Dental caries

Dental caries
Sohail
PGT: 1st yr
Dept of pedodontics
SVS Institute of Dental Sciences.
1

Contents
Introduction
History
Definitions
Etiology
Microbiology
Classification
Histopathology
2
Part - 1
Part - 2

Introduction
• The word caries is derived from Latin, meaning “rot or decay”
• BENJAMIN FRANKLIN stated that:
“HOT things, sharp things, sweet things, cold things rot the teeth and make
them look like old things”.
• Dental caries is a multifactorial disease requiring the presence of a susceptible
host, cariogenic microflora and a diet conducive to enamel demineralization.
3

► Dental caries or tooth decay is one of the most common of all disorders,
second only to common cold.
► The first study about dental caries was published in 1870 and has continued
uninterrupted to the present.
► Some isolated populations like Eskimos, some African natives, and
inhabitants of rural India are “immune” to dental caries because they are not
exposed to western food habits.
4

5
Historical overview of concepts in understanding
dental caries

Evidences of dental lesions compatible with caries have been observed
1. In Paleozoic fishes (570-250 million years)
2. Mesozoic herbivores dinosaurs (245-65 million years)
3. Pleistocenic animals (1.6-0.01 million).
• Caries has also been detected in bears and other wild animals and it is
common in domestic animals
6
(Pinto & Exteberria, 2001; Palamra et al., 1981), (Gorrel, 2006; Shklair, 1981; Wiggs & Lobprise, 1997).

Homo rhodesiensis cranium 7
A fossil found in 1921 in Broken Hill, Northern
Rhodesia (Zambia)
The specimen shows extensive dental caries and
coronal destruction.
Except for five teeth, all the rest is affected by
rampant caries and several crowns were almost
completely destroyed.

10,000 B.C 8
• In the Mediterranean region, Arabia and India the increase of caries began
early between the 7th and 5th millennium BC.
• In Nautufians from the Levant region, the phase of hunter gatherers
(10,500-8300 BC) shows 6.4% of caries frequency whereas Neolithic
populations(8300-5500 BC) show 6.7% (Eshed et al., 2006).
• In the Indo region the caries frequency range between 1.4-1.8% in the
earliest populations, but in the site of Harappa (5000 BP, Pakistan) from
the Early Bronze Age the caries frequency is 12% (Lukacs, 1992, 1996)

• 1728- Pierre Fauchard, a French physician, wrote “Le Chirurgien Dentiste.”
• Fauchard rejected the tooth worm theory of dental caries.
• Instead, he described enamel hypoplasia as “an erosion of the enamel” and
recommended that hypoplastic areas be smoothed using files
9

The Restorative Era:
1850–Present
• At the International Medical Congress held in London in 1881, Miller and
Underwood proposed that dental caries development was dependent on the presence
and proliferation of “organisms.” (Searle F 1884, Barrett W 1885)
10

In 1881, Dr. W. D. Miller presented the results of his experiments (Miller W 1883)
• Bacteria produced the acids that led to the demineralization of enamel and dentin.
• He also noted that bacteria did not need to be present in enamel or dentin to
initiate demineralization.
• Miller’s research led to a storm of debate and controversy.
11

• Environmentalists won over those who argued that the structure of teeth play a
major role in the caries process (Johnson CN 1918).
• The nutrition-caries hypothesis was partially discredited by the finding that
populations who were malnourished had lower caries prevalence than those who
were well nourished (Massler M, Schour I 1947).
By the mid-1920’s 12

• Also discrediting that hypothesis were findings from the Vipeholm Dental Caries
Study,
• ‘frequent consumption of sugar increases the risk of developing dental caries’
(Gustafsson B, et al 1954).
• Mellanby (1934)- reviewed on literature of caries and noted that incidence was
invariably less in primitive races than in modern man.
13

Definition(s): 14
“Microbial disease of the calcified tissues of the teeth, characterized by
demineralization of the calcified tissues and destruction of the organic
substance of the teeth”
-Shafer
“An infectious microbiological disease of the teeth that results in localized
dissolution and destruction of calcified tissues”
- Sturdevant
“A localized post eruptive pathological process of external origin involving
softening of the hard tissue and proceeding to the formation of a cavity”
-WHO

ICDAS Definition: 15
DENTAL CARIES:
Is the localized destruction of susceptible dental hard tissue by acidic by-products
from bacterial fermentation of dietary carbohydrates. It is a bacterial driven,
generally chronic, site-specific, multifactorial, dynamic disease process that results
from the imbalance in the physiologic equilibrium between the tooth mineral and the
plaque fluid; that is, when the pH drop results in net mineral loss over time.
The International Caries Detection And Assessment System (ICDAS II)and the International
Association For Dental
Research. Available at: https://www.icdas.org. Accessed February, 2010.

17
• There was no universally accepted opinion of the etiology of
dental caries, and various theories have been proposed.
• Early theories
• Endogenous theories
• Exogenous theories

Vital theory: 20
• Proposed by Hippocrates, Celsus, Galen and Auicenna.
• A vital theory of tooth decay was advanced towards the end of the 18th
century which postulated that tooth decay originated like bone gangrene,
from within the tooth itself.

Exogenous theories: 21
Chemical (acid) theory:
• In 17th and 18th century, there emerged, the concept that teeth were destroyed
by acid formed in the oral cavity. The acid implicated were inorganic like
sulfuric, nitric, citric acids formed by decomposition of food in saliva.
• Robertson (1835) proposed that dental decay was caused by acid formed by
fermentation of food particles around teeth.

22
• Dubos (1954) postulated that microorganisms (animal culae) can have toxic and destructive
effects on tissue.
• Early microscopic observation of scrapings from teeth and of the carious lesions by Antoni
Van Leeuwenhoek (1632-1723) indicated that microorganisms were associated with the
carious process.
• In 1843, Erld described filamentous parasites in the membrane removed from teeth. A few
years later in 1847 Ficinus, a physician also observed filamentous organisms in the enamel
cuticle (surface protein membrane of teeth) and in carious lesions.
Parasitic (septic) theory:

Endogenous theories:
• Millers chemicoparasitic theory
• Proteolytic theory
• Proteolytic chelation theory
• Sucrose chelation theory
23

Miller’s chemicoparasitic theory: 24

25
• The essential features of Miller’s work which helped in developing the chemicoparasitic
theory are:
• That 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 those associated with fermentation, namely lactic, butyric,
acetic, formic, succinic and other acids.
• Carbohydrates food material lodged between and on surfaces of teeth is the source of the
acid which demineralizes the lime salts of the tooth.

26
Miller summarized his theory as follows:
• Dental decay is a chemoparasitic process consists of 2 stages: decalcification or
softening of the tissues and dissolution of the softened residue.

27
• Limitations
• Did not explain sub-surface demineralization
• Failed to justify rampant caries
• Did not explain caries in impacted tooth
• Phenomenon of arrested caries is not explained
• Smooth surface caries is not accounted in this theory

PROTEOLYTIC
ENZYMES
• PROTEOLYTIC THEORY :
Organic
Inorganic
28
Gottlieb (1947) Friable and Nuckells (1947) and Pincus (1950).
Acidogenic
bacteria

PROTEOLYSIS-CHELATION THEORY :
Schatz and Martin in 1955.
PROTEOLYTIC
ENZYMES
CHELATION
Organic
Inorganic
29

30
• Egglers – Lura(1967) proposed that sucrose itself can cause dissolution of
enamel by forming an ionized calcium saccharate.
• Calcium saccharates and calcium complexing intermediaries requires inorganic
phosphate which is subsequently removed from the enamel by phosphorylating
enzymes.
Sucrose chelation theory-

31
• The most widely accepted theory till date continues to be the acidogenic theory put forth
by Miller with recent addition.
• This can be explained by Keye’s triad which has been modified into a tetrad.
Current concept :

Tooth
Substrate
Microorganism
KEYE’S TRIAD ( 1960 )
Caries
32

HOST
BACTERIA
TIME
NUTRITION
Caries
CARIES TETRAD( Newburn -1982 )
33

• THE HOST :
- The tooth
- Salivary factors
- Muscular activity
- Habits
- Group suceptibility
- Age
- Environment
• THE MICROORGANISMS :
- Bacterial plaque
• THE MEDIUM :
- Diet
Contributing factors to the caries process: 35

36
Morphology and position
• A susceptible host is one of the factors required for caries to occur.
Host factor : Tooth

37
• Certain surfaces of a tooth are more
prone to decay.
Eg : In mandibular I molar the most prone
areas in order are occlusal, buccal, mesial,
distal and lingual.

• These differences in decay rates of various surfaces on
the same tooth are in part due to morphology,
example lingual groove of maxillary incisors.
38

POSITION OF TOOTH IN THE ARCH:
• Malaligned(buccally/lingually placed)
• Out of position
• Rotations.
39

40
Armstrong et al - relation of caries to the chemical composition of teeth
No differences were found in the calcium, phosphorous, magnesium and carbonate
contents of enamel from sound and carious teeth.
• Significant differences in fluoride content of sound and carious teeth however have
been reported by these same workers.
• They have found the fluoride content of enamel and dentin from
Sound teeth 410ppm and 873ppm but
Carious teeth 139ppm and 223ppm only.
Composition of the tooth:

41
• Surface enamel is more resistant to caries than sub surface enamel.
- Brudevold et al
• Surface enamel is highly mineralized and tends to accumulate greater
quantities of fluoride, zinc, lead and iron than sub surface enamel.

43
• 99% - H2O.
• 1% - a) Inorganic –
Main K, Na, Ca, Cu, HCO3- and inorganic phosphate.
• Others :b)Organic :
• Fluoride, sulfate, thiocyanate iodide and magnesium.
• Carbohydrates – glucose.
• Lipids – Cholesterol, lecillinin.
• Nitrogen –ammonia, nitrites, urea and amino acids.
• Miscellaneous – peroxide.
• Enzymes – carbohydrates (Amylase maltose), proteases trypsin
• Oxidases (catalase, oxidase)
Compositionofsaliva:

44
Daily volume - 0.5 – 1 litre secreted of which
 90%- major salivary glands.
 10%- minor salivary glands.
- 50%produced during chewing and
- 2-10% during sleep
Salivary secretion rate-
• Normal unstimulated/resting - 0.3-0.5ml/min.
• Normal stimulated - 1-2ml/min.
Secretionof
saliva:

Role of saliva as a modifying factor in
dental caries: 45
The principle properties of saliva that protect the teeth against caries:
Dilution and clearance of dietary sugars.
Neutralization and buffering of the acids in plaque.
Supply of ions for remineralization.
Both endogenous and exogenous antiplaque and antimicrobial factors.

46
A number of antibacterial factors such as lysozyme, lactoperoxidase,
lactoferrin and immunoglobulin A are present in saliva.
• Lysozyme: This has the property of cleaning the cell wall of certain
microorganisms, thereby causing their lysis.
• Lactoperoxidase: (milk, tears, saliva):Known to be inhibitory towards
streptococci and lactobacilli.
They oxidize thiocyanate in the presence of hydrogen peroxide.
• Lactoferrin: Strong ion-binding capacity thereby removing bacterial iron and
making it unavailable to the bacteria.
Antimicrobial properties of saliva:

47• Immunoglobins (IgA)
It is the predominant immunoglobin present in saliva secretory IgA is an
effective agglutinin.
It inhibits adherence and prevents colonization of mucosal surfaces of teeth
by organisms facilitating their disposal by swallowing.
Other salivary protein with protective penetration.
a) Glycoproteins:
Depending on their linkage
• Mucinous
• Serous

CHEMICAL NATURE OF THE TOOTH :
%
F , Ca , Sn CARIES
SUSCEPTIBILITY
48

•CARIES BIOFILM
Microbiology & histopathology of dental caries
49

Biofilm and the carious process
50

Dental plaque biofilm
 Dental plaque is a structurally and functionally
organized biofilm.
 Dental plaque has been defined as the diverse
community of micro-organisms found on a tooth
surface as a biofilm embedded in a matrix of polymers
of host and bacterial origin.
( Marsh 2004.)
51

Quorum sensing 52
oRegulation of expression of
specific genes through the accumulation
of signaling compounds that mediate
Intercellular communication
o Mediated by a competence stimulating
Peptide (CSP) in S.mutans.
o Csp is directly involved in biofilm
Formation
oThis quorum sensing system also functions
to regulate acid tolerance in S.mutans
Biofilms.

Plaquesites Fissure plaque-mainly mutans streptococci
Smooth surface plaque
Approximal plaque –mainly
G+ve rods esp. Actinomyces
spp.
53

Development of dental plaque
0-4h
• Pellicle formation
• Attachment of single bacterial cells
4-24h
• Growth of attached bacteria leading to formation of
distinct microcolonies.
1-14d
• Microbial succession and co-aggregation
2 weeks or
older
• Climax community and mature plaque (2 weeks or older ).
• Detatchment
55

Initial
colonizers :
S. Sanguinis , S. oralis, S. mitis biovar 1,
S.gordonii – 56% of initial flora. Also
Actinomyces spp. , & G-ve bacteria
present.
Cryptitopes–
important factor
in regulation of
colonization
56

Current hypotheses to explain role of
bacteria in the etiology of caries 57

Specific plaque hypothesis
 Proposed that out of the diverse collection of species
present in plaque only a relatively small number were
directly involved in causing disease. (Loesche,1976).
 Benefit: focusing studies on the
control of specific microbial targets .
 Association of mutans streptococci
with dental caries is not unique.
58

Non-specific plaque hypothesis
 Proposed that disease is
the outcome of the overall
activity of the total plaque microflora.
 In this way, a heterogenous
mix of microorganisms
could play a role in disease.
59

Ecological plaque hypothesis –key features
The selection of pathogenic
bacteria is directly coupled to
changes in the environment
• and
Diseases need not have a specific
etiology; any species with the
relevant traits can contribute to
the disease process
60

•Relatively unaffected, SUBSURFACE
DEMINERALIZATION seen
•Special properties of enamel, with greater
mineralization-not accepted
•Higher fluoride content
•Greater amount of insoluble protein
•Protection by pellicle/plaque-remineralization
•Moreno model-Ca & Phosphate that diffuse from
subsurface are precipitated in outer surface layer
(DCNA 1999)
62

pH 6.8 6.0 5.5 5.0 4.5 4.0 3.5 3.0
8.0 6.8 6.0 5.5 5.0 4.5 4.0 3.5 3.0
Critical pH
of HA
Demineralisation- remineralisation cycle
Critical pH
of FA
D
HA
dissolves
Ca,HPO42
OH
FA form
R
FA
HA, FA
dissolves
H+
exhausted/
neutralized
H+ + po4
HPO42-
Saliva and plaque
HA, FA form
calculus Re/demineralisation caries erosion
63

Definitions :
• Cariogenic foods : are those that contain fermentable substrates that can be
metabolized by oral bacteria to cause a decrease in plaque pH < 5.5 and
result in demineralization of tooth enamel and ultimately caries .
• The Cariogenic Potential – “ a foods ability to foster caries in humans under
conditions conducive to caries formation”.
65

Carbohydrate nomenclature :
Monosaccharides :
Glucose (dextrose )
Fructose( fruit sugar )
Galactose
Invert Sugar(1:1 glucose and fructose)
Disaccharides:
Sucrose (table sugar)
Maltose
Lactose (milk sugar)
Trehalose (mushroom sugar)
Natural and manufacured oligosaccharides.
Polysaccharides(>10 units)
Starch
Ref :D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285.
67

1D. Form of carbohydrate :
• Directly related to Adhesiveness ( sticky) of the foods .
• Form effects the length of time that teeth are exposed to sugar-containing
foods .
• And there is high retention for foods which are adhesive .
Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-Producing Potential. J
Dent Res Supplement to No. 6 , Vol 49 1970
2. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management .
Blackwell Munksgaard 2003.
69

• Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-Producing
Potential. J Dent Res Supplement to No. 6 , Vol 49 1970
70

1D. Form of carbohydrate :
• Further suggested that chemical composition of the food is
possibly more significant than physical parameters from the
standpoint of cariogenicity.
• Interplay of physical and chemical factors influences food
carcinogenicity.
• Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-
Producing Potential. J Dent Res Supplement to No. 6 , Vol 49 1970
71

Position of carbohydrate in a meal sequence. 72

1E. Position of carbohydrate in a meal sequence.
• Position of a food product with in a meal sequence or a snack can alter its
cariogenic properties.
• For e.g. both cheese and peanuts have shown to reduce the acid reduction after the
previous intake of sucrose – containing foods .
• Cheese – stimulates saliva , releases calcium , and tyramine increases salivation.
Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management .
2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994.
73

• Rugg-Gunn et al 1981 studied the position of sugar containing items in the
sequence of foods was investigated in a test breakfast consisting of three items
– soft – boiled egg, crisp bread and butter , and a cup of sugared coffee.
• If the sugared coffee was taken before or between the non – acidogenic or
slowly fermented items, the acidogenicity was reduced.
• However the greatest reduction in acidogenicity was obtained when the
sugared coffee was taken throughout the meal .
74

Combination of Carbohydrates.
75

1F.Combination of Carbohydrates.
• Starches can increase the cariogenic properties of sugar if they are
consumed at the same time.
• The stickiness of starch enhances the retention time of sugar as well as the
clearance rate , resulting in a prolonged pH fall.
Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its
Management . Blackwell Munksgaard 2003.
76

1Aa. Sugars :
Technically the term applies to two classifications of
carbohydrates.
1. Free form monosaccharides.
2. Disaccharides.
Ref :
1. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6th edition , 2004, Pearson
Prentice Hall.
2. D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285.
78

1Aa. Sugars : Sucrose arch criminal of dental caries - :
• Sole substrate in synthesis of extracellular (water-soluble and water-
insoluble) glucans mediated by microbial glycosyl transferases .
- glucans - major component of the structural intermicrobial matrix of
dental plaque.
- enhances ability of mutans streptococci to accumulate on smooth
surfaces of teeth.
Ref : 1.D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285
2. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6th edition , 2004,
Pearson Prentice Hall.
79

1Aa. Sugars : Sucrose arch criminal of dental
caries - :
• Review by Zero in 2004 showed that sucrose was more cariogenic
than other dietary sugars in rat caries model :
-strain of streptococcus mutans
-generally associated with smooth surface caries
Ref : 1.D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285
2. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6th edition , 2004, Pearson Prentice Hall.
80

Classic evidence from humans supporting the role of sugar in dental
caries :
D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285.
81

HUMAN CLINICAL STUDIES:
The Vipeholm studies:
• The Vipeholm study (Gustaffson et al 1954) is probably the biggest example study in the
field of dental caries ever undertaken.
• 436 inmates of vipeholm hospital – Sweden.
82

• Does increase in carbohydrate intake cause increase in dental caries..??
• If So..?? 1.)Is the caries activity influenced by
• Ingestion of non sticky sugars at meals
• Ingestion of sticky sugars at meals
• Ingestion of sticky sugars in between meals
2.) Does decrease in sugar intake reduce the incidence of caries.?
83
Purpose of the study

• There was one control group and six experimental groups.
• Dental examination system was developed.
• Five bite-wing films were taken annually, together with models and
photographs.
• Caries was diagnosed
84Method

Control group:
60 males - avg age group of 34.9 yrs
Low carbohydrate, high fat diet free from refined sugar
(For 2 years)
85
Caries activity – suppressed
After 2 years
Ordinary diet – 110 gms of sugar (at meal times) Small but significant rise in caries

8657 males – 300 gms of sugar solution at meals for 2 yrs and later reduced to 75 gms
SUCROSE GROUP:
No significant increase in caries
BREAD GROUP:
41 males and 42 females
Sweet bread with 50 gms of sugar once per day (2 yrs) no caries
4 portions of sweet bread during 4 meals Significant increase in caries

87CHOCOLATE GROUP:
47 males – 300 gms of sugar solution at meals (first 2 years)
Reduced to 110 gms supplemented with 65 gms of milk chocolate between meals (next 2 yrs)
Result: caries increment was low in first two years and increased in later 2 years.
CARAMEL GROUP:
First 2 years – control group of 62 males
Next 2 years – 22 caramels daily in 2 portions between meals.
Fifth year – withdrawal of caramel
Result: increase of caries incidence followed by fall

88
8 toffee group:
40 males
First year – low carbohydrate
Second year – 8 toffees daily (during meals)
marked rise in caries increment
24 toffee group:
48 males – 24 toffees in between meals for 3rd and 4th years
Withdrawal of toffees – 5th year
Result: greatest increase in caries during 3rd and 4th years followed by decline in 5th year

Conclusion of the study:
• Increase in sugar definitely increases caries activity
• Risk is greater if consumed in form that stays on tooth surface for longer time
• Increased risk if consumed between meals
• Upon withdrawal the risk gradually decreases
• Increase in clearance time of sugar increases caries activity
89

Studies on groups of people eating low amounts of sugar:
Hopewood house is a home in rural New South Wales, Australia housing about 80
children of low socio-economic back ground.
Dental examinations were conducted annually between 1947 and 1962 and thorough
dietary surveys were made (Sullivan and Harris 1963).
The dental surveys revealed a very low prevalence and severity of dental caries, much
lower than children of the same age and socio-economic back-ground attending state
schools in South Wales, who were examined using the same methods.
90
Hopewood house study

Spartan diet: strict natural diet with occasional egg serving
Entire vegetable and raw
Absence of meat and sugar were significant features of this study.
Meals: vitamin concentrates, nuts and honey(rarely)
End of 10 years: 13 yr old children had mean dmft of 1.6 per child
91

The Turku sugar studies:
The object was to study the effect on dental caries increment of
nearly total substitution of sucrose in a normal diet with either
fructose or xylitol.
• The 125 subjects were allocated to 3 groups-sucrose (S), fructose (F), and
Xylitol (X).
• The caries examination was conducted
• Two standardized bite-wing radiographs were taken
• Both precavitation and cavitation lesions were recorded, for both primary and
secondary caries.
92

Sugar and sugar containing foods were provided free during the two-
year study. All subjects were asked to avoid sweet fruits such as dried
figs, raisins, and dates, since the sugars in these foods could not be
substituted.
The increments in the F and S groups being approximately equal at the end
of the first year but during the second year the development of the S group
caries increment continued at the same rate while virtually no increase was
observed in the F group.
Little caries occurred in the X group and that which developed was
cancelled out by the healing of precavitation lesions by the 24th month,
resulting in a zero or near zero two-year increment.
93

While the X diet was clearly less cariogenic than the S or F diet, it cannot
be concluded that the F diet was less cariogenic than the S diet.
Results of serum analyses and liver-function tests indicated that Xylitol or
fructose did not alter metabolic parameters of liver function compared
with a normal sucrose diet.
94
RESULTS

1Ad. High – fructose corn syrup(HFCS) .
• Produced mainly for economic reasons for use in beverages.
• Chemically similar to invert sugar (50% fructose plus 50%
glucose.
• HFCS and invert sugar do not cause any production of
extracellular polysaccharides in the oral cavity.
• Cariogenecity of invert sugar 20-25% less than that of sucrose .
95

1Ae.Sugars in medicines.
• Medicines such as cough drops , throat lozenges , vitamin
preparations and antibiotic syrups.
• 70% sugar.
• Consumption of these several times a day , often before bedtime
results in a fall in pH of plaque.
97

1Ae.Sugars in medicines.
• They pose a threat to the dental health especially of children..
• Thus sugar formulations containing artificial sweeteners should be
encouraged - Sorbitol , hydrogenated glucose syrups ( lycasin ) and
saccharin used
98

1B.Total sugar consumption: 99

1B.Total sugar consumption:
• The relationship between total sugar consumed and dental caries is strong.
• A study done by Sreenby et al in 1982.
• Data on the prevalence of dental caries for 6- and 12-year-old children in,
respectively, 23 and 47 nations.
• For the 12 year-old-children there is a significant positive correlation between the
per capita availability of sugar and dental caries.
Ref: 1.Sreebny LM. Sugar availability, sugar consumption and dental caries. Community Dent Oral
Epidemiol. 1982 Feb;10(1):1-7.
100

• WHO suggested that the availability, and presumably the ingestion, of 50 g of
sugar per day may represent an outer limit of "safe" or "acceptable" sugar
consumption in regard to dental caries.
101

• The World Health Organization and Committee on Medical Aspects of Food
Policy (COMA).
• Recommended that free or non-milk extrinsic sugars intake should be below
10% of total energy intake.
• Strongly implicated sugars as the main causative factor in dental caries.
Ref: 1.Sheiham A. Why free sugars consumption should be below 15 kg per person per year in
industrialised countries: the dental evidence. Br Dent J. 1991 Jul 20;171(2):63-5.
102

• The dose-response curve for sugar and caries is approximately sigmoid (S-
shaped).
• At levels of sugar consumption below 10 kg/person/year the incidence of
caries is acceptably low. Beyond 15 kg the incidence increases more rapidly.
Ref: 1.Sheiham A. Why free sugars consumption should be below 15 kg per person per year in
industrialised countries: the dental evidence. Br Dent J. 1991 Jul 20;171(2):63-5.
103

1C.Intake pattern.
• Most studies point at frequency of eating as being of greater etiological
importance for caries than the total sugar consumption .
• Frequency refers to the number of times per day certain foods are eaten .
105

1C.Intake pattern.
• High intake frequency increases the overall length of time
that the teeth are exposed to sugar containing foods .
Primary evidence :
Vipeholm study - Gustafsson et al 1954
106

Influence of other foods on the relationship between sugar
and caries : 107

1G.Influence of other foods on the relationship between sugar and
caries :
1. Fluoride :
• During frequent administration , fluoride accumulates in dental plaque and has
shown to influence the sugar caries relationship, both as free ions in the plaque
fluid and in bound intracellular matrix .
• Total fluoride concentration 5-10 ng/mg on a wet weight basis.
108

1G.Influence of other foods on the relationship
between sugar and caries :Flouride
• Cutress et al conducted a study in 1995 – with sucrose, 5% and 10% , supplemented with
between 0 and 5 ppm fluoride (F).
• It was found that enamel demineralization was inversely related to the F concentration in
the range 2 to 5 ppm, for both 5% and 10% sucrose.
• Cutress et al also concluded that introduction of flouride has shifted the sugar/caries
sigmoid curve to the right , increasing the safe margin of sugar intake .
Ref:1. T.W. Cutress et al. Effects of fluoride-supplemented sucrose on experimental dental caries
and dental plaque ph. Adv Dent Res 9(1):14-20, February, 1995
109

Ref: D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285
110

1Ab. Starches.
• A review by Lingstrom et al suggested aspects of starchy
foods consumption, deserving greater attention:
- bioavailability of starches in processed foods.
- their retentive properties.
-also in relation to sugars present (starches as co-cariogens).
- their consumption frequency.
- the effect of hyposalivation on their cariogenicity.
- their impact on root caries.
Ref :Lingström P, van Houte J, Kashket SFood starches and dental caries. Crit Rev Oral Biol
Med. 2000;11(3):366-80
111

1B.Type : Other Minerals
• Selenium is associated with a higher prevalence of caries – excessive
selenium disrupts the formation of the enamel matrix and subsequent
mineralization of the tooth.
• Zinc – increases susceptibility to caries if present during tooth formation .
Ref: 1. w.h. bowen. food components and caries. adv dent res 8(2):215-220, july, 1994
2. carole a. Palmer, Diet and Nutrition in Oral Health.Julie Levin Alexander, 2003.
112

Other factors in diet :
• Last item taken in an episode of meal would have the greatest influence on
subsequent plaque Ph.
• If the meal also includes items which do not contain such carbohydrate, then the
sequence and timing of eating periods may influence plaque acidogenecity .
• If food item is a good sialogogue , the saliva stimulated by the subject eating such
an item will be available to neutralise plaque acid .
113

Critical pH-
114
• The critical pH is the pH at which environment of the enamel becomes unsaturated and
in addition that pH at which sufficiently high concentration of un ionized acid are present
to ensure the inward diffusion of enough acid to extend to inner lesion.
• On total depletion of these compounds, the pH can fall below the critical value of 5.5, at
which the aqueous phase becomes undersaturated with respect to hydroxyapatite.

115
• Critical pH values-
-Enamel - 5.2 - 5.5
- Dentin - 6.0
- Cementum - 6.7
-Fluorapetite -4.5

Types of predominant Microflora:
120
Oral streptococci
• Irrespective of the age of plaque and the diet, the predominant
organisms are gram - positive cocci of the genus streptococcus which form
about 50% of the total colony forming units.
• These streptococci have been divided into various groups based on their
colonial morphology and physiological characteristics.
• Oral streptococci have been isolated on mitis-salivaries agar a selective
medium that permits isolation from mixed flora.

Pathogenic properties of cariogenic bacteria
• Rapid transport of fermentable sugar and their conversion to
acids
• Production of Extracellular Polysachharides and
Intracellular Polysaccarides
• Ability to maintain sugar metabolism under extreme
environmental conditions
121

Criteria for Cariogenicity
• An organism must acidogenic
• An organism must be aciduric
• An organism must exhibit tropism for teeth
• An organism must utilize refined sugar (sucrose)
(Newburn, 1983)
122

The caries culprits
• The main microorganism involved in the initial caries process is S. mutans.
• S. sobrunis and lactobacillus are also involved, but must have s. mutans
present to colonize.
• Lactobacillus produces lactic acid at higher concentrations
123

The Mutans Streptococcus
Species Serotype Source
S. mutans c,e,f Human
S. sobrinus d,g,h Human
S. cricetus a Sometimes human, mostly rats and hamsters
S. rattus b Sometimes humans, mostly rats
S. downei h Macaque monkey
S. macacae c Macaque monkey
S. ferus c Rats
124

Microorganisms found in various types of carious
lesions
Pit and fissures s.mutans,
s.sanguis,lactobacillus
sp.actinomyces
Smooth surface caries s.mutans, s.salivarius
Root caries Actinomyces viscosus,
A.naeslundii, s.mutans,
s.sanguis,s.salivarius
Deep dentinal caries Lactobacillus sp,
Actinomyces viscosus,
A.naeslundii
125

Streptococcus mutans
In 1924 Clarke isolated a streptococcus that predominated in
many human carious lesions and he named streptococcus
mutans because of its varying morphology .
They are non motile , catalase-negative, gram –positive cocci
in short or medium chains .
 On mitis-salivarius agar they grow as highly convex to
pulvinate (cushion –shaped)colonies.
These colonies are opaque ;the surface resembles frosted glass.
126

 When cultured with sucrose they form insoluble Polysaccharides.
This property of forming insoluble extra cellular polysaccharides from
sucrose is regarded as an important characteristic contributing to the
caries –inducing properties of s.mutans.
Mutants of s.mutans ,which lack the ability to synthesize insoluble
glucans or to stick to glass surfaces, do not cause smooth surface caries.
127

Streptococcus mutans exhibits several important properties ;
1) synthesizes insoluble polysaccharides from sucrose
2) homo fermentative lactic acid former .
3) colonizes on tooth surfaces
4) more aciduric than other Streptococci
128

The Oral Steptococci and Disease
• S. mutans (dental caries)
• S. sanguis (gingivitis)
• viridans Streptococci
(bacteremia, endocarditis)
130

VIRULENCE FACTORS
Aciduric (Produces lactic Acid )
Acid tolerance
Produces insoluble glucans;
ECP:
 1. Glucans (dextrans) sticky insoluble ;
 2. Levans (fructans) energy
ICP: Energy sources inside Strep;
Accumulation of intracellular amylopectin-like
polysaccharides (carbon/energy reserve)
Adherence: S. mutans cells binds to salivary components
in the pellicles.
131

How does Strep mutans
attach to teeth and cause caries?
132

Attachment of S.mutans on teeth
Initial attachment of S. mutans to tooth pellicle (mediated by adhesin).
Sucrose is broken down into fructose and glucose by glucosyltransferases (GTFs).
Glucose is stored as a glucan polymer (dextran).
Fructose and glucose are both metabolized, resulting in lactic acid accumulation.
S. mutans accumulates as glucosyltansferases (GTFs) adhere to glucans produced by
other bacteria in plaque.
133

Streptococcus sobrinus
• S. sobrinus is thought to enhance caries initiation ,progression and
development.
• Prevalence is more closely associated with high caries activity than that of
S. mutans.
• It has a higher acidogenic capacity compared to S mutans.
• It is unable to synthesize IPS .
• Requires sucrose for attachment and growth in plaque.
134

Streptococcus sanguis.
135
• This is one of the predominant groups of streptococci colonizing on the
teeth. Formerly it was called streptococcus s. b. e because of its involvement in
sub acute bacterial endocarditis.
• Caries from this strain occurs primarily in sulci and is significantly less
extensive than S. mutans.
• On blood agar S. sanguis causes (green) hemolysis.

Streptococci Salivarius
136
• They have been found in the plaque, throat, nasopharynx and oral
mucosa, but their natural habitat in the dorsum of the tongue.
• In humans they have only a minor degree of cariogenic significance.

Lactobacilli are gram positive ,non spore –forming rods that generally grow
best under micro aerophilic conditions.
Isolation and enumeration of oral lactobacilli have been facilitated by use of
selective agar medium which suppresses the growth of other oral organisms by
its low pH (5.4) .
 Lactobacilli are found mostly as transients in the mouth of infants .
 Lactobacilli represents about 1% of the oral flora.
 L. casei and L fermentum are the most common oral species.
 The population of oral lactobacilli is influenced by dietary habits.
 A favorite habitat of lactobacilli is in the dentin of deep carious lesions.
ORAL LACTOBACILLI 137

 Lactobacilli, have been reported in the oral cavity ever since Miller enunciated the
chemo parasitic theory.
In 1925, Bunting and his collaborators claimed that bacillus Acidophilus was the
specific etiological factor responsible for the initiation of caries.
 Subsequent investigators have isolated other types of lactobacilli besides L.
acidophilus in saliva, plaque, and carious lesions.
LACTOBACILLI AND ITS ROLE IN CARIES.
139

Oral actinomyces
 Actinomyces is a gram positive ,nonmotile ,non-spore-forming
organisms occurring as rods and filaments that vary considering in length .
 Filaments are usually long and slender and are branching .
The species that have been found in the oral cavity are:
Facultative anaerobic anaerobic
A. naeslundii A .israelii
A. viscosus Actinomyces meyeri
A. odontolyticus
140

• All species of Actinomyces ferment glucose, producing mostly lactic acid ,lesser
amounts of acidic and succinic acid ,and traces of formic acid.
• Most interest has centered on A.viscosus and A naeslundii because of their ability to
induce root caries, fissure caries ,and periodontal destruction when inoculated into
gnotobiotic rats.
142

Actinomyes is a good plaque former ,capable of adhering to wires and forming
tenacious deposits on the teeth.
 It is the most common group of microorganisms isolated from the subgingival
microflora and from plaque of human root surfaces caries.
 It is found in the supragingival plaque of all children and comprises about 50 % of all
cells present.
 A naeslundii predominates in the tongue ,salivary flora ,and in the plaque of young
children ,while plaque from teenagers and adults has a higher proportions of A
viscosus.
143

End of part-1 .
Thank you.
144

Genetics and dental caries…
• J Evid Based Dent Pract. 2003 Dec; 3(4): 185–189.
• Evidence of a contribution of genetic factors to dental caries risk
• Walter A. Bretz, Patricia Corby, Nicholas Schork, and Thomas C. Hart
147
Subjects:
The literature was searched for evidence of a contribution of genetic factors
to increased or decreased risk for dental caries. A search for global evidence of
caries heritability was carried out using twin studies. Next, separate searches
were carried out for evidence of heritability for 3 potential mechanisms
associated with caries risk that included variation in the quality of the dental
hard tissues, variation in host immune response, and variation in sugar
metabolism

CONCLUSIONS
• Twin studies provide the opportunity to dissect the relative contribution of genetics
and environment on dental caries variation.
• Accordingly, these studies can often suggest, but not prove, biological inheritance.
Current evidence supports the notion that there is an inherited variation in enamel
development that is associated with increased occurrence of dental caries.
• At present, these results are limited to specific populations with overt recognizable
syndromes.
• Evidence is presented that immune complex genes may modulate the presence of
enamel defects and colonization of cariogenic bacteria
148

ANALYSIS
• Twin studies of dental caries have shown that genetic and environmental
factors play significant roles.
• However, estimates of heritability from the reports reviewed display
considerable variability, no doubt, caused by differences in statistical analysis
models, age, gender, sample size, origin of cohorts and measurement of dental
caries phenotype.
• In addition, cohort and case-control studies linking a particular gene to dental
caries are too few and these studies often neglect the role of environmental
factors on dental caries development that could interact with genetic factors to
induce disease
149

Dental caries – part 2
•Contents
• Classification
• Histopathology
150

151
Rate of
progression
Extent
Location
CLASSIFICATION:

According to location:
• Primary caries
• Caries of pit and fissure origin
• Caries of enamel smooth surface origin
• Backward caries
• Forward caries
• Residual caries
• Root surface caries
• Secondary (recurrent) caries
152

153
According to extent:
• a. Incipient (reversible) caries
• b. Cavitated (irreversible) caries

154
According to hard tissue affected:
• a. Enamel
• b. Dentin
• c. Cementum
Others:
• Primary caries & secondary caries
• Nursing caries
• Radiation caries
• Rampant caries

155
ACCORDING TO LOCATION:
Primary caries:
• Primary caries is the original carious lesion of the tooth.
• Accordingly 3 morphologic types of primary caries are evident in clinical
observations.
• Type I – pit & fissure and occlusal surfaces.
• Type II – Smooth surfaces of which there are 2 variants interproximal
and cervical / gingival.
• Root surface caries.

156
• These caries can form in the regions of pits and fissures
• Usually resulting from imperfect coalescence of the developmental enamel
lobes.
• Such caries are not so clinically noticeable until the forces of mastication
fracture the increasing amount of unsupported enamel.
Type I / Pit and fissure caries:

157
• Limited to the – Occlusal surfaces of molars and premolars
- Buccal pits of molars
- Lingual surfaces of maxillary anterior teeth
• Poor self cleansing features
• Usually occurs before smooth surface caries
• Clinically - Black or brown in color
- Slightly soft consistency
- “Catch” the tip of a fine explorer

Caries of enamel smooth surface origin:
158
• Smooth surface caries does not begin as an enamel defect, but rather in a
smooth area of the enamel surface that is habitually unclean and is thereby
continually or usually covered by plaque.

160
Forward caries:
• Forward caries is wherever the caries cone in enamel is
larger or atleast the same size as in dentine.

Backward caries:
161
• When the spread of caries along the DEJ exceeds the caries in
the contiguous enamel, caries extends into this enamel from the
junction and is termed as backward caries.

Recurrent caries (secondary caries):
162
• It occurs at the junction of a restoration and the tooth and may progress,
under the restoration. It is termed as recurrent caries.
• This condition usually indicates that microleakage is present-
-due to poor cavity preparation,
-faulty restoration or a combination of these factors.

Root surface caries:
163
• These kind of caries originate in the dentinal root portion
of a tooth.
• It is predominantly found in the dentitions of older age
groups with significant gingival recession and exposed
root surfaces.
• It initiates on the surface of mineralized dentin and
cementum which have greater organic content.
• For this reason, bacterial flora causing root caries is also
different from flora causing smooth surface caries.

Linear enamel caries :
164
• This is an atypical form of dental caries called linear enamel caries.
• The lesions predominate on the labial surfaces of the anterior maxillary
teeth on the region of the neonatal line.
• Lesion is crescent shape
• Increase caries susceptibility of posterior teeth.
• Recent evidence suggests that neonatal line forms due to transient
hypocalcemia, a normal feature of the neonatal period

Odontoclasia:
165
• Variant of linear enamel caries
• Results in gross destruction of the labial surfaces of incisor teeth
• Cause may be an inherent structural defect

Early childhood caries
• “A suddenly appearing, widespread, rapid burrowing type of caries,
resulting in early involvement of the pulp and affecting those teeth usually
regarded as immune to ordinary decay.”
-Massler
• A complex disease involving maxillary primary incisors within a month
after eruption and spread rapidly to involve other primary teeth.
-Davies (1988)
167

CLASSIFICATION
TYPE 1
ECC
(mild to
moderat
e)
• Carious lesions involving the molars and incisors
• Seen in 2-5 years of age
• Cause is usually a combination of cariogenic semisolid
or solid food and lack of oral hygiene
• Number of affected teeth usually increases as the
cariogenic challenge persists
TYPE 2
ECC
(modera
te to
severe)
• Labiolingual carious lesion affecting the maxillary incisors
with or without molar caries
• Seen soon after 1st tooth erupt
• Cause is inappropriate use of feeding bottle, at-will
breast feeding or combination, poor oral hygiene
TYPE 3
ECC
(severe)
• Carious lesion involve all the teeth, including mandibular
incisors.
• Usually seen in 3-5 years of age
• Cause is combination of factors and poor oral hygiene
• Rampant in nature and involves immune tooth surfaces.
168

NURSING CARIES
• A unique pattern of dental decay in young
children due to prolonged and improper
nursing/feeding habit.
-Winter et al, 1966
169

Etiological
agents in
nursing bottle
caries
Pathogenic
microorganisms
Substrate
(fermentable
carbohydrates)
Host Time
Other
predisposing
factors
170

CLINICAL FEATURES
Mandibular molars: at later stage
Maxillary canines & 2nd molars: facial, lingual, proximal surfaces
Maxillary 1st molars: facial, lingual, occlusal, proximal surfaces
Maxillary lateral incisors: facial, lingual, mesial, distal surfaces
Maxillary central incisors: facial, lingual, mesial, distal surfaces
171

• Mandibular anterior teeth are usually spared because of:
I. Protection by tongue
II. Cleansing action of saliva due to presence of the orifice of the
duct of sublingual glands very close to lower incisors.
172

PROGRESSION OF THE LESION
Initially, a
demineralization dull,
white area is seen
along the gum line on
labial aspect of
maxillary incisors.
These white lesions
become cavities
which involve the
neck of the tooth in
a ring like fashion
Finally, the whole
crown of the incisors
is destroyed leaving
behind brown-black
root stumps.
173

NURSING CARIES
Specific form of rampant caries.
Age of occurrence
In infants & toddlers
Dentition involved
Affects the primary dentition
Characteristic feature
Specific pattern is seen
Mandibular molars are not involved
RAMPANT CARIES
Acute, widespread caries with early pulpal
involvement of teeth which are usually
immune to decay.
Age of occurrence
Seen at all ages
Dentition involved
Both primary & permanent dentition
Characteristic feature
Surfaces considered immune to decay are
involved. Thus, mandibular incisors are
affected
174

Etiology
Bottle feeding before sleep
Pacifiers dipped in honey
Prolonged at-will beast-feeding
Treatment
In early stage- topical fluoride application &
education
Directed toward maintenance of the teeth till
the transition occurs
Prevention
Education of the parents
Etiology
More multifactorial with all the essential factors
involved are not just feeding practices
Frequent snacks, excessive sticky refined
carbohydrates
Decreased salivary flow
Genetic background
Treatment
Require pulp therapy
Long term treatment
Prevention
Dental Health Education at a mass level involving
people of all ages
NURSING CARIES RAMPANT CARIES
175

176
Complication of radiation therapy of
oral cancer lesion
Radiation induced xerostomia
produces caries conducive environment
Carious lesion develops as early as 3 months after onset of xerostomia
May be caused by other factors like salivary gland tumors, autoimmune diseases,
prolong illness
Radiation caries:

Adolescent caries: 177
• Acute caries attack at 11-18 years of age
• Lesion in teeth and surfaces that are relatively immune to caries
• Small opening in enamel with extensive undermining
• Rapid clinical course
• Little or no secondary dentin formation

Arrested caries:
178
• Caries which becomes static or stationary and does not show any tendency
for progression
• Both dentitions are affected
• Lesion appears as large open cavity with lack of food retention
• Superficially softened and decalcified dentin gets burnished and has
brown stained polished appearance - “Eburnation of dentin

179
Senile Caries
• Caries activity that spurts up during the old age.
• They are located exclusively on the root surfaces of the teeth.
• Also seen in association with partial denture clasps.
• Causes: gingival recession, decreased salivary secretion, poor oral hygiene.

Occult Caries / Hidden Caries
180
• Not clinically diagnosed, but detected only on radiograph.
• Seen in persons with low caries index suggestive of increased fluoride
exposure.
• Also called as fluoride bombs or fluoride syndrome

182
G.V.Black’s Classification
Class-I: - Caries on the occlusal surfaces of molars and premolars
- Occlusal 2/3 of the buccal and lingual surfaces of molars
- Lingual surfaces of the anterior teeth
Class-II: - lesions found on the proximal surfaces of molars and premolars
Class-III: - lesions found on the proximal surfaces of anterior teeth, but do
not involve the incisal angle

183
• Class-IV: - lesions found on the proximal surfaces of anterior teeth and
involving incisal angle
• Class-V: - lesions found on the gingival third of the facial and lingual
surfaces of anterior and posterior teeth.
• Class-VI: - were not included in Black’s classification
- Proposed by Siomon
- Lesions on the incisal edge and cusp tips of the teeth

Root caries (New in ICDAS II)
• E = Excluded root surfaces (no gingival recession)
• 0 = Sound (no caries or restoration)
• 1 = Non-cavitated carious root surface— soft or leathery
• 2 = Non-cavitated carious root surface— hard and glossy
• 3 = Cavitated (greater than 0.5mm in depth) carious root surface— soft or leathery
• 4 = Cavitated (greater than 0.5mm in depth) carious root surface—hard and gloss
• 6 = Extensive cavity: an extensive cavity involves at least half of a tooth surface
and possibly reaching the pulp.
• 7 = Filled root with no caries
186

• 9 = Used for the following conditions
• 97 = Tooth extracted because of caries (tooth surfaces will be coded 97)
• 98 = Tooth extracted for reasons other than caries (all tooth surfaces coded
98)
• 99 = Unerupted (tooth surfaces coded 99)
187

• The shared vision for the International Caries Detection and
Assessment System is now that:
• it employs an evidence-based and preventively oriented approach,
• is a detection and assessment system classifying stages of the caries
process,
• is for use in dental education, clinical practice, research and public
health,
• provides all stakeholders with a common caries language,
• has evolved to comprise a number of approved, compatible ‘formats’,
• supports decision-making at both individual and public health levels and
• has generated the International Caries Classification and Management
System, to enable improved long-term caries outcomes.
188

•Knowledge
•Of macroscopic features:
detection & diagnosis of caries
•Of shape of lesion: cavity
preparation
•Characteristics:
•Chronic disease
•Not self-limiting
Cavity formation
subclinical
Total destruction
Light microscopy
Enamel lesion
Mineral loss
(signs, symptoms)
visible
Time
Electron microscopy
198

Dental Caries
Enamel Caries Dentin Caries Cementum Caries
(Root caries)
Smooth surface caries Pit and fissure caries
199

Speed of lesion formation
• Incipient caries to clinical caries: 18 ± 6 months
• Peak rate for incidence of caries: 2-4 yrs (avg 3yrs) after eruption
• Poor oral hygiene, excess sucrose: 3 weeks
• Radiation induced Xerostomia: 3 months
• Occlusal caries require less time than smooth surface
200

Estimating mineral loss
• Clinical considerations
• Refractive indices of Hydroxyapatite, water and air
• Histological considerations
• Microradiography
• Polarized light microscopy
202

ENAMEL CARIES
MACROSCOPIC FEATURES:
White spot lesion
Opaque, chalky white
Surface features-SEM (Thylstrup, 1994) :
• Deepened & irregular Tomes
processes pits
• Irregular cracks & fissures
• Widened intercrystalline spaces
• Fractures of perikymata edges
• Microcavities 203

•Brown spot lesion
•Sites
•Occlusal surfaces:
•Fissure morphology (Newbrun, 1989)
•Starts at both sides of fissure wall
204

• MICROSCOPIC FEATURES:
• Triangular/wedge in shape
• Divided into 4 zones
• Can be viewed in
• Plain transmitted light
• Polarized light-clearer picture
205

Histological features of early enamel caries 206
o Loss of inter-rod substance
o prominent enamel-rods
o Appearance of transverse striations of
enamel rods due to segmental
demineralization
o Accentuation of incremental striae of
Retzius

H/F of Advanced enamel caries
207
• Classified on the basis of pore volume and
mounting media used
 Zone 1 – Translucent zone
 Zone 2 – Dark zone
 Zone 3 – Body of lesion
 Zone 4 – Surface zone
• These zones are from the dentin towards the
outer enamel surface

•ZONE 1:TRANSLUSCENT ZONE
•At the advancing front- 5 -100 µm
•Seen with quinoline
•Pore volume: 1%
•Not always present, sometimes near lateral part
208

•ZONE 2: THE DARK ZONE
•More constant feature-90-95% lesions
•Pore volume -2-4%
•Why is it called dark zone?
•2 theories for small pores
209

•ZONE 3: THE BODY OF THE LESION
•Largest zone
•Pore vol: 5% at periphery, 25% in centre
•Appears translucent in quinoline and dark with water
•Striae of retzius well marked
•old./chronic lesions: bands of well mineralized tissue
•Bacteria in between prisms (rods)
210

•ZONE 4: THE SURFACE ZONE
•20-50 µm
•Pore vol: 1%
•Negatively birefringence in water
•Importance: serves as barrier to bacterial
invasion
211

Smooth surface caries
• The earliest manifestation of incipient enamel
caries is the appearance of an area of
decalcification , beneath the dental plaque, which
resembles a smooth chalky white area.
• There is loss of interprismatic substance, with
increased prominence and roughening of the ends
of the enamel rods.
White spot lesion
212

• Accentuation of incremental striae of Retzius.
• As deeper layers of enamel are involved it forms
a cone shaped lesion with the apex toward the
DEJ and the base toward the surface of the
tooth.
• Eventual loss of continuity of enamel surface –
feels rough to explorer tip.
214

Pit and fissure caries
• Fissures are diverse in shape and size
• Carious lesion starts at both side of fissure rather
than at the base, penetrating nearly perpendicular to
the DEJ.
• Lesion is cone-shaped with base towards dentine
and apex towards enamel surface
215

Progression of enamel lesion
•Caries dissolution along the rods
•Highest degree of tissue porosity is along “Central
Traverse”
•Oldest part-along CT, lesion spreads laterally along the
surface
217

•Central defects of crystals-hollow hexagons
•As dissolution increases, disorganization of crystal
arrangement, invasion of bacteria
218

Ultrastructural changes in enamel caries
•Destruction of crystals at borders & within the prism
•Arcade like defects bounded by rows of resistant crystals- “caries crystals”
•More dissolution in heads and less in tails
219

Remineralization/arrest
•Enamel most susceptible to caries during & after eruption
•1st molar:12-14 months
•2nd molar:14-18 months
•Premolars:1-2 months-less prone
{Backer-Dirks (1966)}
220

•Mechanism of arrest of non-cavitated lesions:
•Maintains original crystalline framework
•Etched crystallites serve as nucleating agents
•Wear & polishing of the partly dissolved external surface-regain of surface hardness
•Remineralized area: brown or black spots
•Mechanism
•Cavitated lesions can also be arrested with proper plaque control (thylstrup)
•New mechanism of remineralization: CPP-ACP
221

Clinical significance of enamel
caries 222

CARIES OF DENTIN
Begins with the natural spread of the process along the DEJ and rapid
involvement of the dentinal tubules. The dentinal tubules act as tracts leading to
the pulp (path for micro-organisms).
Caries advances more rapidly as dentin provides much less resistance to acid attack .
Early Dentinal Changes:
-initial penetration of the dentin by caries dentinal sclerosis,
-calcification of dentinal tubules and sealing off from further penetration by
micro-organisms,
-more prominent in slow chronic caries.
Dentinal
sclerosis
223

DENTINAL CARIES
•Progression of enamel caries to dentin:
5.4% from 11 – 22 yrs (Mejare et al,
1999)
•MACROSCOPIC CHANGES:
•Lateral spread along DEJ
•Cone shaped-apex towards the pulp
•Affected dentin-Brown or black in
colour
224

•MICROSCOPIC CHANGES: (mechanism)
•Caries advancement proceeds through 3 stages
•Acids demineralize the dentin
•Organic matter degenerates
•Loss of structural integrity & bacterial invasion
•1st mild stimuli –defense reaction of dentin-tubular sclerosis/TRANSPARENT ZONE
•Dentin demineralization-when lesion reaches DEJ
•Arrest of caries
•Cavitation of dentin-bacterial invasion
225

226
Zone of
Decomposed
dentin
Zone of
Bacterial
invasion
Zone of
Demineralisation
Zone of
Dentinal
sclerosis
Zone of
Fatty
degener
ation
Retreating
Odontoblastic
process
INFECTED DENTIN AFFECTED DENTIN
Dentinal
caries

• Behind the transparent sclerotic zone, decalcification of dentin
appears.
• In the earliest stages, when only few tubules are involved,
microorganisms may be found penetrating the tubules Pioneer
Bacteria.
227

• This initial decalcification involves
the walls allowing them to distend as
the tubules are packed with
microorganisms.
• Each tubule is seen to be packed
with pure forms of bacteria, eg., one
tubule packed with coccal forms the
other tubule with bacilli.
228

• As the microorganisms proceed further they are distanced from the
carbohydrates substrate that was needed for the initiation of the caries.
• Thus the high protein content of dentin must favour the growth of the
microorganisms.
• Therefore proteolytic organisms might appear to predominate in the deeper
caries of dentin while acidophilic forms are more prominent in early caries.
229

Advanced Dentinal Changes ;
-decalcification of walls, confluence of the dentinal tubules,
tiny “liquefaction foci”, described by Miller are formed by the focal
coalescing and breakdown of dentinal tubules.
These are ovoid areas of destruction parallel to the course of the
tubules which filled with necrotic debris and increase in size by
expanding. The adjacent tubules are distorted and their course is bent
due to this expansion.
230

• The destruction of dentin by decalcification and then proteolysis
occurs in numerous focal areas- leading to a necrotic mass of
dentin of a leathery consistency.
• Clefts present in the carious dentin that extends at right angles to
the dentinal tubules, accounts for the peeling off of dentin in
layers while excavating.
231

Shape of the lesion is triangular with the apex towards the pulp and the base towards the enamel.
Zone 1; Zone of Fatty Degeneration of Tome’s Fibers,(next to pulp)
-due to degeneration of the odontoblastic process. This occurs before sclerotic dentin is formed
and makes the tubules impermeable.
Zone 2; Zone of dentinal sclerosis,
-deposition of Ca salts in the tubules.
Zone 3; Zone of decalcification of dentin
Zone 4; Zone of bacterial invasion
Zone 5; Zone of decomposed dentin due to acids and enzymes.
232

ZONE OF FATTY DEGENERATION:
•Of the Tomes fibres-stained by Sudan red
•Importance:
•Fat contributes to impermeability of dentinal tubules
•Maybe a predisposing factor favouring sclerosis
• Innermost layer of dentinal caries towards pulp
• Due to deposition of fatty tissue in odontoblastic processes
• Seen usually in rapidly progressing caries
• No crystals or bacteria in lumen of tubules
• Intertubular dentin  normal
233

•ZONE OF TUBULAR SCLEROSIS:
•Reaction of vital dentinal tubules & pulp
•Seals off tubules to further penetration by bacteria
•Mineralization process-2 types
•Hydroxyapatite crystals & large rhomboidal crystals (whitlockite)
•Transluscent appearance-transluscent/transparent dentin
• As the microorganisms cause destruction to dentin, initially there is an
attempt to stop the advancement of caries by depositing the minerals.
• There is a deposition of mineral in intertubular dentin.
• Zone is called “transparent zone”
• Odontoblasts also start depositing dentin.
• At the periphery of sclerotic dentin, dead tracts are present.
234

ZONE OF BACTERIAL INVASION
•Initially tubules with single type of bacteria
•Liquefaction foci-beadings, varicosities, moth-eaten,
rosaries
• Decalcification is by bacterial acid diffusion
• Very narrow zone, softer than normal dentin
• Further loss of minerals from inter tubular dentin
• Large crystals within lumen of dentinal tubules
235

•ZONE OF DEMINERALIZATION
•Narrow zone
•Occlusion of tubules Softer than normal dentin
•Few microorganisms in the tubules – “pioneer bacteria”
236

237
Zone of Decomposed Dentin / Infected Dentin
• Outermost zone, large scale destruction of dentin
• Foci of Miller join together
• Areas of dentin decomposition, occur perpendicular to dentinal tubules 
“Transverse Clefts”
• Mechanism of formation of Clefts - not known
• May follow course of incremental lines or
• May result from coalescence of liquefaction of adjacent tubules
• Also may rise by extensive proteolytic activity along interconnecting
lateral branches of odontoblastic processes
• Bacteria shift from dentinal tubules to the peri & inter tubular dentin

Zone of Decalcification with Bacterial Invasion / Turbid Dentin
• Initially only few tubules are involved & micro-orgs also less
• These are acidogenic, pioneer bacteria (initiators), present long before lesion is clinically
detected
• Bacteria multiply within tubules & are seen in advancing front of lesion
• Walls of tubules are thin & when micro-orgs penetrate, they cause
irregularities/distensions of walls  ROSARY BEAD appearance
• Later, bacteria have proteolytic activity, areas of proteolysis appear as spaces containing
necrotic material & bacteria
• These areas  “Liquefaction Foci of Miller”.
• These areas vary in number & are parallel to dentinal tubules
238

Other features
•In slowly advancing lesions
•Sclerotic dentin-very hard, shiny
•Hypermineralized –radioopaque
•In moderately advancing lesions
•Dead tracts
•Reparative/reactionary dentin
•Pulp stones
•In rapidly advancing lesions
•Abscess, necrosis of pulp
240

Zones of dentin (sturdevant)
•ZONES OF DENTIN:
•Zone 1: normal dentin
•Zone 2: subtransparent dentin
•Zone 3: transparent dentin
•Zone 4: turbid dentin
•Zone 5: infected dentin
•AFFECTED DENTIN
•INFECTED DENTIN
•Caries detector – basic fuschin/ 1% acid red (Fusayama, 1979)
241

Secondary / Reactionary dentin
242
• Protective mechanism to protect pulp
• Develops as a result of localized, non-specific irritation to
odontoblasts
• Hyper mineralized,less number of dentinal tubules having irregular &
torturous course

ROOT CARIES
•Occurs in older individuals where
root/cementum is exposed
•Microorganisms penetrate along the clefts,
sharpey’s fibres
•Delamination occurs along incremental
lines
•Brush like appearance
•Radioopaque surface layer seen
•Dentinal tubular reactions
243

Root Caries
Root caries as defined by HAZEN, is a soft, progressive lesion that is found
anywhere on the root surface that has lost its connective tissue attachment and
is exposed to the environment.
-the root surface must be exposed to the oral environment before caries can
develop here.
-Plaque and micro-organisms are essential for the cause and progression of the
lesion, mostly Actinomyces,
-micro-organisms invade the cementum either along the Sharpey’s fibers or
between the bundles of fibers.
244

245• -spread laterally, since cementum is formed in concentric
layers.
• -after decalcification of cementum, destruction of matrix
occurs similar to dentin with ultimate softening and
destruction of this tissue.
• -invasion of micro-organisms into the dentinal tunbules,
finally leading to pulp involvement.
• -the rate is slower due to fewer dentinal tubules than crown
area

246
Histopathology:
• Outer surface of cementum – hyper mineralized, thus more caries resistant
• Resistance due to
• Reprecipitation of minerals from within
• Precipitation of minerals from Plaque
• Clefts formed, through which bacteria penetrate & cause tooth structure
destruction
• Penetration occurs along course of Sharpey's fibers
• Once cementum completely exposed & destroyed, underlying dentin is
involved

1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been stopped.
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.
247

Conclusion :
• Dental caries should be considered as a consequence of ecologically driven
imbalances of oral microbial biofilms.
• An appreciation of ecological principles will enable a more holistic
approach to be taken in caries control.
• A better understanding of the process of biofilm formation ,its genetic
regulation is necessary to the development of novel strategies for oral
disease prevention and control.
248

Conclusion :
• Among the multifactorial etiology of dental caries diet plays an important
role in the occurrence of dental caries. This seminar intended to provide an
overview of the evidence for an association between diet and dental caries
which has already been established and documented by a series of studies.
• But the information available regarding the association of diet and dental
caries under the Indian context and the effect of rapid changes in urbanization
and economic development on the Indian diet is sparse and needs further
research.
249

Conclusion :
The way ahead should be considered under 2 aspects:
1. The extrapolation of the data to the India diet and conditions.
2. The task of diet changes which requires lifestyle changes that would
be challenging to bring about and thus should be an important focus area
for dental public health programs/ approaches in any setting for different
age groups and populations.
250

References :
• Cariology – Newbrun.
• Murray J.J. et al. The prevention of oral disease. 4th Ed.
• Shafer. A textbook of Oral Pathology. 4th Ed.
• S.S.Hiremath.Textbook of Preventive & Community Dentistry.
• Per Axelsson . Diagnosis and Risk Prediction of Dental Caries. 2000,
Quintessence Publishing Co.
• Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its
Management . Blackwell Munksgaard 2003.
251

References :
• T.W. Cutress et al. Effects of fluoride-supplemented sucrose on
experimental dental caries and dental plaque ph. Adv Dent Res 9(1):14-20,
February, 1995.
• Lingström P, van Houte J, Kashket SFood starches and dental caries. Crit
Rev Oral Biol Med. 2000;11(3):366-80 .
• Brian A. et al . Sugar Consumption and Caries Risk:A Systematic Review.
Journal of Dental Education . October 2001. Volume 65, No.10
252

References :
• Gordon Nikiforuk. Understanding Dental Caries.Karger Publishers.
• D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285 .
• Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6th
edition , 2004, Pearson Prentice Hall..
• Carole A. Palmer, Diet and Nutrition in Oral Health.Julie Levin Alexander,
2003.
253

References :
• Marsh P. Dental plaque as a biofilm and a microbial community-
implications for health and disease. BMC Oral Health 2006,6:S14.
• Thomas H.J et al .Managing the complexity of a dynamic biofilm. JADA,
2006;Vol.137;10s-15s.
• Scheie A.A &Peterson F.C.The Biofilm concept:consequences for future
prophylaxis of oral diseases? Crit Rev Oral Biol Med 15(1):4-12 (2004)
254

Questions asked in NTRUHS examination :
• Balanced diet in prevention of dental caries – 20 M – APR 2015
• Early childhood caries – 7 M – 2011
• Diet counselling – 2011 and 2013 for 7M and 20M
• Cariogenecity – 2003
• Rampant caries – 2003
• Bacteriological role in caries – 2002
• Diet for healthy teeth – 2001
• Genetics and dental caries- 2001.
255

• Newbrun stated that “ the dentist of future will still have to treat
caries, but unquestionably the emphasis will be on early diagnosis and
preventive intervention.”
• Times change and we change with time”.
Thank you
256

Dental caries

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