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Den104 > Oral physiology > Flashcards

Oral physiology Flashcards

1
Q

Structure of acinus

A 
12+ Acinar cells around a central lumen.
Zygomen granules (digestive enzymes)
Mucus cells (downstream of acinar cells)
Myoepithelial cells to contract and squeeze stuff into the main duct.
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2
Q

Types of ducts (salivary glands)

A

Intercalated, striated, excretory

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3
Q

The rate of flow vs composition

A

Increased flow = increased conc of NaCl and HCO3

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4
Q

Movement of substances from blood to the lumen of the acinus

A

Na+ to the lumen through tight junctions.
Cl- and HCO3- from blood to acinus via co-transporters e.g. transcellular.
Primary saliva is isotonic

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5
Q

Modification of primary secretion

A

In the duct.
Reabsorption of NaCl
Secretion of K+ and bicarbonate (= high pH).
Ductal cells impermeable to water so final saliva is hypertonic.

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6
Q

What is oral mucosa

A

The soft tissue of the mouth

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7
Q

What is oral mucosa composed of

A

Stratified squamous epithelium

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8
Q

What’s the function of oral mucosa

A

Barrier to bacteria and mechanical irritation and protects against dryness.

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9
Q

The different classifications of oral mucosa

A

Masticatory mucosa, lining mucosa and specialized mucosa

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10
Q

Lining mucosa properties

A

Can be stretched, compressed and is moist.

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11
Q

Location of lining mucosa

A 
Buccal surfaces,
Ventral surface of tongue,
Floor of mouth, 
Labial
Alveolar mucosa,
Soft palate.
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12
Q

Histology of lining mucosa

A

Non-keratinised SSE
Elastic fibres in lamina propria and sub-mucosa = a movable base.
Fordyce spots/granules (misplaces sebaceous glands usually associated w hair follicles)

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13
Q

Masticatory mucosa locations

A

Attached gingiva, hard palate, dorsal surface of tongue

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14
Q

Transduction mechanism for Umami tastant

A

G-coupled protein receptor.

T1Rs = T1R2, T1R3

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15
Q

Transduction mechanism for Sweet tastant

A

G -coupled protein receptor

T1R1, T1R3

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16
Q

Transduction mechanism for Salt tastant

A

Ion channel = NaCl, KCl (inorganic salts)

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17
Q

Transduction mechanism for Sour tastant

A

Ion channel = H+

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18
Q

Transduction mechanism for Bitter tastant

A

G-coupled protein receptor.

TR2’s

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19
Q

Which tastant are we most sensitive to.

A

Bitter

Sour produces most saliva bc needs to buffer the H+

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20
Q

Mechanism of AP from eating food

A
  1. Chewing the food = mechanical and chemical stimulation so saliva released.
  2. Molecules from broken down food dissolve in saliva and enter taste pore.
  3. Molecules interact with Ion channels/protein receptors.
  4. Ca2+ released from stores so increase in conc.
  5. Increase in [Ca] = exocytosis of transmitters.
    6 = AP
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21
Q

Factors affecting taste

A 
Genetics
Saliva composition, quantity, etc.
Disease
Past experience
Olfaction
Adaption
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22
Q

Structure of acinar/secretory system

A

~12 acinar cells (serous) around an intercalated duct
Mucous cells further downstream
+Zygome granules
+myoepithelial cells to squeeze saliva downstream
Intercalated then striated then excretory duct.

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23
Q

Movement of substances from blood to the lumen of the acinus

A

Na+ and water travel straight through.
Na+/K+ enter basolateral membrane, Na+/Cl- exchanged (Cl- in)
HCO3, K+, and Cl- exit to the lumen at luminal membrane.

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24
Q

Movement of substances from the lumen of the duct to blood

A

Luminal membrane: H+/K+ exchanger (H+ in), H+/Na+ exchanger (H+ out), HCO3/Cl- exchanger (Cl- in).
Basolateral membrane/to blood: K+ moves into the duct, Na+ and Cl- move out.
Impermeable to water.

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25
Q

Stephan’s Curve: Rate of drop of pH due to ?

A
  1. Metabolic activity of plaque microbes.

2. Complexity/type of substrate

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26
Q

Stephan’s Curve: pH reached depends on?

A
  1. Type of bacteria e.g. acidogenic = lower pH
  2. The complexity of the carbs
  3. The rate of diffusion e.g. affected by plaque thickness, clearing rate of saliva, etc.
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27
Q

Stephan’s Curve: Time taken for normal pH to return

A
  1. The activity of bacteria inhibited by low pH
  2. Saliva flow and composition
  3. Plaque/rate of diffusion.
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28
Q

What is the critical pH

A

pH where CaPO4 crystals dissolve.

= 1/[Ca] or [PO4]

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29
Q

Benefits of the enamel pellicle

A 
Physical barrier e.g. against abrasion
Barrier against bacteria
Neutralises bacterial acids
Reduces demineralization
Inhibits calculus growth
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30
Q

Properties of parasympathetic saliva

A

A Larger volume as it’s more watery (serous)

Secreted via Ach pathways.

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31
Q

Properties of sympathetic saliva

A

Smaller volume but rich in mucins so feels thick

Via noradrenaline pathways

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32
Q

Problems caused by xerostomia

A

Difficulty/pain eating, swallowing, speaking
More gingival infections/tooth decay/poor oral health
Diminished taste

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33
Q

Advantages of the structure of salivary glands

A
  1. The epithelium of luminal membrane can be accessed non-invasively
  2. Well encapsulated = less spread of vectors.
  3. Non-vital e.g. can be removed.
  4. Cells are well differentiated and slow dividing = a stable population.
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34
Q

Types of acini

A

Serous, mucous, mixed

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35
Q

Serous Acini

A

Dark staining
Nucleus in basal third
Secrete a-amylase and water rich saliva to digest starch.
Small central duct

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36
Q

Mucous acini

A

Light foamy stained appearance.
Nucleus at base
Large central duct
Secretes mucins (glycoproteins) and water for lubrication

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37
Q

Composition of primary saliva

A

Isotonic, NaCl rich plasma like fluid

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38
Q

What does whole saliva contain

A 
Acinar secretions/saliva
Blood
Cell fragments
Microorganisms
Food remnants
Electrolytes
Mucins
Antibacterials e.g. lysozyme
Enzymes
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39
Q

Role/structure of intercalated ducts

A

Cuboidal cells

Secretory duct e.g. connects acini to the larger striated ducts.

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40
Q

Role/structure of striated ducts

A

Basal membrane highly folded into microvilli = more surface area for active transport.
NaCl absorbed, HCO3 and K+ secreted.
Impermeable to water so resulting saliva is hypotonic.
Rich in mitochondria due to all the active transport.

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41
Q

Name 5 salivary glands

A 
Parotid
Sub-mandibular
Sub-lingual
Von-Ebner
Weber's
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42
Q

Parotid gland secretions

A

Serous secretions.

Stenson’s duct (crosses masseter and pierces buccinator before entering the oral cavity)

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43
Q

Von-Ebner’s glands

A 
Minor salivary glands
Serous secretions (the only minor salivary gland not mucus).
Found at the base of tongue, underlying the circumvallate papillae.
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44
Q

Weber’s glands

A

Mucous secretions

Found in tonsils.

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45
Q

Types of damage to salivary glands

A

Obstructive, degenerative, infectious, drug side-effects

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46
Q

Types of damage to salivary glands: Obstructive

A

E.g. calculus stones blocking the ducts

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47
Q

Types of damage to salivary glands: Degenerative

A

E.g. after radiotherapy or due to Sjogren’s syndrome (affects post-menopausal women and their glands)

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48
Q

Types of damage to salivary glands: inflammatory

A

Infection, swelling

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49
Q

Types of damage to salivary glands: Drug side-effects

A

Affect the Ach or noradrenaline pathways

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50
Q

What do acinar cells also secrete

A 
Electrolytes
IgA/IgG
Mucins
Cystatins
Histatines
Statherins
Enzymes e.g a-amylase or lipase
Antimicrobial proteins
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51
Q

What are the functions of Statherins, Histatines, and Cystatins in saliva?

A

All of a mineralization function.
Histatines = buffer
Cystatins = tissue coating
Statherins = Lubrications and vasoelasticity

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52
Q

Sub-mandibular

A

Unstimulated saliva mostly from here.
Mixed e.g. mucous and serous
Wharton’s duct
Deep and superficial lobes separated by posterior surface of mylohyoid muscle.

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53
Q

Sub-lingual

A

Mostly mucous

Joins Wharton’s duct and has some small ducts that go directly to the mouth.

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54
Q

What affects saliva composition/amount

A 
Age
Time of day
Gender
Diet
Drugs
Gland size/type
Stimulation type and duration
Circadian rhythm (24h cycle)
Flow rate
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55
Q

the role of saliva

A 
Lubrication and tissue coating
A solvent for taste
Digestive
Defensive
Immunity (antibacterials/antifungal/etc)
Buffering
Remineralisation
Mechanical cleaning
Needed to hold dentures in place
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56
Q

How can we determine the composition of saliva

A

2D/1D electrophoresis

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57
Q

functions of salivary proteins

A

Taste and digestion
Lubrication - mucins
Immunity/defensive - IgA, IgG, lysozymes

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58
Q

Host protective features during periodontal disease/gingivitis

A

A complete layer of epithelium = physical barrier
Saliva flow and contains neutrophils/innate immunity
Crevicular fluid increases and contains neutrophils etc = innate immunity.
For periodontitis, phagocytes etc activated (active immunity)

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59
Q

Histological features of Gingivitis

A

Dilated capillaries = red and bleeding gums
Inflammatory cells
Leaking crevicular fluid (containing neutrophils)
No migration of junctional epithelium
No bone loss

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60
Q

Clinical features of gingivitis

A

False pocketing

Bleeding

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61
Q

Histological features of periodontal disease

A

Migration of jucntional epithelium
Bone loss = wobbly teeth or drifitng teeth
True pocketing (7mm)
Ulceration and bleeding gums
Chronic inflammation = plasma cells, lymphocytes

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62
Q

Clinical features of periodontal disease

A

True pocketing (7mm)
Bone loss - can be checked using a bitewing x-ray
Bleeding
Accumulation of calculus

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63
Q

The appearance of healthy gingiva

A

Pale pink
Firm and stippled
Knife edge gingival margin

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64
Q

The appearance of gums w periodontal disease

A

Red, inflamed and bleeding
Lost the stippled appearance
Rolled gingival margins

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65
Q

Types of gingival disease

A 
Hereditary or acquired.
Plaque-induced or not.
Infective e.g. herpes.
Affected by systemic illnesses etc e.g. pregnancy or diabetes.
Inflammatory or not
hyper or hypoplastic.
Allergic
Traumatic
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66
Q

Chronic periodontitis features

A

Localised or generalized (>30%)
Bad bacteria > good bacteria
Affected by systemic factors e.g. smoking, stress, plaque levels, diabetes.
Progressive bone/attachment loss consistent w local factors

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67
Q

Acute periodontitis

A

Aggressive and rapid bone/attachment loss, not consistent w local factors.
The patient appears to be healthy.
Localised or generalized.
Macrophage/neutrophil abnormalities.

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68
Q

Steps needed in a treatment plan

A
  1. Care of the pain
  2. Prevention (finding and stopping the cause)
  3. Stabilisation
  4. Rehabilitation
  5. Maintenance.
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69
Q

Why do systemic illnesses affect oral health

A

Affect the saliva.
Affect host responses e.g. inflammatory response, antibodies/neutrophils etc.
Affects strength of the tissues e.g. how easily they get infected etc.

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70
Q

Changes in epithelium

A 
Atrophy
Hyperplasia
Hyperkeratinised
Ulcers/loss of epithelium
When epithelium separates from underlying CT
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71
Q

Atrophy of oral epithelium

A

Red fragile epithelium
When rate of loss of cells > rate of new cell production
Reasons = immune mediated, vitamin B12 deficiency, age.

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72
Q

Oral epithelium hyperplasia

A

Appearance = normal, maybe whiter (hyperkeratinised)
When rate of new cell production > rate of loss of cells.
Reasons = trauma, infection/fungal e.g. candidia

73
Q

Oral epithelium hyperkaratinised

A

White appearance

Reasons = immune-mediated, trauma, infection/virus, unknown, etc.

74
Q

Loss of epithelium/ Ulcers

A

Covered in fibrin and neutrophils instead so has a white appearance surrounded by red inflamed surrounding tissues.
Reasons = immune-mediated, infection/virus e.g. herpes, trauma.

75
Q

Separation of epithelium from underlying tissues

A

Blister - can burst to form an ulcer.

Reasons = immune-mediated, virus/infection.

76
Q

Changes to oral connective tissues

A

Inflamed

Hyperplasia

77
Q

Inflamed oral connective tissues

A

Red appearance - increased blood flow
Swollen and firm - due to oedema and increased pressure
Yellow due to the pus
Causes = Trauma, ulcers or gingival/periodontal disease

78
Q

Hyperplastic oral connective tissue

A

Swelling, nodule or lump, normal color or red

Due to trauma e.g. rubbing dentures or hormones.

79
Q

What does red oral mucosa indicate

A

Atrophic epithelium, hyperplastic or imflamed connective tissue.

80
Q

What does a white patch intraorally indicate

A

Hyperkeratosis due to immune-mediated, fungal infection e.g. candida, trauma.

81
Q

Neoplasia definition

A

Unregulated proliferation/replication of cells due to genetic changes

82
Q

Benign neoplasia

A

Cells in a capsule so don’t grow into neighboring cells or metastasize.
Cells resemble the original tissue type - well differentiated
Overlying mucosa looks normal
It compresses surrounding structures.

83
Q

Malignant neoplasia

A

Cells metastasize e.g. not localized and grow, invade and infiltrate into neighboring cells.
Cells don’t resemble original cells.

84
Q

Cancer in glandular tissue

A

Adenoma - spreads via lymph nodes

85
Q

Cancer in connective tissue

A

lipoma, schwannoma - invades the bloodstream and spreads from there.

86
Q

Cancer in epithelium

A

Carcinoma - infiltrates lymph nodes and vessels and spreads

87
Q

Aetiology of neoplasia

A 
Multifactorial:
Age
Nutrition/diet
Alcohol
Smoking
Sunlight/UV (lip)
Genetics
Viruses (HPV)
88
Q

Histology of neoplasia

A

Thicker epithelium bc uncontrolled cell growth
Ragged epithelium/CT edge bc epithelium cells grow into CT
Islands of epithelium break off and lodge in CT e.g. in bone or muscle and stop them working.

89
Q

What occurs during dysbiosis of an early lesion in the mouth.

A

A quiescent site/early lesion in mouth turns into active caries.
Due to a change in the host (e.g. starts smoking, pregnancy) or due to a change in the microbes (e.g. increased plaque levels)

90
Q

Periapical disease definition/summary

A

Infection in pulp (via caries in the enamel/dentine). Causes necrosis of pulp and travels out the apices and infects surrounding tissues.

91
Q

Types of pre-cavitation enamel caries

A

Smooth surface caries

Fissure caries

92
Q

Features of pre-cavitation enamel caries

A

Conical shape
Most spreading at the ADJ
Surface is zone is reistant to demineralisation (until dentine is involved)
Body of lesion = 4-20% demineralised. Demineralisation in the prism cores = enhanced striae of retzius and cross-striations.
Dark zone surrounded by transluscent zone at base of lesion.

93
Q

Pre-cavitation smooth surface caries vs fissure caries

A

Both have a conical shape but smooth surface caries’ apex is towards ADJ and fissure caries’ base is towards ADJ.
Fissure caries starts in the walls of the fissure (not the base).

94
Q

How do caries spread into the dentine

A

Most spread along the ADJ = secondary enamel caries starting from the ADJ.
Acid diffuses through the porous enamel.

95
Q

Dentine/pulp’s reaction to caries

A

Tertiary reactionary dentine forms as the odontoblast cells get reacted and retreat as they detect the stimulus (makes pulp shrink)
Sclerotic dentine = inter and peritubular dentine forms and mineralization of odontoblast processes/calcification of tubules.
Dead tracts = dead odontoblasts and empty tubules.

96
Q

Features of cavitation of a carious lesion

A 
More demineralisation (1st wave) and proteolytic enzymes degrade collagen matrix (2nd wave).
Bacteria invade and grow in tubules and widen them until they collapse = liquefaction foci.
Tubules grow and join = transverse/dentine clefts.
97
Q

Types of arrested caries

A

Type 1 = dentine caries self cleanses

Type 2 = enamel caries/white spot lesion remineralises

98
Q

The 3 zones of the body of the cavitation

A

Demineralisation = sterile e.g. no bacteria (furthers from the enamel/ center of the body)
Bacterial penetration = bacteria invade and grow in tubules.
Destruction = liquefaction foci, transverse clefts, discolouration.

99
Q

Cementum/dentine caries

A

Starts at the amelocemental junction.
The direction of tubules is towards apex and pulp so difficult to see and treat.
PDL means infection can go straight to cementum/dentine.

100
Q

The colonisation of bacteria onto teeth

A

Host-bacteria adhesion: irreversible if just chemical/physical interactions e.g. not specific protein-protein. Bacteria adhere to acquired pellicle via IMF, protein-carb interactions, etc.
Bacterial-bacterial adhesions - co-aggregations.
Growth and multiplication.

101
Q

Source of nutrients for the bacteria in plaque

A

The waste of other bacteria
By-products of the breakdown of stuff e.g. salivary glycoproteins.
Urea/ammonia
Dietary constituents - diff bacteria work together to break up food quicker.

102
Q

Progression of plaque formation

A
  1. decrease in host response
  2. primary adherance
  3. metabolism = a change in environment
  4. bacterial succession
  5. climax community
103
Q

Progression of caries through the tooth

A
  1. White spot lesion - reversible using fluoride and better oral health.
  2. Early coronal lesion collapses the enamel surface.
  3. Caries progresses into dentine and then pulp.
104
Q

Caries management

A
  1. Assessment e.g. plaque score (disclosing tablet), diet diary, x-rays to identify the causes and how to stop them - preventative.
  2. Diagnose and come up with a specific treatment plan for that patient.
  3. Inform the patient and of their options etc.
  4. Restoration/treat the symptoms.
  5. Future prevention e.g. oral hygiene instructions, topical fluoride application.
  6. Review and assess at each visit and recall time specific to each patient.
105
Q

Types of caries risk factors

A 
Primary = stuff that affects the biofilm directly e.g. saliva, oral-health, bacteria.
Modifying = indirectly affect the biofilm e.g. SES, job, background, etc.
106
Q

Pulp pathology types

A 
Inflammatory = pulpitis
Degenerative = fibrosis, calcification, internal resorption.
107
Q

Pulp pathology causes

A

Infectious = via caries or fracture
Trauma = a blow, cold/hot
Chemical = fillings
Mechanical

108
Q

Pulpitis

A 
Chronic = usually due to infection. Open or closed.
Acute = usually due to trauma. Open or closed e.g. if due to a fracture or a blow.
109
Q

Periapical pathology types

A 
Inflammatory = periapical periodontitis
Reactive = Hypercementosis
110
Q

Periapical pathology causes/ aetiology

A

Infectious = Periodontitis or via root canal e.g. pulp necrosis.
Trauma, chemical or mechanical

111
Q

Periapical pathology on a non vital tooth w periapical periodontitis

A

Chronic periapical granulation = Periapical cyst = Chronic abscess.
Acute periapical abscess = Acute alveolar abscess = Chronic abscess or Cellulitis (face infection).
Chronic periapical granulation can lead to acute periapical abscess and vice versa.

112
Q

Non-invasive diagnosisi of caries techniques

A

Radiographs
Caries detection dye that stains demineralizing areas
Laser fluorescence or transillumination
Interproximal impression.

113
Q

Periodontal tissue injuries

A 
Avulsion = tooth falls out
Intrusion/extrusion = tooth pushed in or out
Concussion = inflammation of PDL only
Luxation = tooth displaced e.g. lateral or buccal
Subluxation = tooth not displaced but is mobile.
114
Q

Soft tissue injuries

A

Abrasion
Laceration
Contusion

115
Q

Types of tooth fractures

A 
Uncomplicated # = just in enamel/ a bit chipped off
Complicated # = enamel-dentine
Root # = just through root
Enamel infraction = crack in the enamel
Crown-root #
116
Q

Trauma to primary teeth and effects on primary teeth

A

U1’s most common site, infarcation, due to accidents.

Effects on primary teeth = discolouration, early/delayed exfoliation.

117
Q

Trauma to primary teeth’s effect on secondary teeth.

A 
Discoloration or enamel opacity
Hypoplasia/incomplete enamel development
Early/delayed eruption and diff order.
Abnormal root morphology/dilaceration.
Benign tumors.
118
Q

Trauma to secondary teeth and effects

A

U1’s most common, due to RTA, assault or sports injury
Effect on tooth = pulp death, discoloration, fracture, inflammation, hypersensitivity
Effect on patient = image, time, money, pain

119
Q

Epidemiology

A

Study of distribution, risk factors and outcomes of a disease on a population (i.e. not individuals)

120
Q

How to decide if an oral health condition is of public health importance

A 
Frequency, severity, and distribution.
Study epidemiology, prevalence (people w it/people at risk) and incidence (new cases/people at risk).
Use an index to measure the disease.
Impact on individuals and society.
Prevention and treatment options etc.
121
Q

What index is used to measure caries

A 
DMFT/DMFS = permanent (teeth/surfaces)
dmft = decidiuous teeth
122
Q

Pros of DMFT

A

DMFS > DMFT bc bigger range and more specific
Used for a long time so accepted and a lot of data to compare to.
Easy to use and view data etc.

123
Q

Disadvantages of DMFT

A

Age-specific so hard to compare across populations e.g. w/ aging populations or not.
Irreversible and cumulative
Doesn’t take into account:
- The severity of disease e.g. a small filling or a crown.
- How the tooth was lost e.g. trauma or decay
- The dentist’s treatment style
- Improvements in oral health
- Further treatments
- Treated or untreated decay

124
Q

Index for measuring gingivitis

A

Plaque and bleeding score.

Plaque is more unreliable bc patient can brush teeth before coming to the dentist.

125
Q

Index for measuring periodontitis

A

Loss of attachments e.g. recession or probing depths.

126
Q

Non-carious tooth loss types and risk factors

A

Attrition, erosion, abrasion
Risk factors = anything that affects pH or saliva e.g. diet and medication. Teeth-brushing habits, acid reflux, teeth strength, etc.

127
Q

Measuring non-carious tooth loss

A

O’Sullivan index

  • A-F sites in the mouth (buccal, lingual, occlusal, buccal+occlusal, lingual+occlusal, multi).
  • 0-5, 9 severity (9=crown/can’t tell).
  • +/- = amount of mouth affected.
128
Q

Oral cancer risk factors and effects on people/society

A

Risk factors = smoking, alcohol, sun, diet
Effects on individuals =
- death
- Time off work etc
- Surgery = physical and functional changes
- Radiotherapy = diminished tase, saliva and worse oral health.
Effects on society =
- NHS
- People not working/dead.

129
Q

Centric Relation

A

The most anterior-superior position of the condyle in the glenoid fossa. Movement here is rotation around the horizontal axis.

130
Q

RCP

A

Retruded contact position

Occlusion when TMJ is in centric relation.

131
Q

ICP

A

Max cuspal contact.
Posterior teeth in contact, anterior teeth in light contact (posteriors have more molars and are sturdier so can withstand forces of mastication whereas anterior’s can’t)

132
Q

Why is ICP important to maintain

A

Stops teeth drifting or over-erupting because there’s cuspal contact.

133
Q

Protrusion of mandible

A

Condyle moves forward.
Incisor guidance - the palatal surface of upper incisors guides the mandible.
Anterior teeth in contact but not posteriors.

134
Q

Sideways movement of the mandible

A

Canine guidance (only canines on the working side are in contact).
Canines > posteriors:
- Have a better morphology so less likely to fracture/recession/bone resorption when a sideways force applied (than posteriors).
- Longer larger root so can withstand force
- Further from the muscles and TMJ/hinge so less force applied to them than posteriors.
- More innervated. Masseter only works when posteriors are in contact, to protect anterior teeth.

135
Q

Class I jaw

A

“Normal”
Molars = mesiobuccal cusp of U6 sits in buccal groove of L6.
Incisors = Lowers occlude at or below the upper cingulum

136
Q

Class II jaw

A

Small mandible, large maxilla.
Molars = mesiobuccal cusp of U6 occludes in front of L6 buccal groove.
Incisors Division 1 = Uppers are at a normal inclination or proclined, so overjet increased.
Incisors Division 2 = uppers are retroclined so deep overbite.

137
Q

Class III jaw

A 
Molars = mesiobuccal cusp of U6 sits behind the buccal groove of L6.
Incisors = lowers occlude in front of uppers.
138
Q

Anterior guidance/protrusion with a Class II jaw

A

Division 1 = Mandible needs to protrude more so more occlusal contact between incisors so careful when doing incisal edge restorations.
Division 2 = Mandible needs to open more before protruding so more contact between lowers and posterior surface of uppers so careful when doing restorations here.

139
Q

Anterior guidance/protrusion with a Class III jaw

A

Contact between all the teeth = bad.

140
Q

Mandible movements dictated by

A

The position of the condyle in the fossa
Condylar guidance (from fossa to eminence)
Teeth guidance

141
Q

How can fluoride act on teeth in general

A 
Topically = directly affects the enamel on the tooth
Systemically = incorporated into the enamel structure when the tooth was developing.
142
Q

Effects of fluoride on teeth

A
  1. Replaces the OH- in calcium hydroxyapatite to make calcium fluoroapatite which is less soluble in acids.
  2. In bacteria, it affects some reactions e.g. glycolysis (less glycolysis = less acid)
  3. Catalyst for remineralization
  4. When demineralization happening, HA is lost so F binds to the Ca and PO4 lost and redelivers them to the tooth.
143
Q

Sources of fluoride

A

Natural e.g. food and drinks
Added to stuff e.g. toothpaste, water, salt, milk
Supplements
Dental treatments

144
Q

Water fluoridation pros

A

Breaks SES barriers e.g everyone can have it.
Proven to reduce caries (by 15%)
Easy to give to a large population and cheap
Safe

145
Q

Water fluoridation cons

A

Associated with some health problems e.g. fluorosis
Mass medication means people don’t have a say
Not the same as naturally fluoridated water
Only benefits children because their teeth are still developing.

146
Q

Problems caused by excess fluoride

A

While developing = fluorosis. More porous, weaker enamel that appears chalky white w striations and brown in severe cases.
A high F dose is toxic e.g. can cause respiratory problems. > 1 mg/kg is can cause nausea and vomiting.

147
Q

Fluoride in dentistry

A

toothpaste - high F toothpaste can be prescribed to high risk patients (2800 ppm if >10yrs, 5000ppm if >16yrs).
Normal toothpaste = 1000ppm for <3yrs, 1350-1500ppm for 3-6yrs.

fluoride varnish - given to children and high risk patients/on high risk sites or white spot lesions. V V V high [F]

supplements - need to be prescribed. Not for < 6 months. Only effective until 6 years/while teeth are developing.

mouthwash - alternate time to brushing. 0.05% daily, 0.2% weekly.

148
Q

What are white spot lesions and why do they appear white

A

Signs of demineralisation but not necessarily caries. White because the enamel becomes more porous as it loses minerals e.g. PO4 and Ca.

149
Q

Are caries an infectious disease

A

No, because you need more than just the right bacteria to cause caries.

150
Q

What are the requirements for caries to occur

A

Change in host response/susceptible tooth
Bacteria
Sugar

151
Q

Historical theories of cariogenesis

A
  1. Acidogenic - the acid produced from fermentation of sugars causes caries
  2. Proteolytic - enzymes break down the matrix.
152
Q

Dental plaque benefits and how it can cause caries.

A

Stops other bacteria colonising the tooth surface
If exposed to lots of acid frequently, the good acid sensitive bacteria get inhibited and the aciduricity and gram-negative anaerobic bacteria get selected for
= bad bacteria > good.

153
Q

How to prevent the process of plaque becoming cariogenic

A

Prevent the low pH environment e.g. use fluoride and no snacking/sweeteners etc.
Stop the bacteria colonizing using antibacterials.

154
Q

Cariogenic properties of mutan strep

A

Sugar transport systems are v efficient.
Aciduricity
Acidogenic
Make EPS and IPS.

155
Q

What is dental plaque

A

Matrix of polymers with bacteria embedded into it.

156
Q

What is the enamel pellicle

A

Selectively absorbed salivary proteins.

157
Q

Plaque matrix’s role in making EPS

A

Produces enzymes glucosyl and fructosyl transferase that breaks down sucrose into fructose and glucose.
The glucose then joins w other glucose molecules to make a chain w side chain etc.
More side chains = more rigid = more insoluble.
These chains = EPS

158
Q

EPS functions

A
  1. Sticky so harder to physically remove plaque from tooth.
  2. Sticks the microcolonies together.
  3. Diffusion barrier keeps low pH trapped near tooth.
  4. Makes it harder for immune cells and antibiotics to get in.
  5. Store of energy - glucan chains can be broken down if needed (via glucanase)
  6. Creates spaces b/w the bacteria so more sugars can diffuse in.
  7. Reduces surface area of bacteria so less Ca can stick to them so less Ca released when low pH = less buffering.
159
Q

IPS roles

A

When there’s lot of sugar availible, bacteria cells lay down IPS in their cells which can be broken downa nd used as an energy source during times of low sugar availibiltiy.

160
Q

What carciogenic properties of bacteria are most useful/needed

A

Aciduricity and acidogenicy.

161
Q

How does sugar get fermented when there’s little glucose availibility

A

Permease used to allow glucose to enter cell (ATP dependent)
Pyruvate to Acid pathway uses a diff pathway that makes a diff acid (acetate, via PFL instead of LDH)

162
Q

How does sugar get fermented when there’s a lot of glucose availability

A

PEP.PTS pathway used to get glucose into the cell.

LDH used to make lactate from pyruvate.

163
Q

How do artificial sugars work and give an example of one?

A

Xylitol.
Compete/use up the PEP.PTS when they’re taken into the cell but don’t undergo phosphorylation so not ATP or acid made but the PEP.PTS is still used up.

164
Q

How does aciduritity work?

A

The bacteria cells still work best intracellularly at a normal pH.

  1. Active pump system removes lactic acid and works best at low pH.
  2. Protein pump and glucose permease work best at low pH.
  3. Bacteria makes alkalis to neutralize the acid/increase pH e.g. breaks down arginine into ammonia.
  4. Pumps out acids actively and passively (gradient)
165
Q

What in the saliva neutralizes the acid

A

HCO3, K+

166
Q

How is dental tartar formed

A

Saliva pools and the ions can ppt out into the teeth but if ou aren’t brushing your teeth, it will solidify.

167
Q

Problems with restorative materials

A

Water damages them:

  • Poor surface retention e.g don’t stick well so gaps can form between it and the cavity walls and bacteria can live in these spaces.
  • Water disrupts the setting process (polymerisation)
  • Water absorbed into the material causes it to swell, weaken and crack.
168
Q

How can you diagnose a salivary stone/sialolith e.g. investigations to do

A 
Sialography, radiography
ultrasound to see any soft tissue swellings
Intra/extraoral examinations
Take a history
Measure flow rate
169
Q

What is a mucocele

A

Damage to the salivary duct so when it tries to secrete saliva, it bursts

170
Q

What is it called when there is damage to a salivary duct that causes it to burst if it tries to secrete saliva

A

mucocele

171
Q

What is a swollen parotid gland called

A

Suppurative parotitis

172
Q

Pediatric dentist’s patients

A

Specialist medical condition
- at higher risk of complications

Specialist dental condition

  • abnormal facial bone growth e.g. cleft palate
  • abnormal teeth e.g. morphology, position, number
  • severe trauma
  • excessive dental or periodontal health
  • oral pathology e.g. infections, abscess, etc.

Behavioral or learning disability
- In pediatric clinics, the dentist is more trained and has more time.

Special cases e.g. safe-guarding, language communication barrier.

173
Q

Preventative dentistry in paeds

A

Can be done on an individual or large population (water fluoridation).
Healthcare is important - educate, advice, preventative treatments.
Must be the first thing considered when treating a patient, and must be specialized for that patient esp w high-risk cases.
Should be evidence-based.

174
Q

Benefits of preventative dentistry

A

Improves patient’s quality of life.
Better outcomes for the dentist
Cheaper for NHS etc.

175
Q

Methods of prevention of oral conditions

A 
Fissure sealants
Smoking cessation
Mouthguards
Dietary advice
Mechanical/chemical removal of plaque or calculus
Regular screening (for cancer)
Early intervention
Fluoride
176
Q

What sugars are most/least cariogenic

A

Sucrose (fructose and glucose) is most cariogenic.
Added sugars or non-milk extrinsic sugars are bad
Lactose and intrinsic sugars e.g. in fruits aren’t a threat.

177
Q

How can sugar be eliminated from the mouth

A

Chewing
Saliva rinsing
Using foods/elements e.g. cheese, fluoride, phosphates, xylitol (in chewing gum)

178
Q

What does clearance time depend on

A 
Time of day
Age
The stickiness of the food
Conc. of the sugar
Saliva flow rate

Den104 (8 decks)

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