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Symposia > Year 1 > Flashcards

Year 1 Flashcards

0
Q

Describe the basics of tooth embryology

A
  1. Dentine is formed by cells called odontoblast
  2. Enamel is formed by cells called ameloblast
  3. Initially; (Ameloblast) | (Odontoblast)
  4. | = amelodentinal junction; the site of the future enamel-dentine junction (EDJ)
  5. Ameloblast is lost before the teeth erupts
  6. Odontoblast continue to produce dentine through out life
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1
Q

Describe the basic anatomy of tooth

A 
Clinical crown; 
1. Enamel
2. Contour lines
3. Dentin
Anatomical crown;
1-3
4. Gingival crevice (sulcus)
5. Epithelium
6. Attachment epithelium
Root;
7. Pulp
8. Odontoblast
9. Alveolar bone
10. Periodontal ligament
11. Noncellular and cellular cementum
12. Apical foramen
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2
Q

Describe properties of enamel

A
  1. Covers anatomical crown
  2. 96% hydroxyapatite crystals
  3. 4% proteins and water
  4. Hardest calcified matrix of the body (also very brittle)
  5. Incapable of renewing itself and repair (acellular)
  6. Insensitive
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3
Q

Describe the properties of dentine

A
  1. Hard tissue portion of pulp-dentine complex
  2. Forms bulk of tooth
  3. Characterised by multiple closely packed dentinal tubules that transverse it’s entire thickness
  4. Contains cytoplasmic extension of odontoblast
  5. 65-70% hydroxyapatite
  6. 20-25% organic material (collagen and glycoproteins)
  7. 10% water
  8. Capable of repair by odontoblast
  9. Sensitive
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4
Q

State the order of deciduous teeth eruption (including dates)

A

Man central incisor (6.5) > Man lateral incisor (7) > Max central incisor (7.5) > Max lateral incisor (8-9) > Second molars (10-12) > First molars (12-16) > Canines (16-20)

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5
Q

State the order of permanent teeth eruption (including dates)

A

First molars (6-7) > Man central incisor (6-7) > Max central incisor (7-8) > Man lateral incisor (7-8) > Max lateral incisor (8-9) > Man canine (9-10) > Max first premolar (10-11) > Man first premolar (10-12) > Max second premolar (10-12) > Man second premolar (11-12) > Max canine (11-12) > Man second molars (11-13) > Max second molars (12-13) > Third molars (17-21)

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6
Q

Compare deciduous and permanent teeth

A

Deciduous teeth:

  1. Are smaller (except E)
  2. Have a whiter and more opaque enamel
  3. Have crown that is lighter in colour
  4. Have anterior teeth that are more bulbous
  5. Have more pointy cusps
  6. Have shorter roots, less stronger and lighter in colour
  7. Have anterior teeth with roots that are longer than their crown
  8. Have posterior teeth with more divergent roots
  9. Have smaller pulp chambers
  10. Have enamel that bulges at cemento-enamel junction
  11. Fissures are shallower
  12. Do not have premolars
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7
Q

How many root(s) and root canal(s) does each tooth has?

A
  1. Max/Man central incisor; 1 : 1
  2. Max/man lateral incisor; 1 : 1
  3. Max/man canine; 1 : 1
  4. Max first premolar; 2 : 2
  5. Max second premolar; 2 : 1/2
  6. Man premolars; 1 : 1
  7. Max first molar; 3: 3
  8. Max second molar; 3 :3
  9. Man first molar; 2 : 2/3
  10. Man second molar; 2 : 2/3
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8
Q

What is the difference between x-ray and radiographs?

A

X-ray is the process in which radiographs are produce. Thus radiograph is the film we obtain from the process.

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9
Q

What do radiolucency and radiopacity indicate?

A

Radiolucency indicates that x-ray can pass through easily thus producing blackening.
Radiopacity indicates x-ray is absorbed producing no or little blackening.

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10
Q

What determines how many x-rays are absorbed by a material or tissue?

A
  1. Atomic number (the bigger the size of the atom the more x-ray they absorb)
  2. Density
  3. Thickness
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11
Q

How do tooth structures appear on a radiograph?

A
  1. Enamel is highly calcified: high radiopacity
  2. Dentine is less calcified: lower radiopacity than enamel
  3. Pulp not calcified: high radiolucency
  4. Periodontal ligament is made of tissues: high radiolucency
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12
Q

What is the purpose of bitewing radiograph?

A
  1. For caries diagnosis

2. For showing periodontal bones

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13
Q

What is the purpose of periapical radiograph?

A

For periapical diagnosis (around the root apex)

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14
Q

What are the types of extra oral imaging and their respective purposes?

A
  1. Panaromic radiograph: shows entire dentition. It’s main uses are;
    a) to identify large or remote abnormalities that are not suitable for seeing on intraoral radiographs
    b) to identify the presence and position of developing teeth for patients with need for orthodontics
  2. Cephalometric radiograph: shows dentition and skull. For patients with both dental and skeletal problems
  3. Cone beam computed tomography (CBCT): shows 3D view of dentition
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15
Q

What are errors in development of teeth?

A
  1. Hyperdontia: extra teeth

2. Hypodontia: missing teeth

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16
Q

What is the oral mucosa?

A

Oral mucosa is the moist mucous membrane lining the mouth. It consists of;

  1. Epithelium containing glands secreting mucous
  2. Underlying connective tissues (lamina propria)
  3. Muscularis mucosa
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17
Q

What are the roles of the oral mucosa?

A
  1. Mechanical protection from compression and shearing forces
  2. Barrier to microorganism, toxins and antigen
  3. Immunological defence
  4. Glands for lubrication, buffering and antibody secretion
  5. Rich innervation for touch, proprioception, pain and taste
  6. Entry of food
  7. Mastication
  8. Deglutition (swallowing)
  9. Speech (modification of sound)
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18
Q

What are the 3 types of oral mucosa?

A
  1. Masticatory mucosa
  2. Lining mucosa
  3. Specialised mucosa
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19
Q

What is masticatory mucosa and where would you find it?

A

Keratinised stratified squamous epithelium with a thick lamina propria usually bound to an underlying bone. It covers structures like;

  1. Hard palate
  2. Gingival mucosa
  3. Dorsum of tongue (not sure)
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20
Q

What is lining mucosa and where can you find it?

A

Non keratinised stratified squamous epithelium with a loose lamina propria and often a sub mucosa. The sub mucosa is made up of dense irregular connective tissue which contains blood vessels, nerves, minor salivary gland and fat. It covers structures like;

  1. Cheeks
  2. Lips
  3. Alveolar mucosa
  4. Floor of mouth
  5. Ventral surface of tongue
  6. Soft palate
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21
Q

What is specialised mucosa and where is it found?

A

Non keratinised thin epithelium (shows short papilla). It covers specialised gustatory mucosa on the dorsum surface of tongue.

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22
Q

State the boundaries of the oral cavity?

A

It extends from oral fissure to pharynx.

a) Roof: hard and soft palate
b) Wall: alveolar arches and their teeth
c) Floor: tongue

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23
Q

Define the following;

  1. Free gingiva
  2. Attached gingiva
  3. Interdental papilla
  4. Mucogingival junction
  5. Labial frenulum
A
  1. Lies unattached around cervical region of teeth
  2. Tightly adheres to the bone around roots of teeth
  3. Extension of the attached gingiva that fills the space between adjacent teeth
  4. Demarcation between firm, pink attached gingiva and moveable, red alveolar mucosa
  5. Fold of tissue on the midline that links labial mucosa and alveolar mucosa
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24
Q

What are the four basic types of tissues?

A
  1. Epithelium
  2. Connective
  3. Muscle
  4. Nervous
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25
Q

Where is epithelium found, what role does it play and what does it consists of?

A
  1. Covers body surfaces, lines cavities and tubes, forms glands
  2. Plays a role in protection and mediates selective diffusion, absorption and secretion
  3. Consists of closely bound cells supported by a basement membrane
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26
Q

State the 6 types of epithelium with their major function and where they are found?

A
  1. Simple squamous epithelium
    a) Exchange of nutrients and gases
    b) Alveoli, blood vessels (endothelium)
  2. Non keratinised stratified squamous epithelium
    a) Protection and barrier
    b) Oral cavity, oesophagus
  3. Keratinised stratified squamous epithelium
    a) Protection and barrier (waterproof)
    b) Skin
  4. Simple cuboidal epithelium
    a) Secretion and absorption
    b) Glands,kidney tubules
  5. Simple columnar epithelium
    a) Secretion and absorption
    b) Gastrointestinal tract
    c) May have modification like micro villi
  6. Pseudostatrified ciliated columnar epithelium with goblet cells
    a) Mucocilliary escalator
    b) Trachea, large respiratory airways
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27
Q

What are specialised connective tissues?

A
  1. Bone
  2. Blood
  3. Cartillage
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28
Q

What are types of connective tissue proper, state their properties and where they are found?

A
  1. Loose (areolar) connective tissue
    a) Ground substance is predominant
    b) Few collagen and elastic fibres
    c) Cells: fibroblast, adipocytes, macrophages
    d) Found under epithelium and lines body surfaces
  2. Dense irregular connective tissue
    a) Little ground substance
    b) Collagen fibres predominate (ARRANGED HAPHAZARDLY)
    c) Resists excessive stretching and distension
    d) Found in dermis
  3. Dense regular connective tissue
    a) Little ground substance
    b) Densely packed collagen fibres (ARRANGED IN PARALLEL ROWS)
    c) Found in tendons and ligaments
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29
Q

What is the histological arrangement of oral mucosa?

A

Oral mucosa = Epithelium + lamina propria (fibroblast + macrophages + capillaries + ECM)

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30
Q

What is basal lamina, state it’s purpose and what does it consist of?

A
  1. Basal lamina is a sheet of protein laid down
  2. Epithelium cells are all connected to the basal lamina
  3. Basal lamina controls what molecules passes through to the connective tissues and prevents cell migration
  4. It consists of;
    a) Type IV collagen (forming a network)
    b) Laminin (adhesive glycoprotein)
    c) Proteoglycans (have ability to bind growth factors. Also involved in cell signalling. They stick cells to each other and to the ECM)
31
Q

State the 5 types of cell-cell junctions in epithelium?

A
  1. Tight junction
  2. Adherens junction
  3. Desmosomes
  4. Gap junctions
  5. Hemi desmosome (only one that binds cell to basal lamina)
32
Q

Where do bacteria reside in the oral environment?

A
  1. Mucosa: buccal epithelium can harbour bacteria
  2. Tongue: dorsum surface
  3. Teeth
  4. Saliva
  5. Gingival crevicular fluid
33
Q

Define dental plaque

A

Diverse community of microorganism found on the tooth surface as a biofilm, embedded in an extracellular matrix of polymers of host and microbial origin

34
Q

State the 5 steps in the formation of dental plaque and what happens in each state.

A
  1. Pellicle formation;
    Salivary proteins and glycoproteins are adsorbed forming a surface conditioning film ‘The Acquired Enamel Pelicle’
  2. Attachment;
    Microorganisms that are passively transported by saliva to the tooth experience a weak physiochemical forces towards the acquired pellicle. Bacteria then connect to each other and to the pellicle with their fimbrae.
  3. Colonisation of pioneer microorganism;
    The pioneer population start to divide and form micro colonies. Consists of mainly STREPTOCOCCI. The attachment involves specific interaction called ‘Adhesin Receptor Interaction’ (ACI).
  4. Co aggregation;
    Plaque micro flora becomes more diversified (increasing portion of gram -ve bacteria). Some microorganism that were initially unable to colonise are able to attach to already-adherent pioneer species bu further ACI knows as ‘Coaggregation’.
  5. Mature biofilm;
    A biofilm with a 3D structure is produced. Some of the adherent bacteria synthesise extra cellular polymers that contribute to plaque matrix. Bacterial composition will vary at distinct anatomical site.
  6. Detachment from surfaces;
    Some bacteria are able to detach itself to be able to colonise elsewhere
35
Q

What are the common oral flora (in health)?

A
  1. Gram +ve cocci most numerous (Streptococcus)
  2. Gram +ve rods (Lactobacillus)
  3. Gram -ve rods (Prevotella)
  4. Gram-ve cocci (Veillonella)
  5. Spirochaetes (Treponema)
36
Q

What are the 4 factors that influence the oral flora?

A
  1. Saliva
  2. Gingival crevicular fluid (GCF)
  3. pH (acid = carcinogenic bacteria, alkaline = periodontopathogens)
  4. Redox potential
37
Q

How does plaque bacteria obtain energy?

A
  1. Plaque bacteria catabolise carbohydrates to obtain glucose which is used as an energy source.
  2. Endogenous source of carbs: saliva and GCF
  3. Exogenous source of carbs: diet
  4. Plaque bacteria transports sugars into their cells via PEP-PTS
  5. There are two enzymes involved: fructosyltransferase (ftf) and glucosyltransferase (gtf).
  6. Ftf = sucrose > fructan (rapidly turned off in plaque) + glucose
  7. Gtf = sucrose > glucan (kept in biofilm until needed) + glucose
  8. Stereptococcus is very good at 7. and thus it is an effective carcinogenic bacteria
38
Q

How does plaque bacteria produce acid?

A
  1. To obtain energy, plaque bacteria catabolise glucose and the by product of this process is acid
  2. This process begins with Glycolysis = glucose > 2x pyruvic acid.
  3. Enolase is an enzyme involved in this process and fluoride inhibits enolase
  4. Pyruvic acid then can undergo either one of these two:
    a) Cellular respiration = pyruvic acid > acetyl coA > energy (via Krebs cycle)
    b) Fermentation = pyruvic acid > organic acid (lactic acid, acetic, formic etc) This creates an acidic environment that is bad for teeth
39
Q

Explain pathogenicity of Streptococcus mutans?

A
  1. Ability to transport sugar effectively
  2. It produces acid as a by product of glucose catabolism
  3. Ability to survive at low pH
  4. Ability to store carbohydrate
40
Q

What are the bacteria involved in periodontal disease and how do they cause PD?

A

Pocket formation from;

  1. Direct action of anaerobic bacteria such as Prevotella and Treponema
  2. Indirectly from immune response
41
Q

What are the 4 injurious agents?

A
  1. Physical; heat, cold, radiation
  2. Chemical; acid, alkali
  3. Infectious; bacteria, fungi, viruses
  4. Immunological; antigen-antibody complex
42
Q

What are the cardinal signs of inflammation?

A
  1. Heat
  2. Pain
  3. Redness
  4. Swelling
  5. Loss of function
43
Q

What are the 4 important events that occur during inflammatory response?

A
  1. Vasodilation causes increased blood supply to area = increased supply of cells and factors to area
  2. Activation of endothelial cells lining causes increased expression of adhesion molecules (causes endothelium to be more ‘sticky’ to white blood cells thus promoting migration of leukocytes from blood to tissue)
  3. Increased vascular permeability making it easier for cell and protein to pass through walls of blood vessels to enter tissue
  4. Chemotactic factors are produced thus attracting cells from blood stream into the tissue
44
Q

What is the role of inflammation?

A

To recruits cells and other factors from the bloodstream to the tissues to aid the removal of pathogens and dead cells/tissues

45
Q

The first step of the inflammation process is the recognition of pathogen and activation of tissue macrophage. What are the factors produced upon activation?

A
  1. Prostaglandin; derived from arachidonic acid
  2. Platelet Activating Factor (PAF)
  3. Cytokines; Interleukin 1 (IL1), IL8 and Tumor Necrosis Factor (TNF)
46
Q

What are the effects of the factors produced during macrophage activation?

A
  1. Increase vascular permeability: TNF, prostaglandin and PAF (causes platelets to releases histamine which also increases vascular permeability)
  2. Activate endothelial cell: IL1 and TNF
  3. Chemotaxis: IL8
47
Q

What are the other pathways activated during inflammation?

A
  1. Kinin pathway; produces bradykinin which causes a) pain b) vasodilation c) increased vascular permeability
  2. Coagulation pathway; fibrinogen > fibrin > fibrinopeptides (chemotactic for phagocytes)
  3. Complement pathway; series of pro-enzymes and related factors that sequentially activate each other resulting in production of biologically active proteins
  4. Mast cell activation; when activated undergo degranulation and release histamine, heparin and proteolytic enzymes. Also synthesises prostaglandin (vasodilation) and leukotrienes (attract neutrophils, increase vascular permeability)
  5. Fibrinolytic pathway; fibrin degradation products induces vascular permeability
48
Q

What are cellular inflammatory mediators?

A
  1. Pre formed and stored waiting for inflammatory response
  2. Actively synthesised in response to inflammation
  3. Eg; vasoactive amines (histamine), arachidonic acid metabolises (prostaglandin and leukotrienes), PAF, cytokines (IL1, IL8, TNF), nitric oxide (from endothelial cells) and neutrophil factors
49
Q

What are plasma derived inflammatory mediators?

A
  1. Normally present in blood and activated by inflammatory response
  2. Eg; kinin system, coagulation cascade, complement pathway, fibrinolytic pathway, mast cell activation
50
Q

How are neutrophils involved in the inflammatory response?

A
  1. Due to vasodilation, blood flow becomes slow and allows the neutrophils to bump along the endothelium.
  2. Known as “Rolling” or “Margination” as cells travel along margins of endothelium
  3. Neutrophils line themselves along the edges of endothelium known as “Pavementing of neutrophils”
  4. Neutrophils bind firmly to endothelium
  5. Neutrophils squeezes between endothelial cells and pass through into tissue space.
  6. Neutrophils will travel along the IL8 gradient (process of chemotaxis where the IL8 is most concentrated at the centre of infection)
  7. The neutrophils will engulf the pathogens via phagocytosis
  8. Neutrophils will kill the pathogen via two methods;
    a) Fusing their toxic filled granules with pathogen and releasing their toxic content via degranulation
    b) Oxidative mechanism which produces free radicals (also kills themselves in the process)
  9. Macrophage will arrive at site of infection to clear away the dead neutrophils > formation of pus
51
Q

What are types of inflammation?

A
  1. Serous; esp in body cavities
  2. Haemorrhagic; severe damage to blood vessels
  3. Fibrinuous; pronounced activation of coagulation system
  4. Purulent; infection with pus forming organisms
52
Q

What is chronic inflammation?

A

Active inflammation of prolonged duration in which tissue destruction and attempts at healing are proceeding simultaneously.

53
Q

What are causes of chronic inflammation?

A
  1. Persisting acute inflammation
  2. Infection with certain microorganism
  3. Prolonged exposure to toxins
  4. Autoimmune reaction
54
Q

What are the 4 injurious agents?

A
  1. Physical; heat, cold, radiation
  2. Chemical; acid, alkali
  3. Infectious; bacteria, fungi, viruses
  4. Immunological; antigen-antibody complex
55
Q

What are the cardinal signs of inflammation?

A
  1. Heat
  2. Pain
  3. Redness
  4. Swelling
  5. Loss of function
56
Q

What are the 4 important events that occur during inflammatory response?

A
  1. Vasodilation causes increased blood supply to area = increased supply of cells and factors to area
  2. Activation of endothelial cells lining causes increased expression of adhesion molecules (causes endothelium to be more ‘sticky’ to white blood cells thus promoting migration of leukocytes from blood to tissue)
  3. Increased vascular permeability making it easier for cell and protein to pass through walls of blood vessels to enter tissue
  4. Chemotactic factors are produced thus attracting cells from blood stream into the tissue
57
Q

What is the role of inflammation?

A

To recruits cells and other factors from the bloodstream to the tissues to aid the removal of pathogens and dead cells/tissues

58
Q

The first step of the inflammation process is the recognition of pathogen and activation of tissue macrophage. What are the factors produced upon activation?

A
  1. Prostaglandin; derived from arachidonic acid
  2. Platelet Activating Factor (PAF)
  3. Cytokines; Interleukin 1 (IL1), IL8 and Tumor Necrosis Factor (TNF)
59
Q

What are the effects of the factors produced during macrophage activation?

A
  1. Increase vascular permeability: TNF, prostaglandin and PAF (causes platelets to releases histamine which also increases vascular permeability)
  2. Activate endothelial cell: IL1 and TNF
  3. Chemotaxis: IL8
60
Q

What are the other pathways activated during inflammation?

A
  1. Kinin pathway; produces bradykinin which causes a) pain b) vasodilation c) increased vascular permeability
  2. Coagulation pathway; fibrinogen > fibrin > fibrinopeptides (chemotactic for phagocytes)
  3. Complement pathway; series of pro-enzymes and related factors that sequentially activate each other resulting in production of biologically active proteins
  4. Mast cell activation; when activated undergo degranulation and release histamine, heparin and proteolytic enzymes. Also synthesises prostaglandin (vasodilation) and leukotrienes (attract neutrophils, increase vascular permeability)
  5. Fibrinolytic pathway; fibrin degradation products induces vascular permeability
61
Q

What are cellular inflammatory mediators?

A
  1. Pre formed and stored waiting for inflammatory response
  2. Actively synthesised in response to inflammation
  3. Eg; vasoactive amines (histamine), arachidonic acid metabolises (prostaglandin and leukotrienes), PAF, cytokines (IL1, IL8, TNF), nitric oxide (from endothelial cells) and neutrophil factors
62
Q

What are plasma derived inflammatory mediators?

A
  1. Normally present in blood and activated by inflammatory response
  2. Eg; kinin system, coagulation cascade, complement pathway, fibrinolytic pathway, mast cell activation
63
Q

How are neutrophils involved in the inflammatory response?

A
  1. Due to vasodilation, blood flow becomes slow and allows the neutrophils to bump along the endothelium.
  2. Known as “Rolling” or “Margination” as cells travel along margins of endothelium
  3. Neutrophils line themselves along the edges of endothelium known as “Pavementing of neutrophils”
  4. Neutrophils bind firmly to endothelium
  5. Neutrophils squeezes between endothelial cells and pass through into tissue space.
  6. Neutrophils will travel along the IL8 gradient (process of chemotaxis where the IL8 is most concentrated at the centre of infection)
  7. The neutrophils will engulf the pathogens via phagocytosis
  8. Neutrophils will kill the pathogen via two methods;
    a) Fusing their toxic filled granules with pathogen and releasing their toxic content via degranulation
    b) Oxidative mechanism which produces free radicals (also kills themselves in the process)
  9. Macrophage will arrive at site of infection to clear away the dead neutrophils > formation of pus
64
Q

What are types of inflammation?

A
  1. Serous; esp in body cavities
  2. Haemorrhagic; severe damage to blood vessels
  3. Fibrinuous; pronounced activation of coagulation system
  4. Purulent; infection with pus forming organisms
65
Q

What is chronic inflammation?

A

Active inflammation of prolonged duration in which tissue destruction and attempts at healing are proceeding simultaneously.

66
Q

What are causes of chronic inflammation?

A
  1. Persisting acute inflammation
  2. Infection with certain microorganism
  3. Prolonged exposure to toxins
  4. Autoimmune reaction
67
Q

Which bones contribute to the hard palate?

A
  1. Palatine process of maxilla

2. Horizontal plates of palatine bone

68
Q

What is vibrating line?

A

Demarcation between vibrating and non vibrating parts of the palate. Slightly posterior to junction between hard and soft palate

69
Q

Name the 3 foraminas of the hard palate and what passes through them?

A
  1. Incisive foramen; nasopalatine nerve and great palatine artery
  2. Greater palatine foramen; GP nerve and GP artery
  3. Lesser palatine foramen; LP nerve and LP artery
70
Q

State the origin, insertion, nerve and action of tensor veli palatini

A

O: Spine of sphenoid and auditory tube
I: Median palatine raphe
N: V3 of trigeminal
A: tenses the soft palate and opens the auditory tube

71
Q

State the origin, insertion, nerve and action of levator veli palatini

A

O: Inferior surface of temporal bone
I: Median palatine raphe
N: Pharyngeal of vagus nerve
A: Elevates the soft palate

72
Q

State the origin, insertion, nerve and action of palatoglossus

A

O: Palatine aponeurosis
I: Side of tongue
N: Pharyngeal plexus of vagus
A: Elevates posterior part of tongue and draws the soft palate to contact the tongue

73
Q

State the origin, insertion, nerve and action of palatopharyngeus

A

O: Palatine aponeurosis
I: Lateral wall of pharynx
N: Pharyngeal plexus of vagus nerve
A: Moves palate back & down and the pharynx forward and up

74
Q

State the origin, insertion, nerve and action of musculus uvulae

A

O: Palatine aponeurosis
I: Mucosa of uvula
N: Pharyngeal plexus of vagus
A: Shortens and broadens uvula

Symposia (5 decks)

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