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1. Symposium on
Cariology
Contents
 Introduction– Unique features of Dental caries & its Measurement
 Caries in pre-historic times
 Caries in contemporary isolated population.
 Effect of Environment factors on dental caries.
 Effect of demographic factors on the prevalence of dental caries.
 World scenario
 Current trends in Caries incidence & changing trends.
 Indian scenario
 Conclusion.
Host factor in dental caries
G. Kayalvizhi
PG in dept of Pedodontia
• Early theories and recent concepts in etiology of dental caries
• Host factors in dental caries
Tooth
Saliva
Immune factor

2. Etiology of dental caries
Early theories
The legend of the worm Ancient Sumerian text (5000 BC )– worm that drank the blood from the
teeth and fed on the roots of the jaws Homer and Guy de Chahuliac (1300-1368 ) – fumigation
Antony van Leeuwenhoek 1700 – “taken out of corrupt tooth”.
Endogenous theories
1) Humoral theory (Greeks)
 4 elemental fluids- blood, phlegm, black bile and yellow bile,4 humors – sanguine,
phlegmatic, melancholic, and choleric.
 Galen – local and general medicaments, astringents and tonic remedies.
 Hippocrates – stagnation of food
 Aristotle - soft ,sweet figs
2) vital theory (end of 18th
century) – originating within tooth itself e.g. –deep carious lesions
Exogenous theories
1) Chemical (acid )theory - Parmly 1819 (inorganic)
a) putrefaction of protein ammonia nitric acid
b) food in saliva – sulfuric, nitric or acetic acids
Robertson ( 1835) and Regnart (1938) – Expts fermentation of food particles around teeth
2) Parasitic or septic theory
Erdl 1843 – filamentous parasites in surface membrane of teeth
Ficinus 1847 – ‘denticolae’ – decomposition of enamel
Antony van Leeuwenhoek 1700
3) Chemo – parasitic theory – Millers 1889
Basis- oral microorganisms role in acid formation
 Pasteur, Koch, Emil magitot 1867
 Leber and rottenstein 1867 – lepthothrix buccalis
Millers –role of 3 essential factors in caries process
 Oral microorganisms in acid production and in proteolysis
 carbohydrate substrate which the microorganisms fermented
 The acid which causes dissolution of tooth minerals
Summary-
“Dental decay is a chemoparasitic process consisting of 2 stages: decalcification or softening of the
tissues and dissolution of the softened residue”.
Critique of chemoparasitic theory
 Unable to explain the predilection of specific sites on the tooth to DC , plaque.
 Ascertain types of organisms
 Why some populations are caries free?
 Arrested caries?
 Concept of tooth resistance – no support.
4) Proteolytic Theory

3.  Organic or protein elements –initial pathway of invasion of microorganisms.
 Gottlieb 1947, Frisbie 1947 – proteolytic enzymes, staphylococcus aureus, acid produces
chalky enamel.
 Pincus 1950 –proteolytic enzyme attacked cuticle, destroyed prism sheaths.

 Critique of proteolysis theory
 Invasion of microorganisms and their metabolism is not explained
 Initial attack on enamel is proteolytic –no evidence
5)Proteolytic Chelation Theory(Schatz,martin 1955)
 Bacterial Destruction of teeth , where the initial attack is essentially on organic components of
enamel breakdown products (chelating property) dissolve minerals in enamel.
 Complexing agents – acid anions, amine, amino acids, peptides, polyphosphates and
carbohydrate derivatives.
Critique of this theory
 Proteolysis is not an important step
 <1% of mature enamel is organic, upon degradation conc of chelator dissolve 96%
mineral?
Other theories
 Sulfatase theory –Pincus 1950
Bacterial sulfatase hydrolyse mucoitin sulfate of enamel/chondroitin sulfate of dentin produce
sulfuric acid- decalcification.
 Phosphate sequestration theory (Lura1967)– inorganic phosphate was taken up by bacteria
from plaque - disturbance in Po4 equilibrium - loss of po4 from enamel.
Silverstone et al 1981 - bacteria
- saliva
- foodstuff
- crevicular fluid
Nikiforuk 1985–primary and secondary factors
Geddes 1991- saliva
 Fejerskov and Manji model 1990
(Dental plaque and determinants)
Determinants - time
- fluoride
- diet
- microbial species
- saliva
- sugar and buffer
Confounders- socio-economic and behavioral factors
Johnson (1991) and Brathall (1996) – biological factors
 Brathalls cariogram- diet, bacteria, host

4.  Slavkin square 1999
 Bokhout et al 2000- 3 component causes ,other factors depend on saliva. Fl, oral hygiene,
diet.
 Baelum and Fejerskov 2003 - Confounding variables as determinants
Brathall
cariogram 1996
Factors contributing to susceptibility of dental caries (Slavkin et al)
 Genetics of mother, father and child
 Genetics of infectious microorganisms
 Transmission of infectious microorganisms and age of the child
 Mucosal immunity and saliva
 Diet and nutrition
 Biofilms and microbial ecology
 Relative susceptibility of individual teeth
 Relative prevention measures
 Early detection of caries
I . Tooth related factors
Physical characteristics of teeth
 Tooth morphology
 Tooth surfaces
 Tooth size
 Tooth types and arch form
 Tooth composition
Mesial and distal surfaces of 1st
molars
 Mesial surface of 2nd
molars, distal surface of 2nd
PM
 M and d surfaces of max 1st
premolar
 D surface of canine and M surface of mand 1st
Pm
 Approximal surface of max incisors
Tooth surfaces
 Mand 1st
molar – O,B,M,D,L
 max 1ST
molar – O,M, P,B,D
 Max lateral incisors – palatal surface
 Tooth size
 Grahnen and ingervall 1963 – smaller teeth associated with less caries incidence
 Hunter 1967 –larger teeth were more caries susceptible.
 Stern and curzon 1975 – population and individual basis.
 Carvalho et al 1989 – plaque accumulation over 48hrs is 5times more in fissures of erupting
1st
molars.

5. Tooth types and Arch form
 Most susceptible permanent teeth are mand 1st
m - max1st
molar - max and mand 2nd
molar -
2nd
PM - 1ST
PM - mand incisors and canine
 Primary teeth - 2nd
primary molar- 1st
primary molar- primary canines.
 Irregularities in arch form ,crowding and overlapping of teeth
Tooth composition
Inorganic constituents (Patel and brown 1975)
Development of enamel crystallites
 Long plates /ribbons
 mature in width and thickness
Enamel crystallites
PRISM
(Ameloblasts)
 Caries resistance
(cevc etal 1980)
Crystalline phase of dental tissues
 Hydroxyapatite crystals
 Flourapatite –
OH-F bonds
crystal solubility
Surface chemistry of enamel
 Preeruptive stage – enamel surface crystals are in dynamic equilibrium with adjacent tissue
fluid envt. (trace elements)
 Post eruptive stage – equilibrates with saliva, GCF and ingested fluids (physicochemical
change)
 Early - water and protein – CA, P, Carbonate
 Preeruptive stages – till eruption (maturation)
 Posteruptive – increase in f ,reduction in carbonate
Difference in composition between surface and subsurface enamel
Surface enamel
- Low conc of water
- High conc of mineral salts( reduced acid solubility) Isaac etal 1958
 Subsurface enamel
- Reduction in surface area
- Increasing diffusion distances
Enamel surface is more caries resistant than subsurface - hypothesis
 Brudevold and soremark 1964 – surface enamel is harder
 Mineral content, Water fluoridation
 Post eruptive maturation- nitrogen and fluoride
- density and permeability
 Frank, herdly and phillipe 1965- small microdefects (TEM)
 Thyslstrup and fejerskov 1981 –
unaffected surface layer?? SEM – openings in outer enamel surface through eroded focal holes
Moreno and zahradni 1974 – pumping mechanism

6. Inner enamel surface zone saliva
Effect of trace elements on caries activity
(Navia 1972)
TALE OF TWO CITIES
1) 2 isolated mountain villages- Columbia
SA, Don mateas, Heliconia( Fl -0.1ppm)
 cu, mn, fe higher in Don mateas (high caries prevalence)
 Heliconia (ca,mg,mo,v)
 In new zealand,
Napier city(5-8yr)low caries- mo, al,ti
Hastings- Cu ,mn, B ,Sr
DETERMINANTS OF TOOTH SUSCEPTIBILITY TO CARIES
CARIES IMMUNE TEETH- DO THEY EXIST?
 Structure and composition of teeth influence the initiation and rate of progression of caries.
 Diet low in cariogenic potential, absence of cariogenic flora.
 Water fluoridation, fluoride preparations.
 Nature of carious mechanism
Host resistance
 Difficult to define, Conclusion cannot be drawn
 Kilian and Brathall 1994 – dental caries does not lead to acquired immunity
1) mucosal immune system has evolved to maintain a natural balance with members of the commensal
flora of the body and not to eliminate them.
2)S mutans releases a protein with immunosuppressive properties.
Immune Factor
Non-specific and specific immune factors –
 limit microbial colonization of the oral surfaces
 Prevent the penetration of noxious substances and damage to underlying tissues.
 Non specific immune factors in saliva- lysozyme, lactoperoxidase, lactoferrin, high mol wt
glycoprotein ( lack immunologic memory, not subject to specific stimulation )
 GCF - PMN leucocytes
Specific host immune factors
 Major and minor salivary glands- secretory IgA
(IgM, IgG)
IgA – 65-75% IgA1 susceptible to proteases
- IgA2 resistant to proteases
GCF - IgG, IgA
MS do not colonize the mouth in infant and toddlers till maturation and expansion of host immune
networks.
a) Lag in expansion of lymphocytes
b) Poor oral hygiene
II . Role of saliva as a modifying factor in dental caries
 Functions of saliva
 Constituents of saliva

7.  Salivary clearance from the oral cavity
 Salivary flow and dental caries
 Neutralisation and buffering of plaque
 Demineralisation and remineralisation of tooth surfaces( ca, p ,fl, )
 Antimicrobial properties
 Acquired pellicle
Sources of saliva
 Parotid glands - (25%) serous
 Submandibular gland – ( 60% )mainly serous
 Sublingual gland – (5%)mainly mucous
 Minor salivary glands – mucous (soft palate), 10% of total volume of saliva
Functions of saliva
 Specific and non- specific defense in oral cavity
 Vital to the Integrity of mineralized tissues
 Protection of teeth from caries
 Dilution and clearance of dietary sugars
 Buffering effect
 Remineralise teeth ( ions)
 Antimicrobial factors
 Direct antibacterial activity - interfere with their ability to produce acid
lysozme
Lactoferin- bacteriostatic and bactericidal
Salivary peroxidase
GCF, mucins
Major functions of saliva ( sreenby 1992)
Antimicrobial Properties
 Role in Maintaining balance within ecosystem associated with tooth surfaces
 NON IMMUNOGLOBULIN PROTEINS
- Lysozyme
- lactoferrin
- salivary peroxidase system
- Myeloperoxidase system
- agglutinins (mucins, IgA, fibronectin)
- histatins
- PRP
 IMMUNOGLOBULINS
Secretory IgA ,IgG, IgM
Proline rich proteins (PG)
 Selectively mediate bacterial adhesion on tooth surfaces.
 function - PRP (-ve) binds with ca (tooth)
Outer ends (proline and glutamic acid) bind to harmless and protective normal microflora of teeth
 Primary colonisation (24 hrs)
 Secondary colonisation (galactose amine structures)

8. Lysozymes
Nasal secretions and tears by fleming1922
 Major and minor SG,GCF and salivary leucocytes
 Direct antimicrobial effect
 Strongly cationic – lysis of bacterial cells, SM, viellonella
 Bind to HA
 Alters glucose metabolism- aggregation
Lactoferrin
 Iron binding glycoprotein
 Secreted by SG, PMN leucocytes
Function – “nutritional immunity”
 high affinity for fe (microorganisms)
 S mutans (bacteriostatic and bactericidal)
Salivary peroxidase
 PG,SMG
 Antimicrobial activity (Produce hypothioyanate – inhibit glycolysis)
 Protection of host proteins and cells from hydrogen peroxide toxicity
High mol wt glycoprotein (P – 0.001%)
Mucins (MG1 and MG2)
1) - Tissue Coating(MG1)
 Protective coating about hard and soft tissues
 Primary role in formation of acquired pellicle
 Concentrates anti-microbial molecules at mucosal interface
2) -Aggregation of bacterial cells (MG2)
 Mucin -coated bacteria may be unable to attach to surface
3)-Bacterial adhesion
 React with bacterial adhesins, thereby blocking them
 Statherins
 Supersaturation of calcium phosphates maintain enamel integrity (demineralisation)
 Statherins prevent precipitation or crystallization of supersaturated calcium phosphate in ductal
saliva and oral fluid (remineralisation)
 Produced by acinar cells in salivary glands
 Also an effective lubricant
 Histatins
 Bind to HA, prevent cap ppt from supersaturation of saliva and inhibit crystal growth –
enhancing stability of HA
Cystatins
 Submandibular gland
Salivary amylase
 Maior SG
 Promotes adherence of oral streptococci to HA (Indirectly produces glucans)

9.  Substrate for oral bacteria (glucose and maltose)
Salivary agglutinins
 Interact with unattached bacteria – clumping of bacteria
 Neutralises toxins and enzymes
Effects of IgA and IgG responses in relation to protection of tooth surfaces ( Kilian and Brathall 1994)
Salivary flow rate
 1ml of whole saliva- > 200 million microorganisms
 300 diff species
 Unstimulated saliva- 0.3ml/min
 Stimulated – 0.8-3.0 ml/min
 Ca conc increases- flow
 Englander etal1958 - inverse
 Shannon and terry 1965,– no correlation bet flow and caries (PG, SMG)
 Whole saliva
– Jenkins 1964 flow rate and fasting pH of plaque
Salivary flow and dietary carbohydrates
 VOLUME OF SALIVA – 500-620ml gustaffson1954
 Frequency of consumption (solid) – caries
 Von der fehr 1970 – liquid
 Starch containing foods
STEPHEN’S CURVE
Salivary clearance from the oral cavity
Healthy balance between host defense and microbial attack disturbed by
 Extensive growth of bacteria
- unstimulated salivary flow rate- 0.3ml/min
- Plaque- 10-20mg/day
 Excessive intake of fermentable carbohydrate
 Systemic diseases
Sugar clearance from oral cavity
 Swenander- lanke (1957) – consumption of carbohydrate foods, conc of sugar in saliva fell.
 Dawes (1983) – computer model
- volume of saliva
- unstimulated SSR
 Sreenby et al (1985) – sugar solutions were cleared in 2 stage pattern proportional to shifts in
SSR.
- Rapid – 1st
6min
- Slow
Neutralisation and buffering of acids
 Bicarbonate
 Macromolecular proteins
Arginine rich protein – arginine+ammonia
 Urea (parotid)
urea- ammonia- increases plaque pH
 Phosphate (unstimulated rate)
Bicarbonate

10. Salivary bicarbonate (parotid gland)
Greater secretion rates of stimulated saliva
ph rises and buffering power increases
 Ingestion of sugar – paraffin wax /chewing gum
 Plaque from Caries resistant - > buffering effect
 Lab and chairside tests (Dentobuff strip system)
 Heinz et al 1983 – males and females (low pH)
 Positive correlation between SSR and buffering effect
 Inaccessible sites
Critical pH
 The pH at which any particular saliva ceases to be saturated with calcium and phosphate;
below this value, the inorganic material of the tooth may dissolve. range of 5-6, average 5.5.
Role of calcium
 Submandibular /sublingual twice parotid
 Depending upon pH Calcium – bound and ionized form
Free ionized calcium
 < pH 4 - establishes equilibrium between cap of hard tissues and surrounding fluid
 pH is normal – 50%
 Lowered salivary pH – increase ca
Bound form –
 Firmly bound to inorganic ions to small organic ions
 low SSR low bicarbonate low ca bicarbonate complex
 Plaque and pellicle - ca conc( binding sites, ppt ca salts)
 As plaque Ph increases – ionized ca in saliva ,plaque and pellicle will reach equilibrium
Role of inorganic phosphate
 Submandibular 1/3 that in parotid but 6times higher than in minor mucous glands.
 Phosphoric acid, primary, secondary and tertiary inorganic phosphate ions
 10% bound with ca and proteins, 10% -pyrophosphate
(inhibitor of cap ppt)
 Demineralisation – lower pH of saliva, lesser tertiary ions (HA ion product)
 SSR - total inorganic phosphate
 Functions – its contribution to solubility products (cap)
- role in maintenance of tooth structure
- Minor role in salivary buffer
Role of fluoride
 Ionized and bound form
 Incorporated into enamel
crystals
 Reduce acid production in dental plaque
 Initial fl conc will be higher in saliva pellicle and plaque- caF will be formed
 Salivary fl clearance- F to basal level( prolonged)

11. - swallowed F partly reenters saliva
- higher F in pellicle and plaque than saliva
- F conc in pellicle undersaturated with respect to CaF (dissolves)
Acquired pellicle
 0.1-1.0 µm thick , formed by selective adsorption of HA-reactive salivary proteins, serum
proteins and microbial products such as glucans and GTF.
 It acts as a diffusion barrier, slowing both attacks by bacterial acids and loss of dissolved
calcium and phosphate ions
 Form a base
 Protective barrier
 lubricating film
 Regeneration capability
References
 Nikiforuk
 Newbrun
 Text book of clinical cariology – thysltrup andd fejerskov
 Diagnosis of caries – axelson
 Cariology DCNA1999
 Oral health and prev dent 2005
 BDJ 1993
 CRIT REV ORAL BIOL MED 1993
 Cariology today – guggenheim
 JADA1989
Can ecological catastrophe of microflora lead to dental
diseases?
conclusion
References
 Cariology: Ernest Newbrun, 3rd
edt.
 Diagnosis & risk prediction of dental caries: vol 2. Per Axelson.
 Understanding Dental caries: Vol 1- Gordon Nikiforuk.
 Cariology Today: Guggenheim B
 Scheie AA:Mechanismof denta plaqueformation. Adv Dent Res.1994;8:246-53.
 Harper DS, Loesche WJ. Growth & tolerance of human dental plaque bacteria. Arch Oral
Biol.1984;29:843-8.
 Trahan L. Xylitol- a review of its action on mutans streptococci & dental plaque—its clinical
significance. Int Dent J.1995;45:77-92.
 Marrquis RE. Oxygen metabolism, oxidative stress & acid-base physiology of dental plaque
biofilms. I Ind Microbiol,1995;15:198-207.
Diet And Dental Caries
Dr G. Kayalvizhi
PG in Dept of Pedodontia
 Introduction
 Definitions

12.  Unique forms of food
 Sugars and dental caries
 Interventional and non-interventional studies
 Longitudinal and cross sectional studies
 Starch and dental caries
 Cariogenecity of foods
 Role of fats, proteins, vitamins
 Diet - the customary allowance of food and drink taken by any person from day to day.
Unique forms of food
 Monosaccharide
 Disaccharides
 polysaccharides
Physical properties of foods and cariogenecity
 Mechanical- Hardness, cohesiveness, viscosity, adhesiveness
 Geometric- particle size and shape
 Others- moisture and fat content
 Affect- food retention, food clearance, solubility and oral hygiene
Recommended-
 improves cleansing action
 Increase salivary flow
 Reduce the retention of food
Sugars and dental caries
 Metabolic fate of carbohydrates in plaque
 Oral sugar clearance
 Frequency of eating
 Effective concentration of sugar
 Relationship bet sugar and dental caries
Dietary sugars and caries
SUCROSE-ARCH CRIMINAL (Newbrun 1969)
 Effect on plaque
 substrate for cariogenic microflora
 Sucrose polymers bulk of plaque
attachment of bacteria
 High free energy, high specificity of enzymes
SUGARS – THE ARCH CRIMINAL (zero 2004)
Frequency of eating
 Weiss and trithart 1960- 1000 children (candies, cookies)- DMFT rates
 Konig et al 1968- caging system in animals
 Fanning et al 1969- school canteen
 Effective concentration of sucrose
CAGE SYSTEM – KONIG ET AL

13. Sugar clocks
(Johansson and Birkhed 1994)
Oral sugar clearance
 Salivary rinsing, masticatory muscle activity
 Lagerlof et al – 20% sucrose, solid foods
 Retentive, sticky, sweet foods with less self cleansing property.
Effective concentration of sucrose
 Natural sugar in fruits (50-60%) – occlusal surfaces
 Processed cane sugar (5-50%)- maximum acid production- plaque flora gets saturated
 King et al 1955 – addition of sucrose – no drop in pH
Relationship bet sugar intake and caries
a) b) Newbrun 1982- S- shaped curve
c) Woodward and walker 1994- linear
d) Zero 2004- individuals with good oral hygiene and regular fl exposure, higher level of sugar can be
tolerated
Relationship bet sugar and dental caries
STEPHEN’S CURVE
10% sucrose solution- 40min
INTERVENTIONAL STUDIES
 VIPEHOLM STUDY
 HOPEHOOD HOUSE STUDY
 TURKU SUGAR STUDY
EXPERIMENTAL CARIES STUDY
NON INTERVENTIONAL STUDIES
 EPIDEMIOLOGICAL STUDIES
 CROSS- SECTIONAL STUDIES
 OBSERVATIONAL STUDIES
Interventional studies
1) Vipeholm study, Lund (Sweden) 1945- 1954
 1930,Hojer and Maunsbach, Gustafson 1954
 Purpose- to determine the effects of frequency and quantity of sugar intake on the formation of
caries.
 Institutionalized patients (436- 32yrs) were divided into 6 experimental and 1control group
 Poor oral hygiene, twice normal sugar
Seven groups
 Control group - low sugar diet only at meals
 Sucrose group - high- sugar diet (300g) mostly in drinks with meals
 Bread group - sweetened bread at meals (sugar- ½ or equal to normal)
 Caramel group- 22 sticky candies
2 portions at meals (carbohydrate study I)
4 portions between meals (carbohydrate study II)
 8- toffee group
 24-toffee group- throughout day, twice normal total intake of sugar

14.  Chocolate group- milk chocolate- 4 portions bet meals( CSII)
Studies were divided into 3 phases
 clinical experimental studies of the relation bet diet and caries
 Supplementary studies
 Special studies (Hojer and Maunsbach 1954)
Preparatory period (1945- 1946)
pts were selected, recording methods
I Clinical experimental studies
1) Vitamin study (1945-1946)
Vit A,C,D, 1mg Fl tab
Basic diet- sugar (1/2) + starch = low caries
2) Carbohydrate study
To examine how caries activity was influenced by the ingestion of carbohydrates under controlled
conditions
Study 1 (1947- 49)
SUGAR - solution/ sticky form at (new bread) /bet meals( toffees)
Study 2 (1949- 51)
Types of sweets were similar
Preparatory and vitamin period- low sugar= 0.34 carious lesions/pt/yr
Carbohydrate I- twice the normal amt of sugar, only at meals
Carbohydrate II- normal amt of sugar only at meals/ at and bet meals
Results
Little effect- sweet drinks with meals
bread
sugar in non sticky
 Moderate increase in caries- chocolate (4times) bet meals
 Dramatic increase- 22 caramels
8 / 24 toffees bet or after meals
Effect of frequency and CHO intake
(Davies 1955)
Influence of carbohydrate type and frequency on dental caries
II Supplementary and special studies
Supplementary study
Quensal et al 1954 – reliability of the method in determination of caries, caries activity was
statistically significant in all groups (sticky)
Special studies
1) Biochemical studies
(Lundquist 1952, Swenander lanke 1957)
sugar content of blood and urine, pH viscosity, buffer capacity, ca p conc in saliva and oral sugar
clearance.
2) Microbiological studies
(Grubb and Krasse 1953, 1954)
Differences in lactobacilli and carbohydrate
caries promoting diet=>caries, high LB count

15. Other studies
a) Consumption of sweets and caries activity in school children an Hungarian farm workers.
b) studies on the inhibition of acid production by substance produced by chocolate bean.
3) Genetic study (Book and Grahnen 1953)
Parents and siblings of caries free recruits - low caries prevalence, no diff bet oral hygiene and
dietary habits.
IMPLICATIONS
 “ALL THE SWEETS YOU LIKE BUT ONLY ONCE A WEEK”
 sugar substitutes
 Malmo study 1976- consumption of sugar (sticky) form bet meals= >caries incidence + high
LB count
 Vipeholm study - Citation classic
conclusion
 Increase avg sugar consumption(30-330g/day) showed very little increase in caries(0.27-0.43
cs/yr) provided additional sugar was consumed at meals in solution
 In patients with poor oral hygiene - caries
 Varies from person to person
 Subsides- withdrawal of sugar containing foods
 Great risk –Sugar (retained on tooth surf)
 Greatest risk- bet meals, form
 Increase in duration of Sugar clearance from the saliva
Limitations
 No possibility of matching the age
 Initial caries
 Mentally handicapped- instructions
 Dietary regimes of various groups
Hopewood study in Bowral, N.S.W, Australia
 1942, 80 children, 7-14 yrs (10yr period)
 Vegetarian diet- carbohydrates (whole meal bread, whole meal porridge, biscuits, wheat germ,
fruits ,vegetables, dairy products)
 1948- 49 – meat
 Vitamin concentrates, nuts and honey
 Unfavorable oral hygiene, insignificant fl, meals controlled = Toothsome diet
Results- 13yr old (DMF) -1.6(53%) HH
-10.7(0.4%) general
Turku sugar study, Finland
(Scheinen and Makinen 1975)
 AIM - To compare the cariogenecity of sucrose, fructose and xylitol. (1972-1974)
BASIS- Xylitol is a sweet substance not metabolised by plaque organisms.
125 subjects (115), 27.6yrs (15-45yr)
3 groups – sucrose (S), fructose (F) and xylitol (X)
 Examination- clinically, radiographically
 Precavitational and cavitational lesions
 primary and secondary caries

16. Results
1) Early white spot lesions-
 Sucrose group- DMFS- 3.6
 After 1 yr- sucrose and fructose= equal
xylitol= no caries
 2nd year- sucrose- increase
fructose- unchanged
Xylitol- zero
 Xylitol- non cariogenic / anticariogenic
2) cavitation- low DMFS –xylitol than sucrose and fructose.
Development of primary and secondary caries (24 mon)
conclusion
 Substitution of xylitol for sucrose in normal Finnish diet resulted in low caries incidence.
 Reduced the number of most microorganism
 second 1yr trial –
to test the effects of xylitol gum
 102 subjects- 22.2yrs
 2 groups (chewing gum)
1) sucrose (4.2 sticks/day)
2) xylitol (4.9 sticks/day)
Saliva- remineralistion
Xylitol- anticariogenic effect
IV. Experimental Caries Study
Von der fehr 1970-buccogingival enamel caries
 23 days,50% sucrose solution (9 timesdaily)
 After 30 days- oral hygiene and fl rinses.
 Critical factor- duration and frequency
Loe et al 1972- 3 weeks, chemical plaque control twice daily (CHX) but no Fl, no caries
conclusion
 Sugar is modifying risk factor
 Dental plaque is a etiological factor
 Clean teeth- no caries
Non interventional human studies
 Subjects are free to choose whatever diet they please, correlation bet caries increment and
dietary factor is low.
 Based on dietary recall
 No control over amount/ frequency of sugar intake
I. Epidemiological studies
Sugar consumption in selected countries in1977
Sugar consumption in Sweden 1960-1990
 During world war II in Europe and Japan – wartime food restrictions
15kg- 0.2kg
nutrition
Marthaler 1967 – (1941-1946)- less decay

17.  Sreenby 1982 – international data
6yr (23 nations), 12yr (43 nations)
<50gms- <3 DMFT
 Confectionary workers and bakers
II. Cross sectional studies
 Goose1967, Goose and Gittus 1968, James et al 1957, Winter et al 1966, 1971
labial incisor caries and sugared pacifiers
 Granath et al 1976,1978- level of sugar, Fl
Oral hygiene (6yr, 4yr)
 Hausen et al 1981 – 2000 finish school children, least caries prevalence- sugar exposure
 Marthaler 1990- sugar main threat
 Wendt et al 1995,1996- 700 infants,1-3yr
Bottle fed/breast fed>12mon
Less fl toothpaste
Oral hygiene and diet
III. Observational studies
 Axelsson and El Tabakk 2000- 685, 12yr old (period of 2yrs) with poor oral hygiene, sugar
diet.
 Rugg- Gunn et al (1984) North thumberland, England and Burt et al 1988 in Michigan
Assessed frequency and grouping of foods
Starch and dental caries
 Swenander lanke 1957
 Dietary starch - mixture of starch products with apparently widely varying potentials to serve
as substrates for bacterial acidogenesis in plaque and hence induce cariogenesis.
a) Intraoral bioavailability of starch
 Polymers of glucose
 Starch molecules- starch granules
(grains and vegetables)
 Gelatinization (8-100
c)
 Starch
dextrin and glucose (mormann and muhleman1981)
 Modifiers – starch protein, starch lipid interactions
b) Applications to cariology
 Starch consumption, frequency and retention
 Stickiness of starches in human mouth
(Bibby etal 1957,Gustafson 1953,Caldwell 1975)
 Kashket et al 1991 – increased starch food particles
 Lingstorm et al 1997 – high cariogenic potential
2) Studies of starch caries issues with humans
 Classic vipeholm study
 Hopewood house experiments

18.  Turku sugar studies
 HFI individual study
Draw backs
1) Frequency of consumption
2) plaque pH lowering potential
3) bioavailability
Hopewood house study
 Lacto vegetarian diet
 3 meals with milk upon rising and milk/fruit after dinner
 Low caries
Vs and HHS – not caries inducive
Turku sugar study
 3 groups- sucrose, fructose, xylitol
 Xylitol- little / no caries
Newbrun et al 1980
 HFI (hereditary fructose tolerance)= little caries
 Little sucrose(2.5g/d), total carbohydrate (160g/d)
Rugg gun et al 1987 – (2yr)
 High starch/ low sugar diet- no reduction caries
Sreenby 1983, 1996- 12yr children
 Various starches + little sucrose=low
Schamschula et al 1978-
 Starch diet+ sugar + frequency= caries
Studies of starch caries issue with animals
 classic animal model (van Houte 1980,1994)
MS free rats fed with high sucrose diet
sucrose replaced by starch – fissure caries
 Bowen et al 1980- starch sucrose diet
 Processed starches
 Amylopectin and amylose
 Firestone et al 1984- cooked wheat starches
pH remained low for longer periods
• Co-carcinogen
Starch and dental caries???
Non cariogenic or cariogenic???
 Non cariogenic
 Starch products can be , but frequently are not, as effective as sucrose in inducing enamel
caries
1) lower bioavailability of starches
2) diminished delivery of glucose and maltose to plaque bacteria.

19.  Co- carcinogen
 Enhanced retentiveness of starchy foods
“It is premature to consider starches in modern diet as safe for teeth”
Cariogenecity of foods (ADA 1985)
 Cariogenic potential- a foods ability to foster caries in humans under conditions conducive to
caries formation. (Stamm et al 1986)
 Diet counselling
 methods to assess
Animal models, plaque acidity models, demineralization and in vitro models.
 Influenced by- sugar content, protective factors, consumption pattern and frequency
(Bowen et al 1980)= CPI
Edgar 1985-
 food factors- Amt and type of CHO, food pH, buffer, consistency , retention in mouth, eating
pattern, factors modifying enamel solubility.
 Cultural and economic factors- availability and distribution
Can foods be ranked according to their cariogenic potential??
 Foods – 2 categories ( Switzerland ) acidogenic / non- acidogenic
 Cheddar cheese
 non fat dry milk solution
 10% sucrose solution, fruit beverage
 caramel. cracker, potato chip. SLS
 Milk chocolate, sugar cookie, corn and wheat flake.
Minimum pH obtained with reference foods (schachtele and Jensen)
Caries promoting potential
Snack foods – acidogenic potential Edgar 1981
Cariogenecity of foods
 Based on acidogenic potential
Raw vegetables<nuts<milk<corn chips<fresh fruit<ice cream<French fries<dried fruit.
 Retention
High sugar foods- caramel, chocolate bars
Sucrose+ cooked starch
Cariogenecity- food composition, texture, solubility, retentiveness, and rate of salivary clearance than
sucrose alone
Role of vitamins in dental caries
Vitamin B1- thiamine
Caries promoting effect
Vitamin B6 (pyridoxine)
 Cole et al 1980 – reduce caries in rats
 High doses - drug (pregnant women and children)
 Local effect?
 Affect growth rates, metabolism and microbial composition of dental plaque (by stimulating/
inhibiting microbial species)
Role of fats in dental caries
Post eruptive consumption- reduce caries

20. Mechanism ??
 Protects the enamel surface by fatty film
 Reduces the contact bet CHO and bacteria
 Antimicrobial action? (Williams et al 1982)
 Replace carbohydrates (Michigan 1994)
 Rapid clearance of carbohydrates from oral cavity.
Role of proteins in dental caries
 Shaw 1970 and Navia 1979-
protein deficiency during dental development in rats - caries susceptibility
 Experimental and control rat pups on cariogenic diet
Mechanism?
Posteruptively – direct action on plaque met
Short exposure time in mouth
Replace CHO
weak proteolytic activity in mouth
xylitol
 Metabolism by microorganisms- lacks enzyme to utilize xylitol
 Frequency – 3 times a day
 Timing- long term
Caries prevention
 Turku 1975- 90% reduced
 Gallium 1981- 70%- candies
 Isokangas 1987- gum
 Makinen et al 1995 (Belize study) – pellet and sticky gums
sorbitol
 Fermented by microorganisms (Slow- SM)
 Substrate for microorganisms
 Diffuses out acid
 Slack et al 1964- 48% reduction
 Birkhed and bar 1991- acidogenecity reduced
 Glass et al 1983,szoke et al 2001- gum
 Von loveran 2004- between /after meal
sweeteners
 Non caloric
 Not fermented by oral microorganisms
Saccharin- (Grenby et al 1991)
 active cariostatic property
 Inhibit bacterial growth
Aspartame (NutraSweet)- reduce caries
SOFT DRINKS AND CARIES
Potentially cariogenic
 10% sucrose

21.  Carbonic and phosphoric acids- pH 2.4-2.5
(transitory)
 Oral sugar clearance is rapid
Apple and orange juice- heavily buffered
Protective food components
 Fluoride
 Phosphates- capo4 toothpaste, ACP-CPP
 Fatty acids- replace carbohydrates (Michigan 1994)
 Arginine rich peptides and pyridoxine (basic)
 Calcium lactate
 Dietary acids and flavors (foods and beverages)
 Tea and starch
 Aged cheddar cheese- antiacidogenic effect
 Chocolate ad extracts, glycyrrhizin/ liquorice
 Sugar substitutes
REFERENCES
 DIAGNOSIS OF CARIES- AXELSSON
 CARIOLOGY – NEWBRUN
 CARIOLOGY TODAY- GUGGENHEIM
 UNDERSTANDING DENTAL CARIES- NIKIFORUKH
 CARIES RESEARCH 2004
 J DENT RES 2001
 ACTA ODONT SCAND 1975
 DCNA 1999
 DCNA 2003
Dental caries process
Dr G. Kayalvizhi
 Time factor in caries development
 Classification of dental caries
 Macroscopic, microscopic and ultra structural changes
Caries in enamel
Caries in dentin
 Caries in cementum
TIME FACTORS IN CARIES DEVELOPMENT
 Average time from incipient caries to clinical caries is
18 +
- 6 months (Parfitt et al 1956)
 Von der Fehr 1970 – 3 weeks
 In Xerostomic patients caries can be detected clinically within 3 months (Brown et al 1976)
 2-4 years post eruption decline
 Enamel dentine
3 years

22. Classification of dental caries
1) Based on morphology (anatomic site)
Pit and fissure (type I)
Smooth surface (type II) – interproximal, cervical
Root surface
G.V.Black's Classification
Class I- Cavities occurring in pit and fissure defects in occlusal surfaces of bicuspids and molars,
lingual surfaces of upper incisors, and facial and lingual grooves
Class II- Cavities in proximal surfaces of bicuspids and molars.
Class III- Cavities in proximal surfaces of incisors and cuspids not requiring removal of incisal angle.
Class IV- Cavities in proximal surfaces of incisors and cuspids that require removal of incisal angle
Class V- Cavities in gingival third of labial, lingual, or buccal surfaces.
Class VI- (not a true Black classification ) Cavities in incisal edges and smooth surfaces of teeth
above the height of contour.
2) Based on severity and rate of caries progression
(Klein and palmer 1941)
3) Clinical forms of caries based on severity
 Incipient caries
 Occult caries
 Cavitation
4)Based on progression
Arrested caries
Recurrent caries
Rapidly progressive- Radiation caries
5) Based on chronology
 Infancy caries
 Adolescent caries
 Adult caries
6) Based on hard tissues involved
Enamel, dentin, cementum
7) Root caries based on extent of lesion
(Billings 1966)
(8) The shape and depth of lesion can be scored on a four- point scale ( W.H.O)
 D1 – clinically detectable enamel lesions with intact (non-cavitated) surfaces
 D2 – clinically detectable “cavities” limited to enamel
 D3 - clinically detectable lesions in dentin
(with and without cavitation)
 D4- lesions into pulp
9) Clinical carious lesions related to type, localisation, size and depth, shape (Axelsson 1994)
10) Based on site and size- Mount G.J 1997
A) Site
 Site 1 –pit and fissures of posterior teeth, buccal, palatal grooves, erosion lesions

23.  Site 2 – approximal surface
 Site 3 – gingival third
B) Size
 Size 0 - small
 Size 1 (mild)- lesions which have progressed just beyond remineralisation
 Size 2 (moderate) – larger lesions with adequate tooth structure
 Size 3 (enlarged) –tooth structure and restoration are susceptible to fracture
 Size 4 (severe) – extensive loss of tooth structure
 2.3 on #12
11) Radiographic classification of caries
1) Occlusal caries
 Incipient occlusal caries- cannot be seen on a dental radiograph
 Moderate Occlusal Caries –
extends into dentin and is seen as a very thin radiolucent line
 Severe Occlusal Caries
large radiolucency
2) Interproximal caries - radiograph
Macroscopic changes in enamel
 Early changes – enamel demineralisation
 White spot lesion - first visual clinical representation
Clinically detectable- depth of 300-500 µm
 White spots- Intact and smooth / rough surface
Backer- dirks 1966 – does not progress to frank cavitation - arrested / reversed
Reversible stage of clinical caries process / partially arrested lesion
White spot should not be referred to as a PRECAVITATED lesion, suggesting that it will eventually
lead to cavitation, but as a NON- CAVITATED lesion. (Ismail 1997)
Fissure caries
Smooth surface lesions
Microscopic changes of enamel
Silverstone 1973
 Translucent zone
 Dark zone
 The body of the lesion
 Surface layer
FOUR ZONES OF ENAMEL CARIES
 Translucent zone- enamel breakdown, structureless
 Dark zone- “Positive zone”
filled with air, brown discoloration
pore volume – 2-4%
 Body of the lesion- well marked prism structure, Increase in unbound water and organic
content
 pore volume - 25%

24.  Surface layer- 20 & 100µm thick
Pore volume in 4 zones of enamel
ZONAL CHARACTERSTICS OF ENAMEL CARIES
Crystal diameter in lesion of enamel caries compared to normal enamel
Silverstone 1983
Enamel caries process - demineralisation
I Production of organic acids by plaque
Microorganisms
 Homofermentative bacteria- lactic acid
 Heterofermentative bacteria- mixture of organic acids
 Plaque pH – saliva, bacterial, dietary
II Diffusion of acids into the tooth
 Organic acids – Dissociated ( H+ , A-
) Enamel Crystals
- undissociated (HA ) - subsurface
Plaque fluid (H+
) pellicle Enamel
(pore size- 1.4 - 2.4nm)
Ultrastructural changes in enamel
1) Preferential loss of interprismatic substance
2) Two main types of crystal damage during carious dissolution
Schematic representation of the dissolution of hydroxyapatite crystal
Direct dissolution of enamel surface
I stage (early caries process)
Softening of enamel surface subsurface lesion
Anderson and Elliot 1992
 Surface layer is protected by presence of demineralisation inhibitors
 Difference in anatomic structure and composition
 Stable ca po4 phase in surface layer
Moreno and zahradni 1974 – pumping mechanism
Inner enamel surface zone saliva
Graphic representation of a block of enamel
1) Intact block showing enamel surface and sub-surface
2) Beginning of demineralization creates pores in the enamel resulting surface roughness and loss of
shine.
3) As demineralization progresses,
the pores increase and with remineralization the pores decrease
5) In the final stage, the carious process has progressed to the point where sufficient amount of
enamel matrix has been lost and the inward collapse of the remaining surface layer.
Caries in dentin
Rate of progression to dentin – factors

25.  Overall estimated caries risk of the individual
 Rate at which enamel lesions have developed
 Size and depth of enamel lesion
 Post eruptive age of enamel
 Preventive programs
Macroscopic changes of dentin
 Cone shaped
 Backer-Dirkis 1966- 50% -11-15yr
 67% in 9-15yrs
 Bille and carsten 1989- 14% - 13-14yr
 Mejare et al 1999 – 5.4% 11-22yrs
Microscopic changes of dentin
Proceeding from the lesion inward to normal dentin the various zones are: chronic
 Zone of Decomposed dentin
• Zone of Bacterial invasion
• Zone of Demineralisation
• Zone of Dentinal sclerosis
• Zone of Fatty degeneration
DENTINAL CARIES
 Zone of decomposed dentin
Degenerating dentinal tubules, mixed oral flora, structureless matrix
 Zone of bacterial invasion
Lumen distended- liquefaction foci
beading, moth eaten, rosary
 Zone of demineralisation
Superficial layer- few bacteria
Deep- sterile
 Zone of dentinal sclerosis /hypermineralised zone
Deep dentinal lesion progressing at slow rate
Reprecipitation of crystalline material- blocks advancing carious lesion
 Zone of fatty degeneration ?
Reparative dentin
Fusayama and co-workers (1979)
Outer/ first carious layer
collagen fibres- irreversibly denatured, crosslink decreased.
Inner/second carious layer- reversible
Ultra structural changes in dentin
 Superficially, Crystals seen in zone of sclerosis
 Two types- HA crystals, Caries crystals
 Outer carious layer- few collagen fibers lost cross band
marked demineralisation of ITD, PTD disappears
 Inner carious layer –apatite crystals bound to CF, retain cross bands, ITD is partially
demineralised, reduced thickness of PTD
Root caries

26.  Cementum and dentin
 Slowly progressing carious lesion
 Cementum caries- saucer shaped, step wise process
 Demineralised clefts, penetrate sharpeys fibers
 Radioopaque surface layer
 Tablet shaped crystals of HA
 Advanced lesion- root dentin (sclerosis)
Rate at which caries forms – clinical significance
 Initiation and development – evaluating caries activity
 Speed of progression – rapid, slow
 Occlusal – smooth surface lesions
 Larger individual variations
 To treat / not to treat – clinical and radiographic assessment
References
Cariology- Newbrun
 Understanding dental caries –Nikiforukh
 Cariology – DCNA1999
 Diagnosis and risk prediction- Axelsson
 Textbook of clinical cariology- Thylstrup and fejerskov
 Restoration Of Teeth- G.J Mount
Caries Diagnosis
Objectives
 Various methods available today.
 To quantify the progress of caries .
Contents
• Visual examination
• Tactile examination
• Conventional Radiographs
• Digital radiography
• Trans-illumination
• DIFOTI
• UV illumination
• Near-IR light imaging
• Quantitative light fluorescence
• Diagnodent
• Endoscope/ Video-scope
• Ultra sound imaging
• Electronic caries meter
• Caries detection dyes
• Conclusion & References
Terminology

27. Diagnosis: the art or act of distinguishing one disease from another
Visual & Tactile examination
 limited to, occlusal pits and fissures
 variations -- tooth surface create reflections, light spots, dark spots, and contain stains
 create difficult conditions for visual decay detection
 Use of dental explorer and mirrors
White spot lesions
RADIOGRAPHY
DIGITAL RADIOGRAPHY
Digital subtraction radiography
Fiber Optic trans-illumination, FOTI
 Friedman & Marcus (1970)– detection of approximal caries.
 Basis : decayed matr- scatters light more strongly – lower index of light transmission.
 very Low sensitivity(0.13) & high specificity(0.99).
 Can detect En– crazing, cracks in tooth.
DIFOTI diagnostic imaging unit.
 Non invasive
 No radiation
 detects early caries ,hidden caries
 no film, film processing, mounting, and storage.
Ultraviolet Illumination (UV I)
 optical contrast b/n carious region(CR)& the surrounding sound tissue.
 mineral content – natural fluorescence under UV
 CR appears as dark spot against a fluorescent background.
 More sensitive than simple visual & tactile methods( Alfano & Yao,1981)
Imaging of occlusal dental caries (decay)
with near-IR light at 1310-nm
 Demineralization (decay) can be easily differentiated from stains, pigmentation, and
hypomineralization (fluorosis).
 the high transparency of the enamel -- imaging at greater depth.
 show high contrast between sound and demineralized areas.
 detection of subsurface decay hidden under the enamel.
Laser auto-fluorescence (LAF)
 Visible light within Blue-Green region (488nm)– Argon ion laser.
 Smooth-surface and fissure caries-early stage ( Bjelkhagen et al 1982)
 .Fluorescence in En –yellow range(540nm) –yellow high pass filter

28.  Deminr
areas appear dark in this situation
 Quantification of mineral loss - natural initial smooth surface caries : <1mm dia with a lesion
depth <5- 10 microns
 differential water content of early fissure caries & sound occlusal enamel ---carbon dioxide
laser to reveal such lesions.
Quantitative light/ laser induced fluorescence[QLF]
 Diagnostic tool – in vivo/ invitro quantitative assessment of dental caries, plaque, calculus &
staining.
Ultra-Sound Imaging.Adv Dent Res 7(2):70-79, 1993
 Introduced Ng et al (1988)
 Detecting early caries of smooth surface.
 Ultra sound pulse echo technique.
 Enamel surface & relative DEJ echo difference
• < 57% difference of sound En mineral content– body of lesion.
Endoscope/Videoscope
 Based on fluorescence—400-500nm
 Viewed through a specific broad band gelatine filter—caries lesion – dark spots.
 White light endoscopy
 Integrated camera --- Videoscope—expert independent examiners opinion.
Electrical resistance (ER)
 Pincus, 1951-- thr electrical impedance.
 Electrical conductivity --- function of porosity
 En deminr
-- porosity + saliva = conductive pathways for electrical current.
 > deminr
-- conductivity
 Vanguard electronic caries detector—probe in fissure + hand held earth
 Rock & Kidd (1988) in vivo- compared with H/L section –sensitivity0.70 & a specificity 0.85
 Regarded as only diagnostic tool with acceptable performance.
Dye penetration method:
 Used to visualize – subject from routine background.
 Dyes– minimal reqr
criteria :-
• Absolutely safe for intra oral use.
• Specific and stain tissues intended to stain.
• Easily removable & not permanent staining.

29.  Dyes used for detection of Carious Enamel
 Procion dyes
 Calcein dyes
 Brilliant blue
 Procion dyes:
• Stains enamel-
• sometimes irreversible– reacts with N2 & OH-
groups of En & acts as fixative.
 Calcein dyes
• Complex with Ca & remains bound to lesion
• Fluorescent dye ., Zyglo ZL 22 for invitro only
• Visible by UV illumination.
 Brilliant blue.
• Used to enhance the diagnostic quality of fiber optic transillumination.
Modified dye penetration method
 I2 penetration method – En porosity– Bharkos et al
 Pot. Iodide—applied for specific time– affected enamel.
 No of micro pores – estm & indicates– permeability of En.
Dyes used for detection of Carious dentin.
 Histopathologically
 Infected & affected dentin.
 0.5% basic fuschin in propylene glycol
 Deminr
dentin – denatured collagen – stains
 Acid red & Methylene blue.
Reference
A review of modern non-invasive systems for caries detection. Derek J Moore & Nairn, H F
Wilson. CPD Dentistry 2001; 2(3):86-90
Diagnosis of Occlusal Caries: Part I. Conventional Methods. Dorothy McComb,. Laura E. Tam.
J Can Dent Assoc 2001; 67(8):454-7. Part II:- J Can Dent Assoc 2001; 67(8):459-63.
The current status of laser applications in dentistry.LJ Walsh*Australian Dental Journal 2003;48:
(3):146-155.
Occlusal caries: wherefore art thou? D. C. Attrill,and P. F. Ashley Br Dent J 2001; 190: 440-443
Caries-Detector Dyes —How Accurate and Useful Are They? Dorothy McComb. Journal of the
Canadian Dental Association. 2000, Vol. 66, No. 4
Kavo dental products. www.kavousa.com
Imaging of occlusal dental caries (decay) with near-IR light at 1310-nm Christopher M. Bühler,
Patara Ngaotheppitak and Daniel Fried. Vol. 13, No. 2
Early childhood caries
Dr G. Kayalvizhi
Pg in dept of Pedodontia
Contents
 Definition , terminologies

30.  Classification
 Prevalence
 Etiology
 Clinical features
 Prevention
 Management
 Conclusion
 References
“Nothing is so shocking to a dentist as the examination of a child patient suffering from rampant
caries”
Stages of nursing bottle caries - Veerkamp & Weerheijm 1995-
Classification - Caries pattern
Rule 1982-
Occlusal, posterior prox, ant prox, Facial and lingual
Caries analysis system (Douglass et al 1994)
 Fissure pattern
 Maxillary anterior pattern
 Posterior proximal pattern
 Posterior bucco-lingual smooth pattern
Johnson and colleagues – 3 main patterns
I lesions associated with developmental defects
A) pit & fissure defects
B) Hypoplasia
II smooth surface lesions
A) Facio - lingual lesions
B) approximal molar lesions
C) Both
III rampant caries – 14 teeth
Definition (NIDCR – 1999)
 ECC– “The presence of 1 or more decayed (non-cavitated or cavitated lesions), missing (due to
caries), or filled tooth surfaces in any primary tooth in a child 71 months of age or younger”. (AAPD)
 S-ECC - children with atypical, progressive, acute or rampant patterns of dental caries
Proposed case definitions of ECC & S-ECC - Drury et a1999)
Classification of ECC – 3 basic forms
Prevalence
 True prevalence ?
 preschool age – not accessible
 Infant feeding habits
 Difficult to examine
 Criteria
Etiology – 4 variables

31. Etiology of ECC
 Microorganisms
Transmission of s.mutans
 Kohler 1978 – mother to child, spoon , sucrose containing dish.
 Berkowitz et al 1981 –105
CFU
 Van houte et al 1982 - saliva and plaque
 Caufield et al 1993 – window of infectivity
2) Fermentable carbohydrates
 Nursing bottle + sugar
 Pacifier dipped in honey
 Syrupy sweet vitamin preparations
 Fruit juices and carbonated beverages
 Bovine and human milk
 Nutrient content of different milk sources
Breast milk
 lactose, less buffering capacity, low fl , vitamin c
 cariogenic? – at will, sugars
Bovine milk
 ca, p, protein, whey, riboflavin, thiamin, ( Weiss and bibby 1966)
 Cariogenic? –prolonged, sugars
3) Teeth
 Number of erupted teeth – s.mutans– 5yr old (Carlson 1975)
 Rapid rate of progression - Thin enamel layer
 Immature teeth - Hypoplastic Defects
4) Time
 Berkowitz et al 1985 – eruption of teeth
 Frequency and amount of exposure of offending liquid
 Duration of the deleterious habit – beyond weaning period
 At will /at night breast feeding
Other risk factors
 Malnutrition
 Low birth weight
 Excess of lead, fe deficiency
Clinical features
 Sequence of involvement
Max central incisors,max laterals,
max 1st
molars (f,l,o), max canine
2nd
molars (f, l, p), mand molars
Stages of early childhood caries
Normal
Very mild:
mild demineralization usually at gingival crest and no cavitation
Mild: moderate cavitation
Predictors of ECC & Risk assessment
 Case history

32.  Clinical examination
Ist
dental visit
 Microbial sampling
Prevention
 Parent education
 Identifying high risk patients
Parent education
 alternative to nocturnal feeding
 Weaning methods – diluting liquid, cup- 12mon
 Avoid sweetened pacifiers
 Sharing of utensils
 Clean gum pads - teeth
3 stages in development (Berkowitz 1985)
 primary infection
 Prenatal care
“Treat the parent before the child”
 Kohler 1982 – mothers program
Diet counseling, professional cleaning, Naf mouth rinse, excavation & restoration
- Antimicrobial agents – CHX, FL
- xylitol
2) Accumulation of organisms secondary to CHO ingestion - Eliminate CHO ingestion
- Chemotherapeutic – fall asleep pacifier
- Fl, chx
3) Demineralization and cavitation of tooth surface
Prevention of rampant caries in children and adolescents
Fluoride treatment (0.3-0.7ppm)
Diet counselling in dental practice
Before counseling
 Explain the patient the reason for counseling
 Dental health diet score
 Food intake – diet diary
Scoring the four food groups
Nutrient score
Scoring the sweets - Decay- promoting potential
Totaling the scores
4 food group score
 72 – 96 -------- excellent
 64 – 72 -------- adequate
 56 – 64 -------- barely adequate
 56 or less ------ not adequate
sweet score
 5 or less ------- excellent

33.  10 ------- good
 15 or less ------ ‘WATCHOUT’ zone
The counseling visit
4) Reasons for diet
5) Education about the role of diet
6) Cariogenic potential of diet
7) Adequacy of diet listed in diet diary
8) Diagnosis of problem
9) Diet prescription
10) Compare old and new diet
11) Summary
12) Follow- up
Dietary recommendations
Combining and sequencing of foods
 Sugary foods + protein+ limited fats
 Fermentable carbohydrates +non sugary item
 Inclusion of milk, non fat yoghurt, cheese
 Peanuts + apple juice
 Drink water
Management
Aims
 emergency
 Arrest and control of carious process
 Preventive procedures
 Restoration and rehabilitation
Depends on
 Parent Motivation
 Extent of decay
 Age and co-operation of child
management
modify etiological factors
 Discontinuation of habit –
- identifying the offending habit and eliminating it
 Restorative management – symptomatic
- asymptomatic
Dentition stabilization
Early carious and WSL
 White spot lesion – topical fl
 Gross caries removal - Temporisation with GIC
 Pits and fissures
Definitive treatment

34. Pulpotomy
Pulpectomy
Extraction
Final restoration
Full coverage restorations
Restorative strategies / treatment protocol
 Early caries with minimal loss of enamel
 topical fl- weekly
 Extensive cavitation with no pulpal involvement
Ant teeth - acid- etch composite
- Pedo strip crowns
- GIC
Post teeth – post composite, GI cermet, SSC, amalgam
Extensive cavitation with pulpal involvement
pulpotomy/ pulpectomy – permanent restoration
Extraction – space maintainer
References
 Community dent oral epidemol 1998
 Community dent oral epidemol 1999
 J public health dent 1999
 Pediatric dent 1995
 Dcna 2000
 J dent res 1993
 Text book of Pediatric dentistry – shobha tandon
 Stephen wei
 Nutrition - nizel
/ OPTICS EXPRESS
“caries prevention”
Thejokrishna.P
Post-Graduate student
Dept of Pedodontics & Preventive dentistry
Bapuji Dental College & Hospital
Davangere: 577 004
“An ounce of prevention is worth a pound of dental cure”.
-Old Dental Public Health Proverb
Oral diseases--- “The Neglected Epidemic”
Primary prevention
 Employs strategies & agents to forestall the onset of disease, to reverse the progress of the
disease, or to arrest the disease process before secondary preventive treatment becomes necessary.

35. Caries prevention
Approach at various levels
 Primary level
 Health promotion
 Specific protection
 Secondary level
*early diagnosis & prompt treatment
 Tertiary level
*disability limitation
*rehabilitation
Dental professional
health promotion
 Patient education
- education to pregnant mother
 Plaque control program
 Diet counseling
 Recall reinforcement
 Dental caries activity tests
Patient education
 Parent education and motivation
“If we are to have a good child patient we must first educate the parents. A dentist who fails to do so is
not using every means available to him in management to the child.”
purpose
 Emotional problems of children in r/t dental treatment.
 Insight of parental influences
 Attitude of parent----behavior mgt techn
 Estb good rapport
 Educate– various dental problems & diseases & their sequelae
Education to pregnant and lactating mother
Plaque control programme
Nutrition
Flouride
Timing of visit
Feeding practice
Importance of weaning
Bottle feeding
Cleaning activity of oral cavity
Recall reinforcement
Dental caries activity test
Diet counseling
Objectives
-correction of diet imbalances—effects genr
& oral health
-modification of dietary habits– isolate sucrose intake– educate its importance
- Acceptable substitute

36. Dietary screening & assessment questionnaire.
Caries prevention
Approach at various levels
 Primary level
 Health promotion
 Specific protection
 Secondary level
*early diagnosis & prompt treatment
 Tertiary level
*disability limitation
*rehabilitation
Dental professional
specific protection
 Application of topical Fl
 Supplement/rinse prescription
 Pit & fissure sealants
Pit & Fissure sealants
 Deep retentive pits and fissures
 Stained pits and fissures with minimum appearance of decalcification
Questionable enamel caries in pit and fissures
Active lesions in other sites
 Caries pattern with more than 1 lesion per year
 If morphology of pit and fissures are at risk of caries
 Routine dental care with active preventive dentistry program
 Community based sealant.
Contra-indications
 Well coalesced, self cleansing pits and fissures
 Presence of radiographic and clinical evidence of caries
 partially erupted teeth.
 Isolation not possible
 Life expectancy of tooth is limited.
 Dentinal caries
 Lack of preventive practices
Individual approach [self administered ]
Health promotion
Diet planning
Demand for preventive services
Periodic dental visits
Individual approach [self administered ]
Specific protection
Appropriate use of Fl
 Fl water
 Fl prescription
 Fl dentifrice
 Oral hygiene maintenance

37. Community approach
health promotion
 Dental health education programs
 Promotion of research
 Oral health policy
 “Safe for tooth concept”
Community approach
specific protection
 Community or school water fluoridation
 School Fl mouth rinse or tablet program
 School sealant program
Caries prevention
Approach at various levels
 Primary level
 Health promotion
 Specific protection
 Secondary level
*early diagnosis & prompt treatment
 Tertiary level
*disability limitation
*rehabilitation
Secondary prevention
Secondary level employs routine treatment methods to terminate a disease process and/or to restore
tissues to as near normal as possible.
Individual
 Self examination and referral utilization of dental services.
Community Services
 Periodic screening & referral
 Provision of dental services
Dental professional
 Complete examination
 Prompt treatment of incipient lesions
 Preventive resin restorations & ART
 Simple restorative dentistry
 Pulp capping
Complete examination
Proper classification
Prompt treatment of incipient lesion
 Remineralizing agents
-topical Fl
-ACP-CCP
PRR is the conservative answer to the conventional “extension for Prevention”
This extension prevents future caries formation but does so at the expense of losing substantial healthy
tooth structure.
The PRR preserves the sound tooth structure.

38. Caries prevention
Approach at various levels
 Primary level
 Health promotion
 Specific protection
 Secondary level
*early diagnosis & prompt treatment
 Tertiary level
*disability limitation
*rehabilitation
Tertiary prevention
It employs measures necessary to replace lost tissues and to rehabilitate patients to the point that
physical capabilities and/or mental attitudes are as near normal as possible after the failure of
secondary prevention.
Dental professional
 Complex restorative dentistry
 Pulpotomy
 RCT
 Extraction
 Removable & Fixed prosthodontics.
 Minor tooth movement
 Implants
Community
 Disability limitation
Provisional of dental services
Rehabilitation
 Utilization of dental services
“Prevention of premature death, disease, disability, and suffering should be a primary goal of any
society that hopes to provide a decent future and a better quality of life for its people”
 References
Primary Preventive Dentistry, 6th
edition, Norman O Harris &Franklin Garcia- Godoy.
Preventive resin restorations: indications, technique, and success-Quintessence Int1992;23:307-15.
 Dental treatment during pregnancy: a preventive approach-JADA1985:110;362-67.
 Infant oral health care: a rationale-J Dent Child:1986;257-69.
 Essentials of preventive & community dentistry: Soben Peter, 2nd
edition.
 Text book of Pedodontics: Shobha Tondon
Caries Risk & Risk profiles
Dr. Thejokrishna.P
Post-Graduate student

39. Dept of Pedodontics & Preventive Dentistry.
Bapuji Dental College & Hospital
Davangere
Changing oral health perspectives
 Changes in disease level among different populations
 Increased understanding of caries pathogenesis process
 Material & Operative technique development
 Changes in patient behavior & requests.
Contents
 Changing oral health perspective
 Definition – risk, caries risk
 Epidemiological and Clinician’s view point
 Repeated restorative cycle.
 Association Vs Prediction &Risk assessment
 Need for high-risk strategy.
 Factors associated with a high caries risk individuals
 Why measure caries risk?
 Factors that cause high risk condition
 Diagnosis & evaluation of high-risk subjects.
 Clinical investigation for caries risk diagnosis
 Microbiologic & biochemical test
 Cariogram model—treatment planning
 Principles for caries etiologic treatment.
 Risk groups & treatment protocol
 Conclusions & references
Epidemiological view point
Clinician view point
Prevention.
• “The central role that restorative treatment has played in caries management will probably
be lost in the future.” Anusavice 1995
Minimal intervention techniques
G.Kayalvizhi
Pg in dept of pedodontia
Bapuji dental college and hospital
Davangere
Contents
 PRINCIPLES OF MINIMAL INTERVENTION RESTORATIVE DENTISTRY
 FACTORS INFLUENCING THE MINIMAL INTERVENTION

40. RESTORATIVE DENTISTRY
 MINIMAL INTERVENTION TECHNIQUES
EARLY LESIONS
ADVANCED LESIONS
Minimal invasive preparation techniques
 ART
 Air abrasion
 Sonic oscillation
 Laser
 Ozone
 Chemo mechanical excavation
 Enzymatic digestion
 Smart prep
Minimally invasive dentistry
 Def – maximal preservation of healthy dental structures
 Goal – extend the life of restored teeth with as less intervention as possible.
 Fillings are not curative – (Black 1908)
PRINCIPLES OF MINIMAL INTERVENTION RESTORATIVE DENTISTRY - WORLD
DENTAL FEDERATION 2000
 Control the disease through reduction of cariogenic flora.
 Remineralize early lesions.
 Perform minimal intervention surgical procedures, as required.
 Repair, rather than replace, defective restorations.
10 commandments of Minimally Invasive Dentistry
Burnhal- Grigereit in 1995
1) Always follow the philosophy of minimally invasive dentistry.
2) Perform the least amount of dentistry needed in any situation.
3) Never remove more tooth structure than is absolutely required to restore teeth to their
normal condition.
4) Always use dental materials that conserve maximal tooth structure over time.
5) Use only dental materials that have been researched by leading dental schools and research
institutions and that are recommended by leading practicing dentists.
6) Use only the strongest and longest lasting materials to reduce the need for future repair and
replacement.
7) Keep dental appointments as short as possible to ensure conservative treatment.
8) Use dental procedures that minimize the number of necessary appointments.
9) Select dental laboratories that use minimal invasive materials for the restoration of teeth
10) Use only restorative materials that do not wear opposing teeth more than enamel.
FACTORS INFLUENCING THE MINIMAL INTERVENTION
3 factors

41.  The demineralization- remineralization cycle.
 Adhesion in restorative dentistry.
 Biomimetic restorative materials.
II. ADHESION IN RESTORATIVE DENTISTRY
 Amalgam
 Adhesion – micromechanical, chemical
 Glass ionomer cement – adhesion, anticariogenic
 Resin modified GIC – wear resistant, strength
 Metal modified GIC
 Compomers -
 Composites - strength, low solubility, wear resistance
III) BIOMIMETIC RESTORATIVE MATERIALS
Imitation of nature
Biocompatible
Sealing ability
External surface –withstand load, wear, antibacterial properties, fl release
Internal surface – remineralisation
G.V.Black's Classification
ClassI - Cavities occurring in pit and fissure defects in occlusal surfaces of bicuspids and molars,
lingual surfaces of upper incisors, and facial and lingual grooves
Class II - Cavities in proximal surfaces of bicuspids and molars.
Class III- Cavities in proximal surfaces of incisors and cuspids not requiring removal of incisal
angle.
Class IV- Cavities in proximal surfaces of incisors and cuspids that require removal of incisal
angle
Class V - Cavities in gingival third of labial, lingual, or buccal surfaces.
Class VI- Cavities in incisal edges and smooth surfaces of teeth above the height of contour.
G.V. Black concept
 To remove tooth structure to gain access and visibility
 To remove all trace of affected dentin from the floor of the cavity
 To make room for the insertion of restorative material itself
 To provide mechanical interlocking designs
 To extend the cavities into self- cleansing areas to avoid recurrent caries
CLASSIFICATION OF CARIOUS LESIONS BY SITE & SIZE
Mount G.J 1994
Site 1, Size 1 – pits and fissures, minimal dentin involvement
Site 1 size 2 –G.V. Black class I
( moderate dentin)

42. Site 1 size 3 - G.V. Black class I
(enlarged)
Site 1,size 4 - G.V. Black class II
(extensive lesion)
Site 2,size 1 – contact area, minimal dentin
3 approaches – tunnel. Slot, proximal
 tunnel - 2.5mm apical to crest of marginal ridge
occlusal cavity proximal cavity
1) Tunnel preparation
 Removal of approximal carious tissue via a modest access cavity in the occlusal surface.
 Scandinavia 1980
2 variations
 Closed tunnel – leaves demineralised approximal enamel intact
 Open tunnel
Semi permanent restoration- small lesions
Classification
 Internal tunnel preparation
 Partial tunnel preparation
 Total tunnel preparation
Indications and contraindications
 Small proximal carious lesions
 Large carious lesion
Advantages
 Preservation of marginal ridge
 Less potential for microleakage
 Minimal preparation
 Esthetic
Disadvantages
 Highly technique sensitive
 danger of pulpal involvement
 Uncertain – caries removal
 Risk of marginal ridge #
Preparation and restoration
Initial approach gain access
Completed cavity restoration
Site 2 ,size 1-
2) Slot cavity– close to marginal ridge
Site 2 , size 1-
3) proximal
Site 2 size 2 -G.V Black class II, III
(approximal, moderate dentin) – amalgam, GIC
SITE 2, SIZE 3 – G.V Black class III,II
(ENLARGED APPROXIMAL)

43. Site 2,size 4 – G.V. B lack class IV, II
(extensive)
Site 3 size 1,2,3,4 – G.V Black class V
Atraumatic restorative techniques (ART)
Who benefits from ART ?
Remote communities with no dental services.
Towns and villages without electricity.
Housebound elderly.
Elderly living in nursing homes
The physically or mentally handicapped
Introducing oral care to very young children
 For patients with extreme fear/anxiety
 History
Tanzania in the mid 1980s – university of dares salaam
 1988 Dr.Jo Frencken
 1993- Field trial in Zimbabwe “press finger” technique
 1994 - The World Health Organization introduced ART
Instruments and materials used
Mouth mirror, explorer, tweezers. hatchet, spoon excavator, carver, spatula, glass slab, gloves,
cotton wool rolls and pellets, wedges, plastic strips, and clean water.
glass ionomer restorative material, dentin conditioner, petroleum jelly (Vaseline)
voroscope
IDEAL ART MATERIALS
 be biocompatible
 be tooth colored
 have “forgiving” handling properties
 be insensitive to moisture or desiccation
 harden without special equipment
 form stable bonds to enamel and dentin
 seal margin gaps against bacteria
 release fluoride and/or remineralization agents
 release a chemotherapeutic agent when required to arrest disease
 exhibit excellent durability.
Description of the ART Technique
principal steps
Isolate the tooth with cotton wool rolls
Clean the tooth surface to be treated with a wet cotton wool pellet.
Widen the entrance of the lesion
Remove caries
Provide pulpal protection if necessary
Clean the occlusal surface
7) Condition the cavity and occlusal surface
8) Mix glass ionomer
9) Insert mixed glass ionomer into the cavity and overfill slightly

44. 10) Pressure finger technique
11) Check the bite
12) Remove excess material
13) Cover filling / sealant with petroleum jelly
14) Instruct the patient not to eat for at least one hour.
 Advantages of ART
use of easily available and relatively inexpensive hand instruments
 conserves sound tooth tissue.
 minimizing the need for local anesthesia.
 simple infection control practice
 Glass ionomers – adhesion, fl
 preventive and curative treatment
 ease of repairing defects in the restoration
 low cost
Limitations of ART
 Long – term survival rates for glass ionomer ART restorations and sealants are not yet
available
 one-surface lesions
 hand fatigue
 Hand mixing
 misapprehension that ART can be performed easily
 A misconception by the public that the new glass ionomer “white fillings” are only
temporary dressings.
Permanent teeth
 71% survival (3yr)- Thailand (1991-1994) – chemfill
 Zimbabwe (1994-97)-fuji ix – 84-92%
Primary teeth
 WHO report 1993 – chemfil-80% (1yr)
 Holmgren 1999 – 12-30months -86%
“Is ART really a new approach?”
“Is ART a Myth or Reality?”
Air abrasion
 Utilises kinetic energy from alumina particles entrained in
high velocity stream of air to remove tooth structure.
Development
 1940 - Robert Black
 1950 - Tim Rainey, Father of concept of air abrasive micro dentistry.
 1951- S.S White technology introduced AIR- DENT,
 1990’s- New technology
Equipment – kavo rondoflex, KCP 100,prepstart
Principle – kinetic cavity preparation
 Based on the formula for kinetic energy
E =1/2 mv2
 Enamel ,dentin – KE absorbed, cuts rapidly
 Abrasive particles
- Alo- 27µm, 50µm

45. - polycarbonate resin alumina HA mixtures
 Pressure – 40 -140psi
 Tip size – 0.015” – 0.027”
 Tip distance- <2mm
 Tip angle – 40-1200
Cavity preparation procedure:
Stain the groove
Start with 0.0 11” tip to abrade superficial stain.
Large amounts of soft decay may be removed by a spoon or small round bur in slow speed.
Alternatively, the caries can be desiccated by laser and then air abraded.
Restoration: restorative materials - GIC, Compomers, Composites
check occlusion
Kcp preparations
 Rounded cavosurface margins and internal line angles
 Microscopic roughness
 Abraded enamel surrounding cavity outline
 Closure of dentinal tubules
Application / indications
 Class I,V,III
 Internal cleaning of tunnel preparations
 Removal of temporary cement inside a crown, preparation of metal surfaces inside crown
Contraindications
 Chronic pulmonary diseases - Asthma patients
 Severe dust allergy
 Recent extraction
 Any open wound / cut
 Sub gingival caries removal.
Safety
 Face masks, rubber dam, eye glasses, disposable mouth mirrors, high speed suction
Advantages
 Non traumatic treatment
 Less invasive procedure, preserve more tooth structure.
 Less discomfort to the patient
 No chipping
 No microfracture
 Decreased thermal build up
 No anesthesia
Disadvantages
 Not cost effective
 Lack of tactile sensation
 Non contact based modality - inadequate carious removal.
 Mess & spread Al oxide around the dental operatory.

46.  Impaired direct view- abrasive particles collect on the mirror rapidly blocking the
viewing surfaces.
Sono - abrasion
 Sonicys microunit- Sonic oscillations -<6.5 KHZ
 Elliptical motion
 3 tips- torpedo (1.3mm), small hemisphere (1.5mm), large hemisphere (2.2mm)
uses
 Prepare pre determined cavity outlines ( sonocys approx)
 Finishing cavity preparations
 Remove softened carious dentin (sono – abrasion)
Lasers
 Beam of photons from electromagnetic spectrum, which when focussed in a thin beam-
cut
 Different laser settings- water content (E,D)
 Dual feedback – tactile, auditory
 Lasers + air motor- 40- 60 micron
 Photomechanical effect - vaporises of water – massive volume expansion – explode away
 Excimer laser - Ablation of carious dentin
 Er:YAG Nd:YAG, - cut dental hard tissues (Myers 1988)
 CO2 laser – sealing of fissures (melcu et al 1984)
 Destroy streptococcus mutans
 Resistant to demineralisation
steps
 Gently touch target tissue with tip end
 Direct water stream to target tissue
 Keep tip moving – effective ablation and cooling
 Wide cut – constantly move tip over surface
 Deep cut- move tip up and down
Ozone technology in caries removal
 Ozone - natures most powerful oxidant ( Dr Edward lynch )
 Chemistry of Ozone (o3)5
- part of natural gas mix that surrounds the earth at high
altitude
 Mechanism of action
Principle-
 Niche environment theory
 Concept - Complete elimination of acidophilic bacteria, fungi and viruses , creating a
sterile environment for remineralisation
(alter metabolic products of bacteria)
 10sec (2200ppm) - 99% elimination
Indications
 Primary root carious lesions
 Primary pit and fissure caries
 Early carious lesions around crowns and bridges
Heal ozone TEC 3 unit (cur ozone.)
1) polyurethane console

47. 2) handpiece
Clinical steps in ozone therapy
 Polymer cup is adapted to primary carious lesion
 Ozone gas delivered (10sec) – into cup
 Gas passed through Activated carbon filter
 Fluid(2% naf+5% xylitol) is pumped for 5sec
 Home care kit
 Recall – 3months
Adverse effects – respiratory distress
Advantages
 Kills > 99% micro organisms
 Oxidises caries, speeds up remineralisaion
 Remove organic debris, volatile sulphur compounds
 Whitens discolored caries
 Decreased time, painless, noiseless
 No allergic reaction
 Microorganisms- no resistance
 Cochrane review – no evidence
 Holmes 2003, Baysan 2004- bacteria
Other applications
 Purify water
 Eliminate pollution in air supplies in hospitals
 Decontaminate dental unit water airlines
 Cleaning of root canals
 Tooth whitening procedures
 Treatment of periodontal disease
 Prewashing of surgical sites prior to implant placement
Chemomechanical caries removal
 Chemical softening of carious dentin – gentle excavation
Principle –
 Goldman & kronman (Naocl)
 Sorenson's buffer – glycine, NaoH, Nacl
 glycine + Naocl – NMG (GK- 1019)
 NMAB (GK 101E)
 EARLIER- HP, chlorination
 Recent- oxidation of glycine
Caridex and carisolv
Steps
Advantages
 Safe , no adverse effects on pulp
 Reduced need for LA
 Conservation of tooth structure

48.  Reduced risk of pulp exposure
 Pediatric, medically compromised pts
Limitations
 Need for Rotary and hand instruments
Selective dentin removal
 Limiting dentin removal to lesion itself
 Polyamide bur- cutting elements that abrade or deflect upon encountering dentin
Enzymes
 1989 Goldberg and keil – collagenase
 1999- pronase (non- specific proteolytic enzyme)
Conclusion
“Prevention of extension”
References
 Preparation and restoration of tooth structure- G.J mount
 Minimal intervention- early lesions- quintessence int 2000
 Minimal intervention- advanced lesions- quint int 2000
 ART – j public health dent 1996
 Jada 1994, 551
 Int dent j 2000, 1-12
 Dcna 2002, 185-200