CARIOLOGY

Dr. Florence May Arquillo-Posecion S.Y. 2022-2023

- Rice and corn – high in carbohydrates and
contain sugar
History - Developed drills/tools to try to remove the
Hunt – eat raw rotten parts/ decay

Molar
s

- Cusp pudpod
- Roots damol
- Adapt to the dietary requirement

Prehistoric men – (Mesiodistally) 10.4 – 11 mm,

broader roots A Sumerian text from 5000 BC describes a “tooth
Modern men - 9.6 – 10 mm, narrower roots

worm” as the cause of caries:

Archeologic evidence shows that dental caries is The worm as Hell’s demon: a battle with the “tooth
ancient disease. worm”

1. Paleolithic and Mesolithic ages Chinese doctor Chunyu Yi practiced moxibustion

- 3-8% of population has dental caries
- Eat raw food (no softening of food)
- Flat occlusal table
- Broader roots
- More on periodontal disease
- Does not consume sugar
2.
- 10,000 – 14,000 years ago
- Our ancestors began farming
- 80% of population has dental caries
and acupuncture to relieve dental pain (2500 BC)
- Concoct mouth washes to relieve the pain
- Silver paste dental filling
Like modern people, they went to the doctor. Most
physicians in ancient China were what we would call
“general practitioners”. They took care of all human
Neolithic ailments, including those that affected the teeth.
ages
The biography of the famous doctor Chunyu Yi
(205–150BC), in Records of the Grand Historian,
recorded 25 of his cases, one of which involved

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
dental work. A grandee in the state of Qi was
suffering from tooth decay. Chunyu Yi turned to
acupuncture, inserting needles into the patient’s left
arm, and told him to gargle every day with three
sheng (about 650ml) of an infusion of bitter root, the
exact composition of which has been lost. The patient
became well after five or six days.
According to Chunyu Yi, the cause of the tooth decay
was an attack of “wind” because he slept with his
mouth open. Also, and this is more in line with
modern knowledge of dental hygiene, because he did
not gargle after his meals.
Egypt
The Papyrus Ebers contain references to diseases of
the teeth, as well as prescriptions for substances such
as olive oil, dates, onions, bens, and green lead to be
mixed and applied “against the throbbing of the
bennut blisters in the teeth”
Hesy-Re, an Egyptian scribe, often called the first
dentist. An inscription on his tomb includes the title
“the greatest of those who deal with teeth, and of
physician” (2600 BC)
Greek physician called Esculapius was recognized,
according to Greek literature, to be the inventor of
purgatives and extraction of teeth. Therefore, the first
documented origin of dental surgery can be thought
to be from Esculapius.
Celius Aurelianus mentioned of a leaden instrument
'plumbeumodontagogoon' used for the extraction of
tooth.
500-300 BC
Hippocrates - functions of teeth and eruption of teeth
- first to suggest that food stuck between teeth
was responsible for tooth decay
- pulling teeth that were loose or decayed
- addressed the very common problem of bad
breath, suggestion different ingredients to
use in a mouth wash, such as anise seed,
myrrh, and white wine.
Aristotle - wrote about the eruption pattern of teeth,
treating decayed teeth and gum disease, extracting
teeth with forceps, and using wires to stabilize loose
teeth and fractured jaws
Little Medicinal Book for All Kinds of Diseases and
Infirmities of the Teeth
Bronze age and Iron age – low caries
11th century (Medieval age) – caries rise with the
appearance of sugar cane
 Caries was treated with herbal remedies,
charms and bloodletting.
Stronger cases were treated by tooth extractions
which were done by barbers which were very
successful in these treatments and probably prevented
spread of infections in many cases.
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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Dentistry even had its patroness Saint Apollonia and
prayers to her were meant to heal pain caused from
tooth infection.
History of Dentistry in the Philippines
Age of Enlightenment
 proved to be a critical period for the
advancement of cavity treatments
 medical community of Europe stops
believing that “tooth worm” causes the
caries and blames sugar which was not far
from the truth.
Pierre Fauchard "Father of Modern Dentistry"
- He is widely known for writing the first
complete scientific description of dentistry, Le
Chirurgien Dentiste ("The Surgeon Dentist"),
published in 1728 his book described basic
oral anatomy and function, signs and
symptoms of oral pathology, operative
methods for removing decay and restoring
teeth, periodontal disease (pyorrhea),
orthodontics, replacement of missing teeth,
and tooth transplantation
- first time defined a comprehensive system for
caring for and treating teeth introduced the
idea of dental fillings and the use of dental
prosthesis, and he identified that acids from
sugar led to tooth decay.
Willoughby D. Miller
o formulated the chemo-parasitic theory of
caries (tooth decay)
o This theory held that caries is caused by acids
produced by oral bacteria following
fermentation of sugars.
o The principles of the chemo-parasitic theory
were bolstered by the descriptions of bacterial
plaque on tooth surfaces independently by GV
Black and by JL Williams in 1898
Cariolgy
o the study of dental caries and its
development (cariogenesis)
Dental caries
o WHO - is a microbial multifactorial disease
of the calcified tissues of the teeth,
characterized by the demineralization of the
inorganic portion and destruction of the
organic content
o SHAFER - dental caries as an irreversible
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, which
often leads to cavitation
o Sturdevant - It is an infectious
microbiological disease of the calcified
tissues of the teeth, characterized by a
demineralization of the inorganic portion
and destruction of the organic substance of
the tooth
Consensus Report of a Workshop Organized by
ORCA (European Organization for Caries
Research) and Cariology Research Group of
IADR (2020)
Dental caries is a biofilm-mediated, diet modulated,
multifactorial, non-communicable, dynamic disease
resulting in net mineral loss of dental hard tissues
[Fejerskov 1997; Pitts et al., 2017]. It is determined by
biological, behavioral, psychosocial, and
environmental factors. As a consequence of this
process, a caries lesion develops.
Chapter 2: Review of Oral Anatomy, Histology
and Basic Terminologies
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Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Dental anatomy, histology, physiology and occlusion - External manifestation of incremental lines
are interrelated disciplines that are prerequisites to of Retzuis
understanding cariology. - Wavelike transvers elevations between
grooves
- The grooves are called imbrication lines of
Structures of teeth Pickerill
1. Enamel - Present only in postnatal enamel
2. Pulp-dentin complex
3. Cementum

1. Enamel
- Covers the anatomical crown of the teeth
- Ameloblast (formative cell)
- Hardest tissue of the body

a. Enamel rods
Dentioenamel junction
b. Rod sheath
- Membrana preformativa
c. Interred
- Junction between dentin and enamel
substance
- Scalloped or has a pitted appearance
- Hypomineralized zone

(A) Permanent Tooth – enamel rods – directed

apically
(B) Temporary tooth - enamel rods – directed
Enamel tufts
coronally
Incremental lines of Retzuis
- Brownish bands that illustrate the
incremental pattern of laying down of
enamel
- Comparable to growth rings of the tree
- Appear as tufts of grass that project into the
enamel
- Narrow ribbonlike structure
- Hypocalcified enamel rods and
interprismatic substances that originates
from DEJ to at least 1/3 of the enamel
- Less mineralized, weakened planes

Perikymata

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Enamel lamellae Odontoblasts
- Thin, leaflike structures Predentin
that extends from enamel
surface towards DEJ and Structures in Dentin
even towards dentin 1. Dentinal tubules
- Organic in nature and 2. Peritubular dentin
hypomineralized 3. Intertubular dentin

Enamel cracks
- Narrow fissurelike
structures which are actually outer edges of
the enamel lamella

Types of Dentin
1. Primary dentin
a. Mantle
b. Circumpulpal
2. Secondary dentin
3. Tertiary/Reparative/
Reactive/Response
Enamel spindle
- Thickened end of odontoblastic process that
crosses the DEJ and is entrapped in the
enamel
- Pain receptors

Dead tracts
- Due to disintegration or death of
Grooves – sound coalesce of odontoblasts and empty tubules are filled
developmental lobes of the with air
enamel - White in reflected lift
Fissures – faulty coalesce of - Black in transmitted light
developmental lobes of the - Initial step in formation of sclerotic dentin
enamel

Pit-fissure sealants

2. Dentin Sclerotic/Transparent dentin

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
- Deposition of collagen fibrils and apatite 3. Premolars
crystals in the dead tracts 4. Molars
- Dentinal tubules become more mineralized
like peritubular dentin thus it becomes
transparent Physiology and tooth form:
Reparative dentin 1. Function
 Noxious stimuli 2. Contours
 Death of odontoblasts 3. Proximal
 Formation of reparative dentin contours
 Seal off site of injury and promote healing 4. Embrasures
process of pulp
- Has fewer
Surfaces of teeth
Hydrodynamic theory Crowns of all teeth have five surfaces:
- Various stimuli such as heat, cold, air blast, 1. Facial surface – labial surface of buccal surface
dessication , mechanical or osmotic pressure a. Labial surface – surfaces of incisors and
may affect or cause fluid movement in canines that are towards the lips
odontoblasts b. Buccal surface – surfaces of premolars
- The said movement of fluid disturbs pulpal and molars that face the check
environment and is sensed by plexus of 2. Lingual surface (palatal surface) – all surfaces
raschkow on pulp facing towards the tongue
- Odontoblasts are mechanoreceptors 3. Proximal surface
a. Mesial surface – all surfaces towards
the midline
b. Distal surface – all surfaces away from
the midline
4. Incisal or occlusal surface
a. Incisal surface – surface of incisors and
canines that come in contact with those
in the opposite jaws during the act of
closure
b. Occlusal surface – surface of premolars
and molars that come in contact with
those in the opposite jaws during the act
3. Cementum of closure
- Covers the anatomical roots of the teeth
- Cementoblasts
Landmarks and Structures in Teeth
Types: Depressions of tooth surface
a. Acellular 1. Pit – a sharp pinpoints depression on the
b. Cellular surface of the enamel

2. Fossa – an irregular depression or concavity

3. Sulcus – a long depression on the surface of
Basic Terminologies in Dentistry a tooth
Classes of teeth
1. Incisors
2. Canines

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
4. Groove – shallow linear depression on the
surface of a tooth
a. Developmental groove – shallow
groove or line between the primary
parts of the crown or root
b. A supplemental groove – is less
distinct and does not mark the
junction of primary parts

Elevation on tooth surface Other important terms

1. Cusp – an elevation or mound on the crown
of the tooth
2. Cingulum – lingual lobe of an anterior tooth
and makes up the bulk of the cervical third
of the lingual surface
3. Lobe – one of the primary sections of
formation in the developmental of the
crown.
Mamelons – are three rounded protuberance
found on the incisal ridges of newly erupted
incisor teeth
4. Ridge – linear elevation on the surface of a
tooth
a. Marginal ridge - rounded borders of
enamel that form the mesial and
distal margins of the occlusal
surfaces of posterior teeth and the
mesial and distal margins of the
lingual surfaces of anterior teeth
b. Triangular ridge – is a ridge that
descends from the tips of the cusps
of molars and premolars towards
the center part of the occlusal
surface
c. Transverse ridge – is formed by the
union of buccal and lingual
triangular ridges
d. Oblique ridge – is a ridge obliquely
crossing the occlusal surfaces of
maxillary molars.
Oblique ridge – prominent in maxillary molars
1. Midline – imaginary line dividing the upper
and lower arches into two equal halves
2. Anterior - pertaining to or towards the front
plane of the body
3. Posterior - Pertaining to or towards that
back plane of the body
Division in thirds
To make study and communication easier the crown
and root are divided into 3 halves
a. Division in thirds occluso-gingivally
(Crown)
1. Cervical third
2. Middle third
3. Incisal/Occlusal third
b. Division in thirds facio-lingually (Crown)
Crowns when viewed from front
1. Mesial third
2. Middle third
3. Distal third
Chapter 3: Elements of Dental Caries
“It is an infectious microbiological disease of the
calcified tissues of the teeth, characterized by a
demineralization of the inorganic portion and
destruction of the organic substance of the tooth”
– STURDEVANT

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Definition 2020
- Dental caries is a biofilm-mediated, diet
modulated, multifactorial, non- communicable,
dynamic disease resulting in net mineral loss of
dental hard tissues [Fejerskov 1997; Pitts et al.,
2017]. It is determined by biological, behavioral,
psychosocial, and environmental factors. As a
consequence of this process, a caries lesion
develops.
Diet – Frequency of eating, Amount of Sugar, Type
of sugar
Tooth – Surface morphology, Fluoride exposure
Bacteria – Oral hygiene, Fluorides
CARIES
Composed of:
- Diet, Bacteria, Time, Susceptible surface
Plaque cycle
> Pellicle > Materia Alba > Plaque > Calcular
Deposits >
Pellicle
 Pellicle forms immediately on a clean tooth
surface
 Pellicle is a protective as it slows diffusion of
acids, chelating agents, calcium, and phosphate
ions
 Pellicle enables attachment and colonization of
microbial species in the early stages of biofilm
formation
- assist in remineralization
- bind microorganisms
Development of Bacterial Plaque
1. Pellicle (1 um thick) covers all oral surfaces
within 30 minutes to 1 hour after brushing
2. It becomes colonized by bacteria within 12-24
hours
3. High sucrose diet or frequent ingestion of sucrose
– favors colonization of acidogenic bacteria and
exclusion of non-cariogenic bacteria (e.g., S.
sanguis, S. mitis)
4. Special receptors make it easy for acidogenic
bacteria to adhere and extracellular matrix
facilitates cohesion
5. Metabolism of sucrose results in acid production –
lactic acid from sucrose
6. Plaque pH below 5.5 – period of
demineralization
7. Plaque pH above 5.5 – period of reminalization
Bacteria
1. Acidogenic – ability to produce acid
Lactic acid is major contributor of pH decline in
dental plaque
2. Aciduric – ability to tolerate acid and acidic
environment

Acquired enamel pellicle

 exposure of a cleaned enamel surface to saliva
results in formation of a1-10 um film

Oral Habitats
Habitat Predominant Environmental
species Conditions within
Biofilm
Composition: Mucosa S. mitis Aerobic
- mainly H2O, protein, CA2+ S. sanguis pH approximately 7
- salivary proteins adhere to polar HA surface S. salivarius Oxidation-reduction
potential positive
via polar (especially ionic) interactions
Tongue S. salivarius Aerobic
- since proteins anionic, CA2+ bridging S. mutants pH approximately 7
important S. sanguis Oxidation-reduction
potential positive
Probable functions Teeth (non S. sanguis Aerobic pH 5.5
- protect against acid attack (local buffering) carious) Oxidation-reduction
- facilitate adhesion of gingiva to enamel negative
surface Gingival Fuscobacterium Anaerobic pH variable

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
crevice Spirochaeta Oxidation-reduction may play an important role in caries production.
Actinomyces very negative Actinomyces spp. and non-S. mutans streptococci
Viellonella
may be involved in the initiation of the disease.
Enamel S. mutants Anaerobic pH <5.5
caries Oxidation-reduction
negative
Dentin S. mutants Anaerobic pH <5.5
Plaque Biofilm
caries Lactobacillus Oxidation-reduction  Biofilms builds on the pellicle layer
negative  Key stages of biofilm are (1) attachment and
Root caries Actinomyces Anaerobic pH <5.5 colonization (2) growth and proliferation (3)
Oxidation-reduction maturation and detachment
negative
 Gram positive Cocci, mainly streptococci
are the early colonizers
Mutans s.
Dental plaque, a bacterial biofilm
 Initiator of dental caries
 pellicle becomes plaque upon bacterial
 Acidogenic and aciduric (pH 4.2)
colonization
 Have ability to adhere to pellicle
 adhesion of bacteria
 Can form glucan
 Enamel caries Initially, adhesion is superficial
- like most proteins, bacteria surface has net
negative charge so, CA2+ is important as
Streptococcus mutans Serotypes Associated with
bridging agents
caries
- some have specific attachment sites on
Humans
surface (adhesins)
 Steptococcus mutans
 Steptococcus sobrinus Later, bacteria proliferate & modify plaque
 Steptococcus rattus - rats - salivary proteins (mucins, etc.) bind & are
 Steptococcus cricetus - hamsters modified: e.g., anionic sugars (sialate)
 Steptococcus ferus – wild rats removed
- plaque polysaccharide formation: with
Primates sucrose present, bacteria direct synthesis of
 Steptococcus macacae
 Steptococcus downei
o mutans, dextrans (glucans, i.e, polyglucoses)
o levans (polyfructose)

Dextrans/glucans – structural component of the

Lactobacillus acidophilus plaque matrix that glues certain bacteria to the tooth
- pH 3-4
- Produce lactic acid Levans/fructans – serve as transient reserve of
- dentin caries fermentable carbohydrate (prolonging duration of
acid production)
Actinomyces viscosus
- Root caries Sugar
 Fermentation of sugars lowers biofilm pH
 Lower pH causes shift in biofilm ecology
 10% of subjects with rampant caries in the
 S mutans and lactobacilli proliferate
secondary dentition do not have detectable levels
 More acid production leads to
of S. mutans
demineralization and the sub-surface lesion
 Species in addition to S. mutans, e.g., species of
Veillonella, Lactobacillus, Bifidobacterium,
Calculus: Composition
Propionibacterium, low-pH non-S. mutans
Composition: (dry weight)
streptococci, Actinomyces, and Atopobium, also

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
 80% mineral: CA2+, Pi, Mg2+, carbonate greatly increased caries
amorphous CA phosphate, HA prevalence
Hereditary Marthaler Less caries in individuals that
 rest: plaque matrix, bacteria (fossilized) Fructose Newbrun et al must avoid sucrose and fructose,
Intolerance but not other sugars and complex
Main Sources of Components carbohydrate
 supragingival: saliva Experimenta von der Fehr et Incipient caries can be rapidly
 subgingival: gingival crevicular fluid (GCF), l Caries in al Geddes et al induced by frequent rinsing with
essentially plasma containing neurophils man high concentration sucrose
solutions in the absence of oral
hygiene

Stephan Stephan Demonstrated the relationship

plaque pH between sugar exposure resulting
repsonse in the acidification of dental
plaque and caries experience

Cariogenic foods
- highly fermentable carbohydrate content and
a sticky consistency, break into small pieces
in the mouth, reduce the pH in the mouth to
less than 5.5 and are highly processed

 Sugar and chocolate confectionery

 Cakes and biscuits

 Buns, pastries, fruit pies

 Sponge puddings and other puddings
 Table sugar
 Sugared breakfast cereals
DEIT  Jams, preserves, honey
 lce cream
Table 1 – Classic evidence from human
supporting the role of sugar in dental caries  Fruit in syrup
 Fresh fruit juices
Study Reference(s) Main conclusions  Sugared soft drinks
Vipehlom Gustaffson et al The more frequently sugar is  Sugared, milk-based beverages
study consumed the greater the risk;
sugar consumed between meals  Sugar-containing alcoholic beverages
has much greater caries potential
than when consumed during a
meal Cariogenic foods Noncariogenic foods
Turku sugar Scheinin et al When sugars are almost - Sugar and chocolate - Bread, sandwiches,
completely replaced by non – confectionery toast
fermentable sugar substitutes, - Cakes and biscuits - Pasta, rice
caries increment is dramatically- Jams and jellies Unsweetened/
reduced; fructose is less
- lce cream artificially
cariogenic than sucrose
World war II Toverud Caries decreased and increased - Fruit syrup - Sweetened yoghurt
Takeuchi with sugar consumption during - Sugared soft drinks - Low-sugar breakfast
and after the war respectively - Flavored/sweetened cereals
Hopewood Harris Modern diet more cariogenic than milk - Sugar-free
house vegetarian low sugar diet - Buns, pastries, fruit confectionery
- pies - Fresh fruit
Tristan da Hallowat et al Introduction of a modern diet - Puddings - Water
Cunha Fisher including sugar and refined - Sugared breakfast - Sugar-free drinks
carbohydrate to this remote island

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 CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
- cereals - Milk, cheese
- Peanuts and dry fruits
- raw/boiled/frozen Xylitol
vegetables  is not fermented by mutans streptococcus
- popcorn and fresh corn and “starves” the cariogenic microorganisms
 Xylitol prevents the accumulation of plaque
Cariogenic sugars – Glucose, Fructose on the tooth surfaces.
Sucrose – most cariogenic sugar (fermentable)  Plaque pH does not drop when xylitol
sweetened gum is chewed, but
Non cariogenic sugars - Aspartame, saccharine,
remineralization is enhanced.
acelysulfame A, Xylitol
 Chewing any gum stimulates the flow of
saliva, which enhances the buffering effect

Classification of sugar substitutes Time

A. NUTRITIVE SWEETENERS - 5-20 mins after consumption of sugar, the
I. Monosaccharide polyols pH of the oral environment drops to5.5
a. Sorbitol
b. Xylitol
c. Mannitol Vipeholm study
d. Erythritol - Sugar consumption between meals has a
larger effect on the increasing dental caries
II. Disaccharide polyols activity than sugar consumption during
a. Isomalt (Palatinit) meals
b. Maltitol
c. Isomaltulose Susceptibility to caries
d. Trehalose a. Areas of tooth surfaces
III. Polysaccharide polyols - Pits and fissures vs smooth surfaces
a. Hydrogenated glucose syrup b. Differences of specific teeth
- Molars vs other teeth
B. NON-NUTRITIVE SWEETENERS c. Age periods
a. Saccharin - Childhood vs adulthood
b. Acesulfame - K d. Consistency of saliva
c. Aspartame - Thick and ropy vs thin and serous
d. Thaumatin
e. Cyclamate
Common clinical sites of caries
f. Dulcin
 Base of pits and fissures
g. AldoximeE
 Smooth enamel surfaces that shelter plaque
h. Neotame
o areas cervical to the contact areas
i. Stevia
j. Sucralose o distal surface of most posterior tooth
o areas cervical to the heights of contour
Why is sucrose the most cariogenic among all thẹ on the facial and lingual
carbohydrates?  Root surfaces
".. it is a relatively small molecule and can easily
enter the plaque. Bacteria like to use sucrose for
energy production and the process produces acid.
Risk factors determinants
Sucrose is also used by bacteria to produce
Caries risk factor/determinant is an environmental,
extracellular polysaccharide called dextrans. It will
behavioral, or biological factor confirmed by
help plaque stick to the tooth surface, making it more
temporal sequence, usually in longitudinal studies,
difficult to remove."
which, if present, directly increases the probability of
- Dr. Edward Lo, Faculty of Dentistry,
caries occurrence.
University of Hongkong

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
The risk factor is part of the causal chain [Burt, 2001].

Saliva
- Thick and ropy saliva
- Thin and serous saliva

Primary risk factors

Saliva
1. Ability of minor salivary glands to produce
saliva
2. Consistency of unstimulated (resting) saliva
3. pH of unstimulated saliva
4. Stimulated salivary flow rate
5. Buffering capacity of stimulated saliva Chapter 4: Pathophysiology of Dental Caries
Progression pattern of spread
Diet
6. Number of sugar exposures per day Plaque cycle
7. Number of acid exposures per day > Pellicle > Materia Alba > Plaque >Calcular
Deposits >
Fluoride
8. Past and current exposure Pellicle
 Pellicle forms immediately on a clean tooth
Oral biofilm surface
9. Differential staining  Pellicle is a protective as it slows diffusion of
10. Composition acids, chelating agents, calcium, and
11. Activity phosphate ions
Secondary risk factors  Pellicle enables attachment and colonization of
12. Past and current dental status microbial species in the early stages of biofilm
13. Past and current medical status formation
14. Compliance with oral hygiene and dietary
advice Plaque Biofilm
15. Lifestyle  Biofilms builds on the pellicle layer
16. Socioeconomic status  Key stages of biofilm are (1) attachment and
colonization (2) growth and proliferation (3)
maturation and detachment
Modifiable risk factor  Gram positive Cocci, mainly streptococci are
the early colonizers
Modifiable risk factor is a determinant that can be
modified by intervention, thereby reducing the Caries Lesion Initiation and Progression
probability of caries Dietary sugars Diffuse into the biofilm
 Acidogenic bacteria convert sucrose to
dextran – a polysaccharide that helps from
the sticky biofilm matrix

Sugar
 Fermentation of sugars lowers biofilm pH
 Lower pH causes shift in biofilm ecology
 S mutans and lactobacilli proliferate
 More acid production leads to
demineralization and the sub-surface lesion

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Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Sub-surface lesion
 The sub-surface lesion is reversible
 Less sugar leads to less acid production
 Fewer H- ions, the presence of F- ions, and
saturation of Ca- ions will encourage Ca- to
diffuse back into the lesion
 Continued presence of sugars, acid
production, and demineralization will lead to
cavitation
 The advancing front of the lesion extends
along the enamel-dentin junction

Reparative dentin
As the advancing lesion progresses toward the pulp,
reparative dentin is produced to defend the pulp from
the advancing infection.

The “Caries Balance” Caries in Enamel

Pathological factors Protective factors Caries on pits and fissure
 Acid producing  Saliva flow and - Initially appears as white spot
bacteria components - chalky white, opaque areas that are revealed
 Sub-normal saliva  Remineralization only when the tooth surface is desiccated
flow and/or (fluoride, calcium, and are termed noncavitated enamel caries
function phosphate) lesions
 Frequent  Antibacterials - translucency is lost because of the extensive
eating/drinking of (fluoride, subsurface porosity caused by
fermentable chlorhexidine, demineralization
carbohydrates xylitol)
 Poor oral hygiene  Good oral hygiene
Demineralization Remineralization
(Caries) (No caries)

Progression of Caries Lesion

Peak rates for the incidence of new lesions occur 3
years after the eruption of the tooth.

Poor oral hygiene and frequent exposures to sucrose-

containing or acidic food can produce noncavitated
(“white spot”) lesions (first clinical evidence of
demineralization) in 3 weeks.
- appears stained brown or black
The time for progression from non-cavitated caries to  Soft catch with fine explorer
clinical caries (cavitation) on smooth surfaces is  Shape of the lesion is conical with base at
estimated to be 18 months ± 6 months. the DEJ and apex at the pit or fissure
- At advanced stage a tiny opening maybe
(Occlusal pit-and-fissure lesions develop in less time
observed clinically overhanging enamel
than smooth-surface caries)
breaks or is fractured away
Radiation-induced xerostomia (dry mouth) can lead
to clinical caries development in 3 months from the
onset of the radiation.

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
- Deepest zone; advancing front of the enamel lesion
Caries on smooth surface (B, L, M, D) 2. Dark zone
 At early stage appears as chalky white spot - Does not transmit polarized light
in enamel becomes slightly roughened 3. Body of the lesion
 Decalcified area - Largest portion of the incipient lesion while in a
spreads laterally demineralizing phase
- Presence of bacteria invading in between enamel
rods
4. Surface zone
- Unaffected by caries
- Intact hypermineralized zone

Zones of Dentinal Caries

Zone 1 – subtransparent dentin
Incipient Carious Lesion Zone 2 – transparent dentin
- Earliest sign of a new caries lesion Zone 3 – turbid dentin
- Appearance of chalky white spot on the surface of Zone 4 – infected dentin
the tooth (demineralization of enamel) Affected dentin vs infected dentin
- White spot lesion

Incipient lesion vs Hypocalcified enamel

Incipient lesion will partially or totally disappear
visually when enamel is hydrated (wet) while
hypocalcified enamel is unaffected by drying and
wetting

Zone 1: Subtransparent Dentin

- Zone of demineralization of the intertubular
dentin and initial formation of very fine
crystals in the tubule lumen at the advancing
front
- Damage to the odontoblastic process; no
bacteria are found in this zone
- Stimulation produces pain; capable of
remineralization

Zone 2: Transparent Dentin

- Stimulation produces pain
- No bacteria are present

Zone 3: Turbid Dentin

- Zone of bacterial invasion
- Very little mineral present
- Cannot be remineralized
Zones of Incipient Lesion
1. Translucent zone

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Zone 4: Infected Dentin b. Dentin
- Outermost zone Triangular/triangle, pyramidal/pyramid, conical/ cone
- Consists of decomposed dentin that is with base at the DEJ and apex directed towards the
teeming with bacteria pulp E+D pattern = Diamond pattern
- No recognizable structure to the dentin and
collagen and mineral seem to be absent
- Great numbers of bacteria
- Removal of infected dentin is essential

Infected dentin = Zones 3 and 4

 significantly discolored
Smooth Surface Caries
 can be removed by excavators
a. Enamel
 stained with caries detector
Triangular/triangle, pyramidal/pyramid,
 needs to be removed unless judged to be within
Conical/cone with base at the outer surface of the
0.5 mm of pulp
tooth and apex at the DEJ
Affected dentin = Zones 1 and 2
b. Dentin
 not significantly discolored
Triangular/triangle, pyramidal/pyramid,
 feels hard already
Conical/cone with base at the DEJ and apex directed
 capable of remineralization
towards the pulp

E+D pattern = double Cone pattern,

pulp◀︎◀︎outer smooth surface
outer smooth surface▶︎▶︎pulp
Pattern of Spread
Pit and Fissure Caries
Follows the direction of the enamel rods and dentinal
tubules

a. Enamel
Triangular/triangle, pyramidal/pyramid with base at
the DEJ and apex at the outermost portion of enamel
near pits and fissure

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Classification of Dental Caries
Dental caries is a biofilm-mediated, diet modulated,
multifactorial, non-communicable, dynamic disease
resulting in net mineral loss of dental hard tissues
[Fejerskov 1997; Pitts et al.,2017]. It is determined by
biological, behavioral, psychosocial,
environmental factors. As a consequence of this
process, a caries lesion develops.
 Bases on anatomical sites
 Based on progression
 Based in virginity of the lesion
 Based on extent of caries
 Based on pathway of caries spread
 Based on the number of surfaces involved
 Based on GV Black’s classification
A. Based on Anatomical Sites
a. Pit and fissure caries
b. Smooth surface caries – buccal, lingual,
labial, mesial, distal
c. Root surface caries
B. Based of Progression
a. Acute caries
 is a rapid process involving a
large number of teeth
 lighter colored (soft, light
colored)
 caseous consistency makes the
and excavation difficult
 Rampant caries, nursing bottle
caries, radiation caries
o Radiation – lowers the saliva secretion
b. Chronic caries (slow)
 long-standing involvement,
affect a fewer number of teeth
 Pain is not a common feature
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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
 decalcified dentin is dark brown and leathery E. Based on Pathway of Caries Spread
a. Forward caries
c. Arrested caries (stop) - caries cone in enamel is larger or at
 Caries which becomes stationary or least the size as that of dentin
static and does not show any
tendency for further progression b. Backward caries
 Exclusively seen in caries of - carious process in dentin progresses
occlusal surface with large open much faster than in enamel,
cavity in which there is lack of food so the cone in dentin tends to
retention spread laterally creating
 on the proximal surfaces of tooth in undermined enamel
cases in which the adjacent
approximating tooth has been
extracted

C. Based on Virginity of the

Lesion
a. Initial/primary caries – no restoration
F. Based on the Number of Surfaces
Involved
a. Simple caries – 1 surface

b. Recurrent/secondary caries – recurring again

for several times, discoloration, leakage around
the fillings, obvious loss of restoration, caries
recurring inside the cavity
b. Compound caries – 2 surface

D. Based on Extent of Caries

a. Incipient caries – white spot, involve only the
enamel, chalky white, demineralize area, no hole

c. Complex caries – 3 or more

b. Cavitated caries – obvious loss of enamel, hole

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
G. Based On GV Black’s Classification d. Class IV
a. Class I - Carious lesions that are located on the
- Carious lesions that are located in pits and proximal surfaces of anterior teeth involving
fissures of the occlusal surfaces of molars the incisal angle
and premolars, occlusal 2/3 of the buccal
and lingual surfaces of molars, and the e.1 Class V
lingual surface of anterior teeth - Carious lesions that are
located on the gingival 1/3
b. Class II of the facial and lingual
- Carious lesions surfaces of both anterior and
that are located posterior teeth
on the
proximal
surfaces of
premolars and
molars
- Mesial and
distal surface
in posterior teeth
only

e.2 Class VI
- Simon’s modification
- Lesions involving cuspal tips and incisal
edges
c. Class III
- Carious lesions that are located on the
proximal surfaces of anterior teeth that do
not involve the incisal angle

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023

Exercise

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
- Summarize ICDAS method, identify the

caries occurred on the tooth

Lesion – another term to describe the pathologic
condition on the tooth or the oral cavity
Shifting Paradigms in the Prevention and
Management of Dental Caries International Caries Detection Assessment
System (ICDAS)
ICDAS – Intervention Caries Detection and  degree of severity – how much tooth tissue
Assessment System is affected?
- system to handle dental caries  correlates lesion depth and histological
- assess the patient risk, categories (low, examination
medium, high risk)  2-digits
- suggested treatment to a particular patient o 1st digit = tooth condition
- gives use a simplified management of dental o 2nd digit = severity of lesion
caries
CAMBRA – Caries Management by Risk
Examination Protocol
Assessment
 remove plaque – cleaning procedure
 initial assessment of tooth, wet
Identification, Classification, Prevention and
 dry tooth for 5 sec, re-examine
Management
 Identification of the lesion  use ball-end probe to confirm visual
 Identification of the cause detection – not sharp
 Identification of the risk of the patient
- Doesn’t mean all lesion should be filled Description of ICDAS Scores
Restoration and Sealant Carious Lesion Codes
ICDAS Codes
0 = Not sealed or restored 0 = Sound tooth surface,
 It is an International convention for “staging”
no or slight change after
Caries, after Detection, and the being able to prolonged air drying
1 = Sealant, partial
Assess lesion activity and monitor with a
System 2 = Sealant, full 1 = First visual change in
 It has been developed in response to the lack of enamel seen after
a modern, evidence-based, preventiveoriented 3 = Tooth-colored prolonged air drying
System that can be employed across: Practice, restoration
Research, Epidemiology & Education 2 = Distinct visual
 It has come from a broadly based International 4 = Amalgam restoration changes in enamel
Group with academic, ORCA, FDI, ADA, and
NIH input 5 = Stainless steel crown 3 = Localize enamel
breakdown, no dentin
6 = Porcelain, golf, PFM involvement
crown or veneer
4 = Underlying dark
7 = Lost or broken shadow form dentin (not
restoration captivated into dentin)

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 CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023

8 = Temporary restoration 5 = Distinct cavity with

visible dentin

6 = Extensive distinct
cavity with visible dentin

ICDAS CODE 0 ICDAS CODE 3

 Sound tooth  localized enamel breakdown but no dentin
- Wala guba exposed
- Dry and wet – no lesion seen - only enamel tissue is affect
- Staining only and no demineralized area

ICDAS CODE 1
 opacity seen only when tooth is dry
 confined to the pit and fissure
 differentiate with coffee/tea stains or fluorosis
as these conditions are symmetrical and tend
to be generalized than localized
- demineralized area is seen when dry

ICDAS CODE 2
 opacity seen even when tooth is wet
 on PF, opacity wider than the pit and fissure
dentin exposed
 no enamel breakdown – no loss / cavity
- seen the demineralized area when wet and
more opaque when dry

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
ICDAS CODE 4
 presence of shadow or discolored dentin
 more noticeable when surface is wet
- pit and fissure of molars and premolars
- brown, black or gray is seen

ICDAS CODE 5
 Cavitation exposing dentin involving less than
half of the tooth surface
- Obvious cavitation, has hole

CAMBRA
Caries Management By Risk Assessment
ICDAS CODE 6
 Extensive cavity
 Deep and wide
- More than half the tooth surface
- Dark staining dentin

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
 CUSTOMIZED strategy for management of
caries taking into consideration various risk
factors, protective factors patient is exposed to
and disease indictors

- More on protective factors – change of

balance
- Balance = moderate risk
- Tip the balance to low risk category

Disease Indicators (WREC)

 White spot lesions - Incipient
 Restorations placed in the last three years as a
result of caries activity – napastahan,before,
clue the patient have caries
 Enamel approximal lesions (confined to
enamel only) visible on dental radiographs –
cannot be seen by naked eye but can be seen
in xrays
 Cavitation of carious lesions showing
radiographic penetration in to dentin

Risk Factors (BAD)

 Bad bacteria – acidogenic, aciduric or
cariogenic – some countries do bacterial
analysis to verify what causes the caries
 Absence of saliva – hyposalivation or
salivary hypofunction
 Destructive lifestyle habits – frequent
ingestion of fementable CHO, and poor oral
hygiene – interview
Protective Factors (SAFE)
 Saliva and sealants
 Antimicrobials or antibacterials (xylitol)

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 CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
 Fluoride and other products that enhance
remineralization (Calcium phosphate 1. Low Risk - no dental lesions, no visible plaque,
technologies) optimal fluoride use, and regular dental care
 Effective lifestyle habits 2. Moderate Risk - dental lesion in previous 12
months, visible plaque, suboptimal fluoride,
Caries Risk Assessment Form irregular dental care.
Featherstone et al, CDAJ, 2007 1. High Risk - one or more cavitated lesions,
Circle Yes’s visible plaque, suboptimal fluoride, no dental
Visualize the balance care, high bacterial challenge, impaired saliva,
Decide on caries risk level: Low, Moderate, High, medications, and frequent snacking
Extreme 2. Extreme Risk - high risk patient with special
needs or severe hyposalivation

Bacteria Frequency Frequency Xylitol

Antimicr
Risk Test (CRT of of and/or
obials Fluoride Sealants
Level test) Saliva Radiograp Periodic Baking
hs Oral Exams Soda
Not May be done OTC fluoride Bitewing Every 12
indicated as a baseline containing radiographs mos to
LOW
RISK

reference for toothpaste every 18- reevaluate

new patients twice daily 24 caries risk
months
Not May be OTC fluoride Bitewing Every 12 Xylitol gum Sealants for
indicated done as a containing radiographs mos to or mints. 2 deep pits and
MODERATE

baseline toothpaste twice every 12- reevaluate sticks of fissures

reference daily + Fluoride 18 caries risk gum or 2
RISK

rinse (0.05% months mints 4x

NaF) daily, or daily
5,000 ppm E

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 CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Chlorhexi Bacterial Fluoride varnish Bitewing Every 6 mos Xylitol gum Sealants for
dine and saliva at initial visit radiographs to or mints. 2 deep pits and
0.12% 10 flow test and P.O.Es every 6-12 reevaluate sticks of fissures
ml rinse initially and Prevident 5000 mos or caries risk gum or 2
HIGH RISK

for one at every Plus or Climpro until no and apply mints 4x

minute P.O.E for 5000 (1.1% NaF) cavitated fluoride daily
daily at new patients twice daily lesions are varnish
bedtime or if there instead of regular evident
for one is suspicion fluoride
week each of high toothpaste
month bacterial
challenge
Chlorhexi Bacterial and Fluoride varnish Bitewing Every 3-6 Baking soda Sealants for
dine saliva flow at initial visit, radiographs mos to rinse. 2 tsp. deep pits and
0.12% 10 test each P.O.E. every 6 reevaluate in fissures
ml rinse initially and and after mos or caries risk 8oz. 4-6
for one at every prophylaxis or until no and apply Times daily.
minute P.O.E perio recall. cavitated fluoride Xylitol gum
EXTREME

daily at 5,000 ppm F lesions are varnish or mints 4x

RISK

bedtime Fluoride evident daily

for one containing
week each toothpaste or
month fluoride trays for
at-home
5000 F gel
daily 5 min. plus
otc F toothpaste
2X daily

- Microcavities – apply CHX + composite

Chlorhexidine
 reduces number of Strep Mutans
 Not effective against lactobaccilus
 Available as mouth rinses, gels, toothpastes,
varnish
 most effective reduction achieved with CHX
varnishes, followed by gels and mouthwashes
basis
- should not be use on a daily basis 1 week –
10 days
- can also destroy microorganisms in the oral
cavity that can kill good bacteria
- too much and long period of time – staining
- For patients >6 years who are classified as being
at high or extreme risk of caries
- 30-s rinse (0.12% everyday of the first week of
every month --- effective in reducing level of
MS)
- Under strict dentist supervision (15 ml 30 min
after brushing & 10-14 days maximum)
Xylitol
 Sugar alcohol
 Accumulates intracellularly in MS and inhibits
bacterial growth
 Habitual consumption results in certain
populations of MS becoming less adherent to
tooth plaque. Easily shed off in the saliva and
hence eliminatd.
 Hampers transmission of colonization from
mother to child
Professional Fluoride Systems
Semi-annual or annual topical fluoride applications –
fluoridation (gargle)
- Widely used in dental offices 1960s, 1970s,
1980s, and now
3 systems were common (2% NaF(Sodium Fluoride),
8% SnF2(Stannous Flouride), 1.23% F APF
(Acidulated phosphate fluoride))
- 30% deduction in caries incidence
- cheap

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CARIOLOGY
Dr. Florence May Arquillo-Posecion S.Y. 2022-2023
Use of one-minute treatments became popular during
1980s
- Lack of supporting data, acceptance by
regulatory bodies
- Convenient for both the patient and the
dental office
Now, Fluoride Varnish use is increasing
- More effective, Easier to apply, More
convenient for the patient and dental office
- expensive
Fluoride Varnishes
 5% NaF
 Best for children under age 6
 Good for partially erupted molars
o Enamel of newly erupted molars are
immature and virtually unetchable
 Effective for white spot lesions
 More effective than topical fluoride gels
- Sticky consistency that can easily stick to the
tooth
- Remineralize incipient lesion
Caries Management
 Dental/medical history
 Clinical exam
 Detect caries lesions early enough to reverse
or prevent progression
o ICDAS
 Assess caries risk
o CAMBRA
 Treatment plan including chemical therapy
 Use fluoride and/or antibacterial therapy
based on observations
 Use minimally invasive restorative
procedures to conserve tooth structure
 Recall and review
Take Home Points
 Dental caries is a disease, not merely a lesion.
Thus we should treat and disease and not the
hole (lesion).
o Try to manage the patient according to
the risk
o Identify what cause the disease – how
you will be able to treat the disease
 Caries risk assessment is an important tool in
the prevention and management of dental
caries
o Analyze how to lessen the caries of the
patient
 Caries management should be personalized
according to the patient’s caries risk and
needs.
o Different from one person to another
o Examine the patient – risk
 Not all carious lesions should be restored.
Caries have the ability to remineralize. See
ICDAS, CAMBRA
 Prevention and maintenance is important
throughout life.
o Fluoride treat and teach the patient
how to manage their oral cavity
 Heal or restore the WREC, avoid the BAD,
live SAFElY
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