1
Q
gingivitis
A
accumulation of plaque in the mouth causing reversible inflammation of the surrounding soft tissue
2
Q
causes of microbial challenge
A
- local plaque retentive factors
= calculus, crowding, overhangs and margins, mouth breathing - systemic modifying factors
= hormones and medication
3
Q
diagnosis of healthy gums
A
- well defined, knife edge margins
- pointed papillas
- stippling in some
- healthy pink colour
4
Q
healthy gingival turnover
A
4-5 days
5
Q
what bacteria will predominate in healthy gingiva
A
aerobes
6
Q
gingivitis sings
A
- puffy rolled gingival margins
- loss of stippling
- redness
- local bacterial plaque changes
- bleeding gums
7
Q
what is amplified in the disease state
A
the immune response
8
Q
what leads to bleeding on probing
A
the epithelium proliferates quickly which can lead to ulcerations and ultimately bleeding
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
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
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
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
13
Q
loss of attachment can be
A
continuous or periodic
14
Q
general rate of loss of attachment
A
- 05-0.1mm/year
- greatly variable among patients
15
Q
the biofilm
A
one or more communities of microorganisms embedded in a glycocalyx, attached to a solid surface
16
Q
glycocalyx
A
glycoprotein and glycolipid covering surrounding the cell membranes of bacteria
17
Q
properties of the biofilm
A
- provides protection for colonising species against environmental pressures and competition
- facilitates the uptake of nutrients and expulsion of metabolic waste (plaque acid)
- develops a physiochemical environment to favour bad bacteria (lowers pH and O2 concentration)
- allows communication between bacteria
18
Q
bacterial virulence
A
the ability to colonise and compete in an ecological niche and to evade host defences to survive
19
Q
ways bacteria evade the host immune system
A
- degrade host immunoglobulin and complement
- leucotoxin production
- tissue invasion
- inhibition of antibody synthesis
20
Q
how are oral bacteria equipped to cause periodontal disease
A
- they easily break down antibodies and cytokines
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
22
Q
what is red complex bacteria
A
- ## identified bacteria highly associated with the presence of periodontal disease
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
24
Q
the theory behind the causation of PDD
A
- 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
25
mechanisms of the host immune response in the oral cavity
1. saliva
2. epithelium
3. GCF
4. inflammatory and immune cells
26
describe the host immune response to bacterial plaque in periodontitis
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
27
protective functions of the antibody
1. inhibition of adhesion and invasion
2. complement activation
3. neutralisation of toxins
4. opsonisation and phagocytosis
28
matrix mellatoproteinases
- family of zinc and calcium dependent proteolytic enzymes
| - break down connective tissue causing tissue destruction
29
3 patterns of bone loss in periodontal disease
1. horizontal
2. vertical
3. furcation
30
measuring bone loss in PDD
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
31
horizontal bone loss
- 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
32
vertical/angular bone loss
- 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
33
reasons for different patterns of bone loss
1. initial shape and thickness of bone
- destruction begins from the most apical point in the plaque
- depends on the thickness of the bone
34
general risk factors for periodontal disease
1. smoking
2. diabetes
3. stress
4. drugs
5. systemic disease
6. nutrition
35
anatomical risk factors of periodontal disease
- enamel pearls and projections
- grooves
- furcations
- gingival recession
36
tooth position risk in PDD
- malalignment creating difficult to clean areas
- crowding
- tipping of teeth
- migration
37
iatrogenic risk factors of PDD
- restorative margins and overhangs
- defective crown margins
- poorly designed partial dentures
- orthodontic appliances
38
normal physiological response to infection or injury of the gingiva
gingivitis
39
pathological inflammatory response associated with tissue destruction
periodontitis
40
early colonisers
commensal aerobes
41
late colonisers
gram negative anaerobes
42
colonisation
microbial presence on a body surface without clinical signs of inflammation or disease
- usually commensal organisms
43
infection
microbial invasion of host tissues causing a reaction
44
asaccharolytic
bacteria metabolism which doesnt break down carbohydrates but proteins and peptides instead
45
gingipains
- proteases produces by P.gingivalis which
1. degrade host enzymes
2. activate MMP's
46
virulence factors of P.Gingivals
1. asaccharolytic
2. gingipains
3. atypical LPS
4. inflammophillic
47
inflammophilic
thrive in inflammatory conditions
48
red complex bacteria
1. porphyromonas gingivalis
2. tannerella forsythia
3. treponema denticola
49
why can lesser pathogens (orange complex) cause PDD
- some factors produced by the bacteria reduce host inflammatory response
- therefore they cause the disease easier
50
contents of saliva which protect the teeth
1. S-IgA
2. lysozyme
3. peroxidase
4. lactoferrin
5. mucins
6. cystatins
7. histamines
51
immune defences in the GCF
1. AMPs
2. cytokines
3. chemokines
4. lactoferrin
5. IgG
52
pathogenesis in the development of periodontal disease
- 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
disease state of gingivitis
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
factors that may cause the symbiosis of the oral microbiome
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
hallmark clinical signs of periodontitis
1. increased pocket depth
2. apical migration of junctional epithelium
3. loss of attachment
56
problems with a lack of neutrophils
- 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
problems with too many neutrophils
- main source of tissue MMPs
- can increase the tissue breakdown associated with chronic inflammation
- leads to excessive bone and attachment loss
58
adaptive immune system in periodontal destruction
- 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
process of alveolar bone loss
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
chronic periodontitis
- destruction of junctional epithelium and connective tissue attachment
- bone destruction and pocket formation
- progressive disease which affects the amount of bone loss
61
aggressive periodontitis
- 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
necrotising ulcerative gingivitis
- NUG
- painful ulceration of the tips of the interdental papillae
necrotic tissue is visible
- associated halitosis
63
necrotising ulcerative periodontitis
- same as NUG but with the presence of connective tissue attachment and bone loss
64
periodontal abscess
- infection in a periodontal pocket
| - can be acute or chronic
65
gingival enlargement
- thickingin of the gingiva
- can occur in response to irritation by;
1. plaque or calcuclus
2. friction or trauma
3. fluctuations in hormones
66
smoking and periodontal disease
- no bleeding on probing as the vessels are constricted by the nicotine
- impaired wound healing
- production of inflammation mediating cytokines
67
drugs which can increase periodontal disease risk
calcium channel blockers
68
actions to take when a patient scores BPE3 or above
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
other terms for non-surgical management of PDD
1. cause related therapy
| 2. hygiene phase therapy
70
aims of non-surgical management of PDD
- arrest the disease process
- regenerate lost tissues
- maintain periodontal health in the long term
- to preserve a functional dentition for life
71
stages in the treatment plan
1. emergency care
2. disease control
3. re-evaluation
4. reconstruction
5. supportive care
72
disease control
1. extract hopeless teeth
2. hygiene phase therapy
3. caries management
4. endodontic therapy
5. provisional prosthesis
73
periodontal therapy in the clinic
1. supra and sub gingival plaque control
2. root surface debridement
3. removal of plaque retentive factors
74
periodontal therapy at home
1. demonstration of how to use oral hygiene aids
2. tooth brushing advice
3. toothpaste recommendations
75
things assessed to determine level of dental health education
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
scaling
the removal of plaque and calculus from the tooth surface
77
root surface debridement
- the actor removing dead, contaminated or adherent tissue or foreign material from the root surface
- instrumentation encompasses scaling and root planing
78
root planing
the removal of contaminated cementum, leaving the tooth root surface hard and smooth
79
scaling instruments
```
hand instruments (manual) and sonic and ultrasonic instruments
- rotating and reciprocating instruments
```
80
advantages of hand instruments
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
advantages of powered instruments
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
assessing treatment
1. inflammation levels
2. bleeding on probing indices
3. reduction in probing depth
4. gain in attachment level
83
probing depth indicates
indicates the difficulty of the treatment and the likelihood of recurrence
84
attachment levels indicate
a measure of the tissue destruction pre treatment and the extent of repair post treatment
85
things which can influence manual probing depths
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
effects of supra gingival plaque control alone
- 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
effects of RSD without supra gingival scaling
- initial reduction in pocket depth and inflammation
- pockets re-colonised by supra gingival plaque species
- disease recurrence
88
effects of RSD combines with supra gingival scaling
- decreased gingival inflammation
- reduction in pocket depth
- gain in probing attachment levels
- marked changes in the sub gingival microflora
89
healing time after PDD treatment
- greatest changes observed in 4-6 weeks after treatment
| - gradual repair and maturation of the tissues over the next 6-12 months
90
full mouth disinfection
- aims to prevent treated pockets becoming recolonised by bacteria
- use of chlorohexidine mouth wash for sub gingival irrigation
- tongue brushing
- mouth rinsing
91
effects of RSD
- reduces microbial challenge
- decreases inflammation
- inoculation with plaque organisms can boost the immune response
92
re-evalutaion should look at
1. patient plaque control
2. bleeding on probing
3. residual probing depth and attachment levels
93
what suggests success of non surgical PDD therapy
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
why does periodontal treatment fail
- poor compliance
- inadequate debridement
- host factors *mainly smoking*
95
limitations to non-surgical therapy
- root morphology preventing clearing
- furcation involvement
- deep pockets
- skill level
- time
96
supportive care
- 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
what can be assessed in a 6PPC
1. probing depth
2. bleeding on probing
3. gingival margin height
4. loss of attachment
5. mobility
6. furcation involvement
98
what is the minimum requirement of a 6PPC
to record all sites greater than or equal to 4mm or more probing depth and bleeding on probing
99
what is probing depth a measure of
the base of the gingival crevice to the gingival margin
100
what is recession measure from
the gingival margin to the cej
101
how is loss of attachment a measured
probing depth + recession
102
is the value for gingival margin + or - in a 6PPC if it goes above the CEJ
-
103
is the value for gingival margin + or - in a 6PPC if it goes below the CEJ
positive
104
how should the PCP probe be inserted to measure accurately
parallel to the long axis of the tooth while maintaining contact with the end of the probe to the tooth
105
how many sites around the teeth are recorded on 6PPC
6 points
| 3 buccal 3 palatal
106
grade 1 furcation involvement
initial involvement
- furcation can be felt on probing
- there is less than one third of the tooth width involved
107
grade 2 of furcation involvement
partial furcation involvement
| - loss of support exceeds one third of the tooth width but does not include the total width of the furcation
108
grade 3 furcation
through and through involvement
| - the probe can pass through the entire furcation
109
grading tooth mobility
0-3
110
grade 0 tooth mobility
physiological mobility at crown level
| - tooth os only moved 0.1-0.2mm in the horizontal direction
111
grade 1 tooth mobility
increased mobility of the crown of the tooth at most 1mm in horizontal direction
112
grade 2 tooth mobility
visually increased mobility of the crown exceeding 1mm in a horizontal direction
113
grade 3 tooth mobility
severe mobility of the crown of the tooth in both horizontal and vertical direction impinging on the function of the tooth
BDS2 Periodontology
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