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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
Periodontal pathogens
Porphyromonas gingivalis Prevotella intermedia Aggregebacter Actinomycetemcomitans
26
3 plaque hypothesis
Specific Non-specific Ecological
27
Non Specific plaque hypotheses
The quantity of plaque matters - gingivitis
28
Specific plaque hypothesis
The quality of plaque matters - aggressive periodontitis
29
Ecological plaque hypothesis
Small number of interacting species may cause destruction (unified theory) - chronic periodontitis
30
Medications that cause DIGO
Calcium channel blockers Phenytoin Cyclosporine
31
Systemic diseases that effect the host response
``` Diabetes Infections Osteoporosis CV disease Haematological diseases ```
32
Inherited syndromes effecting the immune response
``` Leukocyte adhesion deficiencies Checliak - Higashi syndrome Ehlers-Danlos syndrome Hyphophosphatasia Down’s syndrome Papillon-lefevre syndrome ```
33
What % of damage is caused by host response
80%
34
What % of damage is caused by bacteria
20%
35
Nutritional deficiency in periodontal disease
Lack of Vit C / scurvy
36
Pro-inflammatory foods
Saturated fats | Refined carbohydrates
37
Anti inflammatory foods
Fruit and veg
38
Adipose tissues store what
Cytokines
39
Cytokines and adoteases are anti inflammatory or pro inflammatory
Pro inflammatory
40
Increased prevalence in periodontal disease in what race
Chinese Asians Afro-Caribbean’s
41
Systemic risk factors (11)
``` Smoking Diabetes Medications Systemic diseases Nutrition Obesity Race Gender Genetics Stress Hormonal changes ```
42
second biggest risk factor after smoking
Diabetes
43
What % of people have diabetes
5%
44
What is the relationship between perio and diabetes
Bi-directional
45
Test for diabetes
HBA1C
46
AGES stands for
Advanced glycated end products
47
Severity of gingivitis correlates with which hormone
Progesterone
48
Junctional epithelium
``` Highly specialised Non-keratinised Fast turnover 20-30 cells thick Attached via hemidesmasomes ```
49
Compact bone
Oral and buccal cortical plates | Thin compact layer lining the socket
50
Cancellous bone
In between contact layers
51
Gingival fibres (4)
Transeptal fibres Circular fibres Dentogingival fibres Alveolar crest fibres
52
Lamina Dura
A radiographic term denoting the thin plate of compact bone that lies adjacent to the PDL and lines the socket
53
PDL features
``` 0.1-0.3mm wide Constantly breaks down and renewed Cells - fibroblasts, cementoblasts, osteoblasts, osteoclasts Blood vessels Nerves Lymphocytes ```
54
Principal Periodontal Fibres (5)
``` Dento-alveolar crest Horizontal Oblique Apical Interradicular ```
55
Composition of calculus
80% inorganic | 20% organic
56
Inorganic calculus salts
Calcium phosphate Calcium carbonate Magnesium phosphate Fluoride
57
Principal crystalline forms (4)
Calcium hydroxyapatite Magnesium whitlockite Octocalcium phosphate Calcium brush it every
58
Organic portion of calculus
``` Proteins Carbohydrates Non-vital organisms Dead epithelial cells Leukocytes ```
59
When does precipitation of calculus begin
1-14 days after plaque growth | May be as early as 4-8 hrs
60
Theories of calculus formation
Nucleation theory - most likely theory (seeding) | Precipitation theory - precipitation of mineral ions from saliva
61
Attachment of calculus to tooth
Acquired pellicle to irregularities in tooth surface Holes in roots where sharpeys fibres were inserted Direct contact - calcium deposit interlocked with crystals of tooth
62
Stain
Discolouration spot or mark caused by contact with foreign matter Not easily removed
63
Extrinsic
Originating from without Mineralised and can be removed by scaling or polishing
64
Intrinsic stain
Integral part of tooth structure cannot be removed by scaling
65
Examples of extrinsic stain
Metallic Tobacco Food and drink
66
Examples of intrinsic stain
Non vital tooth Tetracycline Fluorosis
67
1989 classifications of periodontitis
``` Adult Early onset Systemic disease ANUG Refractory ```
68
1999 classification of periodontitis
``` Chronic Aggressive NUG/NUP Systemic Periodontal abscess Perio endo legions ```
69
Severity of disease
Mild 1-2mm CAL Moderation 3-4mm CAL Severe >5mm CAL
70
Localised %
<30%
71
Generalised %
>30%
72
Aetiology of periapical abscesses
``` Insult to tooth Acute pulpitis Pulpal necrosis Acute periapical periodontitis Acute periapical abscess Acute chronic ```
73
Aetiology of periodontal abscess
Pre-existing periodontal pocket Foreign body impact ion Compromised immune system Response to incomplete treatment
74
Symptoms of pulpal \ periapical abscess
``` Non-vital Swelling over apex Sinus over apex TTP+++ Bone loss at apex ```
75
Symptoms of periodontal abscess
``` 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
Difficulties in differential diagnosis
``` Pulp vitality Position of swelling sinus TTP Radiographic appearances ```
77
Where can the abscess of upper lateral track to
Upper FPM
78
Immediate tx for acute periodontal abscess
Drainage of abscess achieved by instrumentation LA +RSD ABS not used routinely Systemic medical factors
79
Longterm tx of periodontal abscess
``` OHI Scale + RSD Addressing risk factors Supporting care (Local antimicrobials) Periodontal surgery XLA ```
80
Immediate tx for pericoronal abscess
``` Address acute phas LA and RSD Possible irrigation Systemic ABS if systemic involvement Possible adjustment of occlusion ```
81
Longterm tx of pericoronal abscess
Surgical excision of tissue | Possible XLA of offending tooth
82
Local anastheisa for mandibular molars
IDB + lingual | Long buccal
83
LA for mandibular premolars
Incisive, IDB, Lingual | mental
84
LA of maxillary molars
Posterior superior alveolar nerve
85
LA of Maxillary Incisors
Anterior superior alveolar nerve | Nasopalatine
86
Alternative terms for initial therapy
Cause related therapy Hygiene phase therapy Dental prophylaxis NPT
87
Other phases of periodontal treatment
``` Active phase (periodontal therapy) Supportive care ( long term monitoring) ```
88
Aim of initial therapy
Control dental plaque Sufficiently resolve gingival inflammation Improve other clinical features
89
Objects of initial therapy
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
Adjuncts to initial therapy
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
What do patients need to complete IT
``` Motivation Information Manual dexterity Time Money Support ```
92
Patients role in IT
Effective plaque control Modify risk factors Good attendance for TX
93
Factors that influence patient motivation
Every patients motivation will be different
94
Mouth measures for end point of initial therapy
Reduction of BOP, inflammation, swelling, erythema
95
Clinical response to NSPT
Moderate pockets 4-6 mm ppd - 1m reduction Deep Pockets >7mm ppd - 2 mum reduction Pockets >5mm 1-2mm recession
96
Definition of pseudorecession
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
What biotype is associated with pockets
Thick
98
What biotype is associated with recession
Thin
99
Does recession increase or decrease with age
Increase
100
Intrinsic factors that predispose to recession
Bone - fenestration \ bony dehiscence attached gingiva - width and thickness Biotype
101
Extrinsic factor that predispose recession
``` Mechanical - oral hygiene practices Iatrogenic Factitious Accidentally Chemical Malocclusion ```
102
How does plaque cause recession
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
Class I recession
Recession within the attached ginigiva | Full height papilla
104
Class II recession
Recession at or beyond MGJ | Full height papilla
105
Class III
recession recession at or beyond MGJ Reduced height papilla Apical extent to recession
106
Class IV recession
Recession at or beyond MGJ | Flat gingival contour
107
Management of gingival recession
``` 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
What is gingival overgrowth
Non specific term that means an increase in size of the gingivae seen clinically
109
Gingival hyperplasia
An enlargement due to an increase in gingival tissue seen pathologically
110
Gingival overgrowth may be
Localised or generalised
111
Gingival overgrowth may be
Oedematous or fibrous
112
How do you differentiate between oedematous and fibrous enlargement
Check for pitting oedema
113
Epulis
A localised gingival enlargement
114
Aetiology of gingival overgrowth
``` Plaque DIGO Gingival fibromatotsis Granulomatus disease Idiopathic ```
115
Risk factors for DIGO
age - children and teens more susceptible Males more suceptible Drug dosage does not affect susceptibility Combination of drugs can increase severity
116
Management of DIGO
NSPT | Surgical reduction
117
Management of gingival overgrowth
``` Control plaque to eradicate oedema Consider change in Meds Consider surgical reduction Monitor plaque control Monitor gingival contour ```
118
Management of epulides
Control plaque to eradicate oedema Consider aetiology may regress spontaneously Monitor plaque control Monitor gingival contour
119
What does BOP indicate
Active disease
120
Symptoms of acute hermetic gingivostomatitis
Feeling unwell Fever >39 Raised lymph glands Very sore mouth
121
Signs of acute hermetic gingivostomatitis
Vesicles in mouth Burst to form ulcers Red swollen bleeding gingiva
122
Aetiology of NUG
Predisposing factors + bacteria
123
Symptoms of NUG
V.sore bleeding gingivae Metallic taste Bad breath
124
Periodontal microorganisms in NUG
Fusobacteriium nucleatum Treponema Vicenti Prevotella intermedia
125
Clinical features of NUG
``` Seasonal Dirty mouths Localised\generalised V.painful Spontaneous bleeding Powerful halitosis Ulceration Loss of papillae Sloughing Ischaemic tissues ```
126
Treatment of NUG
Local debridement 6% hydrogen peroxide/0.2% CHX Systemic metronidazole 10 day follow up
127
Treatment of acute periocoronitits
``` Immediate Curette and irrigate Plaque control ABs / analgesics XLA opposing teeth ```
128
Fremitus
Tooth movement when teeth come into contact | Class 2 div 2 - palate
129
Factitious
Factitious gingivitis Gingivitis artefacta Pernicious habits
130
Antimicrobial agents in toothpaste And MW
``` Triclosan CHX Fluoride Stannous fluoride Essential oils Cecile peridium chloride SLS ```
131
Bactericidal
Kill bacteria
132
Bacteriostatic
Inhibit multiplication to allow host defence to destroy
133
When should systemic ABs be used
Aggressive perio NUG/NUP Periodontal abscess
134
What is the main problem with topical antimicrobial therapy
Main problem is achieving a high enough concentration in the pocketfor a sufficient amount of time
135
When would topical antimicrobial agents be used
Isolated pockets >5mm which have not responded to NSPT
136
Periochip
Biodegradable 2.5mg CHX digluconate in gelatine base
137
XaN CHX Gel
Muck adhesive biodegradable gel in xantham gum | CHX glauconite and CHX dihydrochloride 1:2
138
Smoking effects on the host response
``` Reduced PMN chemotaxis Reduced salivary IgA Reduced serum IgG Reduced T-Helper Cells Increase TNF-A ```
139
Which teeth are involved in localised aggressive
First molars | Incisors
140
Which teeth are involved In generalised aggressive
>3 permanent teeth other than first molars and incisors
141
Three bacteria involved in agressive
Aggregebacter actinomycetesmcomitans Porphyromonas gingivalis Prevotella intermedia
142
Management of aggressive
Early diagnosis and recognition
143
What BSP complexity level is aggressive
3
144
Adjunct ABs for aggressive
Combination of MEtronidazole 200mg Amoxicillin 500mg 3x daily 7-10 days
145
Virulence factors
Enzymes Toxins Metabolic waste products
146
Three enzymes in tissue destruction
Collagenase Hyaluronidase Elastase
147
Toxins of tissue destruction
Endotoxins lipopolysaccharides Release from/cell walls of G -ve bacteria when they die Attache loosely to cementum Potent stimulators of the immune response
148
Metabolic waste products in tissue destruction
Ammonia | Hydrogen sulphide
149
Three potential mechanisms for periodontal tissue destruction
Bacteria - invade local ST \ release virulence factors Host response - innate\adaptive immune system Environmental factors
150
The innate immune system
Inborn, non specific, inflammatory response
151
The adaptive immune system
Acquired specific
152
2 parts of the innate response
Fluid | Cellular
153
2 parts of the adaptive response
Anti body mediated | Cell mediated
154
Host defence
``` Saliva GCF Epithelium Inflammatory response Immune response Mediators between inflammation, immunity and tissues ```
155
How does saliva work as part of the immune response
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
What induces inflammatory response and induces neutrophil emigration
IL-1b
157
Three main cytokines
IL-1b IL-6 TNF-a
158
Which t lympocytes destroy antibodies
Cytotoxic
159
What is the fluid reaction
Increase in GCF
160
What is involved in the cellular reaction
PMNs and macrophages
161
What do cytokines do
``` 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
Which cells are antigen presenting
B lymphocytes | Macrophages
163
Good records are what ? 6 Cs S
``` Complete Contemporaneous Clear Concise Correct Constrained Signed and dated ```
164
What records are required with regards to periodontal diagnosis
``` RMH - smoking status BPE FPA Rads + results Study models \ photos ```
165
What inhibits collagenase
Doxycycline
166
What surgery would you do to treat recession
Coronal flap
167
What causes bystander damage
Inflammatory mediators
168
What BPE codes are used on children and why
0,1,2 | False pocketing due to mixed dentition
169
Other names for pregnancy epulis
Pregnancy tumour Pregnancy granuloma Pregnancy associated progenitor granuloma
170
When is best to carry out periodontal treatment on a pregnant woman
Second trimester
171
Can radiographs be taken during pregnancy
Yes if deemed appropriate
172
How long after surgery can you refere back to gdp
12 months
173
When should a FPA be carried out after surgery
12 weeks then annually
174
What is the optimum distance between bone margin and CEJ
2-3mm
175
What radiographs should be carried out for Generalised pockets BPE code 3 4-5mm
Horizontal BWs + PAs
176
What radiographs should be carried out for Generalised pockets BPE code 4 >6mm
Vertical BWs + PAs
177
What radiographs should be carried out for | Symptomatic 3rd molars
OPG + PAs
178
What radiographs should be carried out for | Perio-endo lesions
PAs
179
What should be included in a radiographic report
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
Other features of radiographic reports
``` Overhangs PRF Periapical pathology Root fracture Perio endo lesion Abnormal tooth lengths or morphology Caries ```
181
What is host modulation therapy
Involves reducing the destructive components of the host response in periodontitis so that the periodontal breakdown is reduced and wound healing is enhanced
182
Why is some collagen destruction necessary
To allow polymporphs to travel to bacteria to phagocytose them
183
What destroys collagen in a non-specific manner
MMPS
184
What host response modulators are used as adjuncts to NSPT
NSAIDs Bisphosponates Subantimicrobial dose doxycycline SDD
185
Give an example of SDD
Periostat
186
Periostat
20mg 2x daily for 9 months Inhibits MMP activity Encourages repair and healing

UOL PRD (1 decks)

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