrease in the number of cells! So this prominence of fibres bundles in pulp are due to presence of connective tissue sheaths in a narro* pulp chamber! In addition to decrease in ratio of ground substance to collagen& aged pulps also e/hibited an increase in resistance to proteolytic en$ymes and this decreases collagen solubility& *ater content and chemical to/icity! This above process is a normal process& thus it is even seen in young persons as there is increase collagen fibres& minerali$ation in pulp! Thus even younger individuals may encounter this! 6) Atro5$% from C#ri", #nd O5"r#ti1" -roc"d*r", : Atrophy can also result from caries and operative procedures under such conditions there is decrease in si$e and total number of cells! #ulp underlying larger areas of reparative dentin appears to be more atrophic& having fe*er cell and more collagen fibers! The remaining cells appear shrun%en! #ulp seems to be ,burned out- under such cases! There is increase in dystrophic minerali$ation scattered throughout both the coronal and radicular pulp!

 Minerali$ation is found in the *alls of blood vessels and permanent sheaths! c) Atro5$% From -"riodont#( Di,"#," : Atrophy of pulp is found fre=uently in the individuals *ith advanced periodontal disease! Cells are smaller in si$e Fe*er in number! supply! +) D8STRO-HIC 'INERA4I?ATION : Dystrophic minerali$ation is found in varying amounts and degrees in most of pulps! In some pulps *here there is no caries or operative intervention& the coronal portions are free from minerali$ation! +o*ever in those teeth& the apical portion of pulp& especially in region of collagen fibers contains scattered minerali$ation! ?round substance alteration occurs in the dental pulp because of ageing and result sin decreased reactivity of less soluble macromolecules! changes can lead to dystrophic minerali$ation! Electron microscopy has sho*n beginning of minerali$ation in collagen fibrils occurs long before the minerali$ation can be seen in light microscope! #) 'in"r#(i@#tion : .ormally minerali$ation ta%es place in preformed organic matri/! ut Appleton and 3illiams described small-smooth surface spherical clusters either closely pac%ed around collagen fibres& or in the form of intercellular deposits in fibroblasts! The crystals *ere plate li%e or needle li%e and diffused and varied in different si$es! .o* once the nucleus is deposited further minerali$ation ta%es place by secretion! The e/act reason of the minerali$ation of pulp fibrils is un%no*n! ut the changes that helps in minerali$ation of pulp fibrils seem to occur in Such As a result of impairment of nutritional

mucopolysaccharide content of sheaths around fibrils! It is believed that these mucopolysaccharides becomes sulfated and these sulfated mucopolysaccharides are involved in attrition mechanisms for minerali$ation but other factors are also involved! Minerali$ation is rarely seen in mylar sheaths of nerves! Clder fibrotic pulps attracts mineral salts more rapidly! A minerali$ed pulp *hen e/tirpated& feel *ooden and hard! 6) D%,tro5$ic 'in"r#(i@#tion d*" to c#,", #nd -"riodont#( di,"#,", : Dystrophic minerali$ation also occurs due to caries and periodontal disease! In teeth *ith caries and periodontal disease there is significant increase in coronal dystrophic minerali$ation! c) T""t$ 7it$ C$ronic#((% Inf(#m"d -*(5 : Minerali$ation in the region of previous contains dystrophic li=uefaction and necrosis! SEM studies of chronically inflamed pulp sho*s the presence of pathologic minerali$ation! process! Cells 0 Surface of cells become smooth and folded! Cells degenerate& resulting in hollo* interior various cells included are fibroblasts& odontoblasts& endothelial cells and inflammatory cells! Fibres 0 Fibres sho*s braded appearance initially and the later minerali$ed fibres coalesce to form larger masses! Minerali$ation >Flesh 1;862 0 Some authors say that inhibitors of minerali$ation such as polyphosphates and diphosphonates are removed resulting in minerali$ation! Finally grantorm indicated that al%aline phosphatase in odontoblasts may function as calcium pyrophosphates there by stimulating Ca4K upta%e in pulps! oth cells and fibres are involved minerali$ing

In teeth *ith periodontal disease dystrophic minerali$ation occurs both in coronal and radicular portions of the pulps! 5) DENTIC4ES : (arger minerali$ation are called denticles! 41! These are larger minerali$ed bodies *hich sometimes results from fusion of smaller ones! 44! Denticles can become e/tremely large& at times almost obliterating the pulp chamber of the root canal! C(#,,ific#tion : These can be classified I! II! III! According to structure According to si$e According to location

I! According to Structure 0 According to structure denticles can be B A2 True denticles 2 False denticles The difference is bet*een morphology and not chemical! A2 Tr*" D"ntic(" 0 Is made up of dentin and is lined by odontoblasts! ?enerally they are found in apical portion of pulp! 2 F#(," d"ntic(", 0 Are formed from degenerating cells of pulp that tend to minerali$e These minerali$ing cells coalesce! Then layer upon layer of mineral salts are laid do*n! II9 According to Si@" 0 According to si$e they are B A2 Fine minerali$ation 2 Diffused minerali$ation >Fibrillar minerali$ation2

Former are found more fre=uently in root canals but may also be present in the coronal portion of pulp! III9 According to 4oc#tion : According to location these can be A2 Embedded or interstitial denticles! 2 Adherent denticles C2 Free denticles A9 Em6"dd"d D"ntic(", : These are formed originally in the pulp! Dentin matri/ is deposited and minerali$ation occurs! As more and more dentin is elaborated& the denticles may be completely embedded! Embedded denticles are found mostly in apical portions of the root! They are of clinical importance during endodontic therapy because they can be dislodged during instrumentation and may bloc% the ape/ of the tooth& thus causing difficulties in further treatment and thus bloc%age of apical third of root canal may be attributed mista%enly to the pac%ing of debris! 3hen large denticle are present they may interfere *ith e/tirpation of entire pulp or removal of coronal portion of pulp! 39 Ad$"r"nt D"ntic(", 0 Are those *hich are attached to the dentin but are not completely embedded in it! C9 Fr"" D"ntic(", : Free denticles as those *hich are found lying free in pulp! They are present in large percentage of teeth and so prevalent that almost all the pulps have some minerali$ation *ithin them! They are present in young as *ell as old people! There is a tendency of more and more denticles to be deposited *ith age!

Denticles are even found in teeth in vitro and in teeth *hich have not yet erupted and in deciduous as *ell as permanent teeth! Incidence of denticles is greater in females than males! They are not al*ays detected in radiographs unless they are fairly large! 6) Incr"#," in N*m6"r #nd T$ic<n",, of Co((#g"n Fi6r", (Fi6ro,i,) : Fibrosis means proliferation of fibrous connective tissue! This process results namely in the formation of scar tissue to replace normal tissue lost through in)ury or infection! In uninflamed pulps& collagen fibres are infre=uent or absent in coronal portions of posterior teeth that are free of caries and are not operated on! In anterior teeth the =uantity of coronal collagen is significantly greater! In apical third of root canal there is more collagenous pulp! Hi,to(og% : +istologically older pulps sho*s 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 *here there is increase in number of collagen fibrils! Fibrosis in Coronal #ortion of #ulp Increases under 0 45! Caries 46! Abrasion 47! Attrition 48! Cperative procedure In chronically inflamed pulps& fibrosis is mar%edly increased and blood vessels become prominent and dilated! C(inic#( Corr"(#tion, of Ind*c"d -*(5 Aging :

#ulps of all the teeth are sub)ected to caries& attrition& abrasion& erosion& operative procedures such as cro*n cutting& cavity preparation results in the changes such as @ decrease in number of cells& increase in number of collagen fibers& dystrophic minerali$ation! "olume of these pulps have been reduced by formation of reparative dentin! In regions *here chronic inflammation has been present& the lumina of root canals also have been narro*ed! In general aged tissue cannot defend itself as *ell against in)ury as young tissue! For e/ample& *hen youngster fractures a limb& he usually becomes =uic%ly and *ithin short period of time be is functioning normally! +o*ever fracture in older individual is more serious and recovery is not rapid! Complications may arise more rapidly! #ain 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! ?reater the in)ury to the pulp greater *ill be the aging of the pulp! i!e! more formation of secondary dentin!

Artif#ct, : Some of the artifacts can occur because of poor fi/ation or errors in processing of tissues! These artifacts are B 49! 'eticular atrophy 4:! "acuoli$ation of odontoblastic layer 4;! lister formation 5<! Fatty degeneration A E CHAN ES IN CE'ENTU' : C"m"nt*m : Definition 0

 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 )unction and continues to the ape/! It functions as a medium for the attachment of collage fibers that bind the tooth to the surrounding structure! Ac"((*(#r C"m"nt*m : Acellular cementum is first to be formed and covers appro/imately cervical 5rd and half of the root! This cementum is formed before the tooth reaches the occlusal plane and its thic%ness ranges from 5<-45< Jm! SharpeyAs fibres ma%e up the most structure of acellular cementum! Staging fibres si$e& number and distribution increases *ith function! C"((*(#r C"m"nt*m : Cellular cementum is formed after the tooth reaches the occlusal plane! This cementum contains cells& cementocytes! T$ic<n",, of C"m"nt*m : Deposition of cementum is a continuous process! Cementum deposition is most rapid in apical region! Thic%ness of cementum on coronal half of the root varies from 18-8< Jm! It attains greater thic%ness of 17<-4<< Jm in the apical areas and areas of bifurcation and trifurcation! It is thic%er in mesial surface than distal surfaces because of functional stimulation from mesial drift over time! Average thic%ness of cementum at age of 4< is about ;7 Jm *hich increase at the age 8< upto 417 Jm! H%5"rc"m"nto,i, :

+ypercementosis is abnormal thic%ness 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 overgro*th improves the functional =ualities of cementum is %no*n as cementum hypertrophy! In locali$ed hypertrophy prong li%e e/tensions are formed! condition is formed in teeth path are e/posed to greater stresses! #rong li%e e/tensions provides a larger surface area for attaching fibers& thus finer anchorage of tooth to surrounding alveolar bone is assessed! Etio(og% 0 Etiology of hypercementosis varies 0 Spi%e li%e e/tensions generally results from e/cessive tension from orthodontic appliances or from occlusal forces! Teeth *ith missing antagonists sho* hypercementosis as an effort to %eep pace *ith e/cessive tooth eruption! +ypercementosis of entire dentition may occur in patient *ith pagets disease! A E CHAN ES IN -ERIODONTA4 4I A'ENT : In periodontal ligament aging results in a2 Increased number of elastic fibres b2 Decrease in vascularity c2 Decrease in Mitotic activity d2 Decrease in Fibroplasia e2 Decrease in .umber of collagen fibers f2 Decrease in Mucopolysaccharides g2 Increase in arteriosclerotic changes h2 There is both increase and decrease in the *idth of periodontal ligament! This

Decrease in *idth may be due to lo*er functional demand o*ing to the decrease in strength of masticatory musculature! Increase can be due to availability of fe*er teeth to support the entire functional load! Decrease in *idth can also result from continuous deposition of cementum and bone!

REFERENCES: 19Age related changes of the dental pulp comple/ and their relationship to systemic aging! >oral surgery oral medicine oral pathology&December 1;;1&9419672 &!The effect of ageing on tooth morphology0a study on impacted teeth )! <ral rehabilitation of bulimic patient>a case report2 >=uintessence international&vol54&no 8&4<<1&68;-6972

CONC4USION : Aging is a natural process *hich 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 ta%e care of their teeth one can assure that most of teeth can outlive them! At the end I *ould li%e to say that L aging is going to effect each and every individual on earth except for those who leave the earth before timeL!

REFERENCES : 1! Dorrit 3!.it$an& et al 0 The effect of aging on tooth morphology 0 A study on impacted teeth! Cral Surg Cral Med Cral #athol! 81 0 76-8< 0 1;:8! 4! Donald '! Morse 0 Age related changes of the dental pulp comple/ and their relationship to systemic aging! Cral Surg Cral Med Cral #athol! 94 >82 0 941-966! 5! Age related changes in blood capillary endothelium of human dental pulp 0 An ultrastructural study! International Endodontic Dournal! 58 0 5;7-6<5 0 4<<5! 6! Athena S! #apas& (inda C! .iessen& +o*ard +! Chauncey 0 ?eriatric Dentistry! 7! #oul +olm& #edersen& +arrald (oe 0 ?eriatric Dentistry! 8! Ian arner& Angus 3alls 0 ?erodontology! 9! has%ar S!.! Crbans Cral histology and Embryology! :! Mar$au% 0 #rinciples and practice of operative dentistry!

DEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICS COLLEGE OF DENTAL SCIENCES DAVANGERE.

SE'INAR ON

A E CHAN ES IN DENTA4 TISSUES

-r","nt"d 6% :

Dr. BHAWANPREET SINGH