Written Exam Flashcards

1
Q

What is caries ?

A

Pathological demin of tooth tissues by fermenting bacteria

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2
Q

What is aim of vital pulp therapy?

A

Treats reversible pulpal injury

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3
Q

What are the two subcategories of vital pulp therapy ?

A

Direct

Indirect

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4
Q

What are the types of direct pulp therapy?

A

Pulp cap
Partial pulpotomy ➡️ Cvek pulpotomy
Full pulpotomy

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5
Q

What are the types of indirect pulp therapy?

A

Stepwise (2 steps)
Direct complete (one step)
ART

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6
Q

What are the requirements for successful vital pulp therapy ?

A

Pre op: signs/ symps of reversible pulpitis and radiographically involving more than 3/4 of dentine
Intra-op: haemorrhage controlled, rubber dam caries removal and non toxic materials
Post op: prevention of microbial leakage

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7
Q

What study is the process of stepwise caries removal based upon and what did they find with regards to caries removal?

A

-Murray 2000 and Shovelton 1968
- Deepest layer of softened dentine not infected
- inner layer of softened caries contained collagen NOT affected by bacterial proteases and once protected it can be preserved and remineralised

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8
Q

What are the four procedural requirements of vital pulp therapy

A
  • sterile conditions (rubber dam, sterile burs and water
  • irrigate dentine chips with sterile saline
  • rinse with hypo
  • haemorrhage controlled in healthy pulp
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9
Q

What type of cells are odontoblasts ?

A

They are post mitotic which means they will survive for life of the tooth if damage not too extensive

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10
Q

Which embryonic tooth development structure gives rise to dentine?

A

Dental papilla

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11
Q

If there is a mild injury to the PDC what type of Dentine would be expected to be laid down?

A

Tertiary dentine of the Reactionary type

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12
Q

What molecules are involved in formation of odontoblast like cells following a severe injury ?

A

Growth factors
TGF beta
BMP’s

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13
Q

Which dentine is faster to lay down between reactionary and reparative denting ?

A

Reactionary as you are stimulating the already present cells

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14
Q

What effect does EDTA and CaOH have on growth factors?

A

Can stimulate their release from the dentine matrix

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15
Q

What action does EDTA specifically have on tertiary dentine formation?

A

When cavity conditioned with EDTA it can intensify the response from dentine by solubising the bio active growth factors

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16
Q

What is the critical depth of remaining dentine prevent severe pulpal inflammation?

A

0.5mm

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17
Q

What is critical pH of dentine?

A

6.7

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18
Q

What is the downside of using caries detector dyes?

A

Does not discriminate infected vs affected so can end up over prepping this increased risk of pulpal exposure

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19
Q

What is hard dentine?

A

Resistant to probe penetration

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20
Q

What is firm dentine

A

Can be probed but not removed with hand instrumentation

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21
Q

What is ART and describe when it is used

A

Atraumatic Resto treatment

Cares removed only with hand instrumentation in circumstances where resources are limited

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22
Q

What is the most important factor with regards to ART?

A

A good seal is achieved

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23
Q

What is direct complete/one stage pulp therapy?

A
  • All caries is removed along walls
  • Leave behind hard dentine only leaving residual caries
  • Once caries removed condition with NaOCl or ETDA
  • CaOH/Biodentine or MTA and then definitely
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24
Q

With vital pulp therapy what is the risk of placing comp if less than 0.5mm dentine left?

A
  • increased risk of inflammation response

- etch also opens up dentinal tubules facilitating bacterial penetration

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25
What is benefit of biodentine over MTA
Biodentine does not contain bismuth oxide so reduces risk of discolouring teeth
26
How does two stage caries removal work?
- removal of bulk of soft superficial caries and leave avoid excavation close to pulp - soft discoloured dentine left overlying pulp - Layer of CaOH/MTA placed and then GIC - Re enter in 8-12 weeks remove fills and remainder of dentine until hard dement found - Defin restn
27
What is the benefit of two stage vs one stage during VPT and stepwise caries removal ?
Reduced risk of pulpal exposure and can re enter and re-assess the situation
28
In which clinical circumstances is a pulp cap more reliable in?
DTI over carious exposure
29
What are the disadvantages of pulp therapy?
- Obliteration can occur - Resorption can be seen in cases with trauma - Can get discolouration with MTA
30
What effect does age have on success of VPT?
Young patients do better due to 1. increased blood supply 2. Open root apices 3. Pulp free of age related changes
31
What size of pulp exposure reduces chance of success of VPT?
5mm
32
List 5 ideal properties of materials used for pulp capping
``` stimulate tertiary dentine formation maintain pulp vitality bacteriostatic or cidal radiopaque non toxic bacterial seal provided ```
33
What is the need for mechanical preparation of root canal system according to Hulsman et al 2005?
- Remove nectrotic tissue - Creates access and space for irrigation to root canal system - Preserve integrity of apical canal anatomy - Facilitate obturation - Preserve sound root dentine
34
Pulpal and periapical disease is driven by?
microbes!!
35
What are schilders 1974 5 mechanical objectives?
- Cont tapering funnel from apex to access - Cross sectional diameter should be narrower at every point apically - Root canal should follow original anatomy - Apical foramen remain in original location - Apical opening kept as small as practical
36
Benefit of coronal flare?
Less likely to extrude material | Working length less likely to change throughout
37
Risks of prepping apically first?
Do not know where the file is binding-could be binding in mid part or apically
38
What are the principles of cutting your access cavity?
- Remove ensure pulp root - Do not touch floor - Provide straighline access - Resistance and retention form which will retain temp restn
39
What features will affect determining size of apical preparation?
- Taper: if taper is 0.05 then prep needs to be ISO 30 - Resorption present - Acute apical curvatures - Thin roots-risk of fracture
40
What is gauging?
This is a degree of tightness or looseness of a given instrument
41
What are the biological aims of root canal medicament use?
-Effect on microbes: Kill remaining bacteria and prevent re growth of bacteria -Effect on host: Eliminate exudate, Induce hard tissue genesis and Enti inflammation and analgesic effect -
42
which paper showed empty canals had bacterial re growth?
Bystrom et al 1981
43
What did Strogen et al 1991 show?
The use of CaOH reduced bacterial load inter visa medicament
44
What are the ideal features of inter-visit canal medicaments?
``` Biological: -Broad spectrum activity -Tissue dissolution -Bicompatible Physical: -no detrimental effect on dentine -no detrimental effet on root filling material ```
45
What is the pH of CaOH?
12.8
46
Does CaOH have a low or high solubility in water?
LOW
47
What are the types of root canal prep?
``` HULSMAN et al 2005 Manual Automated Sonic UltraSonic Laser Non instrumented technique (NIT) ```
48
According to Peters 2004 what are the benefits of NiTI vs SS files?
- NiTi has less material removal than SS - Flexural fracture happens after more cycles in NiTi compared to SS - Canal transportation with acute curves due to greater restoring force with SS
49
What are Schilders 1974 4 biological objectives?
- Confine instruments to roots - Do not force necrotic debris apically - removal of all tissue from within root space - Create space of canal medicaments
50
What is the aim of obturation?
Sealing of the root canal system to incarcerate residual bacteria and prevent recontamination
51
Why is it not a hermetic seal?
there is micro and nano leakage occurring
52
What is microleakage?
seepage of fluids debris and microorganisms along the interface between the restoration and walls of cavity
53
Name some of the commonly used root canal filling materials
``` GP Silver points Resilon MTA Pastes ```
54
What is a sealer?
Radiopaque luting agent used in combination with a solid or semi solid core material to fill voids during obturation
55
Who set out 11 properties of ideal sealer?
Grossman 1981
56
According to Schiller 2006 what are the three solvent techniques available ?
Chlorpercha: GP is dissolved in solvents and a paste is created Callahan-Johnson diffusion : canal is flooded with chloroform and GP placed into the canals allowing GP to be forced into inaccessible areas Nygaard -Ostby technqiue: Chlorpercha paste used in combination with GP preventing excess being forced apically
57
What is the downside of the Callahan Johnson diffusion tech according to Schiller 2006?
Lots of shrinkage | GP may be extruded
58
What is the 3 D strategy for treating endo pain
Diagnosis-effective treatment starts with an accurate diagnoses Definitive dental treatment Drugs
59
Differential diagnosis of dental pain according to seltzer and Hargreaves’s 2002?
``` Musculoskeletal Neuropathic Nero vascular (Headaches) System disorders Psychogenic ```
60
What is convergence ?
The central terminal of different Nociceptors will convergence or synapse on the same location in the brain. When site of pain perception is different from the origin of nociceptor activation
61
How to identify origin in cases of convergence?
- By using LA which can block one area | - local palpating may increase intensity of the pain to help distinguish origin from site
62
Wright 2000 showed what regarding referred pain?
Masseter muscle is a common orofacial site refers oral pain to teeth Molars and premolars are more dominant for pain compared to incisors
63
Central sensitisation is?
Concept that central neurones in pain system can become sensitised after peripheral injury
64
What is the risk with endo on chronic pain patients ?
This may increase risk of post op pain severity as they are predisposed to increased risk of pain
65
What is the most common type of orofacial pain?
Odontalgia (Lipton et Al 1993)
66
What are the positive predictors for post endo pain?
Hargreaves’s and Hutter 2002 - pre op pain or TTP - strongest predictor - females more than males - the higher the number of appts the more risk - apical perio - necrotic pulp
67
What are the two main points regarding pre op pain on post op pain ?
Torbinejad 1994 - pre op pain good predictor for post op pain - pain is maximal for first 24-48 hours
68
What are the strategies for definitively treating Endodontic pain?
Pulpotomy Extraction incision and drainage Adjust occlusion
69
How long after performing a pulpotomy would you expect to see reduction in pain?
After 1 day dramatic reduction irrespective of the medicaments used Hasselgren & Reit 1989
70
Why are pulpotomies so effective in pain management ?
- It is a peripheral axonomy - The axons have extensive number of nocicpetors receptors and ion channels in the pulp and dentinal tubules making extirpation very effective
71
In necrotic pain where does pain originate?
Periapical tissues hence pain with mechanical allodynia rather than temperature
72
Why does debridement help in pain management ?
Because you are removing bacteria and their antigens which activate peripheral nociceptors
73
What is the importance of endotoxin on toll like 4 receptors ?
Trigeminal neurones express toll like receptors (Toll 4) therefore bacteria can communicate to patient neurones by endotoxin activating toll 4 receptor thus causing pain
74
What is the effect on occlusal adjustment on pain management?
Rosenburg et al 1998 80% had no pain after adjustment 50% had no pain after placebo adjustment (not removing cusp tissue)
75
Which patients would best benefit from occlusal adjustments for pain management?
- Pre op pain - TTP - No PARL - Vital cases
76
How does incision and drainage help with pain?
- reduces pressure | - removes bacterial products and cytokines
77
What orientation should you incise for D and I?
A vertical direction to reduce number of blood vessels that are transected
78
What three methods do we have for Drugs management for pain relief?
- Pre treat with NSAID or paracetamol - Use of long acting LA - Flexible prescription plan
79
Which group of drugs are most effective in dental pain?
Nsaids 800mg or 600mg and then paracetamol
80
How do NSAIDS work?
Peripheral hypothesis : inhibition of COX-strongest general acceptance Central hypothesis: inhibition of COX
81
What is COX1 enzyme and where is it found?
(COX-1 and COX-2) catalyze the conversion of arachidonic acid to prostaglandin (PG) H2, the precursor of PGs and thromboxane. These lipid mediators play important roles in inflammation and pain and in normal physiological functions COX 1 Present in stomach kidneys and platelets Traditional NSAIDS e.g aspirin preferentially inhibit Cox1
82
What is Cox 2 enzyme ?
COX 2 is inducible and is synthesised in inflamed tissues and cox 2 inhibitors have less GI and renal side effects
83
Name some COX1 NSAIDs?
aspirin indomethacin ibuprofen
84
Name some COX 2 NSAIDS
Etodolac
85
What is the risk with COX 2 inhibitor ?
Increased CV risks
86
What are the main risks of COX 1 inhibitors ?
Increased GI risk
87
What are the advantages of NSAID drugs?
Effective for pain of inflammation origin Less adverse side effects compared wit opioids Less addictive potential No tolerance Possible protection fro Alzheimers disease
88
What are the disadvantages of NSAIDS?
- Ceiling effect therefore would need to add a separate drug class - Adverse side effects e.g GI/Renal/Allergic type - Cannot be used in some patients e.g peptic ulcers/asthma/liver dysfunction
89
What effect do NSAIDs have on patients?
Analgesic Antipyretic inhibition of osteoclasts
90
What type of drug is paracetamol?
Acetaminophen
91
Where is paracetemol converted?
Paracetamol is converted by enzyme FAAH in liver into AM404
92
Where is AM404 mainly made?
In the brain
93
What type of receptor is AM404 similar to?
Canabinoids
94
Paracetamol method of actions are?
Absorbed into CNS and converted into AM404 Inhibits COX 1 splice variant Inhibits prostaglandin production
95
What is the benefit of LA?
Pain management during and after treatment by blocking the development of central sensitisation
96
What is periapcial disease?
reaction between periradicular tissues and noxious stimuli caused by interaction between bacteria and host immune response
97
What is a periapical lesion?
Retreat of bone away from source of infection creating space for body's immune cells to migrate the immediate vicinity
98
What type of tissue is present in a chronic lesion?
Granulomatous tissue-co-existance of healing and inflammation
99
Name some cells found in granulomas
``` PMNS and macrophages T and B cells Eosiniphils and mast cells Endothelial cells and fibroblasts Viral cells ```
100
In cysts are T or B cells more dominant?
B cells
101
Where there are sinus tracts what additional cells are present other than immune cells?
Epithelial cells
102
What is the name for zones of which cells are organised in periapical granulomas?
Zones of fish
103
What are the zones of FISH from external to internal layer
``` Zone of: Stimulation Irritation Contamination Infection ```
104
Which land mark study showed root canal infection is caused by bacteria?
Kakehashi et al 1965
105
What type of organisms cause periapical disease?
Eubacteria Bacterial products e.g LPS and M Protein Viruses Archaea (no nucleus and this prokaryotes)
106
Describe the model of periapical disease?
Bacterial invasion of root canals Non specific inflammation response with fluid exudate PMns and Macrophasges recruited Phagocytosis of bacteria Adaptive immune response with B and T cells in an attempt to wall of the oncoming infection
107
In cases where the infection is new how would this appear radiographically?
Diffuse area as there is no pre existing immunity but chronic lesions the host immune response manages this well resulting in a circumscribed area on the xray
108
What is AAP so TTP?
When the onslaught of pulpal and periapcial inflammation occurs faster than bone resorption can occur creating an accumulation of PMNS and oedema around apical tissues
109
What additional factors are seen in chronic lesions other than immune cells and bacteria?
Cytokines which include interleukins
110
What are cytokines?
These are secreted proteins released by cells in attempt to regulate inflammation - they can be pro or anti inflammation
111
Name some anti inflammatory cytokines
IL4 IL10 IL11
112
Name some pro inflammatory cytokines
IL1 IL2 and TNF alpha
113
How would you describe the variety of microbes in periapical disease?
Polymicrobial
114
What does diversity in PA disease consist of?
Species richness: number of unique species | Species evenness: abundance of each taxa
115
What type of bacteria are more common in acute exacerbations?
Fusobacteria
116
How does the species variety shift as time goes on with periapcial disease?
Lesion becomes | more anaerobic and more gram -ve
117
Between the main canal dentine and apical region which are has the greatest site of bacteria?
Main canal
118
Between the main canal dentine and apical region which are has the greatest impact on periapcial tissues?
Apical region due to its proximity
119
How do facultative anaerobes make ATP?
Either by oxygen or by fermentation in absence of oxygen
120
List ways bacteria can gain entry into the pulp system?
Caries- MOST common Cracks Exposed dentine tubules eg lateral canals Less commonly anachoresis - bacteria from another site
121
Why does internal resorption generally have a better long term prognosis compared with external?
Because there is no communication with PDL in internal
122
What problems do retreatment pose compared with primary treatment?
- Bacteria present more difficult to eradicate with more gram pos present - Iatrogenic errors from primary treatment may hinder access - Tactile sensation of canal altered due to prev treatment
123
Outline the 6 stages of retreatment
1. removal of existing coronal restoration 2. assess restorability using restorability index 3. remove all the root filling but avoid instrumentation 4. Guage canal to understand shape and missed anatomy 5. rectify and modify shape and irrigate 6. obturate
124
Name a restorability index we can use
McDonald and Setchell 2005
125
What are the three main causes of root canal failure?
Infection Non microbial Cyst
126
What are the two types of infection that can cause root canal failure?
Intraradicular and extradicular
127
Between intra and extraradicular infection which is the most common cause of failure?
Intra
128
What type of non microbial causes of failure are there
Foreign body reaction
129
What type of cysts can cause failure
True or bay cysts
130
What happens on a cellular level in foreign body reactions?
Acute inflammation: with present of monocytes and neutrophils Proliferative phase: Fibroblasts and macrophages Fibrotic encapsulation with foreign body giant cells
131
with regards to the bacterial species why are retreamtent more difficult?
-Presence of facultative anarobes eg actinomycete and e faecalis
132
What does e faecalis possess that makes it difficult to eradicate?
Proton pump inhibitor acting against calcium in CaOH
133
What are the success rates for retreatment success rates?
78-85%
134
What are the common causes of RCT failure?
- Leaking restorations - Root fractures - Untreated canals - Inadequately cleaned canals - Iatrogenic errors
135
How can RCT failure be assessed clinically?
Presence of pain Cracks Sinus Mobility
136
What are the options for surgical re endo
Perradicualr sugery e.g apicetomy Corrective surgery e.g root resection Fistulatative surgery e.g I and D or decompress
137
According to Ng et al 2011 , what are the 11 prognostic factors indicative for RCT failure?
1. Presence of pre op lesion 2. Size of pre op lesion 3. Presence of sinus tract 4. Patency 5. Prep as close to apical terminus 6. Extrusion 7. Perforation 8. Flare up 9. coronal sela 10. Not using CXD 2% 11. Re RCT use of EDTA as penultimate rinse
138
Classify iatrogenic errors
1. Access 2. Instrumentation 3. Obturation 4. Other e.g. hypochlorite accident/inhalation
139
How can root peforations be classified
Cause: iatrogenic or pathological Position: Coronal middle apical
140
What three things affect prognosis of root perforations
Size Location: exposure to mouth poorer porngosis Time: the longer between closing perf then the worse
141
What materials do we have for repairing perforations in bone?
MTA which is osteogenic and biocompatible
142
What materials do we have for repairing perforations in the mouth?
GIC
143
If the perforation is in the apical third how would you manage this?
Treat this as a canal and obturate with GP
144
Why don't we use MTA in lesions exposed to saliva?
It will be washed out since long setting time and dissolvable
145
What are the components of dentine?
Inorganic mineralised tissue HAP Collagen mainly type 1 Water
146
What function does water perform in dentine?
Stress absorbing and visco-elastic properties
147
What function does the inorganic mineral content provide to dentine?
rigidity and stregth
148
What function does collagen play ind dentine?
toughness and flexibility
149
Why does dehydrated dentine fracture quicker than hydrated dentine?
Unable to undergo plastic strain
150
What are the three main principles to consider when restoring teeth?
1. Preserve remaining tooth structure 2. Reduce stress and ensure favourably distributed in the remaining tooth 3. Provide a seal against coronal leakage
151
What is a bay/pocket cyst?
Huumonen 2002 | Lumen of the cyst is cont with the infectious source-one the tooth is removed then the cyst will go
152
What is a True/self sustained cyst?
Hummonen 2002 | Cyst is completely lined by epithelium -once tooth removed then cyst will need removal separately