Dental caries: History, Etiology, Histopathogenesis and Clinical types

1. Dental Caries
History, Etiology, Histopathogenesis and
Clinical types

2. ―HOT things sharp things, sweet things, cold things, all things rot
the teeth and make them look like old things‖.

3. CONTENTS
 Introduction
 Definition
 Classification
 Epidemiology
 Etiology – earlier concepts
 Current concepts of caries etiology
 Clinical characteristics of caries
 Histopathology of caries
 References

4. INTRODUCTION
―Rot or decay‖
 pre-historic period,
 prevalence modern times

5. History

6.  History :
•An image from 1300s (A.D.) England depicting a dentist extracting a tooth with
forceps.

7. • Archaeological evidence shows that dental caries is an ancient disease.
• Skulls supposedly dating from a million years ago through the neolithic
period show signs of caries, excepting those from the Paleolithic and
Mesolithic ages.
• The increase of caries during the neolithic period may be
attributed to the increase of plant foods containing carbohydrates.

8. • Neolithic period : hole in a tooth to
relieve an abscess in 5½ minutes.

9.  A Sumerian text from 5000 BC describes a "tooth worm" as the cause
of caries.
 Evidence of this belief has also been found in India, Egypt, Japan, and
China.
 Unearthed ancient skulls show evidence of primitive dental work.
 In Pakistan, teeth dating from around 5500 BC to 7000 BC show
nearly perfect holes from primitive dental drills
 References to caries are found in the writings of Homer and Guy de
Chauliac.

10.  The Ebers Papyrus, an Egyptian text
from 1550 BC, mentions diseases of
teeth.
 During the Sargonid dynasty of
Assyria during 626 BC to 668,
writings from the king's physician
specify the need to extract a tooth
due to spreading inflammation.

11.  Consumption of cooked foods : small
increase in caries prevalence.
 The Greco-Roman civilization, in
 addition to the Egyptian, had treatments
for pain resulting from caries.

12.  Rate of caries : low through the Bronze and Iron ages, but
sharply increased during the Medieval age.
 Periodic increase : caries prevalence : small
 1000 AD

13.  Treatment consisted mainly of herbal remedies
and charms, but sometimes also included
bloodletting.
 The barber surgeons of the time provided
services that included tooth extractions.

14. › Learning their training from apprenticeships, these
health providers were quite successful in ending
tooth pain and likely prevented systemic spread
› of infections in many cases.
› Among Roman Catholics, prayers to Saint
Apollonia, the patroness of dentistry, were meant to
heal pain derived from tooth infection.

15. › There is also evidence of caries increase in
North American Indians after contact with
colonizing Europeans.
› Before colonization,
› North American Indians subsisted on hunter-
gatherer diets, but afterwards there was a
greater reliance on maize agriculture, which
made these groups more susceptible to caries.

16.  By the Enlightenment,
the belief that a "tooth worm" caused caries was no
longer accepted in the medical community.
 Pierre Fauchard, known as the father of modern
dentistry,
was one of the first to reject the idea worms caused
tooth decay and noted that sugar was detrimental to
the teeth and gingiva.

17.  In 1850, another sharp increase in the prevalence of caries
occurred and is believed to be a result of widespread diet changes.
 Prior to this time,
cervical caries was the most frequent type of caries,
but increased availability of sugar cane, refined flour,
bread, and sweetened tea corresponded with a greater
number of pit and fissure caries.

18.  In the 1890s, W.D. Miller conducted a
series of studies that led him to propose an
explanation for dental caries that was
influential for current theories.

19.  He found that bacteria inhabited the mouth and that they produced acids
which dissolved tooth structures when in the presence of fermentable
carbohydrates.

20. › This explanation is known as the
chemoparasitic caries theory.
› Miller's contribution, along with the research
on plaque by G.V. Black and J.L. Williams,
served as the foundation for the current
explanation of the etiology of caries.

21. Definition and Classification
Classifications

22. According to Sturdevant:
Dental caries is a infectious microbiologic disease of the teeth that results in localized
dissolution and destruction of calcified tissues
According to WHO:
It is defined as localized post eruptive pathological process of external origin involving
softening of the hard tooth tissue and proceeding to the formation of cavity.
According to Shafer, Hine,Levy:
It is defined it as a ―microbial disease of the calcified tissues of the
teeth, characterized by demineralization of the inorganic portion and destruction of
the organic substance of the tooth.

23.  G V Black‘s classification
Class I lesions : All pit-and-fissure restorations are Class I,
and they are assigned to three groups, as follows.
They usually have three locations:
the occlusal surfaces of molars and premolars
the occlusal two thirds of the buccal and lingual surfaces of molars and
the lingual surfaces of anterior teeth.

24. Class II Lesions: Restorations on the proximal surfaces of posterior teeth are
Class II.

25. Class III lesions : are found on proximal surfaces of anterior
teeth that do not involve or necessitate removal of the incisal angle.

26. Class IV: Class IV Restorations. Restorations on the proximal
surfaces of anterior teeth that do involve the incisal edge
are Class IV.

27. Class V Restorations: Restorations on the gingival third of the facial or
lingual surfaces of all teeth (except pit-and-fissure lesions) are Class V.

28. Class VI Restorations: Restorations on the incisal edge of
anterior teeth or the occlusal cusp heights of posterior teeth
are Class VI.
They usually start in a traumatic or a formative defect.

29. According to Sturdevents:
He has classified dental caries mainly according to 3 criterion:
– Location.
– Extent.
– Rate.

30. According to Location:
 Primary caries.
 Caries of Pit & Fissure origin.
 Caries of enamel smooth surface origin.
 Backward caries.
 Forward caries.
 Residual caries.
 Root surface caries.
 Secondary (recurrent) caries.

31. › According to Extent:
 Incipient caries (reversible).
 Cavitated caries (irreversible).
› According to Rate (speed) of caries spread:
 Acute (rampant) caries.
 Chronic (slow or arrested) caries.

32. Mount G. J.(1997)classified dental caries based on site and size.
A) Site
 Site 1: includes lesions on pit & fissures of posterior teeth, buccal
grooves of mandibular molars, palatal grooves of maxillary molars
& erosion lesions on incisal edges
 Site 2: includes lesions in contact areas of posterior and anteriors.
 Site 3: includes lesions originating in gingival third of all teeth

33. B) Size
 Size 0: small and early enough to be remineralized lesion with only
residual stain
 Size 1: (mild) includes lesions which have passed just beyond
remineralization
 Size 2: (moderate) includes larger lesions, with adequate tooth structure
to support restoration
 Size 3: (enlarged) includes lesions in which tooth structure & restoration
are susceptible to fracture
 Size 4: (severe) includes lesions which have destroyed a major portion
of tooth structure

34.  Classification according to Mc Ghee
 Superficial caries- surface of enamel affected
 Simple caries – penetration into DEJ
 Deep seated caries – cavity of sufficient depth
 Caries with almost exposed pulp – large well defined cavity
 Caries with pulp involvement
 Caries with perforation laterally or through the floor of the pulp
 Loss of crown of the tooth from caries
 Caries of remaining root

35. WHO Classification
In this classification the shape and depth of the caries lesion scored on a
four point scale
D1. clinically detectable enamel lesions with intact (non cavitated) surfaces
D2. Clinically detectable cavities limited to enamel
D3. Clinically detectable cavities in dentin
D4. Lesions extending into the pulp

36. Etiology of Caries

37. › Etiology : complex problem complicated by many indirect factors that
obscure the direct or indirect causes.
› No universally accepted opinion : etiology
› Numerous references on dental caries including early theories have
attempted to explain its etiology.

38. › The oral cavity houses more than 250 microbial species.
› Unlike oral epithelium, the epithelium of the tooth does not shed and tooth
morphology has many areas inaccessible to physiological clearance mechanisms.
› Thus, a tooth becomes an ideal place for the stubborn adherence for many of
these species.
› This colonization occurs as a string of methodical adhesion, succession,and
progression.

39. Usha C, Sathyanarayanan R. 2009
› Host
• Enamel crystal structure
• Enamel mineral
• Saliva quality
• Saliva quantity
• Immune response
• Host behaviour
• Host attitudes
› Environment
• Plaque quantity& quality
• Enzymes
• Minerals
• Bacterial substrate
• Socioeconomics

40. › Organisms that are capable of adhesion adhere to the salivary pellicle on
the tooth and form a convenient arena for the subsequent aggregation of
other organisms that are incapable of initial adhesion.
› These are all endogenous / host microorganisms, not external infectious
agents. In fact, this natural colonization of the tooth prevents any invasion
by an exogenous organism by way of colonization resistance

41. › There are three major hypotheses for the etiology of dental caries:
› the specific plaque hypothesis
› the nonspecific plaque hypothesis
› the ecological plaque hypothesis
› The specific plaque hypothesis has proposed that only a few specific
species, such as Streptococcus mutans and Streptococcus sobrinus, are
actively involved in the disease.

42. › On the other hand, the nonspecific plaque hypothesis
› maintains that caries : outcome of the overall activity of
the total plaque microflora, which is comprised of many bacterial
species.
› The ecological plaque hypothesis suggests
› caries is a result of a shift in the balance of the resident
microflora driven by changes in local environmental conditions.

43. › S. mutans, e.g., species of Veillonella, Lactobacillus, Bifidobacterium,
Propionibacterium, low-pH non-S. mutans streptococci, Actinomyces, and
Atopobium, also may play an important role in caries production.
› Actinomyces spp. And non-S. mutans streptococci may be involved
in the initiation of the disease.

44. › However, many theories have evolved through years of investigation and
observation;
› the acidogenic theory
› the proteolytic theory
› proteolysis-chelation theory, are among many which have stood the test of
time.

45. Theories of formation of caries:
Early theoires
The legend of worms:
 The earliest reference to tooth decay is from ancient
sumerian text – LEGEND OF WORMS
 Given in 5000 b.c
 Stated that worms are responsible for causation of
caries

46. Endogeneous theories:
 Also called humoral theory
 Proposed by Greek physicians
 Stated that caries produced by internal action of acids and corroding humors
 Imbalance in humors
Vital theory
› Tooth was thought to be source of problem and caries started from within tooth

47. Exogenous theories
 Chemical theory:
 Parmly in 1820
 Stated that dental decay affected externally
 Unidentified chymal agent is responsible

48.  Parasitic theory:
 Theory proposed by Erdl
 First to relate microorganisms as causative agent is Erdl in 1843
 Fincus, in 1847, a German physician attributed dental caries to
‗DENTICOLAE‘
 Generic name proposed to decay related organisms
 Theory stated that living micro organisms caused the disintegration in both
enamel and dentin

49. Septic theory:
 Proposed by Underwood and Miller :1880
 Acid capable of causing decalcification of was actually produced by
bacteria , which feeds on organic fibrils of dentin
Chemico-parasitic theory:
 Also called acidogenic theory
 Proposed by Willought D Miller in 1884
 Stated that dental decay is a chemico-parasitic process

50.  Two stages :
 decalcification of tooth substance
 dissolution of softened residue
 This theory is the back bone of current knowledge of understanding
etiology of dental caries
 Theory has been accepted

51.  Draw backs in theory:
 Prediliction of certain specific sites on a tooth
 Why some populations are caries free ?
 Doesn't explain phenomenon of arrested caries
 Theory implicates the study of role of carbohydrates, micro
organisms, acids and dental plaque

52. Proteolytic theory:
 Although the evidence for the so called acidogenic theory is considerable, an
alternative explanation is the proteolytic theory.
 Bodecker , in 1878, demonstrated – certain enamel structures are made up
of organic material such as enamel lamellae and enamel rod sheaths
 Serves as a path way for entry of micro organisms
 Pincus , in 1948, 1949 proposed that nasmyths membrane and other enamel
proteins or mucoproteins yielding sulfuric acid upon hydrolysis

53. Preoteolysis Chelation theory
› This theory proposed by Schatz et al (1955)
› Simultaneous microbial degradation of the organic components
(hence, proteolysis) and the dissolution of the minerals of the tooth by the
process known as chelation.
› A chelate results from combining an inorganic metal ion with
at least two electron-rich functional groups in a single
organic molecule.

54.  It considers dental caries to be a bacterial destruction of teeth
where the initial attack is essentially on the organic components of enamel.
 The breakdown products of this organic matter have chelating properties and
thereby dissolve the minerals in enamel.

55.  This results in the formation of substances which may form soluble
chelates with the mineralized component of the tooth and thereby decalcify
the enamel at a neutral or even alkaline pH.
 Enamel also contains other organic components besides keratin, such as
mucopolysaccharides, lipid and citrate, which may be susceptible to
bacterial attack and act as chelators.

56. Sucrose chelation theory
 Egglers-Lura (1967) proposed that sucrose itself, and not the acid derived
from it, can cause dissolution of enamel by forming an ionized calcium
saccharate.
 The theory is that calcium saccharates and calcium complexing
intermediaries require inorganic phosphate, which is subsequently
removed from the enamel by phosphorylating enzymes.

57. Auto immune theory
 It suggests that few odontoblasts cells at some specific sites within the
pulp of few specific teeth are damaged by the autoimmune mechanisms.
 For this reason, the defence capacity and integrity of overlying enamel and
dentin in those specific areas are compromised and they can be the
potential sites for caries development.

58. Role of plaque as etiologic factor
 Soft, translucent and tenaciously adherent material
accumulating on the surface of teeth is commonly called as plaque
 90% contains bacteria and its byproducts
 Adherence of micro organisms :
 Few specialized microorganisms primarily streptococci adhere onto the
tooth surfaces
 Bacteria contains receptors
 Adhere to even other filamentous and spiral bacteria forming colonies

59. Plaque communities and habitats :
 Dorsum of tongue : S.salivarius
 Teeth : S.sanguis and S.mitis
Habitat Predominant species
Mucosa S.mitis, sanguis, salivarius
Tongue S.salivarius, mutans and sanguis
Teeth (non carious) S.sanguis

60. › Acids : initially decalcify the enamel have a pH: 5.5 to 5.2 or less and are
formed in the plaque material,
› which has been described as an organic nitrogenous mass of
microorganisms firmly attached to the tooth structure

61. Role of carbohydrates :
 Cariogenic carbohydrates are dietary in origin
 Cariogenicity varies with :
 frequency of ingestion,
 physical form,
 chemical composition,
 routes of administration and presence of other food constituents
 Sticky solid carbohydrates are more cariogenic
 They in detergent foods are less damaging

62.  Ones which are rapidly cleared by saliva are less cariogenic
 Plaque organisms produce little acid from the sugar alcohols sorbitol or
mannitol.
› The acids involved in the initiation of the caries process are normal
metabolic by-products of the microorganisms and are generated by the
metabolism of carbohydrates.

63.  Carbohydrates fed entirely by stomach tube or intravenously are not
cariogenic
 Meals high in fat, protein and salt reduce retentiveness of carbohydrates
 Refined pure carbohydrates are more cariogenic
 Bacteria + sugar + teeth – organic acids = caries

64. Role of micro organisms :
Type of caries Microorganisms
Pit and fissure Mutans, sanguis, lactobacillus, actinomyces
Smooth surface Mutans , salivarius
Root surface A.viscosus, naesulundi, S.mutans and sanguis
Type of caries Microorganisms

65. Streptococcus mutans :
 First isolated by CLARKE in 1924
 Catalase –ve , gram +ve cocci
 Cariogenic strains contain lysogenic bacteriophage
 Serotypes a to h
 Polymerize glucose and fructose moieties of sucrose to glucans and
fructans

66.  Extra cellular polymers
 Homopolymers of glucans – dextran and mutan are synthesized by
S.mutans
 Mutan- important constituent of plaque, less soluble and resistant to acid
attack
 Fructans are highly soluble , degraded by plaque bacteria

67. Lactobacilli :
 Gram +ve non spore forming rods
 Acidogenic and aciduric
 Produce lactic acid
Oral actinomyces :
 Gram +ve filamentous organisms
 A.naesulundi and viscosus – facultative anaerobes
 A. Israeli and odontolyticus – strict anaerobes

68. Role of acids :
 Exact mechanism is not known
 Probably occurs due to enzyme breakdown of sugars
 Acids formed are chiefly lactic acid and butyric acid
 Monosaccharides and disaccharides – greatest fall in pH

69. Current concepts in etiology of caries :
Three primary factors: the host,
the microbial flora
the substrate.
a fourth factor — the time — must be considered in any discussion of the
etiology of caries.
In other words,
Caries requires a susceptible host,
a cariogenic flora and
a suitable substrate that must be present
for a sufficient length of time.

71. Host factors and components
 Tooth composition
morphologic characteristics
position
 Saliva composition
ph
quantity
antibacterial factors
quantity and viscosity
 Diet physical factors (quality of diet)
local factors carbohydrate, vitamin and
fluorine content
 Systemic conditions

72. › Tooth
› Most vulnerable to proximal caries during first 2 years following eruption.
› Continuous increase in incidence of proximal caries in adolescent patient
concurrent with a comparative decrease in incidence of occlusal caries.
› Saliva is another host factor : critical to process.
› It mechanically cleans teeth and clears carbohydrates and acids from plaque.

73. › Neutralizes plaque acids, thus
pH and diffusion gradient for calcium and phosphate.
› As these two minerals return to tooth, remineralization occurs in
combination with fluoride.
› Acquired pellicle is an acellular film that covers tooth surface and allows
oral bacteria to adhere to tooth.

74. › Dietary factors
› Diet is another important component in carious process.
› Diet of highly cariogenic carbohydrates is metabolized readily by plaque
bacteria to produce acids.
› Acids diffuse into enamel as minerals diffuse out from tooth, leading to
cavitation.

75. › It is not only composition of diet that is of concern but also frequency of
‗‗sugar‘‘ challenge.
› If sufficient time between acid challenges occurs, demineralization can be
reversed, with resultant neutralization

76. › Bacterial process (agent factors)
› Acquired pellicle is an acellular film that
covers tooth surface and allows oral bacteria
to adhere to tooth.
› Bacteria in dental plaque are diverse, but
some species are implicated more
specifically.

77. › Two main groups of acidogenic bacteria have
been identified:
S mutans and Lactobacillus.
› Actinomyces isrealli has been isolated from
partially erupted teeth with white spot lesions.

78. Microflora of dental caries
› Pit and fissure caries:
› S mutans, S sanguis, other streptococci Lactobacillus, actinomyces.
› Smooth surface caries: S mutans, S salivarius
› Root caries: A viscus, A naeslundi,
› other filamentus rods, streptococci species.
› Deep lesions: lactobacillus, A viscus, A naeslundii,
› other filamentus rods, S mutans, bacillus, Rothia,
› propionibacterium, Arachnia, Eubacterium.

79. Acc to Orland' and by Fitzgerald, Jordan, and Achard
› Dental caries will not occur in absence of microorganisms.
› Animals did not develop caries even when fed a high-carbohydrate
diet.
› Caries did develop in these animals when they were inoculated with
microorganisms from caries-active animals and then fed cariogenic
diets.

80. › They can produce acid to decalcify tooth
Aciduric
streptococci, lactobacilli,
diphtheroids, yeasts, sta
phylococci, and certain
strains of sarcinae.
S mutans: major and most
virulent of caries-producing
organisms.
• Acids that initially
decalcify the enamel
have a pH of 5.5 to
5.2 or less and are
formed in plaque,

81. › Loesche
› Conducted an review of literature regarding etiology of caries.
› Stated that aciduricity appears to be most consistent attribute of S. mutans
and is associated with cariogenicity.
› S. sobrinus may be more important in smooth-surface decay and associated
with rampant caries.
› Concluded that
S.mutans, S sobrinus, and lactobacilli are human odontopathogens.

82. He also stated that
› aciduricity : most consistent attribute of S. mutans and is associated with its
cariogenicity.
› Also observed that,
› Other aciduric species such as S. sobrinus may be more important in
› smooth-surface decay and are perhaps associated with
› rampant caries.

83. › Acids caries process are normal metabolic by-
products of microorganisms
› Which are generated by metabolism of carbohydrates.
› Outer surface of enamel is more resistant to demineralization by acid than
is deeper portion of enamel,
the greatest amount of demineralization occurs 10 to 15 μm beneath the
enamel surface.

84. Saliva
› which is supersaturated with calcium and phosphate and has acid-buffering
capability,
› diffuses into plaque
› neutralizes acids and repairs enamel.
› Time required for remineralization is determined by :
 age of plaque,
 nature of carbohydrate consumed,
 presence or absence of fluoride.

85. Acc to Llory et al., 1972.
 Despite the continuous flow of saliva,
Dental plaque can accumulate at a rapid rate of (10-20 mg/day) in the
absence of oral hygiene procedures but the rate of plaque accumulation
appears to be even more rapid in patients with xerostomia
› Dental plaque developed for 12 hours or less, enamel demineralization
resulting from a single exposure to sucrose will be remineralized by within
10 minutes.

86. › 4 hours are required for enamel repair resulting from a exposure to sucrose
in presence of dental plaque that is 48 hours old.

87. › Fluoride
 enhances rate of remineralization of enamel by
 saliva, also forms of a fluorhydroxyapatite,
 which increases resistance of enamel to acid attack.

88. › Caries may be considered as a continuous dynamic process.
› Involving repeating periods of demineralization by organic acids of
microbial origin and subsequent remineralization by salivary components
(or therapeutic agents),
› but in which overall oral environment is imbalanced toward
demineralization.

89. Socioeconomic status
 low socioeconomic status has an impact on carious process.
 caries rate among individuals living below poverty level is higher.
 Lack of access to care among poor exacerbates condition because dental
caries is more likely to remain untreated.

90.  Barriers to dental care may include :
I. limited income
II. lack of value placed on dental health
III. lack of knowledge of oral care,
IV. and transportation limitations.

91. Window of infectivity: Caufield 1993
› 7-31 months: Teeth erupt
› Provide virgin habitat for bacteria.
› Second window of infectivity.
(Krass 1967, Edrman 1975)
› 6-12 yrs: Permanent teeth erupt.
› Provide new habitat for bacteria

92. Caries progression
› Time for progression from incipient caries to clinical caries (cavitation) on
smooth surfaces is estimated to be 18 months+/- 6 months .
› Peak rates : 3 years after eruption of tooth. (incidence)
› Poor oral hygiene and frequent exposures to sucrose can produce incipient
lesions in as little as 3 weeks.
› Caries development in healthy individuals is usually slow in comparison to
compromised persons

93. › Radiation induced xerostomia (dry
mouth) can lead to caries
development in as little as 3 months
from onset of radiation.

94. Histopathology of caries

95. Caries of enamel
› In pits and fissures, it spreads in triangular pattern with base towards DEJ
and apex towards surface.
› Microscopically 4 zones are are seen
a) Translucent zone:
b) Dark zone
c) Body of lesion
d) Surface zone

96.  The translucent zone is the advancing
front of the caries.
 i.e the innermost zone
 longitudinal sections and when the teeth
are examined in a clearing agent having
refractive index similar to that of enamel
such as quinoline or balsam.

 The preferential removal of inorganic
salts is evident whereas evidence of
organic material removal is not seen in
the translucent zone.

98. The Dark Zone
 Zone immediately above the translucent zone
 Appears dark
 Exhibits approximately 6% loss of minerals per
unit volume of enamel.
 It shows a +ve birefringence in polarized light
while normal enamel has negative
birefringence.

99. The Body of Lesion
 Occupies major portion of the lesion
 Area of max demineralization
 The body of the lesion is positively
birefringent.
 This is the largest zone which
exhibits enhanced striae of Retzius.

100. The surface layer
 Itis approximately 20-100 um thick
 Thinner in active lesion and
 Thicker in inactive ones.
 Partial demineralization = 10%
mineral loss takes place in this layer.
 Char‘ feature : broadening of prism
sheaths.
Surface layer

101.  The surface layer is approximately 20-
100 um thick it is thinner in active
lesion and thicker in inactive ones.
 Partial demineralization equivalent to
10% mineral loss takes place in this
layer.
 The characteristic feature of this layer
is the broadening of prism sheaths.

102. Stages of Progression of Occlusal caries: Natural lesions present itself as undermining
the enamel
Final outcome:
Necrosis and
periapical
inflamatory
reactions

103. Caries of dentin
 When the carious lesion has
penetrated the enamel,
 it spreads laterally along the dentino
enamel junction, undermining the
enamel.
 The pattern of invasion is depicted as
cone shaped lesion with its base at
the dentino-enamel junction and apex
towards the pulp.

104.  The histopathology of dentinal caries has been studied extensively. The
pathological changes have been divided into various zones :
A. Zone of fatty degeneration of tomes fibers

105. A. Zone of dentinal sclerosis or hypermineralization
characterized by deposition of calcium salts in dentinal
tubules
B.
C. Zone of decalcification of dentin, a narrow
zone, preceding bacterial invasion
D. Zone of bacterial invasion of decalcified but intact dentin
E. Zone of decomposed dentin
Bacterial invasion of dentin
Total destruction of dentin
by caries (necrosis)

106. Ekstrand et al,1991
1: Reactive dentin
2: Sclerotic dentin
3:Zone of demineralization
4:Zone of bacterial invasion
5: Peripheral rod direction

108.  According to sturdavent‘s
 Normal dentin: deepest area is normal dentin, which has tubules with odontoblastic
processes and no crystals are in the lumen
 Sub transparent dentin: zone of demineralization of intertubular dentin initial formation
of very fine crystals, damage to odontoblast process is evident, no bacteria is found
 Transparent dentin: zone of carious dentin that is softer than normal dentin, further loss
of minerals from intertubular dentin, many large crystals are present in the tubule
lumen. Stimulation of this region produces pain. No bacteria present
 Turbid dentin: zone of bacterial invasion widening and distortion of dentinal
tubules, which are filled with bacteria. Very little mineral present and collagen in this
zone is irreversibly denatured

109.  Infected dentin : outermost zone, consists of decomposed dentin that is
teeming with bacteria great number of bacteria present.
 Collagen and mineral absent

110.  Caries of Cementum
 The cemental caries is usually seen where there
is gingival recession and the oral hygiene is
poor.
 Clinically,
 The lesions appear as saucer shaped cavities.
 The micro organisms involved in root
caries, chiefly actinomyces, appear to invade
cementum either along Sharpeys fibers or
between bundles of fibers comparable to
invasion along dentinal tubules.

111. › The dentin involvement of cemental caries is similar to that of dentin
involvement in coronal caries.
› As was noted in coronal dentin, there may be sclerotic response, either
partially or completely, occluding the tubules with mineral crystals.

112. Pit and Fissure caries
 The pits and fissures of newly erupted
teeth are colonized by bacteria
 Bacterial plug
 Large variations in the microflora found in
pits and fissures
 G+ve cocci, S.sangius are commonly
found in pits and fissures of newly erupted
teeth
 S.mutants- carious pits and fissures

113.  Long narrow orifice prevents visiual and tactile examination
 Pit and fissure caries expands as it penetrates into the enamel
 Entry site- smaller
 Actual vision- bigger- making clinical diagnosis difficult
 Occlusal enamel rods bend down and terminate on the dentin- affects a
greater area of DEJ
 Cross section- ‗inverted V‘

114. Smooth surface caries
 Less favorable site for plague attachment,
 plaque develops on smooth surfaces near gingiva
 or under contacts
 Provide extra shelter
 Lesions have a broad area of origin and a conical or
 pointed extension
 Path of ingress- parallel to the enamel rods
 Cross section- ‗V shape‘ with a wide area of origin,
apex towards DEJ

115. Root caries
 Cementum is rougher than enamel and readily
allow deposition of plaque
 Cementum is relatively thin and provides little
resistance to caries
 Root caries have less well defined margins
 U shaped in cross section
 Progress more rapidly due to lack of enamel
covering
 Commonly seen in older persons with gingival
recession

116. Acute Dental Caries
 Runs a rapid clinical course
 Early pulp involvement
 Commonly seen in children and young adults
 Large dentinal tubules- show no sclerosis
 Process is so rapid that there is little time for deposition of reparative
dentin

117.  Initial entrance- small
 Rapid spread of the process at DEJ
 Saliva dose not easily penetrate
 Acid accumulated in the cavity
 Dentin is stained light yellow
 Pain is an common feature

118. Rampant caries
 Characterized by sudden, rapid, almost
uncontrollable destruction of teeth.
 Affecting surfaces of teeth that are relatively caries
free, usually proximal cervical surfaces of the
mandibular incisors.
 A caries incriment in 10 or more new carious lesions
over a period of about 1 year.
 Most often observed in primary dentition and in teen
age.
 Diatery factors affecting oral substrate and oral flora
and physiological factors affecting saliva are
significant.

119. Nursing bottle caries
 Also called nursing caries, baby bottle syndrome, bottle
mouth syndrome
 Affects deciduous dentition
 Causes – usage of nursing bottle containing milk or milk
formula, fruit juice or sweetened water, breast feeding, sugar
or honey sweetened pacifiers
 Clinically- widespread destruction of decidious teeth
 Commonly involves four maxillary incisors followed by
molars and then cuspids
 Severe- only root stumps remain
 Mandibular incisors usually escape – covered and protected
by the tongue

120. Adolescent caries
 Two chronological ages when acute rapidly progressing caries are seen
 4 – 8years and 11 – 18 years
 Acute caries attack in the later stage is termed as adolescent caries
 Seen in teeth or surfaces that are relatively immune to caries
 Small opening in enamel, extensive undermining
 Little time for the formation of reparative dentin
 Important to detect caries at an early stage for preventing it

121. Chronic caries
 Progress slowly
 Tends to involve pulp much later than acute caries
 Common in adults
 Entrance to the caries larger
 Less food retention
 Greater access to saliva
 Allows formation of dentinal sclerosis and deposition of secondary dentin
 Carious dentin stained deep brown
 Cavity is a shallower one , minimum softening of dentin
 Little undermining of enamel, and moderate lateral spread of caries at the dej
 Pain is not a common feature due to secondary dentin deposition

122. Recurrent caries
› Immediate vicinity of restoration
› Inadequate extension of restoration or poor adaptation
› Favours retention of debris
› Renewed caries follows a same pattern as primary
caries

123. › Reccurent caries might occur if all the carious dentin is not removed Besic
in 1943 studied the fate of bacteria sealled in dentinal tubules and found
that lactobacilli die out while streotococci persisted.

124. Arrested caries
 Caries which are static or stationary , does
not show tendency for caries progression
 Both deciduous and permanent dentition
are affected
 Occurs mostly in caries of occlusal
surfaces
 Large open cavity, lack of food retention

125.  Supeficially softened
and decalcified dentin
is gradually
burnished- eburnation
of dentin
 Sclerosis and
secondary dentin
formation occur
 Another form of arrested caries- seen on
the proximal surfaces in which adjacent
approximating tooth is extracted

126.  Brown stained area just below the contact point of the
tooth
 Very early caries which in many cases are arrested after
extraction, thus forming a self cleanseable area

127.  Muhler studied the effects of topical application of stannous fluoride
on caries and gave few acquired characteristics
 Presence of brown pigmentation
 Change from a soft to hard texture
 Change from chalkie whiteness to brown
 No increase in the size of the lesion
 No further progression of the lesion as long as the pigmentation remained
 Also stated that ―smaller the size of the lesion at the time of initial
application of fluorides , greater are the chances of caries arrest‖

128. Radiation caries
 Development of rampant caries in patients
undergoing radiation therapy of head and neck are
called rampant caries
 Del regato, observed the effects of xerostomia was
a complication of radiation caries in1939
 Besides xerostomia an increase in viscosity and pH
of saliva also effects

129.  Frank in 1961, salivary gland system and saliva secretion is of fundamental
importance in maintaining a carious free teeth
 Consequence of irradiation- 3 forms of caries formed
 Given by Frank and Baden in 1965 and 1970 respectively
 1st
type-
• char‘caries type lesion, completely encircling the tooth
• Amputation of the crown is seen
• Sometimes extension to labial buccal and lingual surface

130.  2nd
type-
• Brown to black discolouration of the crown
• Occlusal and incisal surface wear away
 3rd type-
• Begins as a spot depression, spreads from incisal or occlusal surfaces to
labial buccal or lingual surfaces
• Enamel shell is destroyed and coronal dentin is disintegrated leaving a
reduced, irregular, discoloured stump

131. Forward and backward caries
 Considered as a graphical representation of pathway of
caries progression
 First component to be involved is interprismatic enamel
 Disintegrating substances passing through these leads to
undermining of enamel prisms
 Resultant carious surface in enamel is cone shape both in
pit and fissure caries and smooth surface caries
 First component to be involved in the dentin is the
protoplasmic extensionwith in the dentinal tubules
 These extensions are spaced widely near dej butnare
closely spaced near pulp

132.  Caries cone in dentin have apex towards the pulpal surface and base of
the cone towards dej
 Where ever the caries cone is larger in enamel or atleast the size of the
dentin is called forward caries
 SCarious process in dentin progresses in a much faster rate than enamel
 Caries spread laterally creating undermined enamel
 In addition decay attack from dentinal surface
 This is termed as backward caries