oral_biology_theme_4-7_20150331151415 Flashcards
(325 cards)
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)
2
Q
What is Alpha haemolysis?
A
Green ring around bacteria produces hydrogen peroxide = oxidises haemoglobin to methaemoglobin
3
Q
What is Beta haemolysis?
A
Lysis of red blood cells (clear ring around bacteria)
4
Q
What is Gamma haemolysis?
A
No Haemolysis
5
Q
Which oral bacteria are associated with Infective endocarditis?
A
Streptococcus OralisStreptococcus GordoniiStreptococcus SangiusStreptococcus Mitis
6
Q
Which oral bacteria are associated with preterm low birthweight?
A
Fusobacterium nucleatum
7
Q
Which has Lipopolysaccharide… Gram positive or gram negative bacteria?
A
Gram negative bacteria
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)
9
Q
What is a biofilm?
A
A microbial community forming at a phase boundary (generally a liquid to solid interface)
10
Q
Give some examples of where biofilms are found?
A
Catheters, Implants & dental plaque
11
Q
What are the constituents of a biofilm? (7)
A
BacteriaFungiAlgaeProtozoa BacteriophagesEnvironmental DebrisHost components
12
Q
Explain how biofilms accumulate (3)
A
- 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
13
Q
Is biofilm formation across a whole surface uniform or not?
A
No!
14
Q
What is sessile growth?
A
Where cells are attached to a surface or a preformed biofilm
15
Q
What is planktonic growth?
A
Where the bacteria grow in liquid suspension
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)
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
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)
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
20
Q
Explain the 3 methods of antimicrobial resistance within a biofilm:
A
- 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)
21
Q
What enzymes can resistant bacteria secrete to produce a bubble of protection around themselves?
A
Beta lactamases
22
Q
List the advantages of microbial culture (2):
A
- can determine antibiotic resistance- Identify virulence factors
23
Q
List the disadvantages of microbial culture (3):
A
- Slow- Identification is often difficult- Only 50% of the oral flora can be cultured
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
25
What are the disadvantages of the checkerboard (4)?
- Requires careful calibration- Lab based (difficult to adapt for clinical use)- Takes several days to complete- Need cultural organisms to make probes
26
What are the 10 suspected periodontal pathogens?
Aggregatibacter actinomycetemcomitansPorphyromonas gingivalisPrevotella intermediaTannerella forsythiaEikenella corrodensFusobacterium nucleatumParvimonas micraTreponema denticolaCampylobacter rectusStreptococcus intermedius
27
Why is the 16s rRNA DNA conserved and does not change between generations?
It is essential for life, any mutations would stop it working and the cell would die = would not pass on altered genome
28
What are the conserved regions of 16s rRNA used for (2)?
- sequence alignment- Universal primers fo PCR and sequencing
29
What are the variable regions of 16s rRNA used for (2)?
-phylogenetic analysis - detecting individua bacteria (species or strains specific PCR)
30
Which method does microarray use?
Ink spray method (spray specific probe onto specific region of chip)
31
Which two bacteria increase with orthodontic brackets?
T. denticolaS. gordonii
32
Why does plaque have different compositions in different areas?
Different environmental conditions (varying saliva flow, abrasive forces etc.)
33
What is a climax community?
A steady state appropriate for local environmental conditions (predominantly gram negative anaerobic rods)
34
How does dental plaque form? (4)
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
35
What is the overall charge of enamel?
Negative (binds to positively charged molecules)
36
List the different types of bacterial adhesin: (5)
LectinsFimbriaePiliOther cell wall proteinsAnchorless adhesins (leave bacterial cell surface - binds to pellicle then rebinds bacteria)
37
What is atomic force microscopy and how does it work?
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
38
Do different fimbrae exist?
Yes, different protein arrangements - bind different glycoproteins
39
Proline rich proteins:
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)
40
Which protein is expressed on the surface of S. gordonii?
Amylase binding protein
41
What do secondary colonisers bind to?
Often to the primary colonisers
42
What are 3 types of interactions in plaque?
1. cell-substratum adhesion2. Homotypic cell- cell adhesion (to same species)3. Heterotyic cell-cell adhesion (to different species) = complex
43
What is coaggregation?
Occurs in suspension -> most bacteria coaggregate with at least one partner type
44
What is coadhesion?
Occurs with pre-attached cell (to pellicle)
45
What are bacteriocins? Give two examples:
peptide antibioticse.g. Actinobaccilin & Mutacins
46
What is EPS?
Extracellularpolymeric substance
47
What % of total plaque volume does EPS make up?
35
48
What is the role of EPS (4)?
- Facilitates diffusion in and out of plaque- Structural integrity (consolidates attachment of cells)- Communication- Localises acid fermentation products)
49
What are the components of EPS (3)?
Proteins (oral fluids & microbes)Polysaccharides: Glucans (from diet = Linear/branched)Fructans (from diet = Linear)eDNA
50
How is colonisation resistance achieved?
- 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)
51
What is an essential nutrient?
Required in a specific channel form and cannot be synthesised in the body (must come from the diet)
52
Give some examples of an essential nutrient (5):
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)
53
What is a non essential nutrient?
Can be replaced by other nutrients or synthesised by other non-essential nutrients within the body
54
Give some examples of a non essential nutrient (3):
All carbohydratesMost fatsMost amino acids
55
What causes enamel hypoplasia?
Calcium deficiencyVitamin A & D deficiency (regulate calcium homeostasis)
56
What causes enamel fluoridosis?
Excess fluoride
57
At what age is an individual most susceptible to enamel fluoridosis?
6 Months to 4 years
58
In which 3 ways can form affect risk of caries?
- Retention in oral cavity = increased risk- Mastication -> stimulates saliva (decreased risk)- Combined with constituents of HPA -> counteracts the demineralisation by acid
59
What is acidogenic potential?
the ability of a carbohydrate to be broken down into acid
60
What is cariogenic potential?
the ability of a carbohydrate to be broken down by BACTERIA (fermentation) into acid
61
What are intrinsic sugars?
located naturally within the cellular structure of a product (e.g. whole fruit and veg) -> these are good for you!
62
What are extrinsic sugars?
added by the manufacturer, cook or consumer (e.g. fruit juices, honey & syrups) -> potentially harmful - should not exceed 10% of daily energy intake
63
How cariogenic is lactose?
It is the least cariogenic disaccharide (bacteria struggles to convert it into acid)
64
What is Casein?
A component of milk that helps with re-mineralisation (along side calcium & phosphate)
65
Name a caries inhibitor:How does it work?
Apigenin =a naturally occurring flavonoidInhibits S. mutans glucosyltransferases = less S. mutans biofilm formation (necessary for progression of dental caries)
66
What is Apigenin found in?
ParsleyOnionsApplesBasilCelery rootTeaPeasArtichokeFeverfewOrange juiceGrapefruit juiceAlfalfa
67
What is erosion?
The irreversible loss of dental hard tissue by acids in a process that does not involve bacteria
68
What are the features of erosion?
Smooth & shiny surfaceCupping and grooving on occlusal surfaces
69
Why is Citric acid worse at erosion than any other acid?
When the acid dissociates it produces a proton and a citrate anionCitrate anion = Calcium chelator = remineralisation no possible because insufficient calcium in saliva
70
What does vitamin C usually do?
A co-factor in collagen synthesis
71
What are the features (2) of an individual with vitamin C deficiency?
Weakened tissues (soft, swollen and bleeding gums & weakened periodontal ligament)Capillary fragility (bruising)
72
What are the features of Vitamin B deficiencies?
Angular chelitis (deep cracks at corned of mouth & shallow ulcers) = B2, 3 & 12Glossitis (inflamed, painful tongue) = B2, 3, 6 & 12
73
Which health problem is associated with an excess in Sugars?
Oral fungal disease
74
Which health problem is associated with an excess in Vitamin A?
Lung cancer (smokers)
75
Which health problem is associated with an excess in Zinc?
Reduced immune function
76
Which health problem is associated with an excess in Manganese?
Muscle/nerve disorders (elderly)
77
Which minerals compete for absorption?
Calcium competes with Iron (too much calcium in diet = iron deficiency)Iron competes with zinc
78
What are the potential effects of alcohol on oral cancer?
- acts as a solvent for other carcinogens- metabolised => Acetaldehyde = DNA damage (inhibits DNA synthesis and repair)- Abuse is associated with a poor diet
79
Which foods are associated with oral cancer?
- 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)
80
Anticancer agent:
- Non-starchy fruits and vegetables (e.g. citrus, raw fruits & carotenoids = Beta carotene & lycopene) High intake decreases risk by 40-80%
81
What is the critical pH? What happens below this pH?
pH 5.5.Disrupts equilibrium between demineralisation & remineralisation (more demineralisation occurs)
82
What is dental caries?
An infection of bacterial origin that causes demineralisation of the hard tissues and destruction of the organic matter of the tooth
83
What is plaque?
A complex bacterial community embedded within EPS
84
What is plaque fluid?
The aqueous component of EPS
85
How is plaque fluid different to saliva?
It contains Potassium and Ammonium (product of metabolism from microbe within the plaque)Rich in Calcium & phosphate (close proximity to tooth surface)
86
What does the Stephan curve show?
It detects the carcinogenicity of a product
87
How is the Stephan curve constructed in vitro?
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
88
What are the pros of the in vitro method?
- Cheap- Requires little specialised equipment
89
What are the cons of the in vitro method?
- Requires great skill to obtain reproducible results (collect same amount of plaque each time)- Volunteer must allow for sufficient plaque to accumulate
90
How is the Stephan curve constructed in vivo?
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
91
What are the pros of the in vivo method?
- Produces large amounts of real time data- Monitering possible over long time periods- Plaque is not disturbed so can be tested against multiple challenges
92
What are the cons of the in vivo method?
- Equipment is expensive- Sample size is small (due to cost)- Volunteers must have dentition allowing for the placement of a bridge
93
At which pH does plaque buffer?
pH 4.0
94
Which (4) factors determine the lowest pH the plaque reaches?
- 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)
95
What are the 5 methods of caries prevention?
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
96
Which group of bacteria is predominant in health?
Gram +ve Facultativee.g. S. sanguis, S. gordonii, Actinomyces spp, Haemophilus Neisseria
97
Which group of bacteria is predominant in caries (excess sugars in diet)?
Gram +veFacultativee.g. S. mutans, S sobrinus, Actinomyces spp, Lactobacillus spp, S. wiggsiae, Bifidobacteria
98
Which group of bacteria is predominant in periodontal disease (lack of oral hygiene & immune dysfunction)?
Gram -veAnaerobic rodse.g. Porphomonas gingivalis, tannerella forsynthia, treponema denticola, aggregatibacter actinomycetemcomitans
99
Is caries genetic or microbiological (transmissible)?
Bit of bothMainly infectious (hamster experiment)
100
Which microbiota is found in primary enamel caries?
S. mutans & S. sabrinus
101
Which microbiota is found in secondary enamel caries?
Actinomyces spp. & lactobacillus spp.
102
Which microbiota is found in primary root caries?
Actinomyces spp. ( in older people with receding gums)
103
Which microbiota is found in secondary root caries?
Lactobacillus spp, S. mutans & S. sabrinus
104
Which microbiota are associated with early childhood caries?
S. mutansScardovia wiggsiae
105
How does S. mutans contribute to carcinogenicity?
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)
106
What is aciduricity?
Tolerance to acid (cells are able to survive, metabolise & grow even at low pH -> outcompete other bacteria at low pH)
107
Which enzyme synthesises Glucans?
Glucosyltransferases
108
Are water soluble Glucans linear or branched?
Linear
109
Where are water soluble Glucans produced?
Both inside & outside cells
110
What are water soluble Glucans used for?
Short term energy store
111
Are water insoluble Glucans linear or branched?
Branched
112
Where are water insoluble Glucans produced?
Outside the cell only
113
What are water insoluble Glucans used for?
Long term energy store
114
What are the other two functions of water insoluble Glucans in the oral cavity?
- Sticky & hard -> acts as cement- Promotes accumulation of plaque
115
What is a Glucan?
Chains of glucose residues
116
What us a Fructan?
Chains of fructose residues
117
Which enzyme synthesises Fructans?
Fructosyltransferases
118
Are Fructans linear or branched?
Often linear
119
What are Fructans used for?
Rapid energy store (fructose metabolism is even faster than glucose -> 1 step less in glycolysis)
120
Give an example of a Glucan binding protein:Which bacteria express them?
LectinsS. mutans & other streptococci
121
What is the role of Glucan binding proteins?
Cementing agents
122
What is attrition?
loss of tooth substance due to tooth-to-tooth contact (Bruxism)Does not involve -> incisal edge, occlusal surfaces & bacteria
123
What is abrasion?
loss of tooth substance due to friction of foreign body independent of occlusion(E.g tooth brushing and pipe smokers)
124
What is erosion?
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)
125
In which two ways are caries classified?
- 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)
126
What are the different zones in early enamel caries (4)?
1. Translucent zone2. Dark zone3. Body of lesion4. Surface zone
127
What are the different zones in caries of dentine (5)?
1. Sclerosis2. Demineralisation3. Bacterial invasion4. Destruction5. Reactionary dentine
128
What are the two types of abnormal calcification that can occur in the teeth?
- Pulp stones (denticles : True = tubular structure, False = calcified but no tubular structure & Fixed/Free)- Dystrophic
129
In which 3 ways is pulpits managed?
- Pulp capping- Pulp extirpation & endnotes treatment- Tooth extraction
130
What is 1ppm equal to?
1 mg/L
131
Which two bacterial enzymes are inhibited by Fluoride below the pH 5.5?
- 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
How does fluoride inhibit demineralisation?
Absorbs onto tooth surface, draws in Calcium & phosphate to local environment = increased remineralisation (requires Ca & Phosphate)
133
What is the problem with fluoride and carious lesions?
Remineralisation can 'bury' the lesions (bacteria etc. still in there)
134
What are the 3 methods of raising the fluoride content of teeth?
- Water fluoridation (07 - 1ppm)- Fluoride tablets- Clinically applied topical fluorides
135
What is monophosphate?
Covalently bound to fluorideHydrolysis by phosphatases in plaque = only slightly less effective than fluoride itself
136
What are slow release fluoride devices made of?
Co-polymer or Glass
137
When combined with Fluoride what does CPP-ACP produce?
Amorphous calcium fluoride phosphate = more effective at low pH than fluoride & CPP-ACP for remineralisation
138
What does CPP-ACP contain?
Casein (10%), Calcium & Phosphate
139
What are the 4 risk factors for dental fluorosis?
- 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
Why are children more at risk to develop fluorosis than adults?
Their teeth are still developing so fluoride has access through systemic route
141
What are the 4 methods of management for periodical periodontitis?
- Drainage (soft tissue or root canal)- Endodontic treatment- Apicectomy (like root canal but from base - chop of apex)- Extraction of tooth
142
Which tooth is most often associated with pulp polyps? and why?
Upper 6th toothInfection spreads into palate because it has 3 roots
143
What is Ludwig's angina?
A big swelling under the chin (caused by infection of the lower teeth spreading into the sublingual spaces)
144
What is a cyst?
A pathological cavity with fluid, semi-fluid or gaseous contents lined by epithelium (fluid = secretion from the type of epithelium lining it)
145
What is an odontogenic cyst?
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
What is a paradental cyst?
Odontogenic cyst of the wisdom tooth
147
Give an example of a non-odontogenic cyst?
Non-epithelialized primary bone cyst
148
What are the key clinical features of odontogenic cysts?
Symptomless expansion (springy = fluid filled)Egg shell crackling (fragments of the buccal plate)
149
What is the role of sIgA in saliva?
- Aggregate oral micro-organisms- Prevents bacterial adherence to surfaces- Inhibition of bacterial enzymes (e.g. glucosyltransferases)- Neutralises viruses
150
What is the problem with S. mutans whole cell immunisation?
Linked to possible immunologically mediated damage of heart tissue
151
How do S. mutans bind (2)?
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
What is the problem with Antigen I/II immunisation?
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
At which age should we immunise against Caries?
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
What other technique is there to protect against caries?
Manipulation of bacteria (so cannot produce acid -> e.g. replace lactate dehydrogenase with alcohol dehydrogenase = metabolises glucose into alcohol instead)
155
Animal studies have been used to understand (5)
- 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
Which surface structures of P. gingivalis are involved in colonisation (6)?
- Proteases - Fimbriae- Non-proteolytic factors- Iron-capturing proteins- haemagglutinin-Capsule
157
Name some vaccine targets for P. gingivalis (2):
Proteases (Rgp & Kgp peptides) -> blocks active sitesFimbriae (N & C epitope peptides on S. gordonii = produces immunoglobulins against P. gingivalis)
158
What is gingivitis?
Inflammation of the gingival tissues (reversible)
159
What is periodonitits?
Chronic gingivitis with loss of attachment (irreversible)
160
What are the different types of periodontitis?
Localised (juvenile) aggressive periodontitis (LAP)Chronic (slow) periodontitis - in elderly/those who don't brush
161
What is a not very form of gingivitis?
Acute necrotising ulcerative gingivitis (involves specific types of bacteria)
162
What causes which % of the tissue damage in periodontal disease?
20% Bacteria (microbial enzymes directly digesting tissue)80% Host inflammatory response
163
What are the clinical features of periodontal disease?
- 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
Which % of patients are at high risk of progression to periodontal disease?
10%
165
Which % of patients are slowly progressive?
80%
166
Which % of patients are resistant to periodontal disease?
10%
167
What is a false pocket?
Caused by inflammation
168
Classification of periodontitis:
Localised (30% teeth involved)Slow/rapid progression
169
What does gingival crevicular fluid have that saliva doesn't?
Lots more protein, Sodium, Calcium & complement
170
What is a polymorphism?
changes in the nucleotide sequences of genes which may alter its expression (increased or decreased)
171
Polymorphisms in which genes are associate with periodontal disease (6)?
- TNF (Tumour Necrosis Factor)- Interleukin 6- Interleukin 1- Leukocytes Fc Gamma receptor for IgG- Vitamin D- Matrix Metalloproteinases (MMPs)
172
What is the periodontal ligament?
Soft connective tissue joining the cementum to the alveolar bone
173
Where is the periodontal ligament derived from?
The dental follicle
174
What do bisphosphonates cause?
Ankylosis (replace periodontal ligament with bone) -> due to disruption in homeostatic induction of factors = induces odontogenic factors
175
What are the functions of the periodontal ligament (4)?
- Supportive- Remodelling of itself, surrounding bone & cementum- Sensation - Nutrition
176
Which fibres make up the periodontal ligament and what % do they occupy?
Collagen >90%Oxytalan & reticulin <10%
177
What is Type I collagen?
Tropocollagen molecule (2 alpha 1 chains & 1 alpha 2 chain)Low in hydroxylysine & glycosylated hydroxylysine
178
What is Type III collagen?
Tropocollagen molecule (3 alpha 1 chains)Low in hydroxylysineHigh in glycosylated hydroxylysineContains cysteine
179
Which has thinner and more numerous principal fibres embedded within... Alveolar bone or Cementum?
The cementum has more with smaller diameter (due to branching)
180
What are the 5 different groups of principal fibres?
1. Alveolar Crest fibres2. Horizontal fibres3. Oblique fibres4. Periapical fibres5. Inter-radicular fibres
181
What do transeptal fibres do?
Join the neck of 1 tooth to the next over the top of the alveolar crest
182
What are the components of ground substance (3)?
- Glycosaminoglycans (GAGs) - hyaluronic acid- Proteoglycans- Glycoproteins (fibronectin, tenascin & vitronectin)
183
What are the functions of ground substance (5)?
- 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
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.)
- 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
How does periodontal ligament resemble foetal connective tissue (7)?
- 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
What are the functions of fibroblasts (6)?
- 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
What is the embryological origin of periodontal fibroblasts?
Ectomesenchymal/neural crest cells
188
What is the embryological origin of gingivae?
Mesenchymal
189
Which fibroblasts have: higher rate of proliferation?
Periodontal fibroblasts
190
Which fibroblasts have: contacts to overlying epithelial cells?
Gingival fibroblasts
191
Which fibroblasts secrete more collagen type III and less ground substance?
Periodontal fibroblasts
192
Which fibroblasts have: faster collagen turnover?
Periodontal fibroblasts
193
Which fibroblasts have: decreased cell volume?
Gingival fibroblasts
194
Which fibroblasts express MORE alkaline phosphates and cAMP?
Periodontal fibroblasts
195
Which fibroblasts contain less contractile proteins?
Gingival fibroblasts
196
What do fibroblasts synthesise (5)?
CollagenOxytalin/elastin fibresIntermediate cytoskeleton fibres (vimetin)Cytokeratins (only in ageing periodontal ligament)Ground substance
197
How do fibroblasts degrade collagen?
take up collagen into fibroblasts = forms organelles (intracellular collagen profiles) -> contains lysozymal & metalloproteinase type enzymes = break down within cellExtracellular collagen - phagocytosed & digested
198
Loss of collagen in periodontal disease could be due to (3):
- Reduced rate of synthesis- Increased rate of degradation- Decrease in the number of fibroblasts
199
Gain of collagen in gingival fibrosis could be due to (3):
- Increased rate of synthesis- Reduced rate of degradation- Selective deletion/survival/proliferation of fibroblast sub populations (those specialising in rapid collagen synthesis retained)
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How fast is gingival collagen turnover compared to skin, bone and the periodontal ligament?
Faster than skin and boneSlower than the periodontal ligament
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What is granulation tissue?
New connective tissue and blood vessels forming on the surfaces of a wound during healing
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At which site are periodontal ligament stem cells found?
Perivascular (next to blood vessels!)N.B. must migrate to their sites of action
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What is the key problem with observing fibroblasts in vitro?
The method of cell culture influences the data (cells don't do what they normally would in vivo)
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What potential future treatment involves fibroblasts?
Guided tissue regeneration(may need to be from specific tissue - we do not know if there are specific progenitors for each)
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Which signals can activate fibroblasts (5)?
- Hormones- Growth factors (TGFβ, IGF-1, PDGF, BMP-2, BMP-7 & FGF-2)- Cytokines- Bacterial products- mechanical factors
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What does TGFβ do?
Produces collagenIncreases amount of inhibitor enzymes preventing collagen breakdown
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What does PDGF & FGF-2 do?
ProliferationChemotaxis
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What does BMP-2 & BMP-7 do?
Bone formation
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What does Osteoprotegerin (OPG) do to osteoclast formation and activity?
It inhibits (binds to and inhibits RANKL)
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What does cell surface RANKL do to osteoclast formation and activity?
It supports= a cytokine that activates osteoclasts
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Which tissue seals the periodontal ligament from the oral cavity?
Gingival ligament
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What are the epithelial rests of Mallassez?
Remnants of Hertwig's epithelial root sheathSlow turnover -> can develop into cysts or tumours
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From which tissue do the blood vessels of the periodontal ligament originate?
Mainly Alveolar bone (superior and inferior alveolar artery)GingivaeSmall amount from apicies
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Other than the periodontal ligament collagen fibres what other fibres can be found in the periodontal ligament?
Oxytalan fibres
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What is calculus?
Calcified plaque
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Which component of saliva do we incorporate into toothpaste to reduce calculus formation?
Pyrophosphate
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How does calculus attach to the tooth?
Fibronectin (very strong attachment to tooth surface = hard to remove)
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What is intracellular calcification? And which bacteria are involved?
From the inside outCorynebacter matruchotii, Actinomyces israelli & streptococcus salivarius
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What is extracellular calcification? And which bacteria are involved?
From outside inVeillonellae spp.
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What are the different components of gingival connective tissue (5)?
- Collagen bundles- Chondroitin sulfate- Keratin sulfate- Heparin- Hyaluronic acid
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Which bacteria are predominant in health?
Gram +ve (streptococi & actinomyces)Facultative (able to withstand the presence of oxygen)
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Which bacteria are predominant in periodontitis?
Gram -ve (fusobacterium, porphomonas, prevotella, tannerella & spirochetes = treponema)Anaerobic
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Why is microbial diagnosis of periodontal flora limited?
Tests will no identify a specific disease or predict disease progression
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Which bacteria is associated with Localised Aggressive (Juvenile) Periodontitis (LAP)?
Leukotoxic Aggregatibacter (Actinobacillus) actinomycescommitans
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Which bacteria acts as a bridge between early colonisers and late colonisers?
Fusobacterium nucleatum (gram -ve)
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Which bacteria (2) are early colonisers in health?
Streptococcus spp. & Actinomyces spp. (gram +ve)
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What do the transitional complex do in sub gingival plaque?
Set up the periodontal pocket
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What are the names of the 3 key periodontal pathogens?
Treponema denticolaPorphomonas GingivalisTannerella Forsynthia
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In which 3 ways do bacteria become pathogenic?
- colonisation mechanisms- Evasion of host defences- Tissue destruction
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What are the different bacterial colonisation mechanisms (5)?
- Fimbriae- Capsule- Lipopolysaccharide (LPS - from gram -ve only)- Invasion of host cells- Microbial complexing
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In which 2 ways do bacteria evade host defences?
- Leukoaggressins (inhibits chemotaxis, phagocytosis, killing proteases & complement factors)- Antigenic shift (express same protein with a different conformation)
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In which 6 ways do bacteria destroy tissue?
- Collagenases- Hyaluronidases- Sulphur compounds- Lipopolysachharides (LPS)- Acid phosphatases- Epithelial & endothelial cell toxins
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What type of bacteria is aggregatibacter actinomycecomitans?
Gram -veFacultative
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Which serotype of Aggregatibacter actinomycecomitans is associated with LAP and which is associated with health?
Serotype B = LAPSerotype C = health
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What type of bacteria is P. gingivalis?
Gram -veanaerobic
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What are the 3 non specific methods of tissue destruction?
Lipopolysaccharide (LPS) - by all gram -veCapsule (surface associated material - SAM = stimulates bone resorption)Cytotoxins (products of metabolism & short chain fatty acids)
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What method of tissue destruction is associated specifically with Aggregatibacter actinomycecomitans?
Leukotoxin (some strains are highly leukotoxic - serotype B = LAP)4 parts:B & D = transportersA= toxin -> forms pore = cell lysisC = activator
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Which 3 methods of tissue destruction are associate specifically to P. gingivalis?
- 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)
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What do most oral bacteria stimulate in epithelial cells?
IL-8 synthesis
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What does IL-8 do?
involved in attracting T cells = secretion of cytokines & lymphotoxin (immune response)
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How does P. gingivalis reduce IL-8 production?
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
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What are the 3 division of the trigeminal nerve?
- Ophthalmic- Maxillary- Mandibular
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What is the bell mangendie law?
Ventral roots = motor axonsDorsal roots = sensory axons
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What are the two trigeminal roots?
Sensory (larger) Motor
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What are the derivatives of the trigeminal roots?N.B. they are different
Sensory -> neural crest cellsMotor -> basal plate of embryonic pons
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What does the trigeminal ganglion contain (2 + 4)?
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
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Which part of the trigeminal ganglion is sensory and which is motor?
Sensory = whole thingMotor = bottom half
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How do we categories trigeminal primary afferents?
Modality
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What are the different trigeminal modalities (5)?
Touch (M, fast)Proprioception (M, fast)Pressure (M, fast)Temperature (NM, slow)Pain (NM, slow)
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Which types of afferents have their cell bodies in the trigeminal ganglion (8)?
- 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
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What are the two connections of the trigeminal nerve to the thalamus and cortex?
Trigeminal leminscus (crosses in midline)Posterior trigeminothalamic tract
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Which nuclei of the thalamus do the above tracts terminate in?
VPM
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What is microneurography?
Measuring nerve impulses by putting electrodes into nerve trunks (e.g. the infraorbital, lingual & inferior alveolar nerves)
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Which primary afferent can be found in the hand but not the face?
Pacinian corpuscle (deep receptors!)
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What is pericoronitis?
Inflammation of the gingivae/mucosa surrounding an erupting tooth (due to build up of debris)
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What is osteitis?
Dull aching, nagging pain from bacterial infection of bone (dry socket)
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What is a migraine?
A headache caused by abnormal vasodilation of arteries in the ECA
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What is post-herpetic neuralgia?
Sensory loss and enduring pain occurring for months following infection with shingles
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What is trigeminal neuralgia?
pain of the face caused by non-noxious tactile stimulus = intense stabbing pain
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What are Aβ fibres? and what is their conductance velocity?
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
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What are Aδ fibres? and what is their conductance velocity?
High threshold mechanoreceptors5- 30m per sSmall diameter & myelinatedThermal & mechanical
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What are C fibres? and what is their conductance velocity?
Nociceptors and postganglionic sympathetics0.5-1.5m per sNon myelinated= dull burning chronic pain
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When using microneurography in animals at which 2 areas?
Trigeminal ganglionMesencephalic nucleus
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What are the functions of low threshold mechanoreceptors (3)?
- Touch & pressure from teeth- Sensory feedback to trigeminal motor nucleus (contribute to motor control of tongue, buccinators & facial muscles during speech)- Control of salivation
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What is the structure of low threshold mechanoreceptors?
- Numerous nerve endings- Finger like projections which extend between adjacent collagen fibres of the periodontal ligament
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Do mechanoreceptors respond to only a single tooth or can they respond to more than one?
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)
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Do posterior or anterior teeth have the highest threshold?
Posterior teeth
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What is pain?
an unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damageIt is subjective & learned
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What are nociceptors?
Sensory receptors activated by high threshold stimuli (potentially damaging e.g. mechanical, thermal & chemical)
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Which neurotransmitters are released by nociceptors?
GlutamateSubstance PCalcitonin gene related peptide (CGRP)
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What is the transduction mechanism for mechanical nociceptors?
Mechanosensitive cation channel (with diff. thresholds)e.g. TRPA1, ASIC & P2X3
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What is the transduction mechanism for temperature nociceptors?
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
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What is a polymodal nociceptor?
Responds to many different stimuli (expresses many different receptors)
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What is a silent nociceptor?
It is usually unresponsiveCan be activated by neurotransmitters & inflammatory molecules by other receptors= AMPLIFICATION of the nociceptive signal
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What is neurogenic inflammation?
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
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When does neurogenic inflammation occur?
Following sub threshold stimulation of terminals (does not require action potential condition -> not always with pain)
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What are the 3 main sub nuclei & lamina of the Nucleus Caudalis?
- Subnucleus maeginlis (MAR) or Lamina I- Subnucleus gelatinosus (SG) or lamina II & III- Subnucleus magnocellularis (MAG) or lamina IV
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Which receptors receive glutamate? And what speed is this pathway?
AMPA & NMDA receptors Fast excitatory
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Which receptors receive Substance P? And what speed is this pathway?
NK1 receptorsSlow excitatory & vasoactive
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Which receptors receive CGRP? And what speed is this pathway?
CGRP receptorsSlow excitatory & vasodilator
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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?
Pain outweighs pressureLTM & HTM inputs are anatomically separatedCaudalis = proprioception inhibits Main sensory nucleus (temp & pressure) = Pain predominates
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What is hyperalgesia?
Increased response to a stimulus that is normally noxiousPrimary = at site of injury -> often due to inflammationSecondary = occurs in undamaged surrounding tissue
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What is allodynia?
Pain due to stimulus that does not normally provoke pain (e.g. trigeminal neuralgia, phantom tooth pain, atypical odontagia)
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What is peripheral sensitisation?And what does it cause?
Receptors are more sensitive to stimulusPrimary hyperalgesia and allodynia
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What is central sensitisation?And what does it cause?
CNS is more sensitive to impulses from the neuronePrimary & secondary hyperaglesia & allodynia
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What can cause peripheral sensitisation? (3)
- 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)
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What causes central sensitisation?
- 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)
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How can central sensitisation be stopped?
pre-emptive analgesia = stops the irreversible change in nerve terminals
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What stimulation produces pain in enamel?
Hot (<28 degrees)
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What stimulation produces pain in dentine?
- Hot/cold- Mechanical (bur & probe)- Removal of water (osmotic e.g. eating toffee, air stream or absorbent materials)- Changes in hydrostatic pressure
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How much of the width of dentinal tubules do odontoblast processes extend?
No more than 1/3 to 1/2 of the length (up to 100 µm)Mainly over the pill cornu -> not in all tubules!
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What is the lamina limitans?
The protein lining of tubules left behind following decalcification
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What are the two types of interdental sensory receptors?
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
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What happens to nerves towards the peripheral terminals?
They taper and have slower conduction velocities
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When the tooth is heated what happens?
There is expansion of the crown = inward flow in dentinal tubules
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When the tooth is cooled what happens?
The crown shrinks = outward dentinal flow (more sensitive to cold than hot as more sensitive to outward flow)
297
How do we measure pulp blood flow?
A laser doppler probe
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What are the different causes of hypersensitivity in dentine (2)?
- Open tubules on surface of exposed dentine- Smear layer removed from exposed tubules & tubules are opened up by acid drinks & foods
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Whats the incidence of hypersensitive dentine in patients?
57%
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What is hypersensitive dentine?
An increased sensitivity to hot, cold & mechanical stimuli and drying (a form of hyperalgesia)
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What are the possible mechanisms for hypersensitive dentine?
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
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In what ways can dentinal tubules be occluded?
- potassium oxalate (precipitates calcium oxalate crystals and dissolves quickly in saliva)- hydroxyapatite- calcium carbonate with 8% arginine- dentine binding materials (adper single bond plus)
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What does sensodyne contains that reduces sensitivity?
Potassium ions (although experiments have shown that sensitivity quickly returns to normal following use of potassium ions)
304
What is the component reducing sensitivity in other desensitising toothpastes?
Strontium chloride
305
What effect does pulpal inflammation have on the sensitivity of etched dentine?
Increased sensitivity to coldDecrease sensitivity to ressure
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What are the two dimensions of pain?
Sensory (actual pain)Behavioural (response to pain e.g. more angry, cannot sleep etc.)
307
How to prostaglandins induce pain?
They increase the sensitivity of free nerve endings to the nociceptive properties of histamine & bradykinin (responsible for pain development and increasing pain intensity)
308
Are pain related pathways in the face mediated by the brain too?
YesThis can be influenced with medication
309
Which modulation happens to the most caudal part of the trigeminal tract nucleus?
Descending nerve fibresDrugs
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What is Encephalin?
An opioidOur own endogenous morphine = activates inhibitory interneurones & dampens down pain!
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What is myofascial pain?
Muscle pain
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What are the key features of pain due to exposed dentine (5)?
repsonds to hot/cold & sweet/sour stimuliPoorly localised (does not cross midline)Lasts for secondsTooth NOT tender to percussion Tooth still vital
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What are the key features of pain due to pulpitis (4)?
responds to hot/cold & pressurePoorly localised (radiates)Lasts for seconds, minutes or hoursNOT tender to touch
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What is Acute necrotic ulcerative gingivitis (ANUG) caused by? and what are its key features? Who is it most often seen in?
Caused by Gram -ve bacteriaSmellsLoss of interdental papillaeClassically seen in young male smokers
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What are the clinical features of a cracked tooth?
Pain is severe (pulpitis)Pain is exacerbated by biting & thermal stimuliTreatment = extraction
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What clinical feature is caused by malignancy in the sinus and not sinusitis?
Numbness
317
What is a sialolith?
White stones in the salivary glands = causes back pressure and pain
318
What are strictures?
Narrowing of the opening of salivary glands
319
What is osteomyelitis?
Bone inflammationBone dies & overlying tissue is ulcerated due to loss of blood supply from bone = inflammation & pain
320
What happens in pagets disease?
Normal bone cycle of renewal and repair is disrupted = weakening & deformation of the bone
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In TMJ dysfunction what key feature do you often see on the tongue?
Crenation (side of tongue looks like bread knife due to biting of tongue)
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What are the 3 different forms of persistant idiopathic (unknown cause) pain?
- Burning mouth syndrome- Atpyical odontalgia = tooth ache without anything wrong- Atypical facial pain
323
What is an acoustic neuroma?And what symptoms does it cause?
A benign growth in the IAMCompression of nerves (Facial & vestibulocochlear nerve)= Palsy (weakness of muscles), tinnitus, deafness & dizziness
324
What is langerhans cell histiocytosis?
Systemic diseaseInflammation causing localised bone loss, inflammation -> good gum attachment with sudden loss of bone & inflammation
325
What is catastripisation?
Only seeing the worst possible outcome -> start loosing hope!
