4. “For there never yet philosopher
that could endure the
toothache patiently”
4
5. INTRODUCTION
• TEETH ARE TOOLS that have evolved to ensure survival
of species.
• Caries is a biosocial disease rooted in the technology
and economy of our society.
• Dental caries is unique not only in terms of
pathological mechanism ; other aspects, social and
economic , are also worthy of note.
• While it is true that diseases of the teeth and their
supporting tissues do not normally kill humans they
certainly affect the persons efficiency and they can , if
neglected, provoke serious conditions elsewhere in the
body. Their contribution to the general fund of human
misery is legendary.
5
6. DEFINITION
• Localized post eruptive, pathological process of external
origin involving softening of the hard tissue and
proceeding to the formation of a cavity (WHO) .
• Is an infectious microbiological disease of teeth that
results in localized dissolution and destruction of calcified
tissues (STRUDEVANT) .
• Microbial disease of the calcified tissues of the teeth
characterized by demineralization of the inorganic portion
and destruction of organic substance of the teeth
(SHAFER) .
• It is fundamentally a microbiological disease which affects
the calcified tissues of the teeth, beginning first with
localized dissolution of the inorganic structures by acids of
bacterial origin leading to disintegration of organic matrix
(ERNEST NEWBURN) .
6
7. HISTORY
5000 B.C LEGEND OF WORM: Ancient sumerian text- clay tablet
found in euphrates valley in lower meepotomian areas.
2700 B.C Chinese used acupuncture as a treatment for various diseases
including dental diseases.
1819 L.S.PARMLEY- caries began on the enamel surface and
speculated that a chemical agent was involved.
1867 Leber and Rotenstein ─ reported microorganisms and activity
of acid producing bacteria
1871,1873,
1878
Clark,Tomes,Magiot-Bacteria was essential for caries.
1881 Underwood and Milles ─ caries was due to bacteria, affecting
organic and inorganic elements
1882 W.D.Miller ─ Acidogenic theory
1899 G.V Black ─ described dental plaque as “gelatinous plaque”
7
8. 1915 Baumgarner ─ acids produced by bacteria were capable of
destroying the inorganic portion
1915 Glies & klinger- found high no. of microorganisms in persons
with caries.
1924 Clarke ─ isolated streptococcus mutants from carious lesions
1927 Jay and Voorhees ─ found the presence of L.acidopilus was
potent for development of caries
1944,1946 Gottleib & Gottleib, Diamond& Applebaum ─ caries is
essentially a proteolytic process
1951 Manley and Hardwick ─ pointed out that acidogenic and
proteolytic theories need not be separate
1952 Finn ─ stated that lower 1st molar was most frequently affected
8
9. EPIDEMOLOGY:
• Decline in caries prevalence in developed countries.
• Increasing prevalence of caries in less developed
countries.
• Most common epidemiologic measure of caries is
evaluation of measure of permanent teeth that are
diseased, missing or filled (DMF).
Geographical differences:
• More remote areas of world with less access to refined
foods shows decreased incidence of caries.
• Caries often rightly called Disease of the civilization 9
10. Family differences:
• More caries rate seen in siblings of individuals with high
caries rates & less incidence seen in siblings of caries
immune individuals.
• Children of high caries incident parents shows higher caries
incidence.
• Attributed mainly to genetic factors such as tooth
morphology, salivary flow rate and also to dietary habits
and oral hygiene habits of the family.
Race:
• Blacks , chainese & east indians have considerably less
caries than american whites.
• The english are known to have appalingly poor teeth & a
higher caries incidence compared to italians & russians.
10
11. Gender:
• Girls show high caries incidence than boys of same age
till early teens.
• Attributed to earlier eruption of teeth in girls because
of early growth spurt.
• Significant as teeth are maximally susceptible to caries
immediately after eruption.
AGE:
• Even at age six around 20% of the children have caries
incidence in their permanent dentition.
• Most frequently involved is the first permanent molar
(six yr molar)
11
12. Socioeconomic & behavioral factors
• Socioeconomic factors are the major
determinants of oral health of both children and
adults worldwide
• It determines the following factors
1)Social class
2)Income
3)Education
4)Knowledge
5)Attitude
6)Behavior
12
13. CARIES SUSEPTIBILITY IN PERMANENT
DENTITION:
Sites ranked in decreasing order of occurrence
1)Fissure of the molars
2)Mesial & distal surface of first molars.
3)Mesial surface of second molars & distal
surface of second premolars.
4)Mesial & distal surface of maxillary first
premolars
5)Distal surface of canines & Mesial surface of
mandibular first premolars
6)Approximal surface of maxillary incisors. 13
14. Etiology of dental caries:
THEORIES OF DENTAL CARIES
• Worm theory
• Humor theory
• Vital theory
• Chemical theory
• Parasitic / Septic theory
• Acidogenic theory
• Proteolytic theory
• Proteolytic chelation theory
• Sucrose chelation theory
• Autoimmune theory
14
15. Worm theory:
• According to an ancient Sumerian text,
toothache was caused by a worm that drank
the blood of the teeth and fed on the roots of
the jaws.
• This legend of the worm was discovered on
one of many clay tablets excavated near
Euphrates Valley of the lower Mesopotamian
area and estimated to date from about 5000
BC."
• Guy de Cahuliac (1300-1368), the greatest
surgeon of' the Middle Ages, believed that
worms caused dental decay. As a cure he
advocated fumigation with seeds of leek, onion,
and hyoscyamine -used as a hypnotic, sedative,
and smooth muscle relaxant.
• Antony van Leeuwenhoek (1700), the father of
modern microscopy, wrote a letter to the Royal
Society of London describing little worms
"taken out of a corrupt tooth" and said that
they caused the pain in toothache.
15
16. Humor theory
• The ancient Greeks considered that a person's physical and
mental constitution was determined by the relative
proportions of the 4 elemental fluids of the body- blood,
phlegm, black bile, and yellow bile which correspond to the
4 humors-sanguine, phlegmatic, melancholic, and choleric.
All diseases, including caries, could be explained by an
imbalance of' these humors.
• Hippocrates, suggested that both local and systemic
factors were related to the cause of caries.
• Aristotle, noticed that soft, sweet figs adhered to the teeth,
putrified. and produced damage.
16
17. Vital theory
• This theory regarded dental caries as originating within
the tooth itself, analogous to bone gangrene.
• This theory ,proposed at the end of 18th century
remain dominant until the middle of 19th century.
• A clinically well- known type of caries is characterized
by extensive penetration into the dentin, and even into
the pulp , but with barely detectable catch in the
fissure.
17
18. Chemical theory:
• Parmly(1819) rebelled against vital theory and
proposed that an unidentified chemical agent caused
caries.
• Robertson(1835) and Regnart(1938)-carried out
experiments with different dilutions of inorganic acids
(sulfuric and nitric) found that they corroded enamel
and dentin.
• Robertson proposed dental decay was caused by acid
formed by fermentation of food particles around the
teeth.
18
19. Parasitic/septic theory:
• In 1843 Erdl described filamentous parasites in the
surface membrane (plaque) of teeth.
• Later Ficinus, a physician observed filamentous
microorganisms, which he called Denticolae, in
material taken from carious cavities.He implied that
these bacteria caused decomposition of enamel and
then the dentin.
• Niether Erdl nor Ficinus explained how these organisms
destroyed tooth structure.
• Leber & Rottenstein- dental caries commenced purely
as a chemical process but living organisms continued
the disintegration of enamel & dentin.
• Underwood & Miles(1880) – SEPTIC THEORY – Acid
capable of causing decalcification was produced by
bacteria feeding on the organic fibrils of dentin.
19
20. CHEMICO-PARASITIC [ACIDOGENIC] THEORY
• Also known as "Miller's chemicoparasitic
theory" as it was first postulated by
Willoughby. D. Miller in the year 1889 .
• It proposes that "acids formed due to the
fermentation of dietary carbohydrates by oral
bacteria leads to progressive decalcification of
the tooth structures with subsequent
disintegration of the organic matrix".
• Therefore acidogenic theory states that the
process of dental caries involves two stages:
20
21. • According to Miller,
there are four
important factors,
which can influence
the process of
tooth destruction in
the process of
dental caries and
these factors are as
follows:
.
acids
Micro
organisms
Dental
plaque
Dietary
carbohydrates
Tooth decay
21
22. Limitations:
• This theory was unable to explain the predilection of specific sites
on a tooth to dental caries . The initiation of caries on smooth
surfaces was not accounted for by this theory.
• Miller believed that dental caries was caused by multiple species of
bacteria .This is understandable since many bacterial species
possess glycolytic abilities. While current evidence for a specific
bacterial infection in dental caries is tantalizing, the concept is not
disputable.
• This theory does not explain why some populations are caries –
free.
• The phenomenon of arrested caries is not explained by this theory.
22
23. Proteolytic theory:
• States that organic or protein elements of the tooth are
initial pathways of invasion by microorganisms.
• Enamel lamellae were considered as pathways for
microorganisms in the progress of dental caries.
• Acc to Gottlieb & Gottlieb; Diamond & Applebaum
“Caries is essentially a Proteolytic process; the
microorganisms invade the organic pathways & destroy
them in their advance. Acid formation accompanied
proteolysis.
• The concept of the proteolytic theory was further
extended by Pincus in 1949 and he proposed that the
"sulfatase enzyme" liberated by gram-negative bacilli,
hydrolyze the sulfated mucosubstances of enamel
matrix and therefore liberate sulfuric acid, glutamic
acid and aspartic acid, etc. which dissolve the mineral
portion of the enamel as well. 23
24. limitations
• No satisfactory evidence to claim that the
initial attack on enamel is proteolytic.
• Gnotobiotic studies: caries can occur in the
absence of proteolytic organisms.
• To date no one has under physiological
conditions successfully demonstrated
significant loss of enamel tissue through
proteolytic activity.
24
25. Proteolysis chelation theory:
• This theory proposed by Schatez et al (1955)
implies a simultaneous microbial degradation of
the organic components (proteolysis) and the
dissolution of the minerals of the tooth by the
process of chelation.
• The word chelate is derived from the Greek word
chelas meaning claw, and refers to compounds
that are able to bind metallic ions as calcium,
Iron, copper, zinc and other metals by the
secondary valence bonds. The resulting chelates
are non ionic and usually soluble.
• According to the proteolytic chelation theory
dental caries results from initial bacterial and
enzymatic proteolytic action on the organic
matter of enamel without preliminary
demineralization. 25
26. • Such action, the theory suggests produces an initial
caries and a release of variety of complexing agents
such as amino acids, polyphosphates and organic acids.
The complexing agents then dissolve the crystalline
apatite.
Limitations:
• Less than one percent of mature enamel is organic in
nature and the suggestion that this material upon
degradation can give rise to a significant concentration
of chelator sufficient to dissolve upto 96% mineral
matter has no experimental support.
• Also there is no substantial experimental evidence that
the initial carious lesion stems from a break down of
organic matter that is due to proteolytic action.
• While proteolysis chelation is an important biological
phenomenon, its primary role in the etiology of the
dental caries has not been corroborated.
26
27. Sucrose chelation theory:
• Egglers-Lura(1967) proposed sucrose itself & not the
acid derived from it can cause dissolution of enamel by
forming an ionized calcium saccharate.
• The theory states that calcium saccharates & calciium
complexing intermediates require organic phosphate
which is subsequently removed from the enamel by
phosphorylating enzymes.
Limitations
• The concentration of sulfated polysaccharides in
enamel is very small and not readily accessible as a
substrate for enzymatic degradation.
• This is a highly unlikely hypothesis for the degradation
of tooth enamel.
27
28. Autoimmume theory:
• The autoimmune theory of dental caries
suggests that few odontoblast cells at some
specific site within the pulp of few specific
teeth are damaged by the autoimmune
mechanisms. For this reason the defense
capacity and integrity of the overlying enamel
or dentin in those specific areas are
compromised, and they can be the potential
site, for caries development in future.
28
33. Microorganisms:
TYPE OF
CARIES
MICROORGANISM HUMAN DISEASE
PIT &
FISSURE
S.Mutans
S.Sanguis
Lactobacillus species
Actinomyces species
Very significant
Uncertain
Very significant
By chance
SMOOTH
SURFACE
S.mutans
S.salivarus
Very significant
By chance
ROOT
SURFACE
A.Viscosus
A.Naeslundii
S.Mutans
S.Sanguis
Very significant
Very significant
Significant
By chance
DEEP
DENTINAL
CARIES
Lactobacilli species
A.Naeslundii
Other filamentous rods
Very significant
Very significant
Very significant
33
34. Virulence Factors of S. mutans
• Specific adherence to tooth surface using
antigen I/II adhesin and GTF
• Production of extracellular polysaccharides
(dextran)
• Accumulation of intracellular amylopectin-like
polysaccharides (carbon/energy reserve).
• Lactic acid production from sugar metabolism
• High tolerance for acid
• IgA proteases
inactivate secretory IgA by detaching the Fc
region of the immunoglobulin
34
35. Lactobacillus:
• Lactobacilli are Gram +ve, non spore forming
rods that generally grow best under
microaerophillic conditions.
• The earlier notion that lactobacilli are the
main etiologic factor(Bunting et al 1925) in
causing dental caries has been discarded.
• The population is influenced by dietary
carbohydrate content and intake frequency.
• They represent around 1% of oral flora.
• They have low affinity for tooth surface and
are mainly seen in deep dentinal lesions.
35
36. • L.casei and L.fermentum are the most
common oral species.
• Other oral species include L.acidophilus,
L.salivarius(saliva),
L.brevis,
L.buchneri.
• The heavier growth of lactobacilli at active
carious lesions do not imply their causative
role in caries development.Though they can
be considered as secondary contributors.
• Lactobacilli are both acidogenic & aciduric
& could therby multiply in low ph of plaque
& carious lesions.
36
37. Oral Actinomyces:
• Gram positive filamentous anerobes –
• Facultative -A.naeslundii
Anerobic- A.israelii
A.visosus
A.odonotyticus
• Actinomyces sps. Is found significantly in
dental plaque & in increasing proportions
on decayed rooth surfaces.
• A.naeslundii predominates in young
children whereas A.viscosus in teenagers
and adults.
Viellonella:
• Gram-ve cocci found predominantly in
plaque.
• Anticariogenic property. 37
38. Evidence of role of bacteria in dental
caries
• Studies in animals and humans give following
conclusions
1. Teeth free from bacterial infection do not develop
caries.
2. Antibiotics are effective in reducing caries in animals
and humans.
3. Oral bacteria can demineralize enamel invitro and
produce lesions similar to naturally occurring caries.
4. Specific bacteria can be isolated & identified from
plaque from various carious lesions
Classical germ-free studies of Orland et
al
1954
38
39. Dental plaque
• A soft translucent, and
tenaciously adherent
material accumulating
on the surface of the
teeth.
• There are 2 hypothesis
concerning the
pathogenicity of plaque
:
1)Non Specific plaque
hypothesis
2)Specific plaque
hypothesis
39
40. Nonspecific plaque hypothesis:
• In the past, and as an extension of miller’s chemico
parasitic theory, the total plaque was viewed as a
pathogenic structure which had to be eliminated or
reduced if caries was to be prevented.
• If all plaques were similar in their potential to
induce caries, the main difference between health
and disease states might be expected in the
quantitative aspects of plaque accumulation.
• This possibility carries with it the implication that
mechanical debridement should be the dominant
method of disease control(loesche-1982).
• Further specific anti microbial agents should be
limited in their efficacy since the accumulation or
activity of the old plaque requires suppression.
40
41. Specific plaque hypothesis:
• It is based on the observation that plaque is
not always associated with disease.
• Plaques can be identified as pathogenic only
when they are associated with clinical disease.
• As only few microorganisms are capable of
caries production treatment based on this
hypothesis is aimed at elimination of the
specific pathogenic organisms but not total
plaque elimination.
41
42. • Demonstrated for first time in histologic
preparations by Williams (1897).
• It is composed of 80% water & 20% solids.
• Bacteria & salivary proteins comprise 50% of the
dry weight of plaque.
• It also contains carbohydrates(polymers of
glucans, fructans & heterosaccharides) & lipids –
25% of the dry weight.
• Inorganic components- 5-10% of the dry weight.
• The accumulation of plaque on the teeth is a
highly organized and ordered sequence of events.
• Adherent bacteria have special receptors for
adhesion to the tooth surface and also produce a
sticky matrix that allows them to cohere to each
other. 42
44. Properties of Cariogenic Plaque:
• The rate of sucrose consumption was
noticeably higher in cariogenic plaques.
• The rate of lactic acid formation was
considerably higher in cariogenic plaques.
• Bacteria in cariogenic plaques synthesized
more intracellular glycogen-amylopectin-type
polysaccharides.
• Upto 20% of sucrose consumed within 15
minutes was converted into intracellular
polysaccharides by cariogenic plaque.
• Cariogenic plaques formed approximately
twice as much extra cellular polysaccharides
from sucrose as did noncariogenic plaques. 44
45. • Cariogenic plaques contained higher levels of
streptococcus mutans than noncariogenic
plaques.-Noncariogenic plaques harboured
higher levels of S.sanguis and Actinomyces than
cariogenic plaques.
• Noncariogenic plaques had significantly higher
proportion of dextranase producing organisms.
• Noncariogenic plaques had higher levels of
veilonella and contained slightly lower
concentration of lactic acids and slightly higher
conc of acetic and propionic acids.
45
46. Tooth:
COMPOSITION:
• Studies indicate that the surface enamel is more
resistant to caries than subsurface enamel.
• Surface enamel is more highly mineralized lower in
CO2 , dissloves at slower rate in acids , contains less
water and tends to accumulate greater quntities of
flouride zinc lead & iron than the subsurface
enamel.
• These factors apparently contribure to caries
resistance & are partly responsible for the slow
disintegration of surface enamel than the
underlying enamel in initial carious lesions.
46
47. MORPHOLOGIC CHARECTERISTICS:
• Deep narrow occlusal fissures, buccal or lingual pits
Entrapment of food, bacteria, debris
Rapid carious development.
POSITION:
Malaligned, Out of poisition, Rotated teeth
Difficult to cleanse, favour accumulation of food &
debris
Dental Caries 47
49. Role of saliva:
1) Bacterial clearance
2) Direct antibacterial activity
3) Buffer
4) Remineralization
49
50. pH OF SALIVA:
• It is determined mainly by the bicarbonate
concentration.(85%) .
• Phosphates and proteins in saliva constitute the other
buffer systems, but the constitution of these in saliva
are too low to be of significance. So the pH will vary
according to the bicarbonate content.
• The buffering capacity of saliva is a very significant
property affecting the carious process.
• The saliva pH increases with flow rate. It may be
slightly acidic as it is secreted at an unstimulated flow
rate but it may reach a pH of 7.8
• Other salivary components contributing to the ability
of saliva to neutralize the acidity are ammonia, urea
and statherin.
• Sialin is an arginine peptide which is the recently
described pH rise factor present in saliva which rapidly
clears glucose from plaque, increases base formation
and elevates pH in the plaque.
50
51. Concept of critical pH
• pH at which any particular saliva ceases to be
saturated with calcium and phosphorus ions is
referred to as critical pH.
• The critical pH value is 5.5
• Below this value the inorganic constituents
dissolve .
• With conc. of H+ ions, more phosphate ions
leave the solid apatite phase.
• Above this pH the remineralization takes place.
51
52. QUANTITY OF SALIVA:
• The normal secretion is 700 to 800 ml per day. It may
influence caries incidence. This is especially evident in
cases of salivary gland aplasia and xerostomia in which
salivary flow may be entirely lacking with rampant
dental caries the typical result.
VISCOSITY OF SALIVA:
• It depends on the mucin content.A high caries
incidence is associated with thick mucinous saliva.
52
53. Factors affecting mineralization:
Statherin : is an acid peptide
• Contains high levels of proline, tyrosine and
phosphoserine.
• They inhibit spontaneous precipitation of calcium
phosphate salts from supersaturated saliva and
prevents crystal growth favoring remineralization .
Histatins : a group of histadine rich proteins.
• They bind to hydroxyapatite and prevent calcium
phosphate precipitation from a supersaturated saliva
enhancing the stability of hydroxyapatite
53
54. Proline-Rich proteins :acidic proline rich protein.
• Prevents the precipitation of calcium phosphate
from the supersaturated saliva.
• A decrease in the proline rich proteins resulted
in sulcal and smooth surface caries.
Cystatins : they prevent the action of potentially
harmful protease on the soft tissue of the oral
cavity.
• Protects the tooth structure by promoting
super saturation of saliva with calcium and
phosphate.
54
55. Mucins : plays multiple roles
• Salivary mucins are MG1 and MG2.
1. MG1 tightly binds to the tooth surface.
• protects the tooth surface from the chemical and
physical attack including acid change.
2. MG2 can also bind but can be easily displaced
• By aggregation. it promotes clearance of oral
bacteria.
55
56. Bacterial clearance:
• Around 1 – 1.5 l of saliva is secreted by various
glands in a day which lubricates the oral tissues,
bathes the teeth and plaque before being
swallowed.
• Flushing action is adequate to remove virtually all
of non adherent bacteria
• Most effective during mastication or oral
stimulation.
• Large volumes of saliva also dilute and buffer the
plaque acids
56
57. ANTIBACTERIAL AGENTS IN SALIVA:
1)Lactoferrin : Iron binding protein
Prevents iron from being used by the
organism for metabolism.
Organisms susceptible: Aerobic
Facultative anaerobic
bacteria.
2)Lysozyme : has a direct antimicrobial affect.
They bind to the bacterial cell wall and
Destabilizes the cell wall allowing
autolysis to take place.
57
58. 3)Peroxidase : produced from the acinar cells of
the major salivary glands.
The enzyme contains heme and
uses thiocyanate and hydrogen
peroxide produced by the oral
bacteria inhibiting glucose metabolism
in bacteria.
4) Salivary IgA: produced by the plasma cells
present in the salivary glands.
They are multivalent antibodies.
They bind to bacterial surface and prevent
adherence.
58
59. Remineralization:
• Saliva is supersaturated with Ca 2+ and P ions.
• When local pH is high enough(>5.5),
demineralization process may be reversed by
remineralization of damaged tooth structure.
• This results in a dark, harder, pigmented
surface termed as arrested caries.
• On dentinal surfaces, it is termed eburnated
dentin
59
60. Pathophysiology of caries:
• Caries development is not a single event of
lowered pH but caused by of many episodes
of long duration demineralization (lowered
pH).
• The rate of caries progression depends on the
dynamic equilibrium between factors
promoting and opposing demineralization.
60
63. Zones of dentinal caries:
1. Normal dentin
2. Subtransparent dentin
3. Transparent dentin
4. Turbid dentin
5. Infected dentin
63
64. Caries diagnosis
In Greek “Dia” means thoroughly
“ Gignoska” means to know
WHAT IS DIAGNOSIS ?
“ it is the art or act of identifying a disease”
Diagnosis : “is a determination and judgment
of variation from normal”
..As utilization of scientific knowledge for
identifying a disease process and to
differentiate it from other disease
64
66. Visual and tactile examination:
Conventional method for detection
Visual examination is aided by compressed air
Tactile examination ─ mirror and probe
66
67. Radiography:
Radiography has been –gold standard to detect
the dental caries.
Primarily for the detection of lesions on
proximal surfaces of teeth that are not
clinically visible Occlusal caries may also be
detected
once it has progressed into dentin.
67
68. Principle:
Radiographic diagnosis of caries ─ the mineral
content of enamel and dentin decreases, ─
decrease in the attenuation of X-ray
beam as it passes through the teeth→
area appears radiolucent on the radiograph
68
69. Conventional radiography:
• Many techniques available, two types
of techniques are popular and
commonly practiced
IOPA
Bitewing
Bite wing radiography:
• Used to detect proximal caries
• Important to detect incipient lesions
at contact points.
• Cervical margins of restoration
• Alveolar crest height
• Lamina dura
• Size of pulp chambers
69
70. Dyes:
Dye are used to visualize a substance
from its routine background or if
several objects have similar
appearance colouring by dye is to
discriminate between them for
identification.
The observation of dye may be:
Qualitative to observe the colour
or differentiate coloured objects
from non- coloured ones.
Quantitative - Intensity of colour is
to be determined
In caries diagnosis qualitative
examination ie visual appearance
of dye is sufficient.
70
71. Reqirements of dyes…….
Dyes for detection of caries in enamel
Procion
Calcein
Fluorescent dye – studied invitro but invivo…
Brilliant blue – enhance diagnostic quality of
during transillumination
Dyes for detection of caries in dentin:
2 layers of carious dentin
outer carious dentin inner carious
dentin
(Infected, unremineralizable) (uninfected
remineral.)
71
72. Caries detector:
Composition:
• 0.5% Basic Fuchsin + Propylene Glycol.
• technique using basic fuchsin which aids in
differentiating 2 layers of carious dentin was
introduced.
• Dye was considered as carcinogenic
• Replaced by Acid Red 52 ( Acid Rhodamine
B) which functions almost same as fuchsin
when dissolved in 1% solution of propylene
glycol.
Disadvantage:
Level of infection in stained and unstained
dentin at the DEJ were measured – not all
dye stainable dentin was infected
72
73. Caries activity tests:
Caries activity : the increment of active
lesions (new or recurrent) over a slated
period of time.
• Ideal requisites: (SYNDER)
• MAXIMUM CORRELATION
• RELIABILITY AND VALIDITY
• SIMPLICITY
• RAPID RESULTS
• INEXPENSIVE
• NON-INVASIVE 73
74. Various caries activity tests:
• LACTOBACILLUS COLONY COUNT
• CALORIMETRIC SNYDER
• THE SWAB TEST
• S.MUTANS LEVEL IN SALIVA
• DIP-SLIDE METHOD
• SALIVARY BUFFER CAPACITY TEST
• ENAMEL SOLUBILITY
• SALIVARY REDUCTASE TEST
74
76. Bibliography:
1) Sturdevant's Art and Science of Operative
Dentistry-5th edition
2) Cariology Ernest Newbrun- 3rd edition
3) Essentials of Preventive and Community
dentistry- Soben Peter -2nd edition
4) A Textbook of Oral Pathology sixth edition –
shafer’s
5) Principles of preventive & community
dentistry – Soben Peter
76
