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bds 2 > periodontology > Flashcards

periodontology Flashcards

1
Q

gingivitis

A

accumulation of plaque in the mouth causing reversible inflammation of the surrounding soft tissue

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2
Q

causes of microbial challenge

A
  1. local plaque retentive factors
    = calculus, crowding, overhangs and margins, mouth breathing
  2. systemic modifying factors

= hormones and medication

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3
Q

diagnosis of healthy gums

A
  1. well defined, knife edge margins
  2. pointed papillas
  3. stippling in some
  4. healthy pink colour
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4
Q

healthy gingival turnover

A

4-5 days

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5
Q

what bacteria will predominate in healthy gingiva

A

aerobes

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6
Q

gingivitis signs

A
  1. puffy rolled gingival margins
  2. loss of stippling
  3. redness
  4. local bacterial plaque changes
  5. bleeding gums
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7
Q

what is amplified in the disease state

A

the immune response

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8
Q

what leads to bleeding on probing

A

the epithelium proliferates quickly which can lead to ulcerations and ultimately bleeding

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9
Q

what happens in early gingivitis

A
  • slightly increased infiltration of immune cells
  • proliferation of junctional epithelium
  • very few plasma cells infiltrate
  • blood vessels dilate
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10
Q

what happens in established gingivitis

A
  • greatly increased leukocyte infiltration
  • lots of increased proliferation of the junctional epithelium meaning false pockets form
  • plasma cells constitute 20-30% of infiltrating cells
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11
Q

false pockets

A
  • epithelium has proliferated
  • inflammatory exudate causes swelling and therefore the illusion of a pocket is created as the probe end disappears
  • however there is NO LOSS OF ATTACHMENT
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12
Q

true pockets

A
  • apical migration of the junctional epithelium as the source of inflammation is not removed
  • exposes cementum as a site for biofilm accumulation
  • loss of attachment is rarely regained and can result in healthy looking gingiva having deep pockets
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13
Q

loss of attachment can be

A

continuous or periodic

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14
Q

general rate of loss of attachment

A
  1. 05-0.1mm/year

- greatly variable among patients

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15
Q

the biofilm

A

one or more communities of microorganisms embedded in a glycocalyx, attached to a solid surface

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16
Q

glycocalyx

A

glycoprotein and glycolipid covering surrounding the cell membranes of bacteria

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17
Q

properties of the biofilm

A
  1. provides protection for colonising species against environmental pressures and competition
  2. facilitates the uptake of nutrients and expulsion of metabolic waste (plaque acid)
  3. develops a physiochemical environment to favour bad bacteria (lowers pH and O2 concentration)
  4. allows communication between bacteria
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18
Q

bacterial virulence

A

the ability to colonise and compete in an ecological niche and to evade host defences to survive

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19
Q

ways bacteria evade the host immune system

A
  1. degrade host immunoglobulin and complement
  2. leucotoxin production
  3. tissue invasion
  4. inhibition of antibody synthesis
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20
Q

how are oral bacteria equipped to cause periodontal disease

A

they easily break down antibodies and cytokines

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21
Q

evidence which would support bacteria being the causation

A
  • associated bacteria reside in higher concentration in diseased sites
  • reduced numbers of bacteria following periodontal therapy
  • presence of an elevated specific immune response
  • production of virulence factors to evade host defences and invade tissues
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22
Q

what is red complex bacteria

A

identified bacteria highly associated with the presence of periodontal disease

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23
Q

synergistic infection

A
  • relates to the interaction or cooperation of two or more organisations, substances or other agents to produce separate effects
  • gingivitis and periodontal disease are exmaples
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24
Q

the theory behind the causation of PDD

A
  1. presence of bacteria in the biofilm causing inflammation
  2. the extent of the disease is caused by the interaction of the bacteria and the host immune response
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25
Q

mechanisms of the host immune response in the oral cavity

A
  1. saliva
  2. epithelium
  3. gingival crevicular fluid
  4. inflammatory and immune cells
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26
Q

describe the host immune response to bacterial plaque in periodontitis

A
  1. initial periodontal lesion is composed of mainly T lymphocytes which secrete the cytokines to tell other cells what to do
  2. the B cells and plasma cells driven by the cytokines arrive
  3. antibody is produced locally to the site of infection and is usually protective
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27
Q

protective functions of the antibody

A
  1. inhibition of adhesion and invasion
  2. complement activation
  3. neutralisation of toxins
  4. opsonisation and phagocytosis
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28
Q

matrix mellatoproteinases

A
  • family of zinc and calcium dependent proteolytic enzymes

- break down connective tissue causing tissue destruction

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29
Q

3 patterns of bone loss in periodontal disease

A
  1. horizontal
  2. vertical
  3. furcation
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30
Q

measuring bone loss in PDD

A

should look at % of bone lost in relation to length of root
usually the bone sits 1-2mm below the ADJ

some people have short roots however

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31
Q

horizontal bone loss

A
  • usually in thinner areas of bone
  • bone is lost at an even plane across the teeth
  • harder to regenerate due to lack of additional adhesive surfaces for bone to grow from
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32
Q

vertical/angular bone loss

A
  • usually in thicker areas of bone
  • same pattern of loss as horizontal however it doesn’t go all the way through the bone resulting in deeper loss in some areas
  • easier to regenerate
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33
Q

reasons for different patterns of bone loss

A

initial shape and thickness of bone
- destruction begins from the most apical point in the plaque
- depends on the thickness of the bone

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34
Q

general risk factors for periodontal disease

A
  1. smoking
  2. diabetes
  3. stress
  4. drugs
  5. systemic disease
  6. nutrition
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35
Q

anatomical risk factors of periodontal disease

A
  • enamel pearls and projections
  • grooves
  • furcations
  • gingival recession
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36
Q

tooth position risk in PDD

A
  • malalignment creating difficult to clean areas
  • crowding
  • tipping of teeth
  • migration
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37
Q

iatrogenic risk factors of PDD

A
  • restorative margins and overhangs
  • defective crown margins
  • poorly designed partial dentures
  • orthodontic appliances
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38
Q

normal physiological response to infection or injury of the gingiva

A

gingivitis

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39
Q

pathological inflammatory response associated with tissue destruction

A

periodontitis

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40
Q

early colonisers

A

commensal aerobes

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41
Q

late colonisers

A

gram negative anaerobes

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42
Q

colonisation

A

microbial presence on a body surface without clinical signs of inflammation or disease
- usually commensal organisms

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43
Q

infection

A

microbial invasion of host tissues causing a reaction

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44
Q

asaccharolytic

A

bacteria metabolism which doesnt break down carbohydrates but proteins and peptides instead

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45
Q

gingipains

A

proteases produces by P.gingivalis which
1. degrade host enzymes
2. activate MMP’s

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46
Q

virulence factors of P.Gingivals

A
  1. asaccharolytic
  2. gingipains
  3. atypical LPS
  4. inflammophillic
47
Q

inflammophilic

A

thrive in inflammatory conditions

48
Q

red complex bacteria

A
  1. porphyromonas gingivalis
  2. tannerella forsythia
  3. treponema denticola
49
Q

why can lesser pathogens (orange complex) cause PDD

A
  • some factors produced by the bacteria reduce host inflammatory response
  • therefore they cause the disease easier
50
Q

contents of saliva which protect the teeth

A
  1. S-IgA
  2. lysozyme
  3. peroxidase
  4. lactoferrin
  5. mucins
  6. cystatins
  7. histamines
51
Q

immune defences in the GCF

A
  1. AMPs
  2. cytokines
  3. chemokines
  4. lactoferrin
  5. IgG
52
Q

pathogenesis in the development of periodontal disease

A
  • healthy biofilm is symbiotic and lives next to host tissues
  • inflammation is subclinical in health
  • any microbial challenge may disrupt this
    1. if controlled, health will return
    2. if uncontrolled then the inflammation will continue and a dysbiosis will occur
53
Q

disease state of gingivitis

A
  1. increased TLR stimulation
  2. increased production of pro-inflammatory mediates
  3. redness, swelling, bleeding, vasodilation, cell migration
  4. neutrophils remain the predominant cell type
  5. monocytes are recruited and active to differentiate into macrophages
  6. lymphocytes recruited later on to fine tune the immune response
54
Q

factors that may cause the symbiosis of the oral microbiome

A
  1. antibiotics
  2. diseases e.g. diabetes
  3. genetics
  4. activity of salivary proteins
  5. salivary flow rate
  6. innate/adaptive immune factors
  7. oral hygiene
  8. diet
  9. smoking
55
Q

hallmark clinical signs of periodontitis

A
  1. increased pocket depth
  2. apical migration of junctional epithelium
  3. loss of attachment
56
Q

problems with a lack of neutrophils

A
  • patients with leukocyte adhesion deficiency
  • trouble getting neutrophils from the BV to the tissues
  • prone to PDD from a young age as they are the predominant species of immune cells
57
Q

problems with too many neutrophils

A
  • main source of tissue MMPs
  • can increase the tissue breakdown associated with chronic inflammation
  • leads to excessive bone and attachment loss
58
Q

adaptive immune system in periodontal destruction

A
  • B and T lymphocytes present in the early lesion
  • aggregations of CD4 T cells and B cells and dendritic cells
  • unable to regulate symbiotic biofilm so does 2 things
    1. protects by stopping the infection becoming systemic
    2. destructive as the inflammation is induced and increases alveolar bone loss
59
Q

process of alveolar bone loss

A
  1. RANK receptors are expressed on monocytes
  2. in the gingival tissues, B and T cells release RANKL which is free to bind to the osteoclasts which are being brought into the tissues by chronic inflammation
  3. when the monocytes bind RANKL, they differentiate into osteoclasts and destroy the bone
  4. this is because in chronic inflammation there are low levels of OPG to increase bone formation

= net loss of alveolar bone

60
Q

chronic periodontitis

A
  • destruction of junctional epithelium and connective tissue attachment
  • bone destruction and pocket formation
  • progressive disease which affects the amount of bone loss
61
Q

aggressive periodontitis

A
  • severe condition usually affecting younger patients
  • may be associated with family history
  • progression is rapid
  • loss of bone attachment is severe
  • plaque levels may be incosistent with disease progression
62
Q

necrotising ulcerative gingivitis

A
  • NUG
  • painful ulceration of the tips of the interdental papillae

necrotic tissue is visible

  • associated halitosis
63
Q

necrotising ulcerative periodontitis

A
  • same as NUG but with the presence of connective tissue attachment and bone loss
64
Q

periodontal abscess

A

infection in a periodontal pocket
can be acute or chronic

65
Q

gingival enlargement

A
  • thickingin of the gingiva
  • can occur in response to irritation by;
  1. plaque or calcuclus
  2. friction or trauma
  3. fluctuations in hormones
66
Q

smoking and periodontal disease

A
  • no bleeding on probing as the vessels are constricted by the nicotine
  • impaired wound healing
  • production of inflammation mediating cytokines
67
Q

drugs which can increase periodontal disease risk

A

calcium channel blockers

68
Q

actions to take when a patient scores BPE3 or above

A
  1. treat entire sextant and take 6PPC for completed sextant AFTER completion of treatment
    OR
  2. complete 6PPC BEFORE and AFTER treatment and conduct RSD on teeth scoring BPE3
69
Q

other terms for non-surgical management of PDD

A

cause related therapy
hygiene phase therapy

70
Q

aims of non-surgical management of PDD

A
  • arrest the disease process
  • regenerate lost tissues
  • maintain periodontal health in the long term
  • to preserve a functional dentition for life
71
Q

stages in the treatment plan

A
  1. emergency care
  2. disease control
  3. re-evaluation
  4. reconstruction
  5. supportive care
72
Q

disease control

A
  1. extract hopeless teeth
  2. hygiene phase therapy
  3. caries management
  4. endodontic therapy
  5. provisional prosthesis
73
Q

periodontal therapy in the clinic

A
  1. supra and sub gingival plaque control
  2. root surface debridement
  3. removal of plaque retentive factors
74
Q

periodontal therapy at home

A
  1. demonstration of how to use oral hygiene aids
  2. tooth brushing advice
  3. toothpaste recommendations
75
Q

things assessed to determine level of dental health education

A
  1. evaluate the patients reasons for attendance
  2. assess their attitude towards healthcare and their motivation to improve their oral health
  3. explain the nature of the patients disease using visual aids
  4. discuss the findings of the examination
  5. demonstrate the healthy dentition and diseased state in the patients mouth
  6. explain the nature of the treatment and the consequences
76
Q

scaling

A

the removal of plaque and calculus from the tooth surface

77
Q

root surface debridement

A
  • the actor removing dead, contaminated or adherent tissue or foreign material from the root surface
  • instrumentation encompasses scaling and root planing
78
Q

root planing

A

the removal of contaminated cementum, leaving the tooth root surface hard and smooth

79
Q

scaling instruments

A

hand instruments (manual) and sonic and ultrasonic instruments
rotating and reciprocating instruments

80
Q

advantages of hand instruments

A
  1. no cavitation and flushing effect from water coolant
  2. powered instruments produce aerosol
  3. powered instruments tend to leave the surface rougher
  4. there is greater tactile sensitivity with hand instruments
81
Q

advantages of powered instruments

A
  1. may allow better access to furcation regions
  2. may be faster
  3. less demanding on the operator (hand fatigue)
  4. less unwanted tooth tissue removal
82
Q

assessing treatment

A
  1. inflammation levels
  2. bleeding on probing indices
  3. reduction in probing depth
  4. gain in attachment level
83
Q

probing depth indicates

A

indicates the difficulty of the treatment and the likelihood of recurrence

84
Q

attachment levels indicate

A

a measure of the tissue destruction pre treatment and the extent of repair post treatment

85
Q

things which can influence manual probing depths

A
  1. resistance of the tissues
  2. size, shape and diameter of the probe
  3. site of insertion
  4. angle of insertion
  5. presence of obstructions e.g. calculus
  6. patient discomfort
86
Q

effects of supra gingival plaque control alone

A
  • decreased gingival inflammation
  • limited effect on probing depth
  • no change in clinical attachment level
  • no alteration in the sub gingival microflora in deep pockets
87
Q

effects of RSD without supra gingival scaling

A
  • initial reduction in pocket depth and inflammation
  • pockets re-colonised by supra gingival plaque species
  • disease recurrence
88
Q

effects of RSD combines with supra gingival scaling

A
  • decreased gingival inflammation
  • reduction in pocket depth
  • gain in probing attachment levels
  • marked changes in the sub gingival microflora
89
Q

healing time after PDD treatment

A
  • greatest changes observed in 4-6 weeks after treatment

- gradual repair and maturation of the tissues over the next 6-12 months

90
Q

full mouth disinfection

A
  • aims to prevent treated pockets becoming recolonised by bacteria
  • use of chlorohexidine mouth wash for sub gingival irrigation
  • tongue brushing
  • mouth rinsing
91
Q

effects of RSD

A
  • reduces microbial challenge
  • decreases inflammation
  • inoculation with plaque organisms can boost the immune response
92
Q

re-evalutaion should look at

A
  1. patient plaque control
  2. bleeding on probing
  3. residual probing depth and attachment levels
93
Q

what suggests success of non surgical PDD therapy

A
  1. good OH
  2. no bleeding on probing
  3. no pockets greater than 4mm
  4. no increasing tooth mobility
  5. a functional and comfortable dentition
94
Q

why does periodontal treatment fail

A
  • poor compliance
  • inadequate debridement
  • host factors mainly smoking
95
Q

limitations to non-surgical therapy

A
  • root morphology preventing clearing
  • furcation involvement
  • deep pockets
  • skill level
  • time
96
Q

supportive care

A
  • maintain periodontal health
  • detect and treat the recurrence of disease
  • maintain acceptable levels of the disease
  • manage and prevent tooth loss

SHOULD BE EVERY 3 MONTHS

97
Q

what can be assessed in a 6PPC

A
  1. probing depth
  2. bleeding on probing
  3. gingival margin height
  4. loss of attachment
  5. mobility
  6. furcation involvement
98
Q

what is the minimum requirement of a 6PPC

A

to record all sites greater than or equal to 4mm or more probing depth and bleeding on probing

99
Q

what is probing depth a measure of

A

the base of the gingival crevice to the gingival margin

100
Q

what is recession measure from

A

the gingival margin to the cej

101
Q

how is loss of attachment a measured

A

probing depth + recession

102
Q

is the value for gingival margin + or - in a 6PPC if it goes above the CEJ

A

-

103
Q

is the value for gingival margin + or - in a 6PPC if it goes below the CEJ

A

positive

104
Q

how should the PCP probe be inserted to measure accurately

A

parallel to the long axis of the tooth while maintaining contact with the end of the probe to the tooth

105
Q

how many sites around the teeth are recorded on 6PPC

A

6 points

3 buccal 3 palatal

106
Q

grade 1 furcation involvement

A

initial involvement
- furcation can be felt on probing

  • there is less than one third of the tooth width involved
107
Q

grade 2 of furcation involvement

A

partial furcation involvement
loss of support exceeds one third of the tooth width but does not include the total width of the furcation

108
Q

grade 3 furcation

A

through and through involvement
the probe can pass through the entire furcation

109
Q

grading tooth mobility

A

0-3

110
Q

grade 0 tooth mobility

A

physiological mobility at crown level
tooth as only moved 0.1-0.2mm in the horizontal direction

111
Q

grade 1 tooth mobility

A

increased mobility of the crown of the tooth at most 1mm in horizontal direction

112
Q

grade 2 tooth mobility

A

visually increased mobility of the crown exceeding 1mm in a horizontal direction

113
Q

grade 3 tooth mobility

A

severe mobility of the crown of the tooth in both horizontal and vertical direction impinging on the function of the tooth

bds 2 (38 decks)

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