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BDS2 OSCE > Perio > Flashcards

Perio Flashcards

1
Q

what are the hand instruments for supragingival scaling?

A

sickle scalers - mini sickle (red) and H6-H7 (grey or yellow)
universal curette (purple)
go back to images in word doc

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2
Q

design of the universal curette

A

working end is perpendicular to the lower shank
2 cutting edges
rounded toe

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3
Q

design of the sickle scalers

A

triangular cross section
face is perpendicular to lower shank
2 cutting edges
pointed sharp tip

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4
Q

how to use sickle scalers to remove calculus

A

place tip third of cutting edge against tooth
tilt towards tooth to achieve 70-80 degree angle between tooth and blade
apply lateral pressure to engage cutting edge
activate scale by using vertical, diagonal or horizontal pull strokes
use short 2-3mm strokes to maintain control
mainly for anteriors

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5
Q

how to use universal curette to remove calculus

A

place a cutting edge against tooth surface
tilt towards tooth for 70-80 degree angle
apply lateral pressure
use vertical diagonal or horizontal pull strokes
mainly for posteriors but can be used for all - blunter

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6
Q

main techniques used for hand scaling?

A

modified pen grip
finger rest!

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7
Q

why is a finger rest used?

A

on same arch, to maintain control of the instrument
not on soft tissues = unstable
close to the tooth instrumenting on

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8
Q

what is periodontitis?

A

an imbalance between oral bacteria and host response, leading to a loss of alveolar bone

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9
Q

what is BPE?

A

clinical screening method to identify periodontitis.

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10
Q

how do you perform a BPE?

A
  1. divide mouth into sextants 7654|321123|4567
  2. introduce probe along the long axis of the tooth. starting on the most distobuccal surface in sextant 1
  3. ‘walk’ probe around entire gingival margins of each tooth
  4. repeat on palatal side after whole sextant done
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11
Q

what is the BPE probe?

A

the WHO probe
mainly use the C-type

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12
Q

dimensions of the C type WHO probe

A

0.5mm diameter ball
first black band has a 2mm width
second black band has a 3mm width

0-0.5 (B),0.5-3.5,3.5-5.5 (B),5.5-8.5,8.5-11.5 (B)

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13
Q

probing force of C type WHO probe

A

20-25g
enough to blanch a fingernail

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14
Q

what is periodontitis in BPE?

A

whole probe fitting means the pocket has periodontitis. above 5.5mm

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15
Q

what length is the gingival crevice?

A

3.5-5.5mm (black band)

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16
Q

how do you record a BPE?

A

worst code in a sextant is recorded in a grid

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17
Q

are 3rd molars/wisdom teeth included in a BPE?

A

no

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18
Q

can * be used with other codes?

A

yes

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19
Q

what happens if all teeth are missing in a sextant?

A

that sextant scores an X

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20
Q

what happens if only one tooth is present in a sextant?

A

that tooth is probed but the score is included in the adjacent sextant. the sextant with the single tooth then gets an X

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21
Q

describe a code 0 BPE

A

1st black band visible
no BOP
no tooth surface roughness/calculus
periodontal health = no treatment required

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22
Q

describe a code 1 BPE

A

1st black band visible
BOP
no tooth surface roughness/calculus
required treatment - OHI instructions

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23
Q

describe a code 2 BPE

A

1st black band visible
plaque retentive factor present, e.g., calculus or poorly contoured restorations
possible BOP
required treatment: OHI and removal of PRF, e.g., debridement or improvement of restorations

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24
Q

describe a code 3 BPE

A

1st band partially obscured (exceeds 3.5mm)
possible PRFs
possible BOP
required treatment = OHI, removal of any PRFs, possible root surface debridement
treatment to shrink the pocket

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25
Q

describe a code 4 BPE

A

1 band completely obscured (exceeding 5.5mm)
possible PRFs
possible BOP
required treatment: complex periodontal treatment including OHI, PRF removal, DPC, RSD

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26
Q

what is a code *?

A

furcation detected on probing

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27
Q

what is a furcation?

A

where the roots separate on multirooted teeth
bifurcation on lower molars and trifurcation on upper molars

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28
Q

what is the prognosis of furcated teeth?

A

more difficult to keep clean, so longevity of tooth is usually reduced

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29
Q

what does BPE provide us with?

A

not a diagnosis! guidance on next diagnostic and treatment steps. not a treatment plan.

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30
Q

what does reproducibility of BPE depend on?

A

probing pressure
probe thickness
probe angle at gingival margin
presence of subgingival obstacles e.g., calculus
operator skill
patient variables

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31
Q

what teeth are examined in paeds BPE?

A

examine all the 6’s, UR1, LL1 (index teeth)

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32
Q

what codes are recorded for paeds BPE?

A

patients ages 7-11 = BPE codes 0-2
patients aged 12-17 = all BPE codes

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33
Q

what is bleeding an indicator of?

A

bleeding is always an indicator of inflammation

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34
Q

what do you get from using a clinical index?

A

grading the severity of a clinical parameter semi-quantitatively by allocating a numerica; value within a scale of values

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35
Q

describe the gingival index (appearance, bleeding and inflammation)

A

0 - normal appearance, no bleeding or inflammation
1 - slight change in colour and texture (stippling lost), no bleeding, mild inflammation
2 - moderate glazing, redness, oedema and hypertrophy, bleeding on probing, moderate inflammation
3 - marked redness, oedema, ulceration and hypertrophy, spontaneous bleeding, severe inflammation

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36
Q

what does disclosing dye show?

A

highlights plaque
pink is newer black, blue is older plaque (about weeks old)
thus purple, in between is days old

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37
Q

what is the crown height?

A

measured from gingival margin to incisal edge

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38
Q

what, apart from plaque, does plaque dye stain and what must we therefore consider?

A

it also stains proteins
must protect lips since these are rich in glycoproteins so will easily stain

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39
Q

what do the plaque index numbers mean?

A

0 = no plaque
1 = separate flecks of plaque at cervical margins of tooth
2 = a thin continuous band of plaque upto 1mm at the cervical margin
3 = plaque covering > 1mm but < 1/3rd of the crown
4 = plaque covering 1/3rd-2/3rd of the crown
5 = plaque covering >2/3rd of the crown

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40
Q

what is the thin purple line along the gingival margin that comes with disclosing dye?

A

not plaque but tissue protein

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41
Q

why do we use indices?

A

good method of screening
quick to perform
provide a measure of progress longitudinally
medico-legal reasons: progress monitoring is mandatory
useful marker of patient motivation

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42
Q

what are the problems with indices?

A

subjective measurements
can show poor reproducibility
does not directly relate to disease - indirect measurement of plaque
unable to predict future disease
does not take into account quantity of plaque only surface area coverage etc

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43
Q

what do clinical scores show?

A

assignment of a value e.g., % that indicates the presence or absence of a clinical parameter

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44
Q

commonly used clinical scores?

A

plaque score, bleeding score, bleeding on probing

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45
Q

how are plaque and bleeding score represented?

A

number of surfaces (with plaque or bleeding)/total number of surfaces * 100
recorded on chart

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46
Q

what is bleeding on probing an indicator of?

A

bleeding from the base of the pocket is the best indicator of active disease

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47
Q

what shows BOP having poor sensitivity?

A

10-20% of sites than bleed have active inflammation = poor sensitivity

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48
Q

what shows BOP having good specificity?

A

absence of BOP almost 100% indicative of health = good specificity

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49
Q

what is GCF?

A

gingival crevicular fluid

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50
Q

what does GCF originate as>

A

a transudate/exudate of serum
transudate when in health, exudate when in disease

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51
Q

what does GCF carry?

A

markers of gingival/periodontal health

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52
Q

name some GCF biomarkers

A

proteins, peptides, lipids, enzymes, antibodies

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53
Q

what enzyme is carried in GCF which we investigated in the plaque project?

A

alkaline phosphatase

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54
Q

when plaque/calculus forms, neutrophils migrate. why does this occur?

A

to defend the soft tissue/tooth interface against microbes, since there is an interruption of the mucosal integrity and therefore a potential entry portal into the body

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55
Q

what can poor oral hygiene cause?

A

inflammation, halitosis, teeth coated with plaque and deposits, tongue coated and discoloured, bleeding gums, caries (with time and sugar), calculus build up, pocketing

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56
Q

what does a bacterial biofilm full of microbes cause?

A

an immune-inflammatory response

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57
Q

difference between TP and vision brushes

A

TP = short in length, flexible, not ideal for PD
vision = precurved brushes, bend allowing you to clean further down into the gingival crevice and pocket areas

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58
Q

purpose of vision brushes

A

aiming to clean into the pocket to remove the bacterial film off the root surface where it is causing the disease

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59
Q

what is a cross-sectional study?

A

a type of observational study that analyses data collected from a population, or a representative subset, at a specific point in time
one time point so doesnt demonstrate causation, but association between variables

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60
Q

what is a longitudinal study?

A

follows patients over a continued period of time

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61
Q

what is detected in higher levels in GCF during the active phases of periodontitis?

A

bacteria and enzymes, bacterial degradation products, connective tissue degradation products, host-mediated enzymes, inflammatory mediators, ECM proteins

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62
Q

what does GCF collection give an indication of?

A

the host response

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63
Q

what is the relevance of alkaline phosphatase?

A

glycoprotein and membrane bound enzyme
hydrolyses monophosphate ester bonds at alkaline pH’s thus increasing local concentrations of phosphate ions
part of the normal turnover of PDL root cementum formation, maintenance and bone homeostasis

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64
Q

is there more alkaline phosphatase in active periodontal disease?

A

yes

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65
Q

why does the immune response kick in early to protect the teeth?

A

bacteria build up on teeth and form biofilm accumulation

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66
Q

why is the interaction between bacteria and the host dynamic?

A

bacteria build up on teeth to cause the immune response but products of immune response will also feed the bacteria

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67
Q

how do bacteria on teeth vary?

A

vary in bacterial load, species present in biofilm, virulence factors

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68
Q

why does bacteria build up on teeth?

A

because they are non-shedding surfaces

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69
Q

what is a commensal organism?

A

a non-disease causing organism, normally resident flora in a particular environment

70
Q

what is an opportunist pathogen?

A

a commensal organism which, under certain circumstances, may cause disease

71
Q

what are the healthy coloured complexes from socransky et al?

A

yellow (mainly strep), green, purple

72
Q

what is the gingivitis indicative coloured complex?

A

orange

73
Q

what bacteria is present in the orange complex?

A

fusobacterium

74
Q

what are the bacteria in the red complex indicative of severe periodontitis?

A

P. gingivalis, T forsythia, T denticola

75
Q

what is the ecological plaque hypothesis?

A

not about amount or specific bacteria present. about the environment the bacteria are living in and how that drives change within the biofilm, suggesting a complex interdependency between multiple factors

76
Q

how is biofilm formed?

A

acquired pellicle is formed on tooth surface. streptococci start to build up through initial adhesion factors. other bacteria stick to streptococci with a more complex structure. production of various food webs, maturation. dispersion, forming a new biofilm.

77
Q

what makes biofilms dangerous?

A

they are resistance to removal and clearance like surfactants, antibiotics and phagocytosis, protecting the bacteria.
they can transfer genetic material between them, e.g., causing AMR

78
Q

how do you get rid of biofilms?

A

physical removal/disruption by scaling and prophylaxis

79
Q

what are the steps to a bacteria becoming pathogenic?

A

acquisition - host must become infected with the organism
adherence - ability of bacteria to stick to a non-shedding surface
colonisation - organism must acquire nutrients and survive
multiplication - must be able to reproduce itself
avoid elimination - evasion of host defences
virulence factorss - interference with immune response and enzymes etc
invasion of host tisssues

80
Q

what are kochs postulates?

A

in order to implicate a microorganism with disease:
the agent must be isolated from every case of disease
must not be recoverable from non-diseased patient of those with a different form of the disease
following isolation and pure culture, pathogen should induce disease in animal models after inoculation

81
Q

what diseases do kochs postulates work and do not work for?

A

works for mono-infections like TB and HIV
not for periodontitis - not a true infection since there are always bacteria on the teeth

82
Q

describe the flora during health

A

gram positive species, streptococci (pioneer species) and facultative actinomyces

83
Q

describe flora during gingivitis

A

shift towards more gram neg flora. appearance of F. nucleatum, motile rods and spirochates

84
Q

describe flora during periodontitis?

A

predominance of gram neg anaerobic rods, motile rods and spriochaetes

85
Q

what are virulence factors?

A

factors elaborated by microorganisms that confer upon them pathogenicity

86
Q

give examples of virulence factors

A

enzymes - might breakdown host cells
metabolic products - toxic to host cells
toxins - exo and endotoxins

87
Q

what are endotoxins made of and where are they released?

A

LPS
released from cell wall of gram negative bacteria when they die

88
Q

what effect do endotoxins have on cells?

A

produce severe inflammation via complement activation.
activate immune response by acting as antigens
toxic to macrophages
bone resorption
cytotoxic to fibroblasts
inhibit connective tissue attachment
stimulate pro-inflammatory cytokine release

89
Q

where are exotoxins formed?

A

released from living bacteria

90
Q

what effects do exotoxins have on cells?

A

can damage host leukocytes

91
Q

are all clonal types of pathogenic species equally virulent?

A

no, can have virulent and antivirulent strains

92
Q

what is the humoral response?

A

B cell response where antibody travels in liquid (blood, plasma, tissue fluid). antibody does not kill the bug, but macrophages/phagocytes do. not as specific. involves neutrophils

93
Q

what is the cell-mediated response?

A

T-cell response where receptor is carried to the bug by the T cell. This is more specific. When T-cytotoxic cell finds the bug, it’ll kill the bug with perforins.

94
Q

what is a hyper-inflammatory response?

A

produces too much inflammation in response to a particular stimulus. makes people susceptible to periodontitis.

95
Q

why do hyper-inflammatory responses occur?

A

due to elevated inflammatory mediators in tissue and/or blood, despite clinical health

96
Q

what do hyper-inflammatory responses put you at a higher risk of?

A

cardiovascular disease, diabetes, RA, COPD, non-communicable diseases caused by excess inflammation

97
Q

what factors drive a hyper-inflammatory response?

A

genetic exposures
environmental exposures e.g., stress
drug exposures e.g., NSAIDs, corticosteroids
behavioural exposures e.g., exercise diet and nutrition

98
Q

what does a biofilm do to people with clinical health?

A

causes inflammation and then breakdown (because of various enzymes produced by host response) and microulcer formation, resulting in gingivitis, and bleeding from the microulcers

99
Q

what happens with biofilm production in high-risk of hyper-inflammatory response individuals?

A

inflammation is hyper-inflammation, which spreads down to bone rapidly and destroys it

100
Q

what attaches junctional epithelium to enamel of the crown?

A

hemidesmosomes

101
Q

where do blood vessels lie around teeth and what do they carry?

A

lie in the connective tissues
they carry the immune response

102
Q

what fluid passes out of the sulcular and junctional epithelium (permeable)

A

GCF from tissue fluid from blood

103
Q

what is the 1st 2nd and 3rd line defence to bacteria?

A

1st - neutrophils as they pass through epithelium into crevice
2nd - epithelial cells
3rd - various other immune cells e.g., T, B, lymphocytes which are within the connective tissue

104
Q

are neutrophils terminally differentiated cells cells?

A

yes

105
Q

what lineage do neutrophils come from?

A

myeloid lineage. released from bone marrows

106
Q

what is the different between non-oxidative and oxidative phagocytosis?

A

non-oxidative = release enzymes into the phagosome from the lysosomes
oxidative = through the release of oxygen radicals

107
Q

what attracts neutrophils to the infection site?

A

chemotaxis - chemoattractants

108
Q

name some basic functions of neutrophils

A

phagocytosis
cytokine production
degranulation

109
Q

describe the action of neutrophils in the blood

A

infection causes various mediators to be released from tissues which activate the endothelial cells.
neutrophils come and touch and untouch the blood vessel due to speed of blood flow, making and breaking contacts with endothelium which slow them down, and drop out of the midstream of the bloodflow = margination
they move into tissues along the chemotactic gradient

110
Q

what does activate mean?

A

opens up receptors on the inner wall of the blood vessel

111
Q

what makes up the chemotactic gradient?

A

LPS = endotoxic
IL-8 = cytokine
FMLP = product of bacteria
C5a = complement 5 a

112
Q

describe the action of neutrophils when in the tissues

A

they bind to the bacteria and phagocytose them (non-specifically)
if there was an antibody stuck to the bacteria, there is a specific receptor on neutrophil surface which will bind the antibody bound to the bacteria to produce more specific phagocytosis

113
Q

what is the difference in neutrophils taken from perio patients?

A

they are slower

114
Q

describe NADPH oxidase activation of safe killing in neutrophils

A

neutrophil sees bacteria and phagocytoses in. simultaneously the oxygen radicals are generated and pumped into the phagosome to kill the bug. neutrophils have catalase SOD which will convert the radicals into water and oxygen.

115
Q

what would happen if oxygen radicals were released?

A

they would damage the tissues

116
Q

peripheral blood neutrophils in periodontitis patients are hyperactive and hyperreactive. what does this mean for oxygen radicals?

A

more oxygen radicals are produced, so more are released and more tissue damage occurs. particularly when there are bugs!

117
Q

how do neutrophils die to avoid releasing their oxygen radicals?

A

they undergo apoptosis and macrophages will come and remove them

118
Q

what is the role of the epithelial cells of the junctional epithelium?

A

2nd line of defence
physical barrier
rapid turnover (so get rid of bugs)
contains cytokines PGE-2
produces collagenases
produces IL-1, IL-8 and establishes inflammatory response

119
Q

what does PGE-2 do?

A

destroys bone as a side effect

120
Q

what do collagenases do?

A

liquefy the tissues, making it more fluid and helps neutrophils move through tissues

121
Q

where are macrophages derived from?

A

monocytes

122
Q

where are langerhan cells derived from?

A

macrophages become langerhans

123
Q

what is the role of macrophages?

A

engulf bacteria
present MHC-II antigens to lymphocytes
release pro-inflammatory cytokines
produce MMPs (collagenases)
produces leukotrienes (chemokines)

124
Q

what do T and B lymphocytes do?

A

recruit phagocytes, produce more lymphokines, produce antibodies, cytotoxic to bacteria, production of other cytokines

125
Q

role of B cells in adaptive immunity

A

b cell receptor recognition
produce memory cells
antibody producing plasma cells

126
Q

role of T cells in adaptive immunity

A

TCR activation
clears invading pathogens
pro-inflammatory cytokines produced
etc

127
Q

what does IL-1 (cytokine) do?

A

stimulates bone resorption, inhibits bone formation
stimulates PGE-2 synthesis by fibroblasts and monocytes
proliferation of fibroblasts increased and increases collagenase
stimulates other cytokines
causes expression of ICAM-1 receptors on endothelium

128
Q

what does TNF alpha (cytokine) do?

A

increases collagenase production
stimulates PGE-2 synthesis by fibroblasts and monocytes
stimulates production of interleukins
stimulates bone resorption and inhibits bone formation
stimulates other cytokines
causes expression of ICAM-1 receptors on endothelium

129
Q

what do PGE-2 (cytokine) do?

A

increases vascular permeability
inhibits fibroblast proliferation
enhances collagenase production by macrophages
stimulates bone resorption
decreases collagen synthesis
stimulates other cytokines

130
Q

what does LTB-4 (cytokine) do?

A

powerfully chemotactic
stimulates PMNL degranulation
stimulates ROS production

131
Q

why do the gums bleed on probing?

A

because the patient has microulcers and probing causes bleeding

132
Q

what are the effects of PMLs?

A

(if PMNL non-specific response does not eliminate bacteria, further recruitment occurs inflammatory lesion spreads towards ligament and bone)
enzymes released damage host tissues
PGE-2 stimulates collagenase production
ROSs production damages host tissues
ROSs production deactivates important antiproteases
PGE-2 causes recruitment of more inflammatory cells via NFK-B activation

133
Q

effects of epithelial cells

A

(Once epithelial barrier breaks down, microulceration, BOP, and bacterial products can enter connective tissues)
produce PGE-2, IL-1, IL-8, TNF
PGE-2 stimulates collagenase production
other MMPs produced by epithelial cells
PGE-2 causes recruitment of more inflammatory cells via NFK-B activation

134
Q

effects of tissue macrophages

A

(at this stage, the size of the inflammatory lesion starts to lead to ligament and bone loss and gingivitis becomes periodontitis)
LPS binds via LBP to CD14 receptors on PMNLs and macrophages
produces IL-1, TNFalpha and PGE-2
PGE-2 stimulates collagenase production etc
IL-1 stimulates secondary PGE-2 production and second wave of other cytokines
immune response is activated

135
Q

NFK-B inhibition

A

block process with certain antioxidants from diet, so dampens inflammation

136
Q

so why does periodontitis occur?

A

if the immune response becomes unbalanced, you get too many cytokines, oxygen radicals, MMPs produced by immune cells, which destroys connective tissues and bone

137
Q

how does the new classification system differ?

A

loss of ‘chronic’ and ‘aggressive’ - replace with periodontitis
introduction to ‘staging’ and ‘grading’
‘necrotising periodontal diseases’ remains as a distinct category

138
Q

what are the percentage of sites bleeding in code 0,1,2, BPE for health, localised gingivitis and generalised gingivitis (with no evidence of interdental recession)?

A

clinical gingival health <10%
localised gingivitis 10-30% bleeding
generalised gingivitis >30%

139
Q

what does evidence of interdental recession give an indication of?

A

perio disease
majority of buccal recession is toothbrush trauma so look as interdental recession

140
Q

what needs to occur if code 3 BPE if found?

A

with no evidence of interdental recession
radiographic assessment
inttial perio treatment followed by DPC. review after 3 months
if: no pockets >=4mm and no bone loss, go to code 0,1,2 pathway
If: pockets >=4mm and/or periodontal radiographic bone loss, go to code 4 pathway

141
Q

what is the BPE code 4 pathway?

A

(and/or obvious evidence of interdental recession)
radiographic assessment
full periodontal assessment (DPC)

142
Q

results from a full periodontal assessment

A

molar/incisor pattern = periodontitis molar/incisor pattern
<30% of teeth = localised periodontitis
>30% of teeth = generalised periodontitis

143
Q

what is staging?

A

look at the worst tooth and severity of bone loss
radiographic assessment - periapicals of OPT
if not clinically justified, bitewings use CAL or bone loss from CEJ

144
Q

staging stages

A

<15% (or <2mm attachment loss from CEJ) = Stage 1, early/mild disease
coronal third of root = stage 2, moderate disease
mid third of root = stage 3, severe disease
apical third of root = stage 4, very severe disease

145
Q

what is the formula for grading?

A

% bone loss / patients age
(use worst site of periodontal bone loss)

146
Q

what are the numerical values for grading?

A

<0.5 = grade A (slow rate of progression)
0.5-1.0 = grade B (moderate rate of progression)
>1.0 = grade C (rapid rate of progression)

147
Q

stability values

A

stable: BOP <10%, PPD <=4mm, no BOP at 4mm sites
in remission: BOP >=10%, PPD <=4mm, no BOP at 4mm sites
unstable: PPD >=5mm OR PPD >=4mm and BOP

148
Q

what is periodontal health defined by?

A

an absence of clinical detectable inflammation

149
Q

features of periodontal health

A

pg45
attached gingiva, gingival groove, free gingiva
stippling
triangular papilla
muco-gingival junction

150
Q

what should be included in the diagnostic statement for perio?

A
  1. condition (health, gingivitis, periodontitis)
  2. extent (localised/generalised)
  3. severity and rate (stage and grade)
  4. stability (stable, remission, unstable)
  5. risk assessment factors
151
Q

what is included in classifiction of perio?

A

stage and grade
historical disease

152
Q

what is a risk factor?

A

increases probability of a diseases developing in a given individual
affects severity

153
Q

how is risk factor different to causative factor?

A

causative factor is needed to get the disease

154
Q

what are the causative factors of periodontitis?

A

causative factors are host response and bacteria - an imbalance between the 2 = periodontitis

155
Q

local risk factor types

A

patient based or iatrogenic
acquired or developmental
modifiable or non-modifiable

156
Q

what does a risk factor do in periodontits?

A

make bacteria worse or host response worse or both
if it doesnt then it is not a risk factor

157
Q

give examples of local risk factors for periodontitis

A

calculus, bleeding on probing, pocket depth, crowding/tooth position, furcation involvement, bone defects

158
Q

why do smokers gums not bleed?

A

smoking causes vasoconstriction, masking some effects of periodontal disease

159
Q

iatrogenic risk factors

A

overhanging restorations, overhanging crowns

160
Q

what are the periodontal tissues comprised of?

A

gingival tissues
alveolar bone
periodontal ligament
root cementum

161
Q

what is gingivitis?

A

an inflammatory lesion, mediated by host/parasite interactions, that remain localised to the gingival tissues and does not extend to involve the periodontal ligament, cementum or alveolar bone

162
Q

what causes gingivitis?

A

accumulation of microbial plaque
in and around the dento-gingival complex
when removed, resolves inflammatory lesion

163
Q

what is the junctional epithelium permeable to?

A

external (bacterial) material passing into the adjacent connective tissues and bloodstream and to products of internal defence systems (leucocytes, antibodies, proinflammatory cytokines)

164
Q

what is the difference between GCF in health and in disease?

A

health - GCF is a serum transudate containing components of serum and PMNL cells
disease - exudate, containing products of host/parasite conflict

165
Q

what does a clinically healthy periodontium look like?

A

pink, stippled, triangular interdental papilla, firm in consistency, knife-edge gingival margin, probing depths <2mm, no bleeding to probe, no recession, no mobility

166
Q

what factors are used to asses gingival health/disease?

A

gingival colour, gingival contour, BoP, mobility, levels of plaque, calculus, plaque retention factors, long cone periapical radiographs

167
Q

clinical signs of gingivitis

A

erythema (redness due to increased blood flow during inflammation)
oedema (fluid swelling due to blood vessels becoming leaky)
pitting on pressure
loss of contour and stippling (rounding)
false pocketing (due to swelling)
BoP
Bad taste
Halitosis

168
Q

clinical features of periodontitis

A

features of gingivitis
increase in probing pocket depth (due to apical migration of the JE and loss of underlying CT and bone)
increased tooth mobility due to loss of periodontal support
gingival recession (exposed root can become sensitive)
suppuration (pus formation)
drifting of teeth due to loss of underlying bone and forces from tongue and lips

169
Q

what is the mucogingival junction?

A

point at which keratinised gingival tissues meet the non-keratinised oral epithelium

170
Q

what is the probing attachment level?

A

distance from CEJ to base of pocket = amount of PDL lost due to disease

171
Q

what is recession?

A

distance from gingival margin to CEJ
attachment loss = pocket depth + recession
any gingival tissue positioned coronally to CEJ counts as negative recession value

BDS2 OSCE (15 decks)

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