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IRDS exam 2 > Cariology > Flashcards

Cariology Flashcards

1
Q

What is the definition of caries?

A

Demineralization and loss of substance of the hard tissues of the teeth, leading to continued destruction of enamel and dentine, and cavitation of the tooth.

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2
Q

What 3 factors are involved in caries formation?

A

Host and saliva, diet, and microflora

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3
Q

What are the 5 risk factors in caries development?

A
  1. Pathogenic plaque bacteria
  2. Poor oral hygiene
  3. Reduced salivary flow/ Systemic conditions
  4. Bad dietary habits
  5. Anatomic variations: hard to clean areas
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4
Q

What are the 5 protective factors from caries development?

A
  1. Non-pathogenic plaque bacteria
  2. Good oral hygiene
  3. Adequate salivary flow
  4. Good dietary habits
  5. Fluoride, xylitol
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5
Q

What are the 3 functions of enamel?

A
  1. Provides hard, durable surface for teeth
  2. Forms a protective cap for the dentin and pulp
  3. Gives shape of teeth
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6
Q

What are the 2 basic structural units of enamel?

A
  1. Cylindrical enamel rods

2. Surrounding interrod enamel

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7
Q

What are the 2 protective mechanisms of enamel?

A
  1. Tightly compressed crystals- little or no space for acid penetration
  2. Renewal of calcium, phosphates, and fluorides
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8
Q

What is the result of enamel’s protective mechanism?

A

The dynamics of demineralization can be stopped or reversed.

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9
Q

What is enamel?

A

Acellular and predominantly mineralized epidermal tissue.

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10
Q

What is the function of calcium ions in enamel?

A

Transported as “seeds” of hydroxyapatite. They form a site for cystallization. Crystals enlarge and supplant organic matrix.

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11
Q

What is the building blocks of enamel crystal?

A

Molecular units of hydroxyapate

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12
Q

What can diffuse through the semipermeable enamel?

A

Various fluids, ions, and low-molecular-weight substances.

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13
Q

True or False:

Enamel is capable of self-repair.

A

False

Incapable of self-repair, but capable of remineralization.

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14
Q

What is the process of remineralization?

A

After initial stage of mineral loss, enamel fills void with new mineral: alterations in the dynamics of mineralization process through the incorporation of fluoride from various sources.

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15
Q

What is the process of initial demineralization?

A
  1. Enamel exposed to acids for a brief time
  2. Spacing and divergent orientation of crystals result in between rod and interrod enamel
  3. Makes enamel rod differentially soluble
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16
Q

What characteristic of enamel makes it more susceptible to acid penetration?

A

Certain areas of our enamel does not have perfect alignment: more susceptible.

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17
Q

What component of enamel are most susceptible to demineralization and first to be solubilized?

A

Carbonated components of the crystal.

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18
Q

Enamel’s crystalline makeup and rigidity/brittleness makes it more susceptible to what 4 things?

A
  1. Acid demineralization
  2. Attrition (“wear”)
  3. Erosion/abrasion
  4. Fracture
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19
Q

Enamel’s hardness is ___ times that of dentin’s.

A

5

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20
Q

What are the 5 functions of dentin?

A
  1. Forms bulk structure of the tooth
  2. Elastic foundation for the enamel
  3. Provides color (pale yellow)
  4. Protective barrier and chamber for vital pulp tissues
  5. Responds to external thermal, chemical, and mechanical stimuli
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21
Q

Which is harder, dentin or bone?

A

Dentin is slightly harder than bone, but not as hard as enamel.

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22
Q

Root dentin is covered with ________ and crown dentin supports the _________.

A

Covered with cementum and supports the enamel.

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23
Q

What makes up dentin?

A

45-50% inorganic apatite crystals

30% organic matrix

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24
Q

What is the function of intertubular dentin?

A

It is the structural component of the hydroxyapatite-embedded collagen matrix. Forms the bulk of dentin structure.

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25
Q

Where is the peritubular dentin and what are its components?

A

Limited to the lining of the tubule walls. Has little organic matrix but densely packed with minuscule apatite crystals.

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26
Q

What is the difference in composition between enamel and dentin?

A

Inorganic hydroxyapatite: E-96% D- 45-50%
Organic matrix: E- 1% D- 30%
Water: E- 4% D- 25%
*Enamel:Nail::Dentin:Skin underneath

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27
Q

What is the affect of time on intertubular dentin and peritubular lining?

A

Primary intertubular dentin remains dimensionally stable, but peritubular lining gradually increases in width over time.
*pulp chamber gets smaller with age

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28
Q

When is primary dentin formed and under what conditions does it continue to form?

A

It is the first dentin to be formed (by odontoblasts).

Formation continues even after tooth is matured, as long as root apex remains undeveloped and open.

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29
Q

When is secondary dentin formed and what are the effects of its formation?

A

Formed as tooth is maturing. Reduces the volume of the pulp chamber, pulp horns, and root canals.

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30
Q

Where is the tertiary dentin formed and what are its functions?

A

Formed at the dentin-pulp interface. Compensates for the loss of peripheral dentin from caries or injury. May provide superior pulpal seal against noxious diffusion thru tubules.
*The reactionary/reparative dentin.

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31
Q

In what sequential ways does dentin respond to injury or active caries?

A
  1. Immediate inflammatory response
  2. Increased outward flow rate of tubular fluid
  3. Passage of plasma proteins into the dentinal fluid
  4. Direct immune response to bacteria.
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32
Q

What happens during dentin’s immediate inflammatory response?

A

Pulpal vasodilation, increased blood flow, and increased interstitial fluid pressure.

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33
Q

Which two plasma proteins are passaged into the dentinal fluid during dentin’s inflammatory response?

A

Albumin and immunoglobulin passaged between the odontoblast cells into the dentinal fluid.

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34
Q

True or False

The diffusion of exogenous stimuli to the pulp is limited.

A

True and it forms direct immune response to bacteria.

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35
Q

What is tubular sclerosis?

A

Dentin reaction against caries by deposition of mineral within the dentin tubules, resulting in gradual occlusion (clogging of passageway)

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36
Q

How does tertiary dentin respond to caries or trauma?

A

Odontoblasts form tertiary dentin at the pulp-dentin border as a response to stimulus.

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37
Q

What happens to dentin-pulp complex in moderate and slow developing stimuli?

A
  1. It has time to hyper mineralize or sclerose the tubule channels.
  2. Can add new tertiary dentin at the pulp-dentin junction. (PDJ)
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38
Q

What happens to dentin-pulp complex in trauma/ rapid advance of caries lesion/ deep cavity preparation?

A
  1. Numerous open tubules –> vulnerable pulp
  2. Bacteria reaches level of PDJ
  3. Pulpal necrosis
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39
Q

What is pulp?

A

Viscous CT of collagen fibers and organic ground substance supporting the vital cellular, vascular, and nerve structures of tooth.

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40
Q

What are the functions of pulp?

A
  1. Formative: generats dentin (dentinogenesis)
  2. Nutritive
  3. Sensory: Nociception (neural processing of noxious stimuli: pain)
  4. Protective
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41
Q

How does pulp provide nutrition to the teeth?

A

Provides 1. vascular supply and 2. ground substance transfer for metabolic functions and maintenance of cells and organic matrix.

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42
Q

How does pulp protect the teeth?

A

Coordinates inflammatory, antigenic, neurogenic, and dentinogenic responses to injury and noxious stimuli.

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43
Q

What is the composition of pulp?

A

75% water and 25% organic material

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44
Q

How is the pulp vascularized?

A

Through one opening (apical foramen) and it is completely surrounded by rigid dentinal walls.

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45
Q

What are the advantages or disadvantages of pulp?

A

Advantages: protected and isolated. Sensitive but resilient tissue with great potential for healing.
Disadvantages: Limited collateral blood supply. Limited expansion space (bc of enamel) for swelling during typical inflammatory response–> pressure.

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46
Q

What are the zones of the pulpal tissue?

A
  1. Peripheral odontoblastic layer
  2. Cell-free zone
  3. Cell-rich zone
  4. Pulp core
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47
Q

What is the process of demineralization?

A
  1. Bacteria feed on carbohydrates producing acid as byproduct and lowering pH
  2. Acids diffuse into tooth
  3. Acids dissolve carbonated hydroxyapatite crystal
  4. Subsurface lesion (partial demineralization)
  5. Cavitation
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48
Q

Which step of demineralization is reversible and how is it reversed?

A

Subsurface lesion step. Reversed by addition of fluoride, phosphate, and calcium.

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49
Q

Which minerals are lost during demineralization?

A

Calcium, phosphate, and carbonate.

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50
Q

What is the result of remineralization?

A

Hydroxyapatite turns into fluorohydroxyapatite, which is more stable and less acid-soluble crystals than hydroxyapatite.

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51
Q

What is cavitation?

A

Breakdown of outer enamel due to caries, mechanical injuries (mastication), microtraumas (wear), iatrogenic trauma (careless probing). At this point, remineralization is not guaranteed.

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52
Q

Why is cavitation conducive to further demineralization?

A

Difficult to remove biofilm out of cavitated area.

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53
Q

What is the evolution of caries?

A
  1. Adhesion
  2. Colonization
  3. De- & Re-mineralization
  4. White spot
  5. Enamel lesion
  6. Dentin lesion
  7. Pulpal lesion
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54
Q

What is the result of greater demineralization than remineralization?

A

White spot lesion

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55
Q

At point is demineralization still reversible?

A

White spot lesion. Once evolved into enamel lesion, bacteria more protected leading to cavitation.

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56
Q

True or False

Caries is caused by commensal organisms not infecting invaders

A

True

Commensal organism: normal bacteria flora in mouth that normally does no harm.

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57
Q

Where does dental caries take place?

A

On any tooth surface where plaque is allowed to develop e.g. enamel, dentin, and cementum

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58
Q

True or False

Microbial adhesion/colonization is vital to have caries and cause disease

A

False

Adhesion/colonization is vital but not necessarily sufficient to cause disease

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59
Q

What is the carious process once the biofilm forms at tooth surface?

A
  1. Bacteria ferment carbs and produce acid

2. Acids lowers pH ( longer periods of demineralization and not enough time for remineralization

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60
Q

What is the critical pH threshold for enamel? For dentin?

A

Enamel: 5.5
Dentin: 6.5

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61
Q

Is caries a preventable disease?

A

Cannot be prevented, can only control progression of lesions.

62
Q

What are the three factors for prevention of caries?

A
  1. Control of pH in plaque (oral hygiene and diet)
  2. Adequate salivary flow
  3. Exposure to fluoride
63
Q

Where does caries form?

A

Areas of plaque retention that are not exposed to routine removal.
(Pits and fissures, buccal palatal pits, interproximal spaces, gingival to contact area, CEJ, exposed root surfaces, margins of existing restoration, surfaces adj to dentures)

64
Q

What are routine forms of plaque removal?

A

Mastication, attrition (wear), brushing, and flossing

65
Q

What are the 3 types of caries?

A
  1. Primary caries: on unrestored surfaces
  2. Recurrent/Secondary caries: Primary caries next to restoration. Caused by biofilm at tooth surface.
  3. Residual caries: Demineralized and infected tissue left behind by dentist before restoration is placed.
66
Q

What are the causes of primary caries?

A
  1. Increase in consumption of refined carbs
  2. Inadequate exposure to fluoride
  3. Repeated exposure to acids (frequent pH drop)
  4. Hyposalivation (drugs or radiation)
  5. Bottle or nursing
67
Q

What are the two ways in which secondary caries occur?

A
  1. Outer lesion: Similar to primary chemically and histologically. Primary attack on surface of tooth adj to restoration.
  2. Wall lesion: may start on the wall of cavity due to microleakage
68
Q

What are the reasons for secondary false positives?

A

Discoloration or shadowing next to an existing amalgam (corrosion products discolor tooth) or composite restoration (improper cavosurface margins: redetermine after polishing).

69
Q

What can be the cause of residual caries?

A
  1. Spread of caries at the DEJ in restored tooth

2. Failure to remove all diseased tissues

70
Q

How to diagnose residual caries?

A
  1. May be darkly stained or very light in color
  2. Can be hard or crumbly
  3. If cultured, few microorganisms, which may not survive due to sealed restoration’s nutrient cut-off
71
Q

What does smooth surface caries typically look like?

A

Triangular shaped lesion with wider base part on the surface.

72
Q

How do occlusal caries form?

A

Lesion spreads laterally in an undermining manner. Lesion gets wider towards gingival.

73
Q

What is the diff btwn active and inactive caries?

A

Active: Progressive caries (Slow and fast progressing lesion)
Inactive: Lesion that formed years previously then stopped further progression. Shiny, hard, dark.

74
Q

What happens with slowly progression lesion in active caries?

A

More darkly stained (tea or coffee), pulp recession, tubular sclerosis, tertiary dentin formation

75
Q

What are 3 preventative measures for inactive caries?

A
  1. Prevention of plaque accumulation sites
  2. In-office fluoride application
  3. Monitored at every visit
76
Q

What is white spot lesion and where is it most often observed?

A

Initial stage of carious lesion and more often observed under plaque retention sites.

77
Q

What does a white spot lesion look like?

A

Opaque area with a matte and chalky white look. Feels rough, and more visible on dry tooth.

78
Q

Why do active white spot lesions look chalky and rough?

A
  1. Increased enamel porosity due to demineralization and loss of translucence
  2. Irregular surface texture due to outer surface erosion
  3. Dissolution of enamel
79
Q

What does inactive white spot lesions look like and how do you treat it?

A

Shiny surface. Abrasion and polishing exposes more tightly packed crystals. It is more resistant to acid attack (like scar tissue)
May be brown in color.

80
Q

Which one is deeper? White spot lesion visible in wet & dry field or one visible in only dry field?

A

Wet and dry field is deeper

81
Q

Where is dentin’s zone of destruction?

A

Most superficial dentin is decomposed by acids and proteolytic microorganisms.

82
Q

Where is dentin’s zone of penetration?

A

Tubular invasion of bacteria

83
Q

True or False

Demineralized dentin contains bacteria

A

False

Contains no bacteria

84
Q

What are dentin’s dead tracts?

A

It is when lesion progress rapidly and the odontoblast processes are destroyed without producing tubular sclerosis

85
Q

What is liquefaction foci?

A

Breakdown of dentinal tubule due to bacterial invasion.

86
Q

Where are root caries located?

A

Below the CEJ even if root is exposed. Mostly right below CEJ, within 2mm.

87
Q

True or False
Cavitated root caries may be active.
Non-cavitated root caries are inactive.

A

False
Cavitation may be active or inactive.
Noncavitated (early) root caries are mostly active.

88
Q

How do you clinically diagnose root caries?

A

The base of the cavitated area can be soft, leathery, or hard to probing.

89
Q

What is rampant caries?

A

Multiple active carious lesions in same patient. Involves surfaces that would usu be caries-free. May be caused by imbalance of demineralization over remineralization.

90
Q

What are the causes of childhood caries?

A

Botte nursing- prolonged exposure to sugary drinks

e.g. EEC (early childhood caries)

91
Q

What are the 4 modalities in treatment decision making?

A
  1. D1- Clinically detectable enamel lesion with intact surface (Non-operative & preventive Tx)
  2. D2- Clinically detectable cavity limited to enamel (Operative Tx & Preventive Tx)
  3. D3- Clinically detectable lesion in dentin (Operative Tx & Preventive Tx)
  4. D4- Lesion into pulp (Endodontic and Operative Tx & Preventive Tx)
92
Q

What are the 5 factors that call for operative treatment?

A
  1. Cavitated tooth: sensitive to hot/cold and sweet
  2. Occlusal and proximal lesions extend deep into dentin and cannot be reached by toothbrush
  3. Pulp is endangered
  4. Previous attempts to arrest lesion failed
  5. Esthetics
93
Q

What is the most important reason for placing a restoration?

A

To aid in plaque control

94
Q

What is the ranking of caries depth severity according to ICDAS criteria?

A

0- Sound
1- First visual change in enamel (seen only after prolonged air drying or within confines of pit or fissure)
2- Distinct visual change in enamel
3- Localized enamel breakdown (wo clinical visual signs of dentin involvement)
4- Underlying dark shadow from dentin
5- distinct cavity with visible dentin
6- Extensive distinct cavity with visible dentin

95
Q

What are the decision making factors with caries?

A
  1. Caries or staining?
  2. Arrested or Active?
  3. White spots or decalcified areas?
  4. Cavitation only within enamel or involve DEJ?
96
Q

What is the difference between sign and symptom in dentistry?
Signs+ Symptoms= ?

A

Sign is the objective side of determining a problem via the dentist.
Sympton is the subjective side of the problem via the patient.
Signs + Symptoms= Detection

97
Q

What is the difference between detection and diagnosis?

A

Detection identifies signs and symptoms and diagnosis identifies the disease.

98
Q

What are the different caries detection methods(9)?

A

Radiographs, proper lighting (mouth mirror), optical technology (LOOPS), Explorer/Periodontal probe, transillumination, floss, caries detector dyes, photography/intraoral camera, quantitative laser fluorescence technique.

99
Q

What are the advantages of using radiographs?

A
  1. Can see the root and detect an infection
  2. Can see the crown:root ratio
  3. Bitewings are directly perpendicular. If the caries lesion is at a certain depth, with that direction of the lesion, you get the most accurate outline
100
Q

How does illumination work in diagnosis?

A

Light can be reflected thru the contact points of anterior teeth using the dental mirror.
Carious lessons appear as dark shadow outlining the lesion.

101
Q

What magnification is used for work on one tooth?

A

Magnification greater than 2.5. With 4.5, much clearer view, but lose whole picture.
Usually used by endodontists because can focus on one tooth

102
Q

How do you use a mouth mirror in diagnosis?

A

Important that you work in dry, isolated field. If not dry, cannot trust judgement.
When using mirror, reflect operating light onto surface you are looking at. Move mirror to change the effect.

103
Q

What are the advantages and disadvantages of using the explorer?

A

Provides tactile feeling when used with mirror.

But when there’s no cavitation, relatively poor detection capability for occlusal surfaces.

104
Q

True or False

When explorer gets stuck, it is indicative of decay

A

False
May be the anatomic feature. May cause damage to surface and possible implantation of organisms.
“Probing found unreliable in finding fissure caries”

105
Q

How is transillumination used for diagnosis of caries?

A

Applies a very strong source of light to the teeth e.g. high speed light or curing light.

106
Q

What are the advantages of using transillumination?

A

Caries lesions can be easily determined and can see cracks.

107
Q

How is laser fluorescence used in caries diagnosis?

A

Reflection of light gives number with the use of diode laser (655nm), can read 2mm into the tooth.
0-10: healthy tooth (calibrated to 0 w healthy tooth)
11-20: outer enamel caries
21-30: inner half enamel caries
>30: dentin caries
light intensity is an indication of the size and depth of the carious lesion.

108
Q

What should be used in conjunction with laser fluorescence?

A

ONLY in presence of suspected caries, x-rays, clinical exam, DIAGNOdent.
• Mostly used for confirmation of no caries. Gives false positives

109
Q

What factors can laser fluorescence respond to?

A
  1. Plaque and organic plug
  2. Composite and stained margins
  3. Calculus
  4. Food
  5. Hypocalcific enamel and carious enamel/dentin
110
Q

True or False

Shredded dental floss indicates caries

A

False, may show surface irregularities from existing restorations with rough cavosurface margins.

111
Q

How are wedges used for diagnosis of caries?

A

Temporarily allows for tooth separation and provide visualization for proximal lesions. Effective but not commonly used.

112
Q

How are caries detection dyes used for diagnosis of caries?

A

Tooth must be prepared with bur and stain used to differentiate carious lesions. Microbrush for drop of dye for 10 sec then wash and dry. Red stains= caries lesions. Reduce red area and repeat.

113
Q

How does caries detection dyes work?

A

Differentiates between mineralized and demineralized areas.
Stains all porous surfaces (including noncarious deep dentin). In areas with darker and lighter stains, focus on dark stains.

114
Q

Why is the use of digital photography for caries detection not recommended?

A

Intra-oral cameras with probes give higher magnification but, not as accurate and images on screen not as sharp.

115
Q

What does QLF stand for?

A

Quantitative Light-Induced Fluorescence

116
Q

How is QLF used for caries diagnosis?

A

Auto-fluorescence of teeth using blue light to emit green light for differentiation of caries tissues. Fluorescence of the teeth has direct relationship with mineral content of enamel.
Contrasts demineralized from sound enamel. Can also identify plaque, calculus, and staining.

117
Q

What are the 9 functions of saliva?

A
  1. Protection
  2. Swallowing
  3. Cleansing the mouth
  4. Antibacterial/antiviral
  5. Remineralization
  6. Buffering pH
  7. Speech
  8. Mastication
  9. Taste
118
Q

What is the function of saliva’s mucoid coating?

A

Protective factor which acts as barrier to irritants and prevents desiccation (dryness).

119
Q

How does saliva function to retard plaque formation?

A

Flows to clear mouth of food, cellular, and bacterial debris.

120
Q

How does saliva regulate pH?

A

Contents: bicarbonate, phosphate, and amphoteric protein contents. Increase in flow–> increase in pH and buffering capacity.
Parotid raised pH to 7.4
Submandibular raises to 7.1

121
Q

How does saliva participate in tooth maturation?

A

Its content of calcium and phosphate provides minerals to incompletely formed enamel soon after eruption

122
Q

How does saliva protect the structure of teeth?

A

Prevents/retards tooth dissolution and enhances remineralization.

123
Q

What is acquired pellicle and how does it protect teeth?

A

Glycoprotein film formed on tooth surface by saliva, reduces tooth wear due to erosion and abrasion.

124
Q

What are the major and minor salivary glands?

A

Major:
Parotid (Stensen’s Duct), Submandibular (Wharton’s Duct), and Sublingual (Wharton’s Duct)
Minor:
Lingual, buccal, labial palatine

125
Q

What are the types of secretion from the major salivary glands?

A

Parotid: Exclusively serous (watery) type
Submandibular: Serous and Mucus
Sublingual: Predominantly mucus
Others: Mostly mucus
Resting saliva (unstimulated) is primarily mucous coming from SM and SL

126
Q

What are the factors affecting saliva action?

A
  1. Flow rate: time of day, stimulated or to
  2. Type of gland
  3. Nature of the stimulus: tasting or chewing
  4. Duration of the stimulation
  5. Time of the day
127
Q

What are the inorganic component of saliva?

A

Calcium: influenced by salivary flow rate. Conc in submandibular/sublingual 2x higher than parotid
Fluoride: From environment, water, dentifrices (to products to clean teeth), enters saliva from salivary gland tissue
Carbonic acid/bicarbonate system: buffering system in saliva

128
Q

How are teeth remineralized?

A

Takes place via replacement using amorphous calcium phosphate

129
Q

What are the 7 organic components of saliva?

A

Mucins– lubrication; major component of the acquired pellicle
Statherin – inhibition of precipitation of calcium phosphate salts from the supersaturated saliva
Lysozyme – antimicrobial function PRIOR TO ERUPTION; no effect on Strep M
Lactoferrin – sequesters iron; bacteriostatic vs. MS
Peroxidase – antimicrobial function and host protection from H2O2
Histatins, Cystatins, and Agglutins – innate immunity against bacteria, fungi, and/or viruses
Amylase- Splits starch into maltose, maltriose, and dextrins.

130
Q

What are the two forms of mucins? How do they function to protect?

A

Two forms: MG1 and MG2
Hydrophilic, resist dehydration, effective i lubricating and maintaining moist mucosal surface.
Aggregates oral bacterial so it is unable to attach to hard surface.
Protects mucosa/soft tissue and hard tissue from infections.

131
Q

From which salivary glands are statherin found in?

A

Parotid and Submandibular

132
Q

What is the most abundant salivary enzyme?

A

Amylase from parotid and submandibular. As it splits starch, acids form, giving cariogenic potential.

133
Q

What are the specific functions of histatins, cystatins, and agglutins?

A

Histatins: anti-bacterial and anti-fungal
Cystatins: Anti-viral e.g. HIV
Agglutins: Clumps bacteria into large aggregates, so they’re easily flushed away by saliva.

134
Q

What is the difference in unstimulated and stimulated salivary flow rate (mL/min) in normal (awake), low (asleep), and very low (xerostomia)?

A 
Unstimulated:
Normal (Awake): over 0.3
Low (Asleep): 0.1 – 0.3
Very Low (Xerostomia): below 0.1
Stimulated (chewing/eating):
Normal (Awake): over 4.0
Low: 0.7 – 1.0
Very Low (Xerostomia): below 0.7
total 500-600 ml in 24 hrs
135
Q

What is Stephan’s curve?

A

Shows what may happen in dental plaque after food intake with fermentable carbohydrate.
Stephan Curve = pH drops below 5.5 within 5 – 10 mins of sugar consumption, and does not rebound for 60 mins

136
Q

At what pH does demineralization of enamel occur?

A

Demineralization of enamel occurs when pH ↓ <5.5 (dentin= 6.5; flouroapatite= 4.5)

137
Q

What are the factors affected in xerostomia?

A

Saliva, Throat and larynx, lips, nose, tongue, eyes, cheeks, thirst, GI tract, mastication, Swallowing, Speech, and taste

138
Q

How is the saliva, throat and larynx, lips, and nose affected in xerostomia?

A

Decrease in saliva (foamy, viscous, and ropy)
Dryness in throat. Persistent cough.
Lips: Dry, crackled, fissured (chelitis)
Nose: dry, crust formation. Decrease in olfactory acuity.

139
Q

How are tongue, eyes, cheeks, and GI tract affected in xerostomia?

A

Tongue: glossopyrosis (burning) and glossodynia (pain)
Eyes: Dry, burn, itch, lids stuck, blurred vision, light sensitive
Cheeks: dry, butteryfly rash, vasculitis
GI: constipation and GERD (gastroesophageal reflux)

140
Q

What are the xerostomia-associated diseases in swallowing, speech, and taste?

A

Dysphagia: difficulty in swallowing
Dysphonia: difficulty in speaking
Dysgeusia: Reduced taste perception

141
Q

Xerostomia can be detrimental to the teeth in what 2 ways?

A

Rampant caries and tooth erosion

142
Q

What are some systemic factors that reduce salivary flow?

A

Drugs, psychological, Sjorgren’s syndrome, hormones, diabetes, dehydration, neurological disease, pancreatic and liver disturbances, nutritional deficiencies, lupus, AIDS, duct calculi, smoking, and aging.

143
Q

What can be done when medications are taken that reduce salivary flow?

A

If used for more than few weeks, preventive dentistry measures must be taken.

144
Q

What are treatments that reduce salivary flow?

A

Chemotherapy and radiation: reduces and thickens saliva

145
Q

What are conditions that reduce salivary flow?

A

Salivary gland tumors, sialadenitis (inflammation of salivary glands), and nerve damage

146
Q

What is Sjorgren’s syndrome?

A

Autoimmune disease. Abnormal proteins in blood, indicating immune system is reacting against own tissues.

147
Q

What are some preventive measures for reduced salivary flow?

A

Avoid coffee/tea, tobacco/alcohol, spicy or salty foods, toothpaste and mouthwashes with alcohol
Water sips btwn and during meals, chew xylitol gum, use lip balm, use humidifier in room.

148
Q

What are some medicinal preventive measures to prevent reduced salivary flow?

A

Dental appts every 3 months.
Daily applications of 1% sodium fluoride gel OR .05% mouth rinse daily for several years to arrest carious lesions.
AND
Daily application of 1% chlorhexidine gel for 14 days
OR
Chlorhexidine rinse for 1 wk for 8 months

149
Q

What measures can be taken from MD and DDS for reduced salivary flow?

A

MD: change or reduce dosage of medication
DDS: saliva stimulating tablets, saliva substitutes( spray, lozenge, or mouthwash) and calcium phosphate and fluoride ions.
Sprays that provide viscosity or Pilocarpine hydrochloride

150
Q

How does saliva substitutes work?

A

Includes

  1. Agents to increase viscosity: carboxymethylcellulose or hydroxyethylcellulose
  2. Minerals such as calcium and phosphate ions
  3. fluoride
  4. Preservatives: methyl-paraben or propylparaben
  5. flavoring and related agents.
151
Q

What are saliva stimulants?

A

Anhydrous crystalline maltose (ACM) to stimulate saliva production (Sjorgren’s Syndrome)
*Not for pts whose salivary gland has lost function thru radiological treatment.

152
Q

What are prescription products for xerostomia?

A

Pilocarpine. 5 mg tablets. 3-6 tablets per day for 6-12 wks uninterrupted.
Salagen tablets 5 mg tablets, 4x a day (Sjorgen’s)
Cevimeline: Capsule 3x a day

IRDS exam 2 (3 decks)

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