3. Introduction
ā¢ Etiology:
Aetiology or Etiology is the study of causation or
origination.
aitĆa = cause Logia = science or Logy= study
ā¢ Pathology :
is the study of disease
Pathos = Suffering.
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4. Dental Caries :
ā¢ is a prevalent chronic infectious disease
resulting from tooth-adherent cariogenic
bacteria that metabolize sugars to
produce acid, which over time
demineralizes tooth structure.
ā¢ The term dental caries is the results of a
localized chemical dissolution of the
tooth surface caused by metabolic
events taking place in the biofilm (dental
plaque) covering the affected area.
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5. Biofilm:
is an assembly of surface
associated microbial cells
enclose in an extracellular
polymeric substance
material ( Dental Plaque )
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7. Caries Theory:
THE NONE SPECIFIC
PLAQUE
HYPOTHESIS
THE SPECIFIC
PLAQUE
HYPOTHESIS
o in this theory
Streptococcus
mutans it's the main
cause for caries
o S.Mutans + EPS
Acid production
pH
THE EQOLOGICAL
PLAQUE
HYPOTHESIS
o The frequency of
sugar intake leads to
a decrease in PH
lade to shifting the
ecology of the plaque
to a more caries-
conductive
conditions.
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o Different types of
bacteria lead to
carious lesions
o Other streptococcus
species ( S.oralis,
Bifidobacteria,
Lactobacilli )
8. Stephan Curve
o Stephan curve is a graph which
reflected the fall in pH values of
dental plaque before, during
and after food intake
o The pH slowly returns to
original over period of time
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9. Traid of Dental Caries
o Host factor
o Saliva
o Dite
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11. Introduction
Dental plaque is general term for the
complex microbial community found on
Dental caries is the result of the metabolic
activities of bacteria in microbial
communities on teeth termed dental
biofilms (often referred to as dental plaque)
Most of the surface of a tooth is kept free
of bacteria by friction from the tongue,
cheeks, and foodstuffs. However, bacteria
colonize areas of the surface protected
from these frictional forces (plaque
stagnation areas) and form a film of closely
packed bacteria known as dental plaque.
Dental Plaque
11
12. Definition
Definition. Dental plaque is a general term
for the complex microbial community found
on the tooth surface embedded in a matrix
of polymers of bacterial and salivary
origin.The term ādental plaqueā has been
used by the dental profession since G.V.
Black (see Preface) de- fined it at the end
of the 19th century.
Dental caries is the result of the metabolic
activities of bacteria in microbial
communities on teeth termed dental
biofilms (often referred to as dental plaque)
Dental Plaque
12
13. * Biofilm is composed of micro-colonies of bacterial cells
(15-20% by volume), which are distributed in matrix or
glycocalx ( 70- 80% by volume)
* Biofilms have demonstrated presence of water channels
between the micro-colonies.
* These water channels permit the passage of nutrient and
other agents through out the biofilm acting as a circulating
system Some of the functions of the biofilm depend on the
ability of bacteria and micro-colonies within the biofilm to
communicate with each other.
Structure
17. a. Bacterial which is one gram of plaque in a wet condition
contains 2x10 bacteria
b. Non bacterial which include mycoplasma species,
yeasts, viruses.
Microorganisms
18. a. Organic constituents include polysaccharide, proteins
and lipid.
b. Inorganic constituents is mainly calcium and
phosphorus with trace amount of other minerals such as
sodium potassium and fluoride.
Intercellular Matrix
19. pellicle formation
Dental plaque 19
ā¢ Microorganisms do not colonize directly on the
mineralized tooth surface.
ā¢ the pellicle that forms on the ānakedā tooth surface
within minutes to hours.
ā¢ The major constituents of the pellicle are salivary
glycoproteins, phosphoproteins, lipids.
ā¢ Salivary pellicle can be detected on clean surface
within 1 min.
ā¢ By 2 hours, the pellicle is essentially in equilibrium
between absorption and detachment, although
further pellicle maturation can be observed for
several hours.
20. Initial colonization
ā¢ The microbial cell approaches the pellicle-coated
surface, long-range but relatively weak
physicochemical forces between the two surfaces are
generated.
ā¢ There are a specific molecules on the bacterial surface
called adhesion, which interact with receptors present
in the dental pellicle.
ā¢ Within a short time, these weak physicochemical
interactions may become stronger owing to adhesion
on the microbial cell surface becoming involved in
specific, short-range interactions with complementary
receptors in the acquired pellicle.
ā¢ A high degree of surface hydrophobicity may facilitate
attachment.
Dental plaque 20
21. Secondary colonization & plaque
maturation
ā¢ The primary colonizing bacteria adhered to the
tooth surface provided new receptors for
attachment with other bacteria in a process known
as co-adhesion
ā¢ The secondary colonizers also attach to the
established pioneer species via adhesion receptor
ā¢ interactions (termed coaggregation or co-
adhesion)
ā¢ As the bacterial deposits become thicker, a
lowering of the oxygen concentration (increased
anaerobiosis) is one of the factors that help to drive
microbial succession.
ā¢ Examples of these types of coaggregation of F.
Nucleatum with P. gingivalis or Treponema
denticola.
Dental plaque 21
22. Conclusion
ā¢ Dental plaque biofilm cannot be
eliminated permanently.
ā¢ Dental plaque is regarded as one of the
main etiological factors in the initiation
and promotion of periodontal diseases
such as gingivitis, periodontitis, dental
caries.
ā¢ The pathogenic nature of dental plaque
biofilm can be reduced by maintaining
the oral flora with appropriate oral
hygiene methods that includes daily
brushing, flossing, rinsing with anti
microbial mouthrinses.
Dental plaque 22
24. Diet
Diet is etiological factor for caries It
causes disturbance of balance in
the equilibrium between tooth
substance and micro organisms
The major components of die ā
carbohydrates, proteins, fats, fruits,
vegetables, and various
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25. Theories of dental caries :
1_ Dairy products are non cariogenic because
they increase salivary flow unless sugar is
added to them
2- Fats are non cariogenic due to itās oily
medium, thus decreasing plaque adherence
3- proteins are non cariogenic as well, because
itās digested into urea which is not cariogenic
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26. o all modulate the caries process, playing either a
promotional or inhibitory role
oFermentable carbohydrates play a promotional role
in the development of dental caries as they are the
main component of the diet that begin digestion in
the oral cavity by salivary amylase and can be
acted upon by plaque bacteria producing acids on
the tooth surface
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27. Types of sugars
There are three types of
sugars:
conventional sugar
As sucrose, lactose,
glucose, fructose, and corn
syrups
Suger alcohols
as: xylitol
Intense sweetenesr
As aspartame
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28. sucrose is fermented by S. mutans
and itās fermented by glycolysis
process It's the arch criminal of
caries streptococcus do the
following :
1-store intracellular
polysaccharides.
2-extracellular polysaccharides to
bind to enamel surface.
3-Facultative anaerobes.
4-acidogenec and can survive in
acidic medium so more and more of
acid > enamel caries.
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29. oA diet rich in readily
fermentable carbohydrates
promotes the development of
dental caries due to the
efficient metabolism of these
sugars by cariogenic
microorganisms, such as S.
mutans So by diet > resident
bacteria become pathogenic
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30. Factors Modifying the Role of
Sugars in Caries Development:
1- Types of Carbohydrates
2- Frequency of Sugar
Intake
3- Consistency of the
Sugary Food
4- Amount of Sugar Intake
5- Thickness and Age of the
Plaque
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32. Stephan curve
The curve is divided into two phases:
(reflecting the underlying pattern of bacterial metabolism)
a. Initial rapid pH fall from the resting value (approximately
pH 7)
b. Slow recovery of the pH
- The critical pH for enamel is around 5.5
the lowest value at which the most aciduric bacteria can
produce acids ~ 4).
- Cariogenic challenge is the period between critical pH
and minimal pH .
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33. Sugar Alcohols
oThe sugar alcohols that
are most frequently used
as substitutes for sucrose
are xylitol, sorbitol, and
maltitol
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35. Xylitol
occurs naturally in many fruits,
berries, and vegetables and has
been used as a sugar substitute for
many years in confectionery.
Xylitol has long been known to be
noncariogenic in humans and
animals
its ability to decrease the number of
mutans streptococci in saliva and
inhibit formation of dental plaque
has been reported by some
scientists to facilitate
remineralization of early caries, and
to arrest the progress of caries
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36. These two functions were
attributed to two factors:
a) salivation
stimulation
B) form complexes
with calcium and
phosphate ions
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37. main reasons limit the use of xylitol as a
substitute for simple sugars
1- xylitol is relatively
expensive as a bulk
sweetener.
2- it is poorly hydrolyzed in
absorbed from the small
intestine and thus may cause
osmotic diarrhea.
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41. Host factors affecting
dental caries
It can be classified into:
ā¢ Local factors.
ā¢ Systemic factors.
ā¢ General factors.
Host factors affecting dental caries
form through a complex interaction
between bacteria ,fermentable
carbohydrate , teeth and saliva.
42. Local Factors
Tooth Surface:
Tooth surface which favor
plaque retention are prone to
decay these sites are ??
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43. ā¢ presence of deep margins , occlusal pits and
fissures or buccal pits tends to trap food &
bacteria.
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44. primary teeth are more susceptible to caries than
permanent teeth, cause they have proportionally
thinner enamel and dentine compared to
permanent teeth.
45. ā¢ Also tooth with orthodontic appliance , clasps of
partial denture and defective restorations are
more susceptible to caries.
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46. Posterior tooth are more
susceptible to caries than
anterior tooth as washing
process is more harder in
posterior area than in the
anterior and also in upper than
lower.
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48. 1-Global Distribution
( socioeconomic state)
ā¢ Caries has historically been seen in high income
countries with low prevalence in poorer countries.
The most observed reasoned for this pattern is
usually considered to be diet and life style due to
high consumption of refined carbohydrates.
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49. 2- Age and Gender
oDMT (sum of number of decayed ,missed and filled
tooth ) increase by increasing of age
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50. ā¢ Also root caries is
high prevalent
among older
people in high
income countries
as its strongly
associated with
loss of periodontal
attachment.
ā¢ Woman visit
dentist more than
men as woman
has high DMT than
men due to
hormonal changes
and high sugar
and carbohydrate
consumption by
woman
ā¢ Smoker people
are more
susceptible to
caries than non
smoking people
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51. Systemic factors
oUse of multiple medication among elderly
people can promote xerostomia, as itās a
major risk factor for caries among people of
any age especially who have tumours and
receive radiations as saliva plays an
important role in control of caries.
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52. saliva
1. Introduction
2. What's is saliva and its composition
3. Classification of salivary glands
4. Function of saliva
5. Control of salivary secretion
6. Saliva secretion (two-step model)
7. Disease and factors affecting salivation
8. Management of salivary gland hypofunction
9. Role of pellicle
10. Inorganic saliva composition
11. Protein buffer system
12. Saliva buffer capacity & PH regulation
53. The oral is a moist environment ; a film of fluid called
saliva coats its inner surface and occupies the space
between the lining oral mucosa and the teeth.
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This Photo by Unknown Author is licensed
under CC BY-SA
54. What is saliva and its composition
ā¢ saliva is composed of more than 99% water and less than
1% solids , mostly electrolyte and proteins , the latter giving
saliva its characteristic viscosity
ā¢ The daily production of whole saliva ranges from 0.5 to 1.0
litres.
ā¢ 90% of whole saliva is produced by three paired major
salivary glands
ā¢ Parotid
ā¢ Sub mandibular
ā¢ Sublingual gland
ā¢ Other minor salivary glands secrets only some what less
than 10% of secretion.
ā¢ Saliva is called āāthe body mirrorā as it reflect the physiological
state of the body including emotional endocrinal and
metabolic variations.
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57. Classification and anatomy of salivary gland
oThe largest salivary gland is the parotid gland , which are purely serous
gland that produce thin watery amylase-rich saliva
oSubmandibular gland produce around two thirds
oThe latter are mixed glands comprising both mucus and serous acinar
cells although they are mainly serous glands
oThe sublingual glands is the smallest of major glands consisting mainly of
mucous acinar cells so it produce such viscous secretions, although they
only contribute a few percent of volume of whole saliva
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59. ā¢ - Other minor salivary glands is very important as it secretes saliva proteins
which play important role in lubrication.
- They are named according to their location
- labial , buccal ,palatine ,lingual or glossopalatine glands.
- The minor glands are mixed composed of mucous acinar cells except:
Palatine glands ( strictly mucus), Lingual von ebner glands ( serous glands)
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60. Control of salivary secretion
- salivary secretion is controlled by both sympathetic &
parasympathetic stimuli.
- It is secreted in response to neurotransmitter stimuli.
- The sympathetic control of salivary production is via the superior
cervical ganglion. Sympathetic stimulation results in the release of
noradrenaline, which acts upon alpha- and beta-adrenergic
receptors. This results in decreased production of saliva by acinar cells,
increased protein secretion, and decreased blood flow to the glands
61. On the other hand, the parasympathetic outflow is coordinated via centers
in the medulla, and innervation occurs via the facial and glossopharyngeal
nerves. Parasympathetic outflow results in the release of acetylcholine
(ACh) onto M3 muscarinic receptors. This results in increased secretion of
saliva by acinar cells, increased HCO3- secretion by duct cells, co-
transmitters resulting in increased blood flow to the salivary glands, and
contraction of myoepithelium to increase the rate of expulsion of saliva
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66. Pathological factor affecting salivation
Many medications induce complaints of oral dryness and
influence saliva flow rate and composition like :
. Also presence of systemic disease and auto immune disease is
common cause of impaired saliva secretion and compositional
change like Sjogrenās syndrome.
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ā¢ Diuretics may induce compositional changes and inhibit effects of electrolyte
transporters in salivary gland.
ā¢ Another iatrogenic cause is radiotherapy against cancer especially in head
and neck region
67. Management of salivary gland hypofunction
Patient with salivary gland hypofunction are predisposed for caries and
oral mucosal infection so prophylactic dental program is often
necessary . It include careful oral hygiene instruction to improve the
patient oral hygiene and regular follow up (at least every 3 months) at
dental clinic including :
oDental plaque control
oDietary instruction and advice
oRegular application of fluoride to reduce caries activity as also sugar-free
chewing gum containing fluoride
oAdvice patient with hypo salivation to sip water and after meal, mouth should
be rinsed with water
oSome drugs are taken to increase salivation
oAlso some mouth gel , oral sprays or artificial saliva can be used to increase
salivation as it contain carbo methylcellulose , mucins or electrolyte.
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69. Critical PH
oSaliva PH 6.3
oBelow pH5.5 demineralization accures
othe pH value that representing to
situation of (IAP), (SP)
Saliva's ion activity product (IAP) &
Solubility product of hydroxyapatite (SP)
of human tooth
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70. Degree of saturation and critical ph
Saliva's ion activity product (IAP)
(IAP)= (CaĀ²+)10 (PO,Ā³Ā·)Ā¤ (OHĀØ)Ā²
Solubility product of hydroxyapatite (SP) of human tooth
1. If IAP>SP, saliva is supersaturated
REMINERALISATION OCCUR
2. If IAP< SP, saliva is undersaturated
DEMINERALISATION OCCUR
3. If IAP-SP, saliva is saturated NO
REMINERALISATION NO
DEMINERALISATION
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72. Human saliva Buffer system
A-bicarbonate.
osaliva kPa ranges from (6.2-7.6)
kpa 6 rich is equal to the PCO2 in blood
obuffering hydrogen ions equal to around half its concentration at
the ph value for carbonic acid,
Function
o raises the pH of the saliva, and greatly enhances its buffering
power.
odissolve mucus and loosen debris.
oCan overcome acid producing from dental plaque
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73. Buffer system
B-Phosphate
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oThe pK value for this equilibrium is
around 7 in human saliva
ohave their best effects in the range of Ā±1
pH unit around their pK values
Function :pH rising capacity to the buffer
system.
oIf phosphate level decrease + increase
salivary flow this leads to decrease of
contribution of phosphate in buffer
system
74. Buffer system
C-Saliva protein
oeach 1 mm of saliva contain 1 -2mg of proteins
omainly glycoprotein
oLess buffer capacity than phosphate and bicarbonate
Saliva
oprotein either mucous or serous or mixed
Function :
-Give viscosity to saliva
-Forming diffusion
barrier to protect teeth
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75. Buffer system
C-Saliva protein
1.Mucous glycoproteins
2.Serous glycoproteins
3.Calcium binding proteins
4.Digestive enzymes
5.Antimicrobial proteins and peptides
6.Agglutinins
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76. ohave a high molecular weight
o contain more than 60% carbohydrates
Function :
1. mucins help to protect the mucosa from infections.
2. also interact with dental hard tissues
3. may mediate specific bacterial adhesion to the
tooth surface
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Buffer system
C-Saliva protein
1-Mucous glycoproteins
77. Buffer system (saliva protein)
2-Serous glycoproteins
olower molecular weight than mucins
ocontain less than 50% carbohydrate
o liquid fluid composed mainly of water and proteins, such as the
digestive enzyme amylase
Function :
1-protect against invading pathogens
2-breakdown large starch macromolecules
into simple sugar molecules that will be
further digested as they move through the gastrointestinal system.
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78. Buffer system (saliva protein)
3-calcium binding proteins
oserves as a storage for calcium and
phosphate ions, which are required for
remineralization of initial enamel
lesions
Function :
regulate the amount of
free (unbound) Ca2+ in the cytosol
of the cell.
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79. Buffer system (saliva protein)
4-Digestive enzymes
oAmylase is the most abundant salivary enzyme
Function:
clears food debris which containing
starch, from the mouth
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80. Buffer system (saliva protein)
5-Antimicrobial proteins and peptides
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81. Buffer system (saliva protein)
6-Agglutinins
concentration in saliva is less than0.1%, but as little as 0.1 Ī¼g
Function :
interact with unattached bacteria,
resulting in clumping of
bacteria into large aggregates,
which are more easily flushed
away by saliva and swallowed.
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82. salivary flow rate measurement
oClinical examination
-Pt chief complain : should be xerostomia , oral dryness ,
compromised oral function
-pt history : medication , disease and radiation
oTools :
1.Plastic cup
2.watch
3.electronic weight
4.1 g of paraffin (inert chewing material) for saliva stimulation.
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83. salivary flow rate measurement
oPreparation
1. patients must have nothing by mouth, including
smoking, for at least 90 min before the measurement
2.The patient should be seated in a relaxed position with
elbows resting on knees and with the head
3.tilted forward between the arms to allow the saliva to
drain passively from the lower lip into a pre-weighed
plastic cup.
4.Even slight movements of the tongue, cheeks, jaws or
lips should be avoided during the collection period
oAllow the patient to dribble into a
measuring container over 15 min
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84. salivary flow rate measurement
oAfter weighing
othe saliva-containing plastic cup and subtracting the weight
of the cup, the flow rate can be calculated in g/min, which
is almost equivalent to ml/min
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85. Dental pellicle
DEF :
HOMOGENOUS, MEMBRANOUS,
ACELLULAR, THIN FILM OF
BACTERIA COVERS THE TOOTH
SURFACE IT FORMS INTERFACE
BETWEEN TOOTH STRUCTURE &
DENTAL (PLAQUE AND CALCULUS )
86. Dental pellicle
Size :
ranging from 1Ī¼m to 10Ī¼m
āgetting thicker by timeā
Formation time :
Even if removed by the dentist during a
professional cleaning, it will start
forming again within seconds and fully
established within 30 min
- can be detecting by using disclosing
agent
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87. Dental pellicle
Composition :
1.Glycoproteins (e.g.,mucins )
2.phosphoproteins (e.g.,
statherine )
3. lipids
4. Remnants of cell walls from
dead bacteria
5. proline rich protins
6. histidine rich protein
7. enzymes (e.g., amaylaze )
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88. Dental pellicle
1. Protective barrier
-The presence of a pellicle inhibits subsurface
demineralization of enamel
-restricting transport of ions in and out of the dental hard
tissues.
2. Lubricant
responsible for the lubrication of tooth-to-soft-tissue contact
as well as tooth-to-tooth contact.
3. Prevent tissue desiccation
can help defending the teeth from acidic attacks due to its
selective permeability.
4. Substrate to which bacteria attaches
due to the presence of specific receptors and hydrophobic
components
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89. Fluoride
o mineral, is naturally present
in many foods and available
as a dietary supplement.
oform of the element
fluorine.
Function :
-inhibits or reverses the
initiation and progression of
dental caries (tooth decay)
-stimulates new bone
formation
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90. Fluoride
oThe fluoride concentration oral fluid
depends present in the environment, above
all in the drinking water.
o In areas with low concentrations of
fluoride in the drinking water the basal
concentration of fluoride in whole saliva
may be lower than 1 Ī¼mol/l. In
oareas with higher levels of fluoride in the
drinking water thebasal salivary
concentration may be much higher.
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91. Fluoride
oBut large amounts of fluoride can be toxic. I
ot can also result in fluoride-induced tooth
discoloration (fluorosis)
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