CARIOLOGY   INDIAN DENTAL ACADEMYLeader in Continuing Dental Education     www.indiandentalacademy.com
CONTENTS•   INTRODUCTION•   DEFINITION•   CLASSIFICATION•   ETIOLOGY OF DENTAL CARIES—EARLY THEORIES                      ...
• CARIES PROCESS—MORPHOLOGICAL AND  CHEMICAL EVENTS• HISTOPATHOLOGY OF ENAMEL CARIES• DENTINAL CARIES—HISTOPATHOLOGY• ELEC...
INTRODUCTION• TEETH ARE TOOLS that have evolved to ensure survival  of species. Caries is a biosocial disease rooted in th...
• DEFINITION•                   Dental caries is defined as a  progressive, irreversible, microbial disease  affecting the...
•   CLASSIFICATION DENTAL CARIESA : On the basis of clinical features and patterns dental  caries may be classified accord...
• 2) Dynamics i.e according to severity and rate  of         progression of lesions   Based on the severity   Class 1: Ver...
• 3) Chronology i.e according to age patterns  at which lesions predominate     a) infancy caries     b) Adolescent caries...
• 5. Based on treatment and restoration design  ( Therapeutic classification) – G.V. Black classified into   a) class 1 Pi...
e) based on carious surfaces involved, it is classified into       1 simple[1surface]       2 compound [ 2 surface]       ...
Early Theories of caries formation;THE LEGEND OF THE WORM•    The earliest reference to tooth decay and toothache came fro...
ENDOGENOUS THEORIESHUMORAL THEORYThe ancient Greeks consider that a persons physical and mental  constitution was determin...
VITAL THEORYThis theory regarded dental caries as originating within the tooth itself, analogous to bone gangrene.This the...
EXOGENOUS THEORIESCHEMICAL THEORY Parmly[1819] rebelled against the vital theory and  proposed that an unidentified chemic...
PARASITIC[SEPTIC] THEORY In 1843 , Erdl described filamentous parasites in  the surface membrane[ plaque ] of teeth.Shortl...
CHEMICO-PARASITIC [ACIDOGENIC] THEORYThis theory was proposed by W.D MILLER[1890]Essential features of this theoryThat the...
After penetration of enamel, the dissolution of dentin is   brought about in the same manner with the organisms   penetrat...
Limitations of acidogenic theory• This theory was unable to explain the predilection of  specific sites on a tooth to dent...
• This theory does not explain why some  populations are caries –free• The phenomenon of arrested caries is not  explained...
• Proteolytic theory (Gottlieb)The surface coverings found on the tooth in grooves and pits are organic in nature , also e...
They described carious like lesions that were initiated by  proteolytic activity at a slightly alkaline ph and  conceded t...
Limitations:• The above conclusions were made on the basis of the  early histological observations.• An interpretation of ...
• PROTEOLYSIS CHELATION THEORY:This theory proposed by Schatez et al (1955) implies a simultaneous  microbial degradation ...
Limitations:• Less than one percent of mature enamel is organic in  nature and the suggestion that this material upon  deg...
Other Theories of caries etiologySULFATASE THEORYPincus[1950] advanced the sulfatase theory, , whereby bacterial sulfatase...
COMPLEXING AND PHOSPHORYLATING THEORY [LURA-1967]It can be readily demonstrated that uptake of phosphate  by plaque bacter...
LIMITATIONS:Saliva is an abundant source of inorganic phosphate for  bacterial utilization.Hence it is highly improbable t...
CURRENT CONCEPT.Primary factors in the etiology of dental caries  (essential factors).In the epidemiological model dental ...
www.indiandentalacademy.com
HOST factorsComposition Studies of the chemical composition of enamel indicate   that surface enamel is more resistant to ...
MORPHOLOGIC CHARACTERISTICS OF THE TOOTHIt has been suggested that morphology of tooth may influence the   initiation of c...
ESSENTIALITY OF ORAL BACTERIAMicroorganisms are a pre requisite for caries initiation.A single type of organism for exampl...
Cariogenic                   suitableBacterial         +            local          --- organic acidsplaque                ...
CLINICAL FEATURES OF CARIESPIT AND FISSURE CARIESpits or fissures with high steep walls and narrow bases are more  prone t...
And penetrates into the dentin  along the dentinal tubules  without fracturing away the  over-hanging enamel.Thus  there m...
SMOOTH SURFACE CARIEScaries that develops on the proximal surfaces of  teeth or on the gingival third of the buccal and  l...
PROXIMAL CARIESIt usually begins just below the   contact point and appears in   the early stage as a faint   opacity of e...
CERVICAL CARIES• It occurs on buccal, lingual or labial surfaces and  usually extends from opposite the gingival crest  oc...
ROOT [CEMENTUM] CARIESHAZEN defined root caries as- A soft, progressive lesion that is found anywhere on the root surface ...
• This type of caries is  predominately found in  dentitions of older age  groups with significant  gingival recession and...
LINEAR ENAMEL CARIES[ODONTOCLASIA]An atypical form of dental caries, called linear enamel  caries, has been observed in th...
A variant of linear enamel caries in the primary  teeth of children in the far east has been named  odontoclasia.The morph...
www.indiandentalacademy.com
www.indiandentalacademy.com
RAMPANT CARIESOne of the most distressful clinical conditions for both patient and   practitioner is rampant caries in whi...
www.indiandentalacademy.com
RECURRENT CARIES  A carious lesion that develops at the inter-face of a restoration and    the cavo-surface of enamel is c...
www.indiandentalacademy.com
• XEROSTOMIA- INDUCED  CARIES[RADIATION CARIES]• A common complication of radiotherapy of oral cancer lesions is    xerost...
www.indiandentalacademy.com
INFANCY[SOOTHER OR NURSING BOTTLE] CARIESNumerous reports by pediatricians and pedodontists  describe a rapidly progressin...
Infancy caries is most often seen in children with  an unusual dietary history such as an addition of  syrup, honey or suc...
www.indiandentalacademy.com
ADOLESCENT CARIES The acute caries attack seen at 11-18 years of age is   characterized as adolescent caries .ITS CHARACTE...
CARIES AS A SPECIFIC MICROBIAL          INFECTION• Definition of dental plaque:    Plaque is a specific but highly variabl...
EVIDENCE OF BACTERIAL ROLE IN   CARIES ETIOLOGY1.germ free animal do not develop caries.2. antibiotics fed to animals are ...
www.indiandentalacademy.com
PROPERTIES OF CARIOGENIC PLAQUEThe rate of sucrose consumption was noticeably higher in   cariogenic plaques.  The rate of...
Cariogenic plaques contained higher levels of  streptococcus mutans than noncariogenic plaques.-  Noncariogenic plaques ha...
NON SPECIFIC PLAQUE HYPOTHESIS:There is no question, dental caries is an infection.In the past, and has an extension of mi...
SPECIFIC PLAQUE HYPOTHESIS:On experimental evidences it is impressive that qualitative  nature of the flora in plaque dete...
According to this hypothesis , most but not all  carious lesions are due to specific bacterial  species.Further the hypoth...
CONCEPT OF CRITICAL pHThe loss of tooth mineral during caries formation is  caused by the formation of bacterial acids whi...
It has been shown experimentally that both saliva   and plaque fluid caese to be satured at Ph values   in the range of 5-...
. These considerations are specially important in the   very early stages of caries when the outer enamel   is being disso...
Being uncharged , the unionized molecules are less likely to react with apatite than their constuient hydrogen and lactate...
STEPHAN CURVEStephan [1940], using antimony microelectrodes ,  recorded the pH values of dental plaques in situ  before , ...
www.indiandentalacademy.com
Stephan[1944] observed that plaques of  caries-free or caries-inactive individuals  usually had a resting pH of between 6....
• Stephan postulated that there must be microbial  differences between plaques in caries – free and  caries prone individu...
• NUTRITION,DIET AND DENTAL CARIES•  Diet----carbohydrates•  Others[calcium,phosphorus,vit.D,K,B6,  proteins,lipids,trace ...
ROLE OF SUCROSE IN DENTAL CARIES• Many oral bacteria utilize sucrose,glucose,fructose and other  simple sugars to produce ...
EFFECT OF TRACE ELEMENTS ON DENTAL CARIES  ____________________________________________________________  _________________...
MECHANISM OF ACTION OF FLUORIDES IN CARIES REDUCTION1 increased enamel resistance/reduction in enamel solubility2 increase...
EFFECT OF DEMOGRAPHIC FACTORS ON    THE PREVALENCE OF CARIES•   sex•   age•   race•   familial factors•   time factors for...
ROLE OF SALIVA IN DENTAL CARIEScomposition 1. Inorganic constituents:   Positive ions- Ca ,H+,Mg,K   Negative ions- carbon...
• pH of saliva:             It is determined mainly by the bicarbonate concentration.(85%)  .Phosphates and proteins in sa...
• ANTIBACTERIAL AGENTS OF SALIVA:          1.Lactoperoxidase          2.Lysozyme          3.Lactoferrin          4.Ig ALAC...
LYSOZYMEIt is a small ,highly positive, enzyme that  catalyzes the degradation of negatively  charged peptide-glycan matri...
LACTOFERRIN It is an iron binding basic protein which tends to bind and   limit the amount of free iron.Since iron is esse...
• HISTOPATHOLOGY OF DENTAL  CARIES    ENAMEL CARIES   Light microscopic studies of carious  lesions of enamel without cavi...
ZONE 1:TRANSLUCENT ZONE           It is the deepest zone and represents the advancing front of enamel lesion. It is not al...
ZONE2:DARK ZONEIt lies adjacent and superficial to the translucent zone . It  is called dark zone because it does not tran...
ZONE 3:BODY OF THE LESION      It lies between the relatively unaffected surface layer and the    dark zone. It is the are...
ZONE 4: SURFACE ZONE   This zone is relatively unaffected by the carious  attack. It has a lower pore volume than the body...
www.indiandentalacademy.com
ZONES OF DENTINAL CARIES Caries advancement in dentin proceeds through 3 stages. 1 weak organic acids demineralise dentin ...
www.indiandentalacademy.com
ZONE 1:NORMAL DENTIN The deepest area is normal dentin which has  tubules with odontoblastic process that are  smooth and ...
ZONE 2 SUBTRANSPARENT DENTIN• This is a zone of demineralization of inter tubular  dentin and initial formation of very fi...
ZONE3: TRANSPARENT DENTINIt is softer than normal dentin . and shows further loss of  mineral from the inter tubular denti...
ZONE 4: TURBID DENTINIt is the zone of bacterial invasion and is marked  by widening and distortion of dentinal tubules,  ...
ZONE 5 :INFECTED DENTINIt is the outermost zone consists of decomposed  dentin that is teeming with bacteriaThere is no re...
www.indiandentalacademy.com
ELECTRON MICROSCOPIC STUDIES OF CARIOUS ENAMELUltra structural studies of enamel caries have shown that  the intercrystall...
This causes the enamel crystals to assume a hairpin   appearance in a longitudinal view .The finding is most easily explai...
www.indiandentalacademy.com
• At the electron microscope level some enamel crystals at  the periphery of the prism in the body of the lesion are  ofte...
• With this new technique, it has been shown that the  crystals in sound enamel have a diameter of 35-40nm ,  in the trans...
www.indiandentalacademy.com
ENAMEL CARIES AT CHEMICAL LEVEL  •A protective organic film of strongly adsorbed  protein, the acquired salivary pellicle ...
• Production of these organic acids produces a  concentration gradient that causes the hydrogen  ions (H+) and the undisso...
• The undissociated HA and HL form a reservoir  of H+ ions.Dissociation is dependent on the pH  and the concentration of u...
• Fluoride in solution markedly inhibits this  dissolution stage of the process.• This ions and their appropriate  complex...
www.indiandentalacademy.com
• As more enamel disolves and the concentration of  the Ca and PO4 ions increases remineralisation  may occur on the surfa...
• -As Ca and PO4 diffuse outward remineralisation  becomes more and more likely as diffusion slows.• This leads to the for...
If subsurface dissolution continues and repair   cannot keep pace with mineral loss this leads   eventually to more extens...
• CONCLUSIONCaries, because of its uniqueness as a disease,its ubiquitous  nature, and its stubborn resistance to resoluti...
• REFERANCES• TEXTBOOK OF CARIOLOGY—GORDON  NIKIFORUK• TEXTBOOK OF CARIOLOGY—MUNKSGAARD• TEXTBOOK OF CARIOLOGY---SILVERMAN...
THANK Uwww.indiandentalacademy.com
Upcoming SlideShare
Loading in …5
×

dental Cariology /certified fixed orthodontic courses by Indian dental academy

2,800 views

Published on

Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.


Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients

State of the art comprehensive training-Faculty of world wide repute &Very affordable.

Published in: Education
2 Comments
24 Likes
Statistics
Notes
No Downloads
Views
Total views
2,800
On SlideShare
0
From Embeds
0
Number of Embeds
10
Actions
Shares
0
Downloads
0
Comments
2
Likes
24
Embeds 0
No embeds

No notes for slide

dental Cariology /certified fixed orthodontic courses by Indian dental academy

  1. 1. CARIOLOGY INDIAN DENTAL ACADEMYLeader in Continuing Dental Education www.indiandentalacademy.com
  2. 2. CONTENTS• INTRODUCTION• DEFINITION• CLASSIFICATION• ETIOLOGY OF DENTAL CARIES—EARLY THEORIES CURRENT CONCEPTS• CLINICAL FEATURES OF CARIES• CARIES AS A SPECIFIC MICROBIAL INFECTION• CONCEPT OF CRITICAL pH• NUTRITION,DIET AND DENTAL CARIES• EFFECT OF DEMOGRAPHIC FACTORS ON DENTAL CARIES• ROLE OF SALIVA ON DENTAL CARIES www.indiandentalacademy.com
  3. 3. • CARIES PROCESS—MORPHOLOGICAL AND CHEMICAL EVENTS• HISTOPATHOLOGY OF ENAMEL CARIES• DENTINAL CARIES—HISTOPATHOLOGY• ELECTRON MICROSCOPIC STUDIES OF CARIOUS ENAMEL• ENAMEL CARIES MECHANISM AT A CHEMICAL LEVEL• CONCLUSION• REFERANCES www.indiandentalacademy.com
  4. 4. INTRODUCTION• TEETH ARE TOOLS that have evolved to ensure survival of species. Caries is a biosocial disease rooted in the technology and economy of our society. Dental caries is unique not only in terms of pathological mechanism ; other aspects, social and economic , are also worthy of note. The uniqueness of dental caries makes it a fascinating study from a scientific standpoint. As living standards improve the severity of disease usually increases. Dental caries constitutes a very real personal problem to virtually every man, woman and child. While it is true that diseases of the teeth and their supporting tissues do not normally kill humans they certainly affect the persons efficiency and they can , if neglected, provoke serious conditions elsewhere in the body. Their contribution to the general fund of human misery is legendary www.indiandentalacademy.com
  5. 5. • DEFINITION• Dental caries is defined as a progressive, irreversible, microbial disease affecting the hard parts of the tooth exposed to the oral cavity ,resulting in decalcification of inorganic constituents and dissolution of organic components, there by leading to a cavity formation. www.indiandentalacademy.com
  6. 6. • CLASSIFICATION DENTAL CARIESA : On the basis of clinical features and patterns dental caries may be classified according to three basic factors 1) Morphology i.e according to anatomical site of lesions a) Occlusal caries (pit fissure caries) b) Smooth surface caries Interproximal Cervical or gingival c) Root caries d) Linear enamel caries ( Odontoclasia) www.indiandentalacademy.com
  7. 7. • 2) Dynamics i.e according to severity and rate of progression of lesions Based on the severity Class 1: Very mild caries Class 2: Mild caries Class 3: Moderate caries Class 4: Severe caries Class 5: Very severe caries www.indiandentalacademy.com
  8. 8. • 3) Chronology i.e according to age patterns at which lesions predominate a) infancy caries b) Adolescent caries 4)Based on the graphical representation ofpathway of dental caries it is classified into 1) Forward decay 2) Backward decay www.indiandentalacademy.com
  9. 9. • 5. Based on treatment and restoration design ( Therapeutic classification) – G.V. Black classified into a) class 1 Pit and fissure cavities of posterior teeth, the occlusal two- thirds of buccal and lingual surface of molars, lingual surface of maxillary incisors. b)class 2 cavities seen on proximal surface of posterior teeth c)class 3 cavities seen on proximal surfaces of anterior teeth which do not involve the incisal angle d) class 4 cavities seen on proximal surfaces of anterior teeth that involve the incisal angle e) class 5 cavities seen on gingival third of facial and lingual surfaces of all teeth f) class 6 cavities seen on incisal edges of ant teeth and occlusal cusp heights of posterior teeth www.indiandentalacademy.com
  10. 10. e) based on carious surfaces involved, it is classified into 1 simple[1surface] 2 compound [ 2 surface] 3 complex [3 or more surfaces] f) based on whether the lesion is a new one attacking a previously intact surface or whether it is occurring around the margins of a restoration it is classified into primary [virgin] caries secondary [recurrent] cariesg) based on degree and rate of caries progression 1 incipient 2 arrested caries 3 xerostomia induced caries[radiation] www.indiandentalacademy.com
  11. 11. Early Theories of caries formation;THE LEGEND OF THE WORM• The earliest reference to tooth decay and toothache came from the ancient Sumerian text known as The legend of the worm.• It was discovered on a clay tablet, excavated from an ancient city within the Euphrates valley of the lower mesopotamian areas which dates from about 5000 BC.• In Japanese the word for dental caries is Mush-ha, meaning hollow teeth. In china the term for hollow tooth is Chung-choo.• The early history of India, Egypt, and the writing of homer also makes reference to the worm as the cause of toothache.• Fumigation devices consisting of burning of leeks and hyocyamus where used by the Chinese and Egyptians.• An interesting therapeutic method applied by the Chinese about 2700BC for the treatment of various diseases including dental tissues was acupuncture.• Atleast at the subconscious level this theory survives to our day when we refer toothache as a gnawing pain . www.indiandentalacademy.com
  12. 12. ENDOGENOUS THEORIESHUMORAL THEORYThe ancient Greeks consider that a persons physical and mental constitution was determined by the relative proportions of the four elemental fluids of the body.-blood, phlegm, black bile, yellow bile- which correspond to the four humors – sanguine ,phlegmatic melancholic, and choleric.All diseases including caries could be explained by an imbalance of these humors.Hippocrates, the father of medicine, while favoring the concept of humoral pathology , also referred to the accumulated debris around teeth and to their corroding action.He also stated that stagnation of juices in the teeth was cause of toothache www.indiandentalacademy.com
  13. 13. VITAL THEORYThis theory regarded dental caries as originating within the tooth itself, analogous to bone gangrene.This theory ,proposed at the end of 18th century remain dominant until the middle of 19th century.A clinically well- known type of caries is characterized by extensive penetration into the dentin, and even into the pulp , but with barely detectable catch in the fissure www.indiandentalacademy.com
  14. 14. EXOGENOUS THEORIESCHEMICAL THEORY Parmly[1819] rebelled against the vital theory and proposed that an unidentified chemical agent was responsible for caries. He stated that caries began on the enamel surface in locations where food putrefied and acquired sufficient dissolving power to produce the disease chemically.Support for chemical theory came from Robertson[1835] and Regnart[1938] , who actually carried out experiments with different dilutions of inorganic acids[such as sulfuric and nitric] and found that they corroded enamel and dentin. www.indiandentalacademy.com
  15. 15. PARASITIC[SEPTIC] THEORY In 1843 , Erdl described filamentous parasites in the surface membrane[ plaque ] of teeth.Shortly thereafter Ficinus[1847] , a Dresden physician, observed filamentous microorganisms, which he called denticolae, in material taken from carious cavities. He implied that these bacteria caused decomposition of the enamel and then the dentin. Neither Erdl or Ficinus explained how these organisms destroyed tooth structure www.indiandentalacademy.com
  16. 16. CHEMICO-PARASITIC [ACIDOGENIC] THEORYThis theory was proposed by W.D MILLER[1890]Essential features of this theoryThat the microorganisms of the mouth, by secretion of enzymes or by their own metabolism , degrade the fermentable carbohydrate food material so as to form acids.The chief acids formed are namely lactic, butyric, acetic, formic, succinic and other acids.Carbohydrate food material lodged between and on surfaces of teeth is the source of the acid which demineralises the lime salts of the tooth.He believed that starchy foods were more effective than soluble sugars . Thus the enamel is destroyed by the acid of fermentation and the disintegrated enamel is subsequently mechanically removed by forces of mastication. www.indiandentalacademy.com
  17. 17. After penetration of enamel, the dissolution of dentin is brought about in the same manner with the organisms penetrating along the dentinal tubules. The final breakdown of dentin results from the secretion of proteolytic enzymes that digest the organic part of dentin and form a cavity. Significance of Millers observations• He assigned an essential role to 3 factors in carious process.• The oral microorganisms in acid production and in proteolysis.• The carbohydrate substrate which microorganisms fermented• The acid which causes dissolution of tooth minerals www.indiandentalacademy.com
  18. 18. Limitations of acidogenic theory• This theory was unable to explain the predilection of specific sites on a tooth to dental caries . The initiation of caries on smooth surfaces was not accounted for by this theory . Miller, while a disciple of koch who was an avid advocate of specific bacterial etiology of infectious disease nevertheless worked with mixed cultures from saliva and with techniques that did not attempt to ascertain types of organisms present.• Miller believed that dental caries was caused by a multiple species of bacteria this is understandable since many bacterial species posess glycolytic abilities. While current evidence for a specific bacterial infection in dental caries is tantalizing, the concept is not disputable www.indiandentalacademy.com
  19. 19. • This theory does not explain why some populations are caries –free• The phenomenon of arrested caries is not explained by this theory.• Miller believed that in some systemic conditions the inorganic salts within a tooth could be withdrawn and that the organic-inorganic bonds would be weakened.• He did not produce any experimental evidence that the adult tooth is subject to such systemic influences.• The concept of tooth resistance while logical did not have any experimental support www.indiandentalacademy.com
  20. 20. • Proteolytic theory (Gottlieb)The surface coverings found on the tooth in grooves and pits are organic in nature , also enamel contains small but significant amounts of organic materials.These observations and the fact that carious lesions are characterized histologically by pigmentation, the phenomenon that was interpreted, without evidence as being indicative of proteolysis, led to the development of the proteolytic theory proposed primarily by Gottlieb(1947) Frisbee and nuckolls(1947) and Pincus(1950). www.indiandentalacademy.com
  21. 21. They described carious like lesions that were initiated by proteolytic activity at a slightly alkaline ph and conceded that the process involved depolymerisation and liquefaction of the organic matrix of the enamel.Gottlieb 1947 proposed that microorganisms invade organic pathways(lamellae) of enamel and initiate caries by proteolytic action.Subsequently the inorganic salts are dissolved by acidogenic bacteria.Pincus (1950) also maintained that the initial process was the proteolytic breakdown of the dental cuticle, the organic membrane found on all teeth. www.indiandentalacademy.com
  22. 22. Limitations:• The above conclusions were made on the basis of the early histological observations.• An interpretation of a molecular mechanism based on morphological evidence is highly suspect.• To date no one has under physiological conditions successfully demonstrated significant loss of enamel tissue through proteolytic activity.• Enamel is highly structured tissue and the accessibility of organic material to enzymatic action before decalcification is restricted.• Enamel can be dissolved under physiological conditions only by demineralization with acids , chelating or complexing agents www.indiandentalacademy.com
  23. 23. • PROTEOLYSIS CHELATION THEORY:This theory proposed by Schatez et al (1955) implies a simultaneous microbial degradation of the organic components (proteolysis) and the dissolution of the minerals of the tooth by the process of chelation.The word chelate is derived from the Greek word chele’ meaning claw, and refers to compounds that are able to bind metallic ions as calcium, Iron, copper, zinc and other metals by the secondary valence bonds.The resulting chelates are non ionic and usually soluble.According to the proteolytic chelation theory dental caries results from initial bacterial and enzymatic proteolytic action on the organic matter of enamel without preliminary demineralization.Such action, the theory suggests produces an initial carious and a release of variety of complexing agents such as amino acids, polyphosphates and organic acids. The complexing agents then dissolve the crystalline apatite. www.indiandentalacademy.com
  24. 24. Limitations:• Less than one percent of mature enamel is organic in nature and the suggestion that this material upon degradation can give rise to a significant concentration of chelator sufficient to dissolve upto 96% mineral matter has no experimental support.• Also there is no substantial experimental evidence that the initial carious lesion stems from a break down of organic matter that is due to proteolytic action.• While proteolysis chelation is an important biological phenomenon, its primary role in the etiology of the dental caries has not been corroborated www.indiandentalacademy.com
  25. 25. Other Theories of caries etiologySULFATASE THEORYPincus[1950] advanced the sulfatase theory, , whereby bacterial sulfatase hydrolyses the mucoitin sulphate of enamel and the chondroitin sulphate of dentin producing sulfuric acid that in causes decalcification of the dental tissues.LimitationsThe concentration of sulfated polysaccharides in enamel is very small and not readily accessible as a substrate for enzymatic degradation.This is a highly unlikely hypothesis for the degradation of tooth enamel. www.indiandentalacademy.com
  26. 26. COMPLEXING AND PHOSPHORYLATING THEORY [LURA-1967]It can be readily demonstrated that uptake of phosphate by plaque bacteria occurs during aerobic and anaerobic glycolysis and the synthesis of polyphosphates.According to this theory , the high bacterial utilization of phosphate in plaque causes a local disturbance in the phosphate equilibrium in the plaque and the tooth enamel resulting in loss of inorganic phosphate from enamel. soluble calcium- complexing compounds produced by bacteria cause further tooth disintegration . www.indiandentalacademy.com
  27. 27. LIMITATIONS:Saliva is an abundant source of inorganic phosphate for bacterial utilization.Hence it is highly improbable that depletion of phosphate in plaque by oral microbial metabolism results in phosphate withdrawal from enamel www.indiandentalacademy.com
  28. 28. CURRENT CONCEPT.Primary factors in the etiology of dental caries (essential factors).In the epidemiological model dental caries is due to an inter play of three primary factors- the host, the agent, or recruiting factor and environmental influences.Obviously many secondary factors influence the rate of progression of disease. www.indiandentalacademy.com
  29. 29. www.indiandentalacademy.com
  30. 30. HOST factorsComposition Studies of the chemical composition of enamel indicate that surface enamel is more resistant to caries than subsurface enamel. Surface enamel is more highly mineralized and tends to accumulate greater quantities of fluoride, zinc, lead and iron than the underlying enamel.The surface is lower in carbon-dioxide, dissolves at a slower rate in acids, contains less water and has more organic material than subsurface enamel .These factors apparently contribute to caries resistance and are partly responsible for the slower disintegration of surface enamel than of the underlying enamel in initial carious lesions. www.indiandentalacademy.com
  31. 31. MORPHOLOGIC CHARACTERISTICS OF THE TOOTHIt has been suggested that morphology of tooth may influence the initiation of caries. The feature that predispose to the development of caries is the presence of deep, narrow, occlusal fissures or buccal and lingual pits.Such fissures tend to trap food, bacteria and debris and caries may develop rapidly in these areas.Conversely as caries advances, the inclined planes become flattened, providing less opportunity for entrapment of food in the fissures and caries predisposition diminishes. TOOTH POSITION Teeth which are malaligned, out of position, rotated or otherwise not normally situated may be difficult to clean and tends to favor the accumulation of food and debris.This in susceptible persons would be sufficient to cause dental caries www.indiandentalacademy.com
  32. 32. ESSENTIALITY OF ORAL BACTERIAMicroorganisms are a pre requisite for caries initiation.A single type of organism for example enterococcus strain is capable of inducing caries.The ability to produce acid is a pre requisite for caries induction but not all acid producing organisms are cariogenic.Streptococcus strain that are capable of inducing caries are also able to synthesis extra cellular dextrans or levans. Not all strains that produce extra cellular polysaccharides are capable of caries induction.Organisms vary greatly in their capacity (virulence) to induce caries. www.indiandentalacademy.com
  33. 33. Cariogenic suitableBacterial + local --- organic acidsplaque substrateorganic toothacids + mineral ---- loss of enamel(in plaque)demineralized + bacterialtooth(dentin) proteolytic ------ cavitation enzymes www.indiandentalacademy.com
  34. 34. CLINICAL FEATURES OF CARIESPIT AND FISSURE CARIESpits or fissures with high steep walls and narrow bases are more prone to develop caries .Deep narrow pits or fissures favor the retention of food debris and microorganisms, and caries may result from fermentation of this food and formation of acid.Early caries may appear brown or black and will feel slightly soft and catch a fine explorer point.The enamel directly bordering the pit or fissure may appear opaque bluish- white as it becomes under- mined. This under-mining occurs through lateral spread of caries at the dentino- enamel junction. www.indiandentalacademy.com
  35. 35. And penetrates into the dentin along the dentinal tubules without fracturing away the over-hanging enamel.Thus there may be a large carious lesion with only a tiny point of opening in advanced lesions it forms a cone shaped cavity with apex at outer surface and base towards DEJ www.indiandentalacademy.com
  36. 36. SMOOTH SURFACE CARIEScaries that develops on the proximal surfaces of teeth or on the gingival third of the buccal and lingual surfaces www.indiandentalacademy.com
  37. 37. PROXIMAL CARIESIt usually begins just below the contact point and appears in the early stage as a faint opacity of enamel without apparent loss of continuity of enamel surface. The early white chalky spot becomes slightly roughened due to superficial decalcification of the enamel . As the lesion advances it forms a cone- shaped lesion with apex toward DEJ and base towards the enamel surface www.indiandentalacademy.com
  38. 38. CERVICAL CARIES• It occurs on buccal, lingual or labial surfaces and usually extends from opposite the gingival crest occlusally to the convexity of the tooth surface making the self cleansing portion of this surface.• The typical cervical carious lesion is a crescent – shaped cavity beginning as a slightly roughened chalky area that gradually becomes excavated. www.indiandentalacademy.com
  39. 39. ROOT [CEMENTUM] CARIESHAZEN defined root caries as- A soft, progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment.Enamel may become secondarily involved if it is undermined during the progression of the lesion .Dental plaque and microbial invasion are an essential part of the cause and progression of this lesion. www.indiandentalacademy.com
  40. 40. • This type of caries is predominately found in dentitions of older age groups with significant gingival recession and exposed root surfaces.• In the 50-59-year age group almost 60% of patients examined had root surface lesions [Banting and ellen-1976] www.indiandentalacademy.com
  41. 41. LINEAR ENAMEL CARIES[ODONTOCLASIA]An atypical form of dental caries, called linear enamel caries, has been observed in the primary dentition of children, in Latin America and Asian countries.The lesions predominate on the labial surfaces of the maxillary teeth, in the region of neonatal zone .This zone represents the demarcation between pre- and post- natal enamel and is a histological feature of all primary teeth. It is thought to result from the metabolic disturbances associated with the trauma of birth .More recent evidence indicates that the specific metabolic disturbance causing the neonatal line is transient hypocalcemia associated with transient hypoparathyroidism- a normal feature of neonatal period. www.indiandentalacademy.com
  42. 42. A variant of linear enamel caries in the primary teeth of children in the far east has been named odontoclasia.The morphological aspects of this type of caries is atypical and results in gross destruction of the labial surfaces of incisor teeth,.This may be an inherent structural defect in teeth resulting in a rapid carious process www.indiandentalacademy.com
  43. 43. www.indiandentalacademy.com
  44. 44. www.indiandentalacademy.com
  45. 45. RAMPANT CARIESOne of the most distressful clinical conditions for both patient and practitioner is rampant caries in which there occurs a sudden, rapid and almost uncontrollable destruction of teeth.Rampant caries also involves surfaces of teeth that are ordinarily relatively caries-free.A caries increment of 10 or more new caries lesions over a period of about a year is characteristic of a rampant caries attack.Proximal and cervical surfaces of anterior teeth, including the mandibular incisors which are relatively caries free, may be affected.It is mostly seen in primary dentition of young children and permanent dentition of teenagers 11-19 years.Dietary factors affecting oral substrate and oral flora and physiological factors affecting saliva are often significant in the development of rampant caries. www.indiandentalacademy.com
  46. 46. www.indiandentalacademy.com
  47. 47. RECURRENT CARIES A carious lesion that develops at the inter-face of a restoration and the cavo-surface of enamel is called recurrent caries.It may indicate an unusual susceptibility to caries attack , a poor cavity preparation, a defective restoration or a combination of these factors. ARRESTED CARIES It has been described as caries which becomes static or stationary and does not show any tendency for further progression.It occurs almost exclusively in caries of occlusal surfaces and is characterized by a large open cavity in which there is lack of food retention and in which , the superficially softened and decalcified dentin is gradually burnished until it takes on a brown stained, polished appearance and is hard, this has been referred to as Eburnation of dentin.Another form of arrested caries is that seen on the proximal surfaces of teeth in which the adjacent approximating tooth has been extracted.. www.indiandentalacademy.com
  48. 48. www.indiandentalacademy.com
  49. 49. • XEROSTOMIA- INDUCED CARIES[RADIATION CARIES]• A common complication of radiotherapy of oral cancer lesions is xerostomia.• Such patients develop rampant dental caries and confirm the important role of salivary secretions in the maintenance of the integrity of teeth.• Xerostomia is accompanied by major changes in the salivary flow, salivary composition, salivary and serum proteins and a shift towards a more caries-producing micro flora.• Carious lesions appear as early as 3 months after the onset of xerostomia and all patients may be affected irrespective of their past caries history.• Xerostomia may be caused by other factors than radiation like tumors of salivary glands , auto immune diseases, anti- sialogogue drugs , prolonged illnesses etc www.indiandentalacademy.com
  50. 50. www.indiandentalacademy.com
  51. 51. INFANCY[SOOTHER OR NURSING BOTTLE] CARIESNumerous reports by pediatricians and pedodontists describe a rapidly progressing type of dental caries that affects the primary teeth of children, usually during the first 2 years of life and as early as the first year. In children with infancy caries there is a unique distribution of dental decay.The 4 maxillary incisors are affected first, these teeth are anatomically so positioned in the mouth as to be most frequently bathed by a feeding formula.If unchecked, the decay may extend to the maxillary and mandibular molars. Initially the lower ant teeth may not be involved because of the protective environment of the mandibular salivary secretions and the cleansing action of tongue muscles. www.indiandentalacademy.com
  52. 52. Infancy caries is most often seen in children with an unusual dietary history such as an addition of syrup, honey or sucrose to the formula or the use of pacifier dipped in honey or other sweeteners. In addition to improper formula in bottle-feeding, it has been reported that prolonged and unrestricted night-time breast- feeding can result in increased caries rates.The stagnation of milk about the neck of ant teeth and the fermentation of disaccharide lactose contribute to the carious process. www.indiandentalacademy.com
  53. 53. www.indiandentalacademy.com
  54. 54. ADOLESCENT CARIES The acute caries attack seen at 11-18 years of age is characterized as adolescent caries .ITS CHARACTERISTIC FEATURES ARE:• lesions in teeth and surfaces that are relatively immune to caries• Relatively small opening in enamel with extensive undermining of enamel• Rapid penetration of enamel and extensive involvement of dentin• The rapid progression of lesion which does not permit an effective pulpal response with little or no secondary dentin www.indiandentalacademy.com
  55. 55. CARIES AS A SPECIFIC MICROBIAL INFECTION• Definition of dental plaque: Plaque is a specific but highly variable structural entity resulting from colonisation of microorganisms on tooth surfaces, restorations , other parts of oral cavity of salivary components like mucin, desquamated epithelial cells, debris and microorganisms all embedded in gelatinous extra cellular matrix www.indiandentalacademy.com
  56. 56. EVIDENCE OF BACTERIAL ROLE IN CARIES ETIOLOGY1.germ free animal do not develop caries.2. antibiotics fed to animals are effective in reducing the incidence and severity of caries.3. Totally unerupted and unexposed teeth do not develop caries.4. oral bacteria can demineralise enamel and dentin in vitro and produce caries like lesions.5. micro organism have been histologically demonstrated invading carious enamel and dentin. They can be isolated and cultivated from carious lesions www.indiandentalacademy.com
  57. 57. www.indiandentalacademy.com
  58. 58. PROPERTIES OF CARIOGENIC PLAQUEThe rate of sucrose consumption was noticeably higher in cariogenic plaques. The rate of lactic acid formation was considerably higher in cariogenic plaques.Bacteria in cariogenic plaques synthesized more intracellular glycogen-amylopectin-type polysaccharides. Upto 20% of sucrose consumed within 15 minutes was converted into intracellular polysaccharides by cariogenic plaque.Cariogenic plaques formed more lactic acids from stored intracellular polysaccharides.Cariogenic plaques formed approximately twice as much extra cellular polysaccharides from sucrose as did noncariogenic plaques.. www.indiandentalacademy.com
  59. 59. Cariogenic plaques contained higher levels of streptococcus mutans than noncariogenic plaques.- Noncariogenic plaques harboured higher levels of S.sanguis and Actinomyces than cariogenic plaques.Noncariogenic plaques had significantly higher proportion of dextranase producing organisms.Noncariogenic plaques had higher levels of veilonella and contained slightly lower concentration of lactic acids and slightly higher con of acetic and propionic acids. www.indiandentalacademy.com
  60. 60. NON SPECIFIC PLAQUE HYPOTHESIS:There is no question, dental caries is an infection.In the past, and has an extension of miller’s chemico parasitic theory, the total plaque was viewed as a pathogenic structure which had to be eliminated or reduced if caries was to be prevented.If all plaques were similar in their potential to induce caries, the main difference between health and disease states might be expected in the quantitative aspects of plaque accumulation.This possibility carries with it the implication that mechanical debridement should be the dominant method of disease control(loesche-1982). Further specific anti microbial agents should be limited in their efficacy since the accumulation or activity of the old plaque requires suppression. www.indiandentalacademy.com
  61. 61. SPECIFIC PLAQUE HYPOTHESIS:On experimental evidences it is impressive that qualitative nature of the flora in plaque determines the metabolism and the potential for caries production.this view is termed the specific plaque hypothesis.Inherit in this concept is that certain plaques are more cariogenic than others because they contain higher numbers of specific bacterial species that cause caries.The species implicated in enamel caries are S. mutans and lactobacilli and in root caries A.viscosus. www.indiandentalacademy.com
  62. 62. According to this hypothesis , most but not all carious lesions are due to specific bacterial species.Further the hypothesis implies that plaque in some sites is not disease- producing.The concept of specific plaque hypothesis suggests the development and implementation of preventive procedures that treat dental caries as a specific bacterial infection. www.indiandentalacademy.com
  63. 63. CONCEPT OF CRITICAL pHThe loss of tooth mineral during caries formation is caused by the formation of bacterial acids which lower the pH to the point where the hydroxyappatite mineral of enamel dissolves.The concept of critical pH was initially applied to indicate the pH at which saliva was no longer saturated with respect to calcium and phosphate ions , thereby permitting hydroxyappatite to dissolve.However it is now realized that the immediate fluid environment involved in demineralization of a tooth is not saliva but the fluid phase of plaque , now known as ‘plaque fluid.; www.indiandentalacademy.com
  64. 64. It has been shown experimentally that both saliva and plaque fluid caese to be satured at Ph values in the range of 5-6 with an average of 5.5. The critical Ph varies in different plaques depending mainly on the concentrations of calcium and phosphate ions but is also influenced by the buffering power and ionic strength of the environment. However it is unlikely that demineralization would occur above 5.7 and this value has often been accepted as being safe for the teeth www.indiandentalacademy.com
  65. 65. . These considerations are specially important in the very early stages of caries when the outer enamel is being dissolved.As a carious lesion develops , the demineralization occurs within the body of the lesion rather than on the outer surface which retains a higher degree of mineralization . This implies that acids must diffuse into the enamel and dissolve the apatite within the lesion .There is good evidence that unionized lactic acid molecules diffuse more readily into enamel. www.indiandentalacademy.com
  66. 66. Being uncharged , the unionized molecules are less likely to react with apatite than their constuient hydrogen and lactate ions.The critical pH may therefore be the Ph at which the environment of the enamel becomes unsaturated and in addition that Ph at which sufficiently high concentrations of unionized acid are present to ensure the inward diffusion of enough acid to extend the inner lesion www.indiandentalacademy.com
  67. 67. STEPHAN CURVEStephan [1940], using antimony microelectrodes , recorded the pH values of dental plaques in situ before , during and after a glucose rinse.These curves are often referred to as stephan curves and they have 3 main charecteristics.Under resting conditions , the pH of plaque is reasonably constant, though differences can be noted in the individuals .Following exposure to sugars , the pH drops very rapidly[ in a few minutes] to its lowest level and then slowly returns to its original value over a period of approximately 30-60min. www.indiandentalacademy.com
  68. 68. www.indiandentalacademy.com
  69. 69. Stephan[1944] observed that plaques of caries-free or caries-inactive individuals usually had a resting pH of between 6.5 and 7 and they usually remained above pH 5 following exposure to glucose. In contrast , plaques of highly caries – prone persons had a lower resting pH and attained acidities well below pH 5 after exposure to glucose www.indiandentalacademy.com
  70. 70. • Stephan postulated that there must be microbial differences between plaques in caries – free and caries prone individuals. In addition to this , other factors which may affect the extent and rate of pH changes in plaque are the type and concentration of carbohydrates and other substrates ingested , the frequency of ingestion, salivary composition and flow, and the thickness and age of the plaque www.indiandentalacademy.com
  71. 71. • NUTRITION,DIET AND DENTAL CARIES• Diet----carbohydrates• Others[calcium,phosphorus,vit.D,K,B6, proteins,lipids,trace elements]• Product related variables type of carbohydrate concentration of carbohydrate stickiness, retention time• individual related variables frequency of eating oral clearance time www.indiandentalacademy.com
  72. 72. ROLE OF SUCROSE IN DENTAL CARIES• Many oral bacteria utilize sucrose,glucose,fructose and other simple sugars to produce organic acids(lactic,acetic and propionic acid) in sufficient concentration to lower the pH of plaque to levels that may result in some demineralization of enamel.• It is only from sucrose, however, that most bacteria are able to synthesize both soluble and insoluble extra cellular polymers which increase the bulk of plaque and facilitate the attachment of bacteria, especially S.mutans to it.• Unlike other disaccharides such as maltose or lactose, sucrose can serve directly as a glycosyl donor in the synthesis of extra cellular polymers.• The high free energy of hydrolysis of sucrose permits this reaction to proceed without other sources of energy.• This property along with the high specificity of enzymes involved in the synthesis of extra cellular polymers has led some workers to regard sucrose as having a unique role in caries www.indiandentalacademy.com
  73. 73. EFFECT OF TRACE ELEMENTS ON DENTAL CARIES ____________________________________________________________ __________________EFFECT TRACE ELEMENTcariostatic F,PMildly cariostatic M,V,Cu,Sr,B,Li,AuEquivocal effect Be,Co,Mn,Sn,Zn,Br,I.No effect Ba,Al,Ni,Fe,Pd,TiCaries potentiating Se,Mg,Cd,Pt,Pb,Si._______________________________________________________ www.indiandentalacademy.com
  74. 74. MECHANISM OF ACTION OF FLUORIDES IN CARIES REDUCTION1 increased enamel resistance/reduction in enamel solubility2 increased rate of post-eruptive maturation3 remineralisation of incipient lesions4 fluoride as an inhibitor of demineralization5 interferance with microorganisms www.indiandentalacademy.com
  75. 75. EFFECT OF DEMOGRAPHIC FACTORS ON THE PREVALENCE OF CARIES• sex• age• race• familial factors• time factors for caries development after eruption• latitude www.indiandentalacademy.com
  76. 76. ROLE OF SALIVA IN DENTAL CARIEScomposition 1. Inorganic constituents: Positive ions- Ca ,H+,Mg,K Negative ions- carbondioxide,carbonate,Cl, F,phosphate,thiocyanate.2.Organic constituents: Carbohydrate-Glucose Lipids-cholesterol,lecithin Nitrogen –nonprotein- NH3,nitrites, urea and aminoacids. Nitrogen protein-globulin,mucin,total proteinsEnzymes- carbohydrases(amylase,maltase),proteases(trypsin),oxidases(catalase, oxidase) www.indiandentalacademy.com
  77. 77. • pH of saliva: It is determined mainly by the bicarbonate concentration.(85%) .Phosphates and proteins in saliva constitute the other buffer systems, but the constitution of these in saliva are too low to be of significance. So the pH will vary according to the bicarbonate content. The saliva pH increases with flow rate. It may be slightly acidic as it is secreted at an unstimulated flow rate but it may reach a pH of 7.8 .Other salivary components contributing to the ability of saliva to neutralize the acidity are ammonia, urea and statherin. Sialin is an arginine peptide which is the recently described pH rise factor present in saliva which rapidly clears glucose from plaque, increases base formation and elevates pH in the plaque.QUANTITY OF SALIVA: The normal secretion is 700 to 800 ml per day.It may influence caries incidence.This is especially evident in cases of salivary gland aplasia and xerostomia in which salivary flow may be entirely lacking with rampant dental caries the typical result.VISCOSITY OF SALIVA:It depends on the mucin content.A high caries incidence is associated with thick mucinous saliva. www.indiandentalacademy.com
  78. 78. • ANTIBACTERIAL AGENTS OF SALIVA: 1.Lactoperoxidase 2.Lysozyme 3.Lactoferrin 4.Ig ALACTOPEROXIDASE These enzymes participate in killing microorganisms by catalyzing the hydrogen peroxide mediated oxidation of a variety of substances in the microbes.Utilizing thiocyanate ions in saliva, it generate highly reactive chemical compounds that bind and inactivate several intracellular microbial enzyme systems, as well as microbial surface components.It has high affinity for enamel surface and it forms an important defence mechanism, limiting early microbial colonization of tooth surfaces. www.indiandentalacademy.com
  79. 79. LYSOZYMEIt is a small ,highly positive, enzyme that catalyzes the degradation of negatively charged peptide-glycan matrix of microbial cell walls.There is strong evidence that lysozyme, which is highly positively charged, binds to hydroxyappatite and maintains its activity after binding. www.indiandentalacademy.com
  80. 80. LACTOFERRIN It is an iron binding basic protein which tends to bind and limit the amount of free iron.Since iron is essential for microbial growth, this salivary protein is an active host defence mechanismIg A Secretory Ig A is an effective agglutinin because each molecule posesses 4 antigen binding sites.It inhibits adherence and thereby prevents colonization of teeth by organisms, facilitating their disposal by swallowing. www.indiandentalacademy.com
  81. 81. • HISTOPATHOLOGY OF DENTAL CARIES ENAMEL CARIES Light microscopic studies of carious lesions of enamel without cavitation, have revealed four distinct zones, which represent varying degrees of hard tissue transformation, beginning on the dentinal side of the lesion www.indiandentalacademy.com
  82. 82. ZONE 1:TRANSLUCENT ZONE It is the deepest zone and represents the advancing front of enamel lesion. It is not always present.The name refers to its structureless appearance when perfused with quinoline solution and examined with polarized light.In this zone , pores or voids form along the enamel prism [rod] boundaries, presumably, because of the ease of hydrogen ion penetration during the carious process.The pore volume of this zone is 1%[10 times greater than normal enamel] www.indiandentalacademy.com
  83. 83. ZONE2:DARK ZONEIt lies adjacent and superficial to the translucent zone . It is called dark zone because it does not transmit polarized light .This light blockage is caused by the presence of many tiny pores too small to absorb quinoline.The total pore volume is 2% to 4%.It has been referred to as positive zone because it is usually presentExperimental remineralization has demonstrated increases in the size of dark zone at the expense of body of lesionThere is also a loss of crystalline structure in this zone , suggesting of process of demineralization and remineralization.The size of dark zone is probably an indication of the amount of remineralization that has recently occurred. www.indiandentalacademy.com
  84. 84. ZONE 3:BODY OF THE LESION It lies between the relatively unaffected surface layer and the dark zone. It is the area of greatest demineralization.It has the largest pore volume, varying from 5% at the periphery to 25%at the centre.The striae of retzius is well marked in this zone, indicating mineral dissolution along these areas of relatively higher porosity.The first penetration of caries enters the enamel surface via the striae of retzius. The inter prismatic areas and these cross striations provide access to rod cores, which are then preferentially attacked . Bacteria may be present in this zone if the pore size is large enough to permit their entry. Studies using TEM and SEM demonstrated the presence of bacteria invading between the enamel rods [prisms] in the body zone www.indiandentalacademy.com
  85. 85. ZONE 4: SURFACE ZONE This zone is relatively unaffected by the carious attack. It has a lower pore volume than the body of lesion [less than 5%]and a radio opacity compared to the unaffected adjacent enamel.It has been hypothesized that hypermineralisation and increased fluoride content of superficial enamel are responsible for the relative immunity of enamel surface www.indiandentalacademy.com
  86. 86. www.indiandentalacademy.com
  87. 87. ZONES OF DENTINAL CARIES Caries advancement in dentin proceeds through 3 stages. 1 weak organic acids demineralise dentin 2 organic material of dentin particularly collagen degenerates and dissolves and 3 the loss of structural integrity is followed by invasion of bacteria .• Five Different zones have been described in carious dentin.• The zones are more clearly distinguished in slowly advancing lesions. In rapidly progressing caries, the difference between the zones becomes less distinct www.indiandentalacademy.com
  88. 88. www.indiandentalacademy.com
  89. 89. ZONE 1:NORMAL DENTIN The deepest area is normal dentin which has tubules with odontoblastic process that are smooth and no crystals are in the lumen .The intertubular dentin has normal cross banded collagen and normal dense apatite crystals .No bacteria are in the lumens .Stimulation of dentin [eg. by osmotic gradient , a bur, dessication from heat or air] produces a sharp pain www.indiandentalacademy.com
  90. 90. ZONE 2 SUBTRANSPARENT DENTIN• This is a zone of demineralization of inter tubular dentin and initial formation of very fine crystals in the lumen at the advancing front .• Damage to the odontoblastic process is evident• However no bacteria are found in this zone• Stimulation of dentin produces pain, and the dentin is capable of remineralization www.indiandentalacademy.com
  91. 91. ZONE3: TRANSPARENT DENTINIt is softer than normal dentin . and shows further loss of mineral from the inter tubular dentin and many large crystals in the lumen of dentinal tubules .Stimulation of this region produces pain . No bacteria are present.Although organic acids attack both the mineral and organic content of dentin , the collagen cross linking remains intact in this zone .The intact collagen can serve as a template for remineralisation of the intertubular dentin, and thus this region is capable of self- repair provided the pulp remains vital. www.indiandentalacademy.com
  92. 92. ZONE 4: TURBID DENTINIt is the zone of bacterial invasion and is marked by widening and distortion of dentinal tubules, filled with bacteria .There is very little mineral present, and the collagen in this zone is irreversibly denatured.The dentin in this zone will not self- repair this zone cannot be remineralized and must be removed before restoration. www.indiandentalacademy.com
  93. 93. ZONE 5 :INFECTED DENTINIt is the outermost zone consists of decomposed dentin that is teeming with bacteriaThere is no recognizable structure to dentin and collagen and mineral seem to be absent.Great number of bacteria are dispersed in this granular material.Removal of infected dentin is essential to sound . ,successful restorative procedures as well as prevention of spreading of infection www.indiandentalacademy.com
  94. 94. www.indiandentalacademy.com
  95. 95. ELECTRON MICROSCOPIC STUDIES OF CARIOUS ENAMELUltra structural studies of enamel caries have shown that the intercrystalline space increases.This can only happen if some mineral substance from the surface of enamel crystallites is removed or if there is selective dissolution of a separate amorphous calcium phosphate phase between crystals.The surface of a crystals in a carious lesion show slight etching as evidenced by the irregularity of the margins.Evidence for the existence and removal of an amorphous intercrystalline phase is lacking.The most common crystal damage detected in electron microscopic studies is central or core defects due to preferential loss of minerals. www.indiandentalacademy.com
  96. 96. This causes the enamel crystals to assume a hairpin appearance in a longitudinal view .The finding is most easily explained on the basis of existence of lattice defects and or different solubilities between the central core and the exterior of crystals.It is known that dislocations in the form of lattice defects increase in the core of crystals.Chemical reactivity increases at dislocation points, thus causing preferential loss of the crystal centres. It has also been suggested , but not proven , that there is a higher concentration of carbonate in the crystal centre, carbonate is preferentially dissolved in an acidic environment. www.indiandentalacademy.com
  97. 97. www.indiandentalacademy.com
  98. 98. • At the electron microscope level some enamel crystals at the periphery of the prism in the body of the lesion are often seem to be thicker and more electron-dense than in normal tissue.• The larger crystals are thought to be formed in the process of recrystallisation or remineralisation. However, the remaining crystals within the body of lesion zone being smaller than those in sound enamel as a result of acid dissolution• Recently a new microdissection technique coupled with high resolution scanning electron microscopy has revealed [Silverstone,1983] that the crystals in both the dark zone and the surface zone of the lesion are larger in diameter than those of sound enamel. www.indiandentalacademy.com
  99. 99. • With this new technique, it has been shown that the crystals in sound enamel have a diameter of 35-40nm , in the translucent zone there was a small decrease in size to 25-30nm, and in the body of lesion crystal diameter varies from 10-30nm however in the dark zone crystal diameters were found to be in the range of 45-100nm.• The crystals in the surface zone were also seen to be larger than those of sound enamel being 40-75nm in diameter• These observations showed remineralisaton occurring in the dark zone and the surface zone of enamel lesion. www.indiandentalacademy.com
  100. 100. www.indiandentalacademy.com
  101. 101. ENAMEL CARIES AT CHEMICAL LEVEL •A protective organic film of strongly adsorbed protein, the acquired salivary pellicle forms on the surface of enamel mineral.Acquisition of fluoride in surface enamel and loss of carbonate from the enamel surface may contribute to the solubility of the outer enamel surface.• In the presence of a suitable carbohydrate sustrate’such as sucrose ,cariogenic plaque bacteria produce organic acids(lactic,acetic,propionic) localized within the plaque in juxtaposition to enamel www.indiandentalacademy.com
  102. 102. • Production of these organic acids produces a concentration gradient that causes the hydrogen ions (H+) and the undissociated acid(HA or HL,etc) to diffuse into the enamel.• As diffusion proceeds the undissociated acid molecules continually dissociate providing H+ ions .These hydrogen ions are rapidly used up in the reaction with enamel, producing calcium and phosphate and promoting further acid dissociation. www.indiandentalacademy.com
  103. 103. • The undissociated HA and HL form a reservoir of H+ ions.Dissociation is dependent on the pH and the concentration of undissociated molecules.As the HA and HL diffuse,dissociation into H+,L- and A- occurs in an attempt to establish an equilibrium.• -The H+, and to a lesser extent L- and A- ,attack the apatite crystals particularly at vulnerable lattice points such as where carbonate is present.• This causes Ca2+,OH-, PO4- ,F- ,CO3-, Na+ and Mg2+ to be removed from the lattice and to diffuse to the solution phase between the crystals. www.indiandentalacademy.com
  104. 104. • Fluoride in solution markedly inhibits this dissolution stage of the process.• This ions and their appropriate complexes(CaHPO4 ,CaL+,CaH2PO4+ ,etc) will diffuse according to their concentration gradient through the newly enlarged pores of the carious enamel so that Ca and PO4 are lost to the external environment.Mineral loss,or demineralization proceeds as long as sufficient acid is available www.indiandentalacademy.com
  105. 105. www.indiandentalacademy.com
  106. 106. • As more enamel disolves and the concentration of the Ca and PO4 ions increases remineralisation may occur on the surface of existing crystals.• New crystals may also form as CaHPO4 or other PO4 phases.As more HA and HL diffuses and reaches a critical concentration it will cause some of the new crystal forms to dissolve as well as more enamel apatite crystals.• This reactions mostly occur in the demineralised subsurface layers particularly the body of the carious lesion which may be as much as 70% demineralised. www.indiandentalacademy.com
  107. 107. • -As Ca and PO4 diffuse outward remineralisation becomes more and more likely as diffusion slows.• This leads to the formation of an apparently intact enamel surface layer,about 20 to 40 micrometer thick,where the mineral content is higher than the body of the lesion.• This isa remineralisation phenomenon where damaged crystals have been repaired and an equilibrium eventually exists which maintain this surface layer but with some loss of minerals.• The loss of ions to the plaque is balanced by the deposition of ions diffusing outwards from the subsurface www.indiandentalacademy.com
  108. 108. If subsurface dissolution continues and repair cannot keep pace with mineral loss this leads eventually to more extensive damage to crystal structure and cavitation.Dissolution of mineral salts eventually exposes the organic matrix of enamel and dentine to proteolytic enzymes of the oral flora.Proteolysis is important in the breakdown of dentin and cementum,less so in enamel as much of the protein is acid soluble and lost. www.indiandentalacademy.com
  109. 109. • CONCLUSIONCaries, because of its uniqueness as a disease,its ubiquitous nature, and its stubborn resistance to resolution remains as one of man’s most common oldest and singly costliest ailment. The total health handicap due to dental caries is staggering. In western countries there has been a dramatic decline in caries over the past decade.But in the economically developing countries caries prevalence is increasing as dietary habits of industrialized nations are adapted. For this reason, it is important that the subject of dental caries is given as broad a readership as possible. Recognition of the enormity of the problem should spur effects to reduce the ravages, the pain and the cost of this disease. www.indiandentalacademy.com
  110. 110. • REFERANCES• TEXTBOOK OF CARIOLOGY—GORDON NIKIFORUK• TEXTBOOK OF CARIOLOGY—MUNKSGAARD• TEXTBOOK OF CARIOLOGY---SILVERMAN-• CARIOLOGY—[THIRD EDITION]—ERNEST NEWBRUN• A TEXTBOOK OF ORAL PATHOLOGY[FOURTH EDITION]—SHAFER• PRINCIPLES OF PREVENTIVE AND COMMUNITY DENTISTRY-SOBEN PETER• OPERATIVE DENTISTRY[FOURTH EDITION]— STURDEVANT www.indiandentalacademy.com
  111. 111. THANK Uwww.indiandentalacademy.com

×