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UOL PRD > UOL PRD > Flashcards

UOL PRD Flashcards

1
Q

Dental Plaque

A

A soft layer composed mainly of bacteria which forms on the hard structures of the mouth and is present in all mouths

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2
Q

Dental Biolfilm

A

A complex association of many different bacteria in a single environment

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3
Q

Features of Biolfim

A

Bacteria more resistant to environmental changes
Reduced susceptibility to antimicrobial agents
Lower nutritional requirements

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4
Q

Materia Alba

A

Soft accumulation of bacteria, dead cells and food debris that is loosely adhered to teeth

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5
Q

Pellicle

A

A thin layer of salivary proteins

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6
Q

Calculus

A

A hard deposit of mi realised plaque which is invariable covered with a layer of soft plaque

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7
Q

Composition of dental plaque

A

Bacteria
Inorganic
Organic

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8
Q

Organic components of plaque

A

Polysaccharides
Glycoproteins
Lipids

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9
Q

Inorganic components of plaque

A 
Calcium 
Phosphate
Sodium 
Potassium 
Fluoride
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10
Q

Plaque formation

A

Pellicle
initial colonisation by pioneer bacteria
Secondary colonisation
Maturation of plaque

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11
Q

How does the dental pellicle adhere to teeth

A

Electrostatic affinity

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12
Q

Initial pioneer bacteria

A

Gram positive facultative bacteria
Streptococcus sanguis
Actinomycetes viscosus
Streptococcus Oralia

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13
Q

Secondary colonisation bacteria

A 
Fusobacterium nucleatum 
Porphyromonas gingivalis 
Prevotella intermedia 
Prevotella losechii
Capnocytophagya
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14
Q

Tooth associated bacteria

A

Streptococcus sanguis
Streptococcus mitus
Actinomycetes viscosus
Actinomycetes naeslundi

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15
Q

Tissue associated bacteria

A

Gram negative rods, cocci, filaments, flagellated rods, spirochetes

Prevotella intermedia
Porphryomonas ginigvalis
Bacteriodes Forsythus
Aggregebacter actinomycetesmcomitans

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16
Q

Cariogenic bacteria

A

Streptococcus mutans
Actinomycetes sp
Lactobacillus acidophilus

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17
Q

Which study is the evidence of bacteria role in caries

A

1950s Orland and Keyes Germ Free Rats

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18
Q

High risk of caries

A

2-10% proportion of s.mutans in plaque

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19
Q

Low caries risk

A

0.1% s.mutans In plaque

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20
Q

Predominant bacteria in enamel pits and fissures

A

Streptococcus mutans

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21
Q

Predominant bacteria on approximately smooth surfaces

A

Actinomycetes

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22
Q

Predominant bacteria on exposed root surfaces

A

Streptococcus mutans
Actinomycetes
Lactobacillus sp

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23
Q

Local risk factors

A

Influence which sites develop disease

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24
Q

Systemic risk factors

A

Influence which individuals develop disease

Modifies the host response to plaque

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25
Q

Periodontal pathogens

A

Porphyromonas gingivalis
Prevotella intermedia
Aggregebacter Actinomycetemcomitans

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26
Q

3 plaque hypothesis

A

Specific
Non-specific
Ecological

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27
Q

Non Specific plaque hypotheses

A

The quantity of plaque matters - gingivitis

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28
Q

Specific plaque hypothesis

A

The quality of plaque matters - aggressive periodontitis

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29
Q

Ecological plaque hypothesis

A

Small number of interacting species may cause destruction (unified theory) - chronic periodontitis

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30
Q

Medications that cause DIGO

A

Calcium channel blockers
Phenytoin
Cyclosporine

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31
Q

Systemic diseases that effect the host response

A 
Diabetes 
Infections 
Osteoporosis 
CV disease 
Haematological diseases
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32
Q

Inherited syndromes effecting the immune response

A 
Leukocyte adhesion deficiencies 
Checliak - Higashi syndrome
Ehlers-Danlos syndrome 
Hyphophosphatasia 
Down’s syndrome 
Papillon-lefevre syndrome
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33
Q

What % of damage is caused by host response

A

80%

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34
Q

What % of damage is caused by bacteria

A

20%

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35
Q

Nutritional deficiency in periodontal disease

A

Lack of Vit C / scurvy

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36
Q

Pro-inflammatory foods

A

Saturated fats

Refined carbohydrates

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37
Q

Anti inflammatory foods

A

Fruit and veg

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38
Q

Adipose tissues store what

A

Cytokines

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39
Q

Cytokines and adoteases are anti inflammatory or pro inflammatory

A

Pro inflammatory

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40
Q

Increased prevalence in periodontal disease in what race

A

Chinese
Asians
Afro-Caribbean’s

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41
Q

Systemic risk factors (11)

A 
Smoking 
Diabetes 
Medications 
Systemic diseases
Nutrition 
Obesity 
Race 
Gender
Genetics 
Stress
Hormonal changes
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42
Q

second biggest risk factor after smoking

A

Diabetes

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43
Q

What % of people have diabetes

A

5%

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44
Q

What is the relationship between perio and diabetes

A

Bi-directional

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45
Q

Test for diabetes

A

HBA1C

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46
Q

AGES stands for

A

Advanced glycated end products

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47
Q

Severity of gingivitis correlates with which hormone

A

Progesterone

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48
Q

Junctional epithelium

A 
Highly specialised 
Non-keratinised
Fast turnover 
20-30 cells thick 
Attached via hemidesmasomes
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49
Q

Compact bone

A

Oral and buccal cortical plates

Thin compact layer lining the socket

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50
Q

Cancellous bone

A

In between contact layers

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51
Q

Gingival fibres (4)

A

Transeptal fibres
Circular fibres
Dentogingival fibres
Alveolar crest fibres

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52
Q

Lamina Dura

A

A radiographic term denoting the thin plate of compact bone that lies adjacent to the PDL and lines the socket

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53
Q

PDL features

A 
0.1-0.3mm wide
Constantly breaks down and renewed
Cells - fibroblasts, cementoblasts, osteoblasts, osteoclasts
Blood vessels
Nerves
Lymphocytes
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54
Q

Principal Periodontal Fibres (5)

A 
Dento-alveolar crest 
Horizontal 
Oblique
Apical
Interradicular
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55
Q

Composition of calculus

A

80% inorganic

20% organic

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56
Q

Inorganic calculus salts

A

Calcium phosphate
Calcium carbonate
Magnesium phosphate
Fluoride

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57
Q

Principal crystalline forms (4)

A

Calcium hydroxyapatite
Magnesium whitlockite
Octocalcium phosphate
Calcium brush it every

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58
Q

Organic portion of calculus

A 
Proteins
Carbohydrates
Non-vital organisms 
Dead epithelial cells
Leukocytes
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59
Q

When does precipitation of calculus begin

A

1-14 days after plaque growth

May be as early as 4-8 hrs

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60
Q

Theories of calculus formation

A

Nucleation theory - most likely theory (seeding)

Precipitation theory - precipitation of mineral ions from saliva

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61
Q

Attachment of calculus to tooth

A

Acquired pellicle
to irregularities in tooth surface
Holes in roots where sharpeys fibres were inserted
Direct contact - calcium deposit interlocked with crystals of tooth

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62
Q

Stain

A

Discolouration spot or mark caused by contact with foreign matter
Not easily removed

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63
Q

Extrinsic

A

Originating from without

Mineralised and can be removed by scaling or polishing

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64
Q

Intrinsic stain

A

Integral part of tooth structure cannot be removed by scaling

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65
Q

Examples of extrinsic stain

A

Metallic
Tobacco
Food and drink

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66
Q

Examples of intrinsic stain

A

Non vital tooth
Tetracycline
Fluorosis

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67
Q

1989 classifications of periodontitis

A 
Adult 
Early onset 
Systemic disease
ANUG
Refractory
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68
Q

1999 classification of periodontitis

A 
Chronic 
Aggressive 
NUG/NUP
Systemic
Periodontal abscess
Perio endo legions
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69
Q

Severity of disease

A

Mild 1-2mm CAL
Moderation 3-4mm CAL
Severe >5mm CAL

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70
Q

Localised %

A

<30%

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71
Q

Generalised %

A

> 30%

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72
Q

Aetiology of periapical abscesses

A 
Insult to tooth 
Acute pulpitis 
Pulpal necrosis 
Acute periapical periodontitis
Acute periapical abscess 
Acute  chronic
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73
Q

Aetiology of periodontal abscess

A

Pre-existing periodontal pocket
Foreign body impact ion
Compromised immune system
Response to incomplete treatment

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74
Q

Symptoms of pulpal \ periapical abscess

A 
Non-vital
Swelling over apex
Sinus over apex
TTP+++
Bone loss at apex
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75
Q

Symptoms of periodontal abscess

A 
Vital tooth 
Swelling near gingival margin
Drain through pocket 
TTP+
Marginal bone loss 
Deep probing depths 
Evidence of further perio disease 
May be an increase in mobility
76
Q

Difficulties in differential diagnosis

A 
Pulp vitality
Position of swelling
sinus
TTP
Radiographic appearances
77
Q

Where can the abscess of upper lateral track to

78
Q

Immediate tx for acute periodontal abscess

A

Drainage of abscess achieved by instrumentation
LA +RSD
ABS not used routinely
Systemic medical factors

79
Q

Longterm tx of periodontal abscess

A 
OHI
Scale + RSD 
Addressing risk factors
Supporting care
(Local antimicrobials)
Periodontal surgery 
XLA
80
Q

Immediate tx for pericoronal abscess

A 
Address acute phas
LA and RSD
Possible irrigation 
Systemic ABS if systemic involvement 
Possible adjustment of occlusion
81
Q

Longterm tx of pericoronal abscess

A

Surgical excision of tissue

Possible XLA of offending tooth

82
Q

Local anastheisa for mandibular molars

A

IDB + lingual

Long buccal

83
Q

LA for mandibular premolars

A

Incisive, IDB, Lingual

mental

84
Q

LA of maxillary molars

A

Posterior superior alveolar nerve

85
Q

LA of Maxillary Incisors

A

Anterior superior alveolar nerve

Nasopalatine

86
Q

Alternative terms for initial therapy

A

Cause related therapy
Hygiene phase therapy
Dental prophylaxis
NPT

87
Q

Other phases of periodontal treatment

A 
Active phase (periodontal therapy) 
Supportive care ( long term monitoring)
88
Q

Aim of initial therapy

A

Control dental plaque
Sufficiently resolve gingival inflammation
Improve other clinical features

89
Q

Objects of initial therapy

A

A patient who is aware of an improvement of their condition
A month which the health of the periodontium has improved
Teeth that a free from deposits

90
Q

Adjuncts to initial therapy

A

Relief of pain
XLA of teeth with poor prognosis
Endodontics to resolve acute periapical infection
Removal of gross caries - place temporary restorations
Smoking cessation
Management of dentine sensitivity

91
Q

What do patients need to complete IT

A 
Motivation 
Information 
Manual dexterity
Time
Money
Support
92
Q

Patients role in IT

A

Effective plaque control
Modify risk factors
Good attendance for TX

93
Q

Factors that influence patient motivation

A

Every patients motivation will be different

94
Q

Mouth measures for end point of initial therapy

A

Reduction of BOP, inflammation, swelling, erythema

95
Q

Clinical response to NSPT

A

Moderate pockets 4-6 mm ppd - 1m reduction
Deep Pockets >7mm ppd - 2 mum reduction

Pockets >5mm 1-2mm recession

96
Q

Definition of pseudorecession

A

When a tooth erupts it takes some time for the gingival margin to reach its adult position. The gingival position of the margin on a atooth in its adult position the adjacent tooth is placed more coronally

97
Q

What biotype is associated with pockets

98
Q

What biotype is associated with recession

99
Q

Does recession increase or decrease with age

100
Q

Intrinsic factors that predispose to recession

A

Bone - fenestration \ bony dehiscence
attached gingiva - width and thickness
Biotype

101
Q

Extrinsic factor that predispose recession

A 
Mechanical - oral hygiene practices 
Iatrogenic 
Factitious
Accidentally 
Chemical 
Malocclusion
102
Q

How does plaque cause recession

A

Rate ridges enlongate with inflammation
When ridges from the sulcular epithelium join ridges from the oral epithelium the intervening connective tissue is displaced from th blood supply to the epithelium is cut off resulting in atrophy

103
Q

Class I recession

A

Recession within the attached ginigiva

Full height papilla

104
Q

Class II recession

A

Recession at or beyond MGJ

Full height papilla

105
Q

Class III

A

recession recession at or beyond MGJ
Reduced height papilla
Apical extent to recession

106
Q

Class IV recession

A

Recession at or beyond MGJ

Flat gingival contour

107
Q

Management of gingival recession

A 
Inform the patient
Instigate plaque control 
Removal of PRFS
Treat dentine sensitivity 
Restore abrasion / erosion lesions 
Restore carious lesions 
Patient reassurance 
Monitor and maintain
108
Q

What is gingival overgrowth

A

Non specific term that means an increase in size of the gingivae seen clinically

109
Q

Gingival hyperplasia

A

An enlargement due to an increase in gingival tissue seen pathologically

110
Q

Gingival overgrowth may be

A

Localised or generalised

111
Q

Gingival overgrowth may be

A

Oedematous or fibrous

112
Q

How do you differentiate between oedematous and fibrous enlargement

A

Check for pitting oedema

113
Q

Epulis

A

A localised gingival enlargement

114
Q

Aetiology of gingival overgrowth

A 
Plaque 
DIGO 
Gingival fibromatotsis
Granulomatus disease
Idiopathic
115
Q

Risk factors for DIGO

A

age - children and teens more susceptible
Males more suceptible
Drug dosage does not affect susceptibility
Combination of drugs can increase severity

116
Q

Management of DIGO

A

NSPT

Surgical reduction

117
Q

Management of gingival overgrowth

A 
Control plaque to eradicate oedema 
Consider change in Meds
Consider surgical reduction 
Monitor plaque control 
Monitor gingival contour
118
Q

Management of epulides

A

Control plaque to eradicate oedema
Consider aetiology may regress spontaneously
Monitor plaque control
Monitor gingival contour

119
Q

What does BOP indicate

A

Active disease

120
Q

Symptoms of acute hermetic gingivostomatitis

A

Feeling unwell
Fever >39
Raised lymph glands
Very sore mouth

121
Q

Signs of acute hermetic gingivostomatitis

A

Vesicles in mouth
Burst to form ulcers
Red swollen bleeding gingiva

122
Q

Aetiology of NUG

A

Predisposing factors + bacteria

123
Q

Symptoms of NUG

A

V.sore bleeding gingivae
Metallic taste
Bad breath

124
Q

Periodontal microorganisms in NUG

A

Fusobacteriium nucleatum
Treponema Vicenti
Prevotella intermedia

125
Q

Clinical features of NUG

A 
Seasonal 
Dirty mouths 
Localised\generalised 
V.painful 
Spontaneous bleeding 
Powerful halitosis
Ulceration 
Loss of papillae 
Sloughing 
Ischaemic tissues
126
Q

Treatment of NUG

A

Local debridement
6% hydrogen peroxide/0.2% CHX
Systemic metronidazole

10 day follow up

127
Q

Treatment of acute periocoronitits

A 
Immediate 
Curette and irrigate 
Plaque control 
ABs / analgesics 
XLA opposing teeth
128
Q

Fremitus

A

Tooth movement when teeth come into contact

Class 2 div 2 - palate

129
Q

Factitious

A

Factitious gingivitis
Gingivitis artefacta
Pernicious habits

130
Q

Antimicrobial agents in toothpaste And MW

A 
Triclosan
CHX
Fluoride
Stannous fluoride 
Essential oils
Cecile peridium chloride
SLS
131
Q

Bactericidal

A

Kill bacteria

132
Q

Bacteriostatic

A

Inhibit multiplication to allow host defence to destroy

133
Q

When should systemic ABs be used

A

Aggressive perio
NUG/NUP
Periodontal abscess

134
Q

What is the main problem with topical antimicrobial therapy

A

Main problem is achieving a high enough concentration in the pocketfor a sufficient amount of time

135
Q

When would topical antimicrobial agents be used

A

Isolated pockets >5mm which have not responded to NSPT

136
Q

Periochip

A

Biodegradable 2.5mg CHX digluconate in gelatine base

137
Q

XaN CHX Gel

A

Muck adhesive biodegradable gel in xantham gum

CHX glauconite and CHX dihydrochloride 1:2

138
Q

Smoking effects on the host response

A 
Reduced PMN chemotaxis
Reduced salivary IgA
Reduced serum IgG
Reduced T-Helper Cells
Increase TNF-A
139
Q

Which teeth are involved in localised aggressive

A

First molars

Incisors

140
Q

Which teeth are involved In generalised aggressive

A

> 3 permanent teeth other than first molars and incisors

141
Q

Three bacteria involved in agressive

A

Aggregebacter actinomycetesmcomitans
Porphyromonas gingivalis
Prevotella intermedia

142
Q

Management of aggressive

A

Early diagnosis and recognition

143
Q

What BSP complexity level is aggressive

144
Q

Adjunct ABs for aggressive

A

Combination of MEtronidazole 200mg
Amoxicillin 500mg
3x daily 7-10 days

145
Q

Virulence factors

A

Enzymes
Toxins
Metabolic waste products

146
Q

Three enzymes in tissue destruction

A

Collagenase
Hyaluronidase
Elastase

147
Q

Toxins of tissue destruction

A

Endotoxins lipopolysaccharides
Release from/cell walls of G -ve bacteria when they die
Attache loosely to cementum
Potent stimulators of the immune response

148
Q

Metabolic waste products in tissue destruction

A

Ammonia

Hydrogen sulphide

149
Q

Three potential mechanisms for periodontal tissue destruction

A

Bacteria - invade local ST \ release virulence factors
Host response - innate\adaptive immune system
Environmental factors

150
Q

The innate immune system

A

Inborn, non specific, inflammatory response

151
Q

The adaptive immune system

A

Acquired specific

152
Q

2 parts of the innate response

A

Fluid

Cellular

153
Q

2 parts of the adaptive response

A

Anti body mediated

Cell mediated

154
Q

Host defence

A 
Saliva
GCF
Epithelium
Inflammatory response 
Immune response 
Mediators between inflammation, immunity and tissues
155
Q

How does saliva work as part of the immune response

A

Aids the ingestion of bacteria
Contains antibacterial substances lysozome and IgA
Swallowing bacteria > activation of lymphocytes
lymphocytes travel to salivary gland and secrete IgA
Binds to bacteria disrupting their attachment

156
Q

What induces inflammatory response and induces neutrophil emigration

157
Q

Three main cytokines

A

IL-1b IL-6 TNF-a

158
Q

Which t lympocytes destroy antibodies

159
Q

What is the fluid reaction

A

Increase in GCF

160
Q

What is involved in the cellular reaction

A

PMNs and macrophages

161
Q

What do cytokines do

A 
Act like hormones 
Cooperate with other cytokines to enhance their effects 
Initiate and enhance immune response 
Can cause bystander damage 
Strong association with bone resorption
162
Q

Which cells are antigen presenting

A

B lymphocytes

Macrophages

163
Q

Good records are what ? 6 Cs S

A 
Complete 
Contemporaneous 
Clear 
Concise 
Correct 
Constrained 
Signed and dated
164
Q

What records are required with regards to periodontal diagnosis

A 
RMH - smoking status 
BPE 
FPA 
Rads + results 
Study models \ photos
165
Q

What inhibits collagenase

A

Doxycycline

166
Q

What surgery would you do to treat recession

A

Coronal flap

167
Q

What causes bystander damage

A

Inflammatory mediators

168
Q

What BPE codes are used on children and why

A

0,1,2

False pocketing due to mixed dentition

169
Q

Other names for pregnancy epulis

A

Pregnancy tumour
Pregnancy granuloma
Pregnancy associated progenitor granuloma

170
Q

When is best to carry out periodontal treatment on a pregnant woman

A

Second trimester

171
Q

Can radiographs be taken during pregnancy

A

Yes if deemed appropriate

172
Q

How long after surgery can you refere back to gdp

173
Q

When should a FPA be carried out after surgery

A

12 weeks then annually

174
Q

What is the optimum distance between bone margin and CEJ

175
Q

What radiographs should be carried out for
Generalised pockets
BPE code 3
4-5mm

A

Horizontal BWs + PAs

176
Q

What radiographs should be carried out for
Generalised pockets
BPE code 4
>6mm

A

Vertical BWs + PAs

177
Q

What radiographs should be carried out for

Symptomatic 3rd molars

178
Q

What radiographs should be carried out for

Perio-endo lesions

179
Q

What should be included in a radiographic report

A

Image quality
Teeth present
Bone loss %
Pattern of bone loss - horizontal or vertical
Distribution of bone loss - localised or generalised
Calculus present
Furcation involvement

180
Q

Other features of radiographic reports

A 
Overhangs
PRF 
Periapical pathology 
Root fracture
Perio endo lesion 
Abnormal tooth lengths or morphology 
Caries
181
Q

What is host modulation therapy

A

Involves reducing the destructive components of the host response in periodontitis so that the periodontal breakdown is reduced and wound healing is enhanced

182
Q

Why is some collagen destruction necessary

A

To allow polymporphs to travel to bacteria to phagocytose them

183
Q

What destroys collagen in a non-specific manner

184
Q

What host response modulators are used as adjuncts to NSPT

A

NSAIDs
Bisphosponates
Subantimicrobial dose doxycycline SDD

185
Q

Give an example of SDD

186
Q

Periostat

A

20mg 2x daily for 9 months
Inhibits MMP activity
Encourages repair and healing

UOL PRD (1 decks)

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