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oral_biology_theme_4-7_20150331151415 Flashcards

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1
Q

List some Gram positive species of bacteria found in the mouth

A

Streptococcus (S. oralis - up to 50% oral flora, anaerobes in abscesses)Staphylococcus (S. epidermidis)Actinomyces (A. naeslundii - dental plaque)Lactobacillus (L. Acidophilus - increase in carious lesions)Eubacterium (E. brachy - periodontal pockets)

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2
Q

What is Alpha haemolysis?

A

Green ring around bacteria produces hydrogen peroxide = oxidises haemoglobin to methaemoglobin

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3
Q

What is Beta haemolysis?

A

Lysis of red blood cells (clear ring around bacteria)

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4
Q

What is Gamma haemolysis?

A

No Haemolysis

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5
Q

Which oral bacteria are associated with Infective endocarditis?

A

Streptococcus OralisStreptococcus GordoniiStreptococcus SangiusStreptococcus Mitis

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6
Q

Which oral bacteria are associated with preterm low birthweight?

A

Fusobacterium nucleatum

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7
Q

Which has Lipopolysaccharide… Gram positive or gram negative bacteria?

A

Gram negative bacteria

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8
Q

List some gram negative species of bacteria found in the mouth

A

Neisseria (N. Subflava - early tooth coloniser)Veillonella (V. parvula - tongue and dental plaque)Haemophilus (H. Aphrophilus - saliva, mucosal surfaces & dental plaque)Eikenella (E. Corrodens - increase in gingivitis)Capnocytophaga (C. Gingivalis - in periodontal pockets)Aggregatubacter (A. Actinomycetemcomitans - localized aggressive periodontitis)Porphyromonas (P. gingivalis - periodonto pathogen, lots in sub gingival plaque)Prevotella (P. intermedia - high numbers in sub gingival plaque)Fusobacterium (F. Nucleatum - high numbers in sub gingival plaque)Spirochetes (Treponema denticola - periodontopathogen, high nubers in sub gingiva plaque = difficult to culture)

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9
Q

What is a biofilm?

A

A microbial community forming at a phase boundary (generally a liquid to solid interface)

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10
Q

Give some examples of where biofilms are found?

A

Catheters, Implants & dental plaque

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11
Q

What are the constituents of a biofilm? (7)

A

BacteriaFungiAlgaeProtozoa BacteriophagesEnvironmental DebrisHost components

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12
Q

Explain how biofilms accumulate (3)

A
  1. Molecular fouling = conditioning film2. Microfoulding = initial colonisation by bacteria followed by micro algae and fungi3. macrofouling = colonisation by complex molecules (macro algae & invertebrates) = DAMAGE TO UNDERLYING SURFACE
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13
Q

Is biofilm formation across a whole surface uniform or not?

A

No!

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14
Q

What is sessile growth?

A

Where cells are attached to a surface or a preformed biofilm

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15
Q

What is planktonic growth?

A

Where the bacteria grow in liquid suspension

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16
Q

Which changes occur in gene expression of bacteria between the planktonic and sessile phase (5)?

A
  • Morphology- Motility (flagellum)- Growth rate (metabolic -> slows down/stops in biofilm)- Signalling (influences each others growth - still competes)- Antibiotic and disinfectant tolerance (slower metabolism)
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17
Q

Fermenter systems: what is a chemostat?

A

planktonic growth - can have surface suspended within (form biofilm on) or you can have a chemostat to a chemostat with surface

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18
Q

Fermenter systems: what is a constant depth film fermenter (CDFF)?

A

contains a biofilm disc and scraper -> can compare biofilms on different materials or can be removed at different times (Separate recesses)

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19
Q

Problems caused by biofilms (5):

A
  • Equipment damage- Product contamination- Energy losses- Medical infections (catheter, contact lenses etc.)- not easy to treat or remove = COST
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20
Q

Explain the 3 methods of antimicrobial resistance within a biofilm:

A
  1. Transport limitations (neutralised by surface layer)2. Physiological limitations (slow growing state = less susceptible to antimicrobial challenges)3. Spread of resistance phenotype (up regulation. spreading through a variety of mechanisms)
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21
Q

What enzymes can resistant bacteria secrete to produce a bubble of protection around themselves?

A

Beta lactamases

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22
Q

List the advantages of microbial culture (2):

A
  • can determine antibiotic resistance- Identify virulence factors
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23
Q

List the disadvantages of microbial culture (3):

A
  • Slow- Identification is often difficult- Only 50% of the oral flora can be cultured
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24
Q

What are the advantages of the checkerboard (2)?

A
  • Can complete a very large amount of analyses at the same time (40 probes & 40 plaque samples)- Quantitative
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25
Q

What are the disadvantages of the checkerboard (4)?

A
  • Requires careful calibration- Lab based (difficult to adapt for clinical use)- Takes several days to complete- Need cultural organisms to make probes
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26
Q

What are the 10 suspected periodontal pathogens?

A

Aggregatibacter actinomycetemcomitansPorphyromonas gingivalisPrevotella intermediaTannerella forsythiaEikenella corrodensFusobacterium nucleatumParvimonas micraTreponema denticolaCampylobacter rectusStreptococcus intermedius

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27
Q

Why is the 16s rRNA DNA conserved and does not change between generations?

A

It is essential for life, any mutations would stop it working and the cell would die = would not pass on altered genome

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28
Q

What are the conserved regions of 16s rRNA used for (2)?

A
  • sequence alignment- Universal primers fo PCR and sequencing
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29
Q

What are the variable regions of 16s rRNA used for (2)?

A

-phylogenetic analysis - detecting individua bacteria (species or strains specific PCR)

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30
Q

Which method does microarray use?

A

Ink spray method (spray specific probe onto specific region of chip)

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31
Q

Which two bacteria increase with orthodontic brackets?

A

T. denticolaS. gordonii

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32
Q

Why does plaque have different compositions in different areas?

A

Different environmental conditions (varying saliva flow, abrasive forces etc.)

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33
Q

What is a climax community?

A

A steady state appropriate for local environmental conditions (predominantly gram negative anaerobic rods)

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34
Q

How does dental plaque form? (4)

A
  1. Conditioning film (host glycoproteins)2. Linking film (streptococci -> link to other bacteria which can then bind to plaque)3. Coaggregation and conditioning film (actinomyces) = secondary colonisation4. Accumulation and shedding = dynamic and parts removed with saliva
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35
Q

What is the overall charge of enamel?

A

Negative (binds to positively charged molecules)

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36
Q

List the different types of bacterial adhesin: (5)

A

LectinsFimbriaePiliOther cell wall proteinsAnchorless adhesins (leave bacterial cell surface - binds to pellicle then rebinds bacteria)

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37
Q

What is atomic force microscopy and how does it work?

A

Records the force required to break the bonds of bacteria/protein to the probeElevate on end of the probe (measure angle of elevation and hence force with laser)3 points of attachment or bacteria to probe = repeated forces needed to break it off

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38
Q

Do different fimbrae exist?

A

Yes, different protein arrangements - bind different glycoproteins

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39
Q

Proline rich proteins:

A

Major component of the pellicle (readily adsorbs onto hydroxyapatite surfaces -> negatively charged region -> binds calcium)Lots of genetic variants (some glycosylated)Selectively mediate bacterial adhesionDegraded by proteasesTandem repeat of proline -> number of repeats determines which bacteria it preferentially binds (e.g. cariogenic streptococci or health associated bacteria)

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40
Q

Which protein is expressed on the surface of S. gordonii?

A

Amylase binding protein

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41
Q

What do secondary colonisers bind to?

A

Often to the primary colonisers

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42
Q

What are 3 types of interactions in plaque?

A
  1. cell-substratum adhesion2. Homotypic cell- cell adhesion (to same species)3. Heterotyic cell-cell adhesion (to different species) = complex
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43
Q

What is coaggregation?

A

Occurs in suspension -> most bacteria coaggregate with at least one partner type

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44
Q

What is coadhesion?

A

Occurs with pre-attached cell (to pellicle)

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45
Q

What are bacteriocins? Give two examples:

A

peptide antibioticse.g. Actinobaccilin & Mutacins

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46
Q

What is EPS?

A

Extracellularpolymeric substance

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47
Q

What % of total plaque volume does EPS make up?

A

35

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48
Q

What is the role of EPS (4)?

A
  • Facilitates diffusion in and out of plaque- Structural integrity (consolidates attachment of cells)- Communication- Localises acid fermentation products)
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49
Q

What are the components of EPS (3)?

A

Proteins (oral fluids & microbes)Polysaccharides: Glucans (from diet = Linear/branched)Fructans (from diet = Linear)eDNA

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50
Q

How is colonisation resistance achieved?

A
  • adherence to receptors/ligands for adhesion- compete for essential nutrients and co-factors- create microenvironment (e.g. acidic or no O2) = discourages growth of exogenous species- produce inhibitory substances (e.g. bacteriocins)
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51
Q

What is an essential nutrient?

A

Required in a specific channel form and cannot be synthesised in the body (must come from the diet)

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52
Q

Give some examples of an essential nutrient (5):

A

Amino acids (proteins) - adults have 9 essential, children have 12Fats (Mono & poly-unsaturated fats)Macrominerals -> support biochemical processesMicrominerals -> enzyme co-factors (need <100mg/day)Vitamins (enzyme co-facor precursors, hormone precursors, antioxidants)

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53
Q

What is a non essential nutrient?

A

Can be replaced by other nutrients or synthesised by other non-essential nutrients within the body

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54
Q

Give some examples of a non essential nutrient (3):

A

All carbohydratesMost fatsMost amino acids

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55
Q

What causes enamel hypoplasia?

A

Calcium deficiencyVitamin A & D deficiency (regulate calcium homeostasis)

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56
Q

What causes enamel fluoridosis?

A

Excess fluoride

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57
Q

At what age is an individual most susceptible to enamel fluoridosis?

A

6 Months to 4 years

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58
Q

In which 3 ways can form affect risk of caries?

A
  • Retention in oral cavity = increased risk- Mastication -> stimulates saliva (decreased risk)- Combined with constituents of HPA -> counteracts the demineralisation by acid
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59
Q

What is acidogenic potential?

A

the ability of a carbohydrate to be broken down into acid

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60
Q

What is cariogenic potential?

A

the ability of a carbohydrate to be broken down by BACTERIA (fermentation) into acid

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61
Q

What are intrinsic sugars?

A

located naturally within the cellular structure of a product (e.g. whole fruit and veg) -> these are good for you!

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62
Q

What are extrinsic sugars?

A

added by the manufacturer, cook or consumer (e.g. fruit juices, honey & syrups) -> potentially harmful - should not exceed 10% of daily energy intake

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63
Q

How cariogenic is lactose?

A

It is the least cariogenic disaccharide (bacteria struggles to convert it into acid)

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64
Q

What is Casein?

A

A component of milk that helps with re-mineralisation (along side calcium & phosphate)

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65
Q

Name a caries inhibitor:How does it work?

A

Apigenin =a naturally occurring flavonoidInhibits S. mutans glucosyltransferases = less S. mutans biofilm formation (necessary for progression of dental caries)

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66
Q

What is Apigenin found in?

A

ParsleyOnionsApplesBasilCelery rootTeaPeasArtichokeFeverfewOrange juiceGrapefruit juiceAlfalfa

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67
Q

What is erosion?

A

The irreversible loss of dental hard tissue by acids in a process that does not involve bacteria

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68
Q

What are the features of erosion?

A

Smooth & shiny surfaceCupping and grooving on occlusal surfaces

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69
Q

Why is Citric acid worse at erosion than any other acid?

A

When the acid dissociates it produces a proton and a citrate anionCitrate anion = Calcium chelator = remineralisation no possible because insufficient calcium in saliva

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70
Q

What does vitamin C usually do?

A

A co-factor in collagen synthesis

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71
Q

What are the features (2) of an individual with vitamin C deficiency?

A

Weakened tissues (soft, swollen and bleeding gums & weakened periodontal ligament)Capillary fragility (bruising)

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72
Q

What are the features of Vitamin B deficiencies?

A

Angular chelitis (deep cracks at corned of mouth & shallow ulcers) = B2, 3 & 12Glossitis (inflamed, painful tongue) = B2, 3, 6 & 12

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73
Q

Which health problem is associated with an excess in Sugars?

A

Oral fungal disease

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74
Q

Which health problem is associated with an excess in Vitamin A?

A

Lung cancer (smokers)

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75
Q

Which health problem is associated with an excess in Zinc?

A

Reduced immune function

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76
Q

Which health problem is associated with an excess in Manganese?

A

Muscle/nerve disorders (elderly)

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77
Q

Which minerals compete for absorption?

A

Calcium competes with Iron (too much calcium in diet = iron deficiency)Iron competes with zinc

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78
Q

What are the potential effects of alcohol on oral cancer?

A
  • acts as a solvent for other carcinogens- metabolised => Acetaldehyde = DNA damage (inhibits DNA synthesis and repair)- Abuse is associated with a poor diet
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79
Q

Which foods are associated with oral cancer?

A
  • Areca nut (chewed in betel quid leaves)- Raw/uncooked foods contaminated with microbial metabolites (e.g. Peanuts can be contaminated with Aspergillus favus = Aflatoxin B1 = cancer risk)
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80
Q

Anticancer agent:

A
  • Non-starchy fruits and vegetables (e.g. citrus, raw fruits & carotenoids = Beta carotene & lycopene) High intake decreases risk by 40-80%
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81
Q

What is the critical pH? What happens below this pH?

A

pH 5.5.Disrupts equilibrium between demineralisation & remineralisation (more demineralisation occurs)

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82
Q

What is dental caries?

A

An infection of bacterial origin that causes demineralisation of the hard tissues and destruction of the organic matter of the tooth

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83
Q

What is plaque?

A

A complex bacterial community embedded within EPS

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84
Q

What is plaque fluid?

A

The aqueous component of EPS

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85
Q

How is plaque fluid different to saliva?

A

It contains Potassium and Ammonium (product of metabolism from microbe within the plaque)Rich in Calcium & phosphate (close proximity to tooth surface)

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86
Q

What does the Stephan curve show?

A

It detects the carcinogenicity of a product

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87
Q

How is the Stephan curve constructed in vitro?

A
  1. Operator takes 6-7 plaque samples from different sites2. Plaque is homogenised with distilled water3. pH is measured using a micro pH electrode4. This is repeated 5-6 times over a time period
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88
Q

What are the pros of the in vitro method?

A
  • Cheap- Requires little specialised equipment
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89
Q

What are the cons of the in vitro method?

A
  • Requires great skill to obtain reproducible results (collect same amount of plaque each time)- Volunteer must allow for sufficient plaque to accumulate
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90
Q

How is the Stephan curve constructed in vivo?

A
  1. Construct a special bridge incorporating a pH electrode2. Place bridge in volunteers mouth3. Allow plaque to accumulate over the surface of the electrode and monitor the pH
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91
Q

What are the pros of the in vivo method?

A
  • Produces large amounts of real time data- Monitering possible over long time periods- Plaque is not disturbed so can be tested against multiple challenges
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92
Q

What are the cons of the in vivo method?

A
  • Equipment is expensive- Sample size is small (due to cost)- Volunteers must have dentition allowing for the placement of a bridge
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93
Q

At which pH does plaque buffer?

A

pH 4.0

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94
Q

Which (4) factors determine the lowest pH the plaque reaches?

A
  • Microbial composition (aciduric or acidogenic)- Plaque density (saliva accessibility & diffusion rate)- Location (e.g. molar fissures sheltered from natural salivary flow & difficult to fully remove plaque from deepest regions of fissures )- Nature of the fermentable carbohydrate (complex sugars must initially be broken down by salivary amylase before it can be fermented by bacteria = slower metabolism and less acid produced)
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95
Q

What are the 5 methods of caries prevention?

A
  1. Dietary control (e.g. sugar substances -> xylitol = taken up by S. mutans but cannot be metabolised & sorbitol)2. Stimulation of salivary flow3. Reduce plaque build up4. Inhibit demineralisation5. Fluoride
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96
Q

Which group of bacteria is predominant in health?

A

Gram +ve Facultativee.g. S. sanguis, S. gordonii, Actinomyces spp, Haemophilus Neisseria

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97
Q

Which group of bacteria is predominant in caries (excess sugars in diet)?

A

Gram +veFacultativee.g. S. mutans, S sobrinus, Actinomyces spp, Lactobacillus spp, S. wiggsiae, Bifidobacteria

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98
Q

Which group of bacteria is predominant in periodontal disease (lack of oral hygiene & immune dysfunction)?

A

Gram -veAnaerobic rodse.g. Porphomonas gingivalis, tannerella forsynthia, treponema denticola, aggregatibacter actinomycetemcomitans

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99
Q

Is caries genetic or microbiological (transmissible)?

A

Bit of bothMainly infectious (hamster experiment)

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100
Q

Which microbiota is found in primary enamel caries?

A

S. mutans & S. sabrinus

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101
Q

Which microbiota is found in secondary enamel caries?

A

Actinomyces spp. & lactobacillus spp.

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102
Q

Which microbiota is found in primary root caries?

A

Actinomyces spp. ( in older people with receding gums)

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103
Q

Which microbiota is found in secondary root caries?

A

Lactobacillus spp, S. mutans & S. sabrinus

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104
Q

Which microbiota are associated with early childhood caries?

A

S. mutansScardovia wiggsiae

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105
Q

How does S. mutans contribute to carcinogenicity?

A

Sugar transport systems:Efficient even at low pH!1. Sugar ABC transport systems (uses ATP to transport maltose into cell -> glycolysis = energy)2. Phosphoeonolpyruvate phosphotransferase systems (sugar phosphorylated from 2B protein -> enters glycolytic pathway to phosphopyruvate = pyruvate)

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106
Q

What is aciduricity?

A

Tolerance to acid (cells are able to survive, metabolise & grow even at low pH -> outcompete other bacteria at low pH)

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107
Q

Which enzyme synthesises Glucans?

A

Glucosyltransferases

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108
Q

Are water soluble Glucans linear or branched?

A

Linear

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109
Q

Where are water soluble Glucans produced?

A

Both inside & outside cells

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110
Q

What are water soluble Glucans used for?

A

Short term energy store

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111
Q

Are water insoluble Glucans linear or branched?

A

Branched

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112
Q

Where are water insoluble Glucans produced?

A

Outside the cell only

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113
Q

What are water insoluble Glucans used for?

A

Long term energy store

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114
Q

What are the other two functions of water insoluble Glucans in the oral cavity?

A
  • Sticky & hard -> acts as cement- Promotes accumulation of plaque
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115
Q

What is a Glucan?

A

Chains of glucose residues

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116
Q

What us a Fructan?

A

Chains of fructose residues

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117
Q

Which enzyme synthesises Fructans?

A

Fructosyltransferases

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118
Q

Are Fructans linear or branched?

A

Often linear

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119
Q

What are Fructans used for?

A

Rapid energy store (fructose metabolism is even faster than glucose -> 1 step less in glycolysis)

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120
Q

Give an example of a Glucan binding protein:Which bacteria express them?

A

LectinsS. mutans & other streptococci

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121
Q

What is the role of Glucan binding proteins?

A

Cementing agents

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122
Q

What is attrition?

A

loss of tooth substance due to tooth-to-tooth contact (Bruxism)Does not involve -> incisal edge, occlusal surfaces & bacteria

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123
Q

What is abrasion?

A

loss of tooth substance due to friction of foreign body independent of occlusion(E.g tooth brushing and pipe smokers)

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124
Q

What is erosion?

A

loss of tooth substance due to chemical processes (does not involve bacteria)Can be dietary, occupational (lead acid battery atmospheric pollution) & regurgitation of the stomach contents (bulimia)

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125
Q

In which two ways are caries classified?

A
  • site (e.g. pit/fissure, smooth surface/interproximal & root)- rate of progression (e.g. rampant - rapid, affects many teeth and often on normally resistant surfaces; chronic - slowly, defence reaction in pulpodentinal complex, most common in adults & arrested caries - become static)
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126
Q

What are the different zones in early enamel caries (4)?

A
  1. Translucent zone2. Dark zone3. Body of lesion4. Surface zone
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127
Q

What are the different zones in caries of dentine (5)?

A
  1. Sclerosis2. Demineralisation3. Bacterial invasion4. Destruction5. Reactionary dentine
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128
Q

What are the two types of abnormal calcification that can occur in the teeth?

A
  • Pulp stones (denticles : True = tubular structure, False = calcified but no tubular structure & Fixed/Free)- Dystrophic
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129
Q

In which 3 ways is pulpits managed?

A
  • Pulp capping- Pulp extirpation & endnotes treatment- Tooth extraction
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130
Q

What is 1ppm equal to?

A

1 mg/L

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131
Q

Which two bacterial enzymes are inhibited by Fluoride below the pH 5.5?

A
  • Enolase (sugar metabolism via the phosphoeonolpyruvate phosphotransferase systems = less glucose uptake = less lactic acid produced)- ATPase (proton pump, directly affected by fluoride = protons not extruded = inhibits enzymes e.g. Enolase)
132
Q

How does fluoride inhibit demineralisation?

A

Absorbs onto tooth surface, draws in Calcium & phosphate to local environment = increased remineralisation (requires Ca & Phosphate)

133
Q

What is the problem with fluoride and carious lesions?

A

Remineralisation can ‘bury’ the lesions (bacteria etc. still in there)

134
Q

What are the 3 methods of raising the fluoride content of teeth?

A
  • Water fluoridation (07 - 1ppm)- Fluoride tablets- Clinically applied topical fluorides
135
Q

What is monophosphate?

A

Covalently bound to fluorideHydrolysis by phosphatases in plaque = only slightly less effective than fluoride itself

136
Q

What are slow release fluoride devices made of?

A

Co-polymer or Glass

137
Q

When combined with Fluoride what does CPP-ACP produce?

A

Amorphous calcium fluoride phosphate = more effective at low pH than fluoride & CPP-ACP for remineralisation

138
Q

What does CPP-ACP contain?

A

Casein (10%), Calcium & Phosphate

139
Q

What are the 4 risk factors for dental fluorosis?

A
  • Fluoride concentration >1ppm- Consumption of many fluoride products - Fluoride intake from multiple sources- Accidental ingestion of Fluoride toothpaste by children (why we recommend pea sized amount)
140
Q

Why are children more at risk to develop fluorosis than adults?

A

Their teeth are still developing so fluoride has access through systemic route

141
Q

What are the 4 methods of management for periodical periodontitis?

A
  • Drainage (soft tissue or root canal)- Endodontic treatment- Apicectomy (like root canal but from base - chop of apex)- Extraction of tooth
142
Q

Which tooth is most often associated with pulp polyps? and why?

A

Upper 6th toothInfection spreads into palate because it has 3 roots

143
Q

What is Ludwig’s angina?

A

A big swelling under the chin (caused by infection of the lower teeth spreading into the sublingual spaces)

144
Q

What is a cyst?

A

A pathological cavity with fluid, semi-fluid or gaseous contents lined by epithelium (fluid = secretion from the type of epithelium lining it)

145
Q

What is an odontogenic cyst?

A

A cyst of the jaw arising from tissues involved in odontogenesis derived from the rests of Mallessez Contains: air, fluid or semi-solid material

146
Q

What is a paradental cyst?

A

Odontogenic cyst of the wisdom tooth

147
Q

Give an example of a non-odontogenic cyst?

A

Non-epithelialized primary bone cyst

148
Q

What are the key clinical features of odontogenic cysts?

A

Symptomless expansion (springy = fluid filled)Egg shell crackling (fragments of the buccal plate)

149
Q

What is the role of sIgA in saliva?

A
  • Aggregate oral micro-organisms- Prevents bacterial adherence to surfaces- Inhibition of bacterial enzymes (e.g. glucosyltransferases)- Neutralises viruses
150
Q

What is the problem with S. mutans whole cell immunisation?

A

Linked to possible immunologically mediated damage of heart tissue

151
Q

How do S. mutans bind (2)?

A

Glucans (direct to pellicle = become incorporated & congregation with other adhering bacteria = gluten binding proteins)Antigen I/II = binds pellicle, fluid phase salivary components (incorporated into pellicle)

152
Q

What is the problem with Antigen I/II immunisation?

A

1 region produces immunoglobulins for heart -> do not want to use this section(can immunise with peptide lacking this section -> we must use recombinant Ag I/II with this part missing!)

153
Q

At which age should we immunise against Caries?

A

12 months (prior to the window of infectivity at 18 months when maternal antibodies wane)Booster at 5-6 years as teeth start to emerge

154
Q

What other technique is there to protect against caries?

A

Manipulation of bacteria (so cannot produce acid -> e.g. replace lactate dehydrogenase with alcohol dehydrogenase = metabolises glucose into alcohol instead)

155
Q

Animal studies have been used to understand (5)

A
  • Aetiology- Role of specific virulence factors- Mechanisms of colonisation- Effects of cells and inflammatory mediators on tissue responses- Role of other infections in periodontal disease- Role of risk factors in periodontal disease
156
Q

Which surface structures of P. gingivalis are involved in colonisation (6)?

A
  • Proteases - Fimbriae- Non-proteolytic factors- Iron-capturing proteins- haemagglutinin-Capsule
157
Q

Name some vaccine targets for P. gingivalis (2):

A

Proteases (Rgp & Kgp peptides) -> blocks active sitesFimbriae (N & C epitope peptides on S. gordonii = produces immunoglobulins against P. gingivalis)

158
Q

What is gingivitis?

A

Inflammation of the gingival tissues (reversible)

159
Q

What is periodonitits?

A

Chronic gingivitis with loss of attachment (irreversible)

160
Q

What are the different types of periodontitis?

A

Localised (juvenile) aggressive periodontitis (LAP)Chronic (slow) periodontitis - in elderly/those who don’t brush

161
Q

What is a not very form of gingivitis?

A

Acute necrotising ulcerative gingivitis (involves specific types of bacteria)

162
Q

What causes which % of the tissue damage in periodontal disease?

A

20% Bacteria (microbial enzymes directly digesting tissue)80% Host inflammatory response

163
Q

What are the clinical features of periodontal disease?

A
  • inflammation of the gingiva- bleeding on probing- loss of attachment- true pocketing and recession of gums- tooth mobility and drifting (due to loss of bone & no tight cuff)- alveolar bone loss (horizontal & vertical)
164
Q

Which % of patients are at high risk of progression to periodontal disease?

A

10%

165
Q

Which % of patients are slowly progressive?

A

80%

166
Q

Which % of patients are resistant to periodontal disease?

A

10%

167
Q

What is a false pocket?

A

Caused by inflammation

168
Q

Classification of periodontitis:

A

Localised (30% teeth involved)Slow/rapid progression

169
Q

What does gingival crevicular fluid have that saliva doesn’t?

A

Lots more protein, Sodium, Calcium & complement

170
Q

What is a polymorphism?

A

changes in the nucleotide sequences of genes which may alter its expression (increased or decreased)

171
Q

Polymorphisms in which genes are associate with periodontal disease (6)?

A
  • TNF (Tumour Necrosis Factor)- Interleukin 6- Interleukin 1- Leukocytes Fc Gamma receptor for IgG- Vitamin D- Matrix Metalloproteinases (MMPs)
172
Q

What is the periodontal ligament?

A

Soft connective tissue joining the cementum to the alveolar bone

173
Q

Where is the periodontal ligament derived from?

A

The dental follicle

174
Q

What do bisphosphonates cause?

A

Ankylosis (replace periodontal ligament with bone) -> due to disruption in homeostatic induction of factors = induces odontogenic factors

175
Q

What are the functions of the periodontal ligament (4)?

A
  • Supportive- Remodelling of itself, surrounding bone & cementum- Sensation - Nutrition
176
Q

Which fibres make up the periodontal ligament and what % do they occupy?

A

Collagen >90%Oxytalan & reticulin <10%

177
Q

What is Type I collagen?

A

Tropocollagen molecule (2 alpha 1 chains & 1 alpha 2 chain)Low in hydroxylysine & glycosylated hydroxylysine

178
Q

What is Type III collagen?

A

Tropocollagen molecule (3 alpha 1 chains)Low in hydroxylysineHigh in glycosylated hydroxylysineContains cysteine

179
Q

Which has thinner and more numerous principal fibres embedded within… Alveolar bone or Cementum?

A

The cementum has more with smaller diameter (due to branching)

180
Q

What are the 5 different groups of principal fibres?

A
  1. Alveolar Crest fibres2. Horizontal fibres3. Oblique fibres4. Periapical fibres5. Inter-radicular fibres
181
Q

What do transeptal fibres do?

A

Join the neck of 1 tooth to the next over the top of the alveolar crest

182
Q

What are the components of ground substance (3)?

A
  • Glycosaminoglycans (GAGs) - hyaluronic acid- Proteoglycans- Glycoproteins (fibronectin, tenascin & vitronectin)
183
Q

What are the functions of ground substance (5)?

A
  • fairly acidic & binds lots of water- controls collagen fibrillogenesis (promotes attachement, migration and orientation of fibrils)- bind growth factors- supports high tissue fluid pressure- inhibitor of mineralisation
184
Q

Which cells can be found in the periodontal ligament (7)?N.B. type and number of cells depends on functional state of periodontal ligament (changes with inflammation & orthodontics etc.)

A
  • Fibroblasts- Osteoblasts &Cementoblasts- Osteoclasts & Cementoclasts- Undifferentiated mesenchymal cells (possibly also true stem cells)- Defence cells- Epithelial rests of mallassez- Cells of vasculature and nerves
185
Q

How does periodontal ligament resemble foetal connective tissue (7)?

A
  • High rate of cell turnover- Distribution of small collagen fibrils & type of crosslinks- Significant amounts of collagen type III- Large volume of ground substance- Presence of oxytalan fibres- High degree of cellularity- Numerous intracellular contacts between fibroblasts (simple desmosomes & gap junctions)- Biomechanical properties (does not respond to forces)
186
Q

What are the functions of fibroblasts (6)?

A
  • Formation, maintenance & remodelling of gingival & periodontal ligament- Respond to hormones, cytokines growth factors, microbial products and mechanical loading- Synthesise, secrete & degrade proteins- Migration- Contraction- Interact with other cell types/fibroblasts within gingival or periodontal ligament
187
Q

What is the embryological origin of periodontal fibroblasts?

A

Ectomesenchymal/neural crest cells

188
Q

What is the embryological origin of gingivae?

A

Mesenchymal

189
Q

Which fibroblasts have: higher rate of proliferation?

A

Periodontal fibroblasts

190
Q

Which fibroblasts have: contacts to overlying epithelial cells?

A

Gingival fibroblasts

191
Q

Which fibroblasts secrete more collagen type III and less ground substance?

A

Periodontal fibroblasts

192
Q

Which fibroblasts have: faster collagen turnover?

A

Periodontal fibroblasts

193
Q

Which fibroblasts have: decreased cell volume?

A

Gingival fibroblasts

194
Q

Which fibroblasts express MORE alkaline phosphates and cAMP?

A

Periodontal fibroblasts

195
Q

Which fibroblasts contain less contractile proteins?

A

Gingival fibroblasts

196
Q

What do fibroblasts synthesise (5)?

A

CollagenOxytalin/elastin fibresIntermediate cytoskeleton fibres (vimetin)Cytokeratins (only in ageing periodontal ligament)Ground substance

197
Q

How do fibroblasts degrade collagen?

A

take up collagen into fibroblasts = forms organelles (intracellular collagen profiles) -> contains lysozymal & metalloproteinase type enzymes = break down within cellExtracellular collagen - phagocytosed & digested

198
Q

Loss of collagen in periodontal disease could be due to (3):

A
  • Reduced rate of synthesis- Increased rate of degradation- Decrease in the number of fibroblasts
199
Q

Gain of collagen in gingival fibrosis could be due to (3):

A
  • Increased rate of synthesis- Reduced rate of degradation- Selective deletion/survival/proliferation of fibroblast sub populations (those specialising in rapid collagen synthesis retained)
200
Q

How fast is gingival collagen turnover compared to skin, bone and the periodontal ligament?

A

Faster than skin and boneSlower than the periodontal ligament

201
Q

What is granulation tissue?

A

New connective tissue and blood vessels forming on the surfaces of a wound during healing

202
Q

At which site are periodontal ligament stem cells found?

A

Perivascular (next to blood vessels!)N.B. must migrate to their sites of action

203
Q

What is the key problem with observing fibroblasts in vitro?

A

The method of cell culture influences the data (cells don’t do what they normally would in vivo)

204
Q

What potential future treatment involves fibroblasts?

A

Guided tissue regeneration(may need to be from specific tissue - we do not know if there are specific progenitors for each)

205
Q

Which signals can activate fibroblasts (5)?

A
  • Hormones- Growth factors (TGFβ, IGF-1, PDGF, BMP-2, BMP-7 & FGF-2)- Cytokines- Bacterial products- mechanical factors
206
Q

What does TGFβ do?

A

Produces collagenIncreases amount of inhibitor enzymes preventing collagen breakdown

207
Q

What does PDGF & FGF-2 do?

A

ProliferationChemotaxis

208
Q

What does BMP-2 & BMP-7 do?

A

Bone formation

209
Q

What does Osteoprotegerin (OPG) do to osteoclast formation and activity?

A

It inhibits (binds to and inhibits RANKL)

210
Q

What does cell surface RANKL do to osteoclast formation and activity?

A

It supports= a cytokine that activates osteoclasts

211
Q

Which tissue seals the periodontal ligament from the oral cavity?

A

Gingival ligament

212
Q

What are the epithelial rests of Mallassez?

A

Remnants of Hertwig’s epithelial root sheathSlow turnover -> can develop into cysts or tumours

213
Q

From which tissue do the blood vessels of the periodontal ligament originate?

A

Mainly Alveolar bone (superior and inferior alveolar artery)GingivaeSmall amount from apicies

214
Q

Other than the periodontal ligament collagen fibres what other fibres can be found in the periodontal ligament?

A

Oxytalan fibres

215
Q

What is calculus?

A

Calcified plaque

216
Q

Which component of saliva do we incorporate into toothpaste to reduce calculus formation?

A

Pyrophosphate

217
Q

How does calculus attach to the tooth?

A

Fibronectin (very strong attachment to tooth surface = hard to remove)

218
Q

What is intracellular calcification? And which bacteria are involved?

A

From the inside outCorynebacter matruchotii, Actinomyces israelli & streptococcus salivarius

219
Q

What is extracellular calcification? And which bacteria are involved?

A

From outside inVeillonellae spp.

220
Q

What are the different components of gingival connective tissue (5)?

A
  • Collagen bundles- Chondroitin sulfate- Keratin sulfate- Heparin- Hyaluronic acid
221
Q

Which bacteria are predominant in health?

A

Gram +ve (streptococi & actinomyces)Facultative (able to withstand the presence of oxygen)

222
Q

Which bacteria are predominant in periodontitis?

A

Gram -ve (fusobacterium, porphomonas, prevotella, tannerella & spirochetes = treponema)Anaerobic

223
Q

Why is microbial diagnosis of periodontal flora limited?

A

Tests will no identify a specific disease or predict disease progression

224
Q

Which bacteria is associated with Localised Aggressive (Juvenile) Periodontitis (LAP)?

A

Leukotoxic Aggregatibacter (Actinobacillus) actinomycescommitans

225
Q

Which bacteria acts as a bridge between early colonisers and late colonisers?

A

Fusobacterium nucleatum (gram -ve)

226
Q

Which bacteria (2) are early colonisers in health?

A

Streptococcus spp. & Actinomyces spp. (gram +ve)

227
Q

What do the transitional complex do in sub gingival plaque?

A

Set up the periodontal pocket

228
Q

What are the names of the 3 key periodontal pathogens?

A

Treponema denticolaPorphomonas GingivalisTannerella Forsynthia

229
Q

In which 3 ways do bacteria become pathogenic?

A
  • colonisation mechanisms- Evasion of host defences- Tissue destruction
230
Q

What are the different bacterial colonisation mechanisms (5)?

A
  • Fimbriae- Capsule- Lipopolysaccharide (LPS - from gram -ve only)- Invasion of host cells- Microbial complexing
231
Q

In which 2 ways do bacteria evade host defences?

A
  • Leukoaggressins (inhibits chemotaxis, phagocytosis, killing proteases & complement factors)- Antigenic shift (express same protein with a different conformation)
232
Q

In which 6 ways do bacteria destroy tissue?

A
  • Collagenases- Hyaluronidases- Sulphur compounds- Lipopolysachharides (LPS)- Acid phosphatases- Epithelial & endothelial cell toxins
233
Q

What type of bacteria is aggregatibacter actinomycecomitans?

A

Gram -veFacultative

234
Q

Which serotype of Aggregatibacter actinomycecomitans is associated with LAP and which is associated with health?

A

Serotype B = LAPSerotype C = health

235
Q

What type of bacteria is P. gingivalis?

A

Gram -veanaerobic

236
Q

What are the 3 non specific methods of tissue destruction?

A

Lipopolysaccharide (LPS) - by all gram -veCapsule (surface associated material - SAM = stimulates bone resorption)Cytotoxins (products of metabolism & short chain fatty acids)

237
Q

What method of tissue destruction is associated specifically with Aggregatibacter actinomycecomitans?

A

Leukotoxin (some strains are highly leukotoxic - serotype B = LAP)4 parts:B & D = transportersA= toxin -> forms pore = cell lysisC = activator

238
Q

Which 3 methods of tissue destruction are associate specifically to P. gingivalis?

A
  • Colonisation mechanism- Haemagluttinins (cell surface proteins mediating binding of bacteria to receptors - oligosaccharides - on human cells & epithelial cells = 5 known Hag A, B, C, D & E)- Proteases (extracellular = released from the cell e.g. RgpA, RgpB & Kpg = degrade collagen)
239
Q

What do most oral bacteria stimulate in epithelial cells?

A

IL-8 synthesis

240
Q

What does IL-8 do?

A

involved in attracting T cells = secretion of cytokines & lymphotoxin (immune response)

241
Q

How does P. gingivalis reduce IL-8 production?

A

It preferentially invades epithelial cells (invades even if other bacteria are present)It reduces mRNA production of IL-8N.B. only in invasive strains and only when it is hiding (/latent) in epithelial cells -> not in other cells = disease

242
Q

What are the 3 division of the trigeminal nerve?

A
  • Ophthalmic- Maxillary- Mandibular
243
Q

What is the bell mangendie law?

A

Ventral roots = motor axonsDorsal roots = sensory axons

244
Q

What are the two trigeminal roots?

A

Sensory (larger) Motor

245
Q

What are the derivatives of the trigeminal roots?N.B. they are different

A

Sensory -> neural crest cellsMotor -> basal plate of embryonic pons

246
Q

What does the trigeminal ganglion contain (2 + 4)?

A

Cell bodies for majority of trigeminal nerve afferentsAxons for α & γ motor neuronesGlial (supporting cells)Connective tissue cells (fibroblasts, adipose cells etc.)Blood vesselsLymphatic vessels

247
Q

Which part of the trigeminal ganglion is sensory and which is motor?

A

Sensory = whole thingMotor = bottom half

248
Q

How do we categories trigeminal primary afferents?

A

Modality

249
Q

What are the different trigeminal modalities (5)?

A

Touch (M, fast)Proprioception (M, fast)Pressure (M, fast)Temperature (NM, slow)Pain (NM, slow)

250
Q

Which types of afferents have their cell bodies in the trigeminal ganglion (8)?

A
  • Low threshold mechanoreceptors- Thermo-receptors- TMJ mechanoreceptors- Golgi tendon organ receptors (group Ib afferents)- Secondary tendons of muscle spindles (group II afferents)- Tooth pulp afferents- Nociceptors- 55-65% of mechanoreceptors of the periodontal ligament
251
Q

What are the two connections of the trigeminal nerve to the thalamus and cortex?

A

Trigeminal leminscus (crosses in midline)Posterior trigeminothalamic tract

252
Q

Which nuclei of the thalamus do the above tracts terminate in?

A

VPM

253
Q

What is microneurography?

A

Measuring nerve impulses by putting electrodes into nerve trunks (e.g. the infraorbital, lingual & inferior alveolar nerves)

254
Q

Which primary afferent can be found in the hand but not the face?

A

Pacinian corpuscle (deep receptors!)

255
Q

What is pericoronitis?

A

Inflammation of the gingivae/mucosa surrounding an erupting tooth (due to build up of debris)

256
Q

What is osteitis?

A

Dull aching, nagging pain from bacterial infection of bone (dry socket)

257
Q

What is a migraine?

A

A headache caused by abnormal vasodilation of arteries in the ECA

258
Q

What is post-herpetic neuralgia?

A

Sensory loss and enduring pain occurring for months following infection with shingles

259
Q

What is trigeminal neuralgia?

A

pain of the face caused by non-noxious tactile stimulus = intense stabbing pain

260
Q

What are Aβ fibres? and what is their conductance velocity?

A

Low threshold mechanoreceptors30-80m per sRespond best in single direction (response decreases in opposite direction)Slowly adaptingVery low threshold force (displacement of 2-5 µm)Spontaneous discharge (stop my Local anaesthetics)Most located close to the root apex (afferent bodies in mesencephalic nucleus)Respond to movement (tension), not pressure

261
Q

What are Aδ fibres? and what is their conductance velocity?

A

High threshold mechanoreceptors5- 30m per sSmall diameter & myelinatedThermal & mechanical

262
Q

What are C fibres? and what is their conductance velocity?

A

Nociceptors and postganglionic sympathetics0.5-1.5m per sNon myelinated= dull burning chronic pain

263
Q

When using microneurography in animals at which 2 areas?

A

Trigeminal ganglionMesencephalic nucleus

264
Q

What are the functions of low threshold mechanoreceptors (3)?

A
  • Touch & pressure from teeth- Sensory feedback to trigeminal motor nucleus (contribute to motor control of tongue, buccinators & facial muscles during speech)- Control of salivation
265
Q

What is the structure of low threshold mechanoreceptors?

A
  • Numerous nerve endings- Finger like projections which extend between adjacent collagen fibres of the periodontal ligament
266
Q

Do mechanoreceptors respond to only a single tooth or can they respond to more than one?

A

Respond to the stimulation of several adjacent teeth (central tooth gives greatest response) -> possibly due to pressure on 1 causing shuttling of pressure onto neighbouring teeth)

267
Q

Do posterior or anterior teeth have the highest threshold?

A

Posterior teeth

268
Q

What is pain?

A

an unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damageIt is subjective & learned

269
Q

What are nociceptors?

A

Sensory receptors activated by high threshold stimuli (potentially damaging e.g. mechanical, thermal & chemical)

270
Q

Which neurotransmitters are released by nociceptors?

A

GlutamateSubstance PCalcitonin gene related peptide (CGRP)

271
Q

What is the transduction mechanism for mechanical nociceptors?

A

Mechanosensitive cation channel (with diff. thresholds)e.g. TRPA1, ASIC & P2X3

272
Q

What is the transduction mechanism for temperature nociceptors?

A

Transient receptor potential (TRP) channel receptorsHeat gated: VR1 & TRPV1 -> also respond to capsaicinCold gated ( also respond to methanolN.B. behavioural responses are mediated view the hypothalamus

273
Q

What is a polymodal nociceptor?

A

Responds to many different stimuli (expresses many different receptors)

274
Q

What is a silent nociceptor?

A

It is usually unresponsiveCan be activated by neurotransmitters & inflammatory molecules by other receptors= AMPLIFICATION of the nociceptive signal

275
Q

What is neurogenic inflammation?

A

Noxious stimuli received by CPN receptor = action potential (pain)= Peripheral nerve endings release Substance P & CGRP locally = Mast cells (increase Substance P release) & Blood vessels vasodilate & increased permeability

276
Q

When does neurogenic inflammation occur?

A

Following sub threshold stimulation of terminals (does not require action potential condition -> not always with pain)

277
Q

What are the 3 main sub nuclei & lamina of the Nucleus Caudalis?

A
  • Subnucleus maeginlis (MAR) or Lamina I- Subnucleus gelatinosus (SG) or lamina II & III- Subnucleus magnocellularis (MAG) or lamina IV
278
Q

Which receptors receive glutamate? And what speed is this pathway?

A

AMPA & NMDA receptors Fast excitatory

279
Q

Which receptors receive Substance P? And what speed is this pathway?

A

NK1 receptorsSlow excitatory & vasoactive

280
Q

Which receptors receive CGRP? And what speed is this pathway?

A

CGRP receptorsSlow excitatory & vasodilator

281
Q

In dorsal horn we have the gate control theory of pain, this means if we rub ourselves after injury the pain lessens. In the trigeminal spinothalamic pathway what happens?

A

Pain outweighs pressureLTM & HTM inputs are anatomically separatedCaudalis = proprioception inhibits Main sensory nucleus (temp & pressure) = Pain predominates

282
Q

What is hyperalgesia?

A

Increased response to a stimulus that is normally noxiousPrimary = at site of injury -> often due to inflammationSecondary = occurs in undamaged surrounding tissue

283
Q

What is allodynia?

A

Pain due to stimulus that does not normally provoke pain (e.g. trigeminal neuralgia, phantom tooth pain, atypical odontagia)

284
Q

What is peripheral sensitisation?And what does it cause?

A

Receptors are more sensitive to stimulusPrimary hyperalgesia and allodynia

285
Q

What is central sensitisation?And what does it cause?

A

CNS is more sensitive to impulses from the neuronePrimary & secondary hyperaglesia & allodynia

286
Q

What can cause peripheral sensitisation? (3)

A
  • Sensitisation by chemical mediators released by noxious stimuli nearby e.g. prostaglandins, histamine, bradykinin, 5-HT etc.- Neurogenic inflammation (release of Substance P & CGRP)- Altered phenotype of afferents following nerve damage (when activated for long periods of time)
287
Q

What causes central sensitisation?

A
  • prolonged stimulation of C fibres = wind up = increased activation of receptors (n.b. this is not confined to a specific pathway, it can spill over into others)
288
Q

How can central sensitisation be stopped?

A

pre-emptive analgesia = stops the irreversible change in nerve terminals

289
Q

What stimulation produces pain in enamel?

A

Hot (<28 degrees)

290
Q

What stimulation produces pain in dentine?

A
  • Hot/cold- Mechanical (bur & probe)- Removal of water (osmotic e.g. eating toffee, air stream or absorbent materials)- Changes in hydrostatic pressure
291
Q

How much of the width of dentinal tubules do odontoblast processes extend?

A

No more than 1/3 to 1/2 of the length (up to 100 µm)Mainly over the pill cornu -> not in all tubules!

292
Q

What is the lamina limitans?

A

The protein lining of tubules left behind following decalcification

293
Q

What are the two types of interdental sensory receptors?

A

Hydrodynamic receptors (Aβ & Aδ myelinated fibres = in or near dentine -> respond to flow in the dentinal tubules)MORE SENSITIVE TO OUTWARD FLOWEtching increases sensitivity Short latency response to coolingHeat & Chemo sensitive receptors (Aδ & C fibres = responds to heating or chemical stimuli - e.g. bradykinin, capsaicin) Long latency response to heating

294
Q

What happens to nerves towards the peripheral terminals?

A

They taper and have slower conduction velocities

295
Q

When the tooth is heated what happens?

A

There is expansion of the crown = inward flow in dentinal tubules

296
Q

When the tooth is cooled what happens?

A

The crown shrinks = outward dentinal flow (more sensitive to cold than hot as more sensitive to outward flow)

297
Q

How do we measure pulp blood flow?

A

A laser doppler probe

298
Q

What are the different causes of hypersensitivity in dentine (2)?

A
  • Open tubules on surface of exposed dentine- Smear layer removed from exposed tubules & tubules are opened up by acid drinks & foods
299
Q

Whats the incidence of hypersensitive dentine in patients?

A

57%

300
Q

What is hypersensitive dentine?

A

An increased sensitivity to hot, cold & mechanical stimuli and drying (a form of hyperalgesia)

301
Q

What are the possible mechanisms for hypersensitive dentine?

A

Peripheral sensitisation:- tubules open at dentine surface- Decreased resistance to flow of dentinal fluid- Increased sensitivity of the ion transducer channels in receptors (changes in ion composition)- Sprouting of intradental nerve terminals (increased innervation)Central sensitisation: secondary to pulp inflammation

302
Q

In what ways can dentinal tubules be occluded?

A
  • potassium oxalate (precipitates calcium oxalate crystals and dissolves quickly in saliva)- hydroxyapatite- calcium carbonate with 8% arginine- dentine binding materials (adper single bond plus)
303
Q

What does sensodyne contains that reduces sensitivity?

A

Potassium ions (although experiments have shown that sensitivity quickly returns to normal following use of potassium ions)

304
Q

What is the component reducing sensitivity in other desensitising toothpastes?

A

Strontium chloride

305
Q

What effect does pulpal inflammation have on the sensitivity of etched dentine?

A

Increased sensitivity to coldDecrease sensitivity to ressure

306
Q

What are the two dimensions of pain?

A

Sensory (actual pain)Behavioural (response to pain e.g. more angry, cannot sleep etc.)

307
Q

How to prostaglandins induce pain?

A

They increase the sensitivity of free nerve endings to the nociceptive properties of histamine & bradykinin (responsible for pain development and increasing pain intensity)

308
Q

Are pain related pathways in the face mediated by the brain too?

A

YesThis can be influenced with medication

309
Q

Which modulation happens to the most caudal part of the trigeminal tract nucleus?

A

Descending nerve fibresDrugs

310
Q

What is Encephalin?

A

An opioidOur own endogenous morphine = activates inhibitory interneurones & dampens down pain!

311
Q

What is myofascial pain?

A

Muscle pain

312
Q

What are the key features of pain due to exposed dentine (5)?

A

repsonds to hot/cold & sweet/sour stimuliPoorly localised (does not cross midline)Lasts for secondsTooth NOT tender to percussion Tooth still vital

313
Q

What are the key features of pain due to pulpitis (4)?

A

responds to hot/cold & pressurePoorly localised (radiates)Lasts for seconds, minutes or hoursNOT tender to touch

314
Q

What is Acute necrotic ulcerative gingivitis (ANUG) caused by? and what are its key features? Who is it most often seen in?

A

Caused by Gram -ve bacteriaSmellsLoss of interdental papillaeClassically seen in young male smokers

315
Q

What are the clinical features of a cracked tooth?

A

Pain is severe (pulpitis)Pain is exacerbated by biting & thermal stimuliTreatment = extraction

316
Q

What clinical feature is caused by malignancy in the sinus and not sinusitis?

A

Numbness

317
Q

What is a sialolith?

A

White stones in the salivary glands = causes back pressure and pain

318
Q

What are strictures?

A

Narrowing of the opening of salivary glands

319
Q

What is osteomyelitis?

A

Bone inflammationBone dies & overlying tissue is ulcerated due to loss of blood supply from bone = inflammation & pain

320
Q

What happens in pagets disease?

A

Normal bone cycle of renewal and repair is disrupted = weakening & deformation of the bone

321
Q

In TMJ dysfunction what key feature do you often see on the tongue?

A

Crenation (side of tongue looks like bread knife due to biting of tongue)

322
Q

What are the 3 different forms of persistant idiopathic (unknown cause) pain?

A
  • Burning mouth syndrome- Atpyical odontalgia = tooth ache without anything wrong- Atypical facial pain
323
Q

What is an acoustic neuroma?And what symptoms does it cause?

A

A benign growth in the IAMCompression of nerves (Facial & vestibulocochlear nerve)= Palsy (weakness of muscles), tinnitus, deafness & dizziness

324
Q

What is langerhans cell histiocytosis?

A

Systemic diseaseInflammation causing localised bone loss, inflammation -> good gum attachment with sudden loss of bone & inflammation

325
Q

What is catastripisation?

A

Only seeing the worst possible outcome -> start loosing hope!

Yr 2 - oral biology tooth (2 decks)

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