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1st year > plaque related diseases - perio > Flashcards

plaque related diseases - perio Flashcards

1
Q

how do metal ions control plaque?

A

zinc, copper, tin, plaque inhibitory
copper and tin cause intrinsic staining
zinc retained by plaque and inhibits growth

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2
Q

what is new attachment?

A

union of CT with previously pathogenically altered root surface

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3
Q

describe the initial lesion?

A 
24-48 hours after plaque accumulation
gm +ve bacteria, aerobic, saccharolytic
vasodilation, increased omns, gcf
minimal tissue damage
immune response provoked
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4
Q

what is mild perio?
mod
severe

A

1-2mm bone loss
3-4mm bone loss
>5mm bone loss

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5
Q

where does gingival attachment happen in health?

A

begins coronal to the ACJ

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6
Q

what are some oral features of downs syndrome?

A 
prone to destructive perio disease
class III occ
ant open bite
lack of lip seal
large tongue
infection prone
w
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7
Q

what are types of periodontitis as a manifestation of systemic disease?

A

haematological
genetic
NOS

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8
Q

what is the tx of a grade 3 furcation?

A

tunnel prep
root resection
XLA

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9
Q

describe the oral epithelium?

A

stratified squamous epithelium
90% keratinocytes
10% - non k cells - langerhans, melanocytes, lymphocuyes, merkel cells

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10
Q

how do you monitor recession?

A

LOA/ppf charts
photographs
study models

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11
Q

enzymes can be used for what control?

A

supragingival plaque control
can interfere with bacterial attachment
host defences can inhibit bacteria

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12
Q

what is the aim of NS therapy?

A

render roots biologically compatible with ST by eliminating calculus/altered cementum and reducing pathogenic microorganisms

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13
Q

what slow release gels are available to use?

A

dentomycin gel

elyzol gel

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14
Q

what do calcium channel blockers do to the gums?

A

nifedipine, gingival hyperplasia in 30% of cases

amlodipine

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15
Q

what are some clinical signs of healing?

A 
reduced redness and swelling
reduced BOP
healing of ulceration
pinker and firmer gums
shrinkage
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16
Q

for regeneration to occur in perio what is needed?

A

epithelium and CT must be excluded from wound space and not allowed to proliferate and
adequate RSD
repopulation by progenitor cells to form a PDL

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17
Q

what are gingival fibres?

A

circular
dentogingival
dentoperiosteal
alveolgingival

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18
Q

what are NUG risks?

A

poor oh
smoking - vasoconstricts - anaerobic
stress
immunodefiency

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19
Q

what is a furcationplasty?

A 
reflection of flap
removal of deposit and ST from furcation
widen furcation
replace flap 
- can lead to RSC, danger to pulp, hypersensitivity
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20
Q

what happens initially after RSD?

A

initial acute inflammation 24-48 hours after

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21
Q

what are the types of chronic periodontitis?

A

localised

generalised

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22
Q

what is triclosan?

A

non ionic antiseptic
mod inhibition with zinc
anti inflammatory

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23
Q

what fungal infections present orally?

A

gen ging candidosis
linear g erythema
histoplasmosis

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24
Q

what does RSD remove?

A

endotoxins
plaque biofilm
subg calc
outtermost nectrotic cementum

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25
Q

how do immunosuppressants affect the gums?

A

reduced inflammatory response = gngivitis appearance may reduce

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26
Q

what is the junctional epithelium?

A

epithelial attachment to tooth

hemi desomosones anchor basal keratinocytes to basement membrane

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27
Q

what theory expains disease progression?

A

socransky burst theory

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28
Q

what is GTR?

A 
allows bone tissue to regenerate in bony defects 
nonresorbable/bioresorbable membrane
- flap resected
- RSD 
- membrane over defect
- sutured in place for 6 weeks
= new attachment
= 3-6mm gain in attachment levels
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29
Q

what are two types of antimicrobials?

what may they cause?

A

antibiotics and antiseptics

sensitivity, resistance, super infections

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30
Q

when would antiseptic MW’s be used?

A

replace toothbrush when not poss

adjunct to normal mechanical cleaning

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31
Q

what is a tunnel prep?

A

exposes entire furcation - only for mandibular
RSD
inter radicular removed

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32
Q

what is a pregnancy epulis?

A

soft pedunculated granuloma from inflammed papilla
deep red and bleeds easy
anteriors and 3rd month of pregnancy common
plaque and one of - cavity, poor contact, overhang

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33
Q

what happens if NUG is not treated?

A

acute for 2-3 weeks, heals as chronic gingivitis

reoccurs with further ID papillae loss

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34
Q

what bacteria are present in NUG?

A

treponema vincentii
fusobacterium
prevotella

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35
Q

how do you prevent sensitivity?

A
  • occlude dentinal tubules - topical - potassium ions e.g sensodyne, potassium oxalate precipirates calcium oxalate crystals
  • by insulative restoration
  • devitalise tooth - rct
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36
Q

what is perio chip?

A

adjunct for pockets not responding to tx
2.5mg chx in gelatin and water
biodegradable
bisphasic release over 7 days - initially 40% released, 60% released over 7 days

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37
Q

pockets of 4-6mm should see what after RSD?

A

reduced ppd of 0.5mm. 1mm attachment gain

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38
Q

how does cyclosporin affect the gums?

A

hyperplasia in 30% of cases
increased change in women and children
change to tacrimolus

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39
Q

what are the types of plaque induced gingival diseases?

A
  • systemic factors - pregnancy/diabetes
  • medication - hyperplasia
  • malnutrition
  • plaque only
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40
Q

how is perio chip used?

A

placed into pocket after RSD/haemorhage arrest
chip swells and contact with moisture and is retained
eliminates pathogenic bacteria >100days
use 3/12

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41
Q

what are the type of aggressive periodontitis?

A

ocalised

generalised

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42
Q

what does the OCP do to the gums?

A

increased gcf/inflammation

only exacerbates a pre existing condition

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43
Q

what are quaternary ammonium compounds?

A

cetly pyridium chloride

mod plaque inhibitory

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44
Q

what is dentomycin gel?

A

semi synthetic tetracyline
2& minocycline
ppd >5mm
2-3 times with 2 weeks inbetween

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45
Q

in health what is the volume of gcf?

A

low volume

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46
Q

what is NUG caused by?

A

anaerobic fusospirochaetal complex
treponema vincentii
fusobacterium nucleatum
p intermedia

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47
Q

signs of PHgingivostomatits?

A

acuute stomatitis
ulcers
gen malaise

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48
Q

what bacteria are present in:
localised aggressive perio?
generalised aggressive perio?

A

A.a

p.gingivalis

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49
Q

what is hereditary gingival fibromatosis?

A

autosmal dominant - secondary dentition
excess collagen - hyperplastic gingivae localised/generalised
gingivae can delay eruption of the teeth

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50
Q

what are phenolics?

A

listerine

poor oral retention

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51
Q

what does vasoconstriction cause in the mouth?

A

decreased serum IgG levels
decreased T helper cells
imapired mobility and chemotaxis of pmns

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52
Q

what happens if epithelium enters the wound space? how can it be fixed?

A

fast proliferation and blocks fibroblast attachment
- bone graft
conditioning root surface
membranes - GTR

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53
Q

how do NSAIDs affect the gums?

A

inhibit synthesis and release of PG = reduced bleeding and swelling
cant use in tx = GI effects and asthmatics

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54
Q

what do you use to vitality test?

A

ethyl chloride

electric pulp tester

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55
Q

what is the conditions of the perio pocket of a smoker?

A

more anaerobic

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56
Q

what is shrinkage?

A

happens due to factitious injury/perio tx

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57
Q

what are the divisions of risk factors for perio?

A

local

systemic

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58
Q

what is seal/protect?

A

fluoride and triclosan
mechanical blockage of tubules on root surface
resin or light cured

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59
Q

what do snuff, chewing tobacco and betel nut all cause?

A

carcinoma and oral leukoplakia where tobacco is placed

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60
Q

what is GTR?

A

mechanical barrier eliminates ep wound space and repopulated by cells from the PDL and bone - good for bony defects and furcations

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61
Q

what is chronic granulomatous disease?

A

defect in cell killing ability of phagocytes

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62
Q

what is NaF used in?

A

duraphat - encourages secondary dentine - more resistant to decalcification

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63
Q

what is the actions of nicotine?

A
  • lipid sol - enters blood and passes through blood brain barrier
  • vasoconstrictor = reduced blood flow = ischameic tissue and impaired healing
  • increases platelet adhesiveness and thrombosis risk
  • reduced proliferation of RBC/fibroblast/macrophages
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64
Q

what is recession?

A

inflammation free condition characterised by apical retreat of the periodontium and ID papillae remain at normal level

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65
Q

what is the composition of dentine?

A

70% inorganic HA
20% organic - collagen
10% water
and processes of odontoblasts - lying at periphery of pulp and extends into ADJ

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66
Q

what is tertiary/reparative dentine?

A

dentine and a noxious stimulus - NCTSL/caries

odontoblasts lay down more dentine

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67
Q

what is stontium chloride/potassium chloride?

A

strontium ions = strong affinity for calcified tissues/obliterates tubules
sensodyne - 10% StCl , 3.75% KCl

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68
Q

what affect does pregnancy have on the gums?

A

exacerbation of any pre exisiting plaque induced inflammation

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69
Q

what are the colours and bacteria present in each bacteria complex?

A

purple - gm +ve, aerobic, non motile - actinomyces
yellow - strep
green - actinobacillus
orange - fusobacterium, prevotella
red - gm -ve, motile, anaerobic - p gingivalis, treponema

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70
Q

where is nicotine stored in the mouth?

A

stored and released by perio fibroblasts

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71
Q

what is a furcation?

A

horizontal loss of support in areas where roots multi rooted teeth converge

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72
Q

describe the established lesion?

A

CT = all inflammatory exudate
JE = ulcertaed and deeper crevice = true pocket
increased pmns, ig, complement
bac = damage/indirect

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73
Q

what are the blood vessels in the PDL?

A

apical
gingival
perforating

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74
Q

what is shrinkage?

A

orientation of healthy gingival collagen fibres and long junctional epithelium formation

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75
Q

what are some perio risk factors?

A 
uncontrolled diabetes
smoking
poor oh
genetic predisposition
immunodeficiency
virulent bacteria in flora
local factors
alcohol
stress
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76
Q

how do the cells of the JE sit?
what is the JE turnover?
how do cells turnover?
why is it readily permeable?

A

sit parallel to tooth
4-11 day cell turnover
cell div throughout JE and shed into sulcus
no MCG’s and large intercellular spaces

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77
Q

what are oxytalin fibres?

A

elastic and insert into cementum
run oblique and parallel to root surface
maintain potency of blood vessels

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78
Q

what is lichen planus?

A

inflammatory disease of skin/mucous membranes with oral lesions and skin lesions
reticulated form of interlacing white network
erosive - can occur on gingivae most common cause of desquamative gingivitis

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79
Q

why does reduced ppd happen?

A

shrinkage of g tissues, long JE, shrinkage

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80
Q

what is neutropenia?

A

oral ulceration
severe gingivitis and profuse bleeding
rapid perio bone loss

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81
Q

describe oral sulcular epithelium?

A

lines sulcus

non k

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82
Q

what is periostat?

A

subantimicrobial dose doxycycline

collagenase inhibitor

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83
Q

new attachment involves formation of…?

A

long junctional epithelium and gradual closure of the pocket

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84
Q

when diagnosing perio consider what?

A 
severity/extent of disease
severity and pattern of pockets/loa
pts age at onset of disease
signs and symptoms
local irritants
85
Q

what are causes of recession?

A 
fenestration - window in bone
dehisence - complete lack of bone
chronic minor trauma and inflammation
frenum pull
ortho tx
excessive scaling
parafunction
86
Q

what type of bone makes up the tooth socket/lamina dura?

A

bundle bone

87
Q

what are mucotaneous disorders that present in the mouth?

A 
lichen planus
pemphigus vulgaris
lupus erythematous
pemphigoid
erythema multiforme
88
Q

highly susceptible pts have bursts of what type of attachment loss?

A

rapid

89
Q

what does an inflammed pulp cause to the sensitivity?

A

increased sensitivity

90
Q

how do bisbiguanide antiseptics work?

A

broad spec of killing

damage to cell wall

91
Q

what are types of developmental or acquired deformitites and conditions?

A

local factors
mucogingival deformities and conditions around the tooth or edentulous ridge
occlusal trauma

92
Q

oral signs of crohns?

A 
apthous ulcers
cobblestone mucosa
mucosal tag
gingivae are diffuse erythematous enlargement of  attached gingivae
severe periodontitis possible
93
Q

what problems can recession cause?

A

sensitivity
root surface caries
TB abrasion

94
Q

what is leukaemia?

A 
oral ulceration
petechiae
gingival enlargement - infiltration of leukaemia cells
gingival bleeding
infection susceptibility
95
Q

what are types of abscesses of the periodontium?

A

gingival
periodontal
periocoronal

96
Q

what are the types of antibiotics?

A
  1. bacteriocidal - kills bac - penicillin/metronidazole

2. bacteriostatic - inhibits multiplication

97
Q

what is NUG tx?

A

OHI
gentle fm USS
systemic symptoms - metronidazole 200mg 3 days
rev 48hours

98
Q

what antiepileptics can cause gingival problems?

A 
phenytoin
causes gingival hyperplasia in 50% of cases, interferes with fibroblast activity, improved OH = reduced hyperplasia
side effects start at 3 months
worse at anteriors and begins ID
related to serum conc of blood
99
Q

how is alveolar bone resorbed?

A

immune response - cytokines, igs and leukotrienes

100
Q

what are the principle fibres of the PDL?

A 
attachment of cementum to bone
oblique fibres
alveolar crest
horizontal fibres
apical fibres
inter radicular
101
Q

what is the treatment of aggressive perio?

A

tetracycline, RSD

102
Q

what affect does puberty have on the gums?

A

increased prevalence and severity of gingivitis

increased host response to plaque

103
Q

what are local perio risk factors?

A

anatomical
iatrogenic
trauma from occlusion

104
Q

what are mucopolysaccharide disorders?

A

disturbance of mucopolysaccharide metabolism - hurlers/hunters
wide spread, small teeth, delayed eruption with or without gingival enlargement

105
Q

what is perio disease commonly treated with?

A

tetracycline

metronidazole

106
Q

what bacteria are present in gingivitis?

A

fusobacterium

porphyromonas

107
Q

why do smokes exhibit less inflammation than younger smokers?

A

more vasoconstriction and keratinisation

108
Q

what does rsd cause/what changes in the microflora?

A

reduced total no.of organisms

= residual bacteria are gm +ve aerobic

109
Q

what are risk markers of perio disease?

A

mobility

BOP

110
Q

what types of attachment loss occur?

A

rapid progressive attachment loss RAL

gradual progressive attachment loss GAL

111
Q

what are the types of gingiva?

A

free - coronal to ep attachment

attached - tightly bound to underlying bone

112
Q

what is periodontitis associated with scurvy?

A

vit c needed for collagen

scurvy = vit c deficiency

113
Q

how does new attachment occur?

A

pocket epithelium attaches to root surface by formation of a basement membrane and hemidesomosomal attachment, keratinocytes are held to cementum by formation of a long junctional epithelium

114
Q

what is ehlers danlos syndrome?

A

excessive joint mobility
skin hyperflexibility
easy bruising and abnormal scarring
fragile oral mucosa, gingiva bleed easy, fragile teeth that fracture easy, type VIII linked with aggressive perio

115
Q

what is hypophosphatasia?

A 
premature exfoliation of deciduous teeth
bone and cementum changes
inflammation free
shell teeth
perm dentition not affected
116
Q

what do dentinal tubules allow?

A

passage of fluid, chemicals and bacteria

117
Q

what is the tx of a grade 1 furcation?

A

s/p, ohi, furcationplasty

118
Q

what is the aim of treating a furcation?

A

exposure to ease cleaning and induce bone regeneration

119
Q

when is USS not used?

A

pts with pacemaker - EM interferes

contagious diseases - aerosol

120
Q

what isc chediak higashi syndrome?

A

lymphoma like condition with neutropenia, anaemia, thrombocytopenia
severe g + p
premature loss of primary and secondary dentition

121
Q

in health changing to disease what changes?

A

increased crevicular fluid
increased inflammatory and immune cellular infiltrate
less fibroblasts
reduced collagen content

122
Q

what is the correct tx plan order?

A
  1. initial exam and pain relief
  2. intitial NS therapy
  3. re exam and definitive tx plan
  4. correct tx
  5. maintenance
123
Q

what is the tx of a grade 2 furcation?

A 
furcationplasty
tunnel prep
GTR
root resection
XLA
124
Q

what is elyzol?

A

25% metronidazole - kills A.a
active for 24 hours
ppd >5mm

125
Q

what are perio prognostic factors?

A 
systemic health
hereditary factors
aetiology
age related to LOA
smoking status
attitude and co op
126
Q

what is type 1 collagen? and what fibres does it make up?

A

attaches g tissue to bone

circular, trans septal, dento gingival, dento periosteal, crestal

127
Q

caution with what antibiotics if pt has liver disease?

A

clindamycin

metronidazole

128
Q

what does hypogammaglobulinaemia cause?

A

high suscpetibility to infection

129
Q

what cellular changes does smoking cause orally?

A

reduced salivary IgA and serum IgG antibodies to fusobacterium and P intermedia
T helper lymphs
neutrophil function

130
Q

what is sarcoidosis?

A

granulomatous condition
swelling of parotid gland and lymph nodes
gingivae can be hyperplastic or granulomatous

131
Q

what is NUG/ANUG?

A

endogenous infection

systemic changes predispose the gingiva to invasion by bacteria in intraoral flora

132
Q

what is stannous F?

A

enzyme poison - inactivates enzymes in process

induces mineralisation in tubules = calcific barrier on surface

133
Q

what is dentine receptor mechanism?

A

odontoblasts have a sensory function

when stimulated will communicate with nerve plexus and cause pain

134
Q

why might recession happen at lower ants?

A

thin buccal bone

frenum pull

135
Q

what are some side effects of chx?

A 
unpleasant taste/taste alteration
staining
increased calc formation
redness/burning/erosion of mucosa
parotid gland enlargement
136
Q

what is root amputation?

A

remove compromised root whilst conserving crown

137
Q

where is dentine more sensitive?

A

adj and pulp

138
Q

what are clinical signs of recession?

A

stillmans cleft - v shape in gum

mccalls festoon - gum has rolled margin

139
Q

what is : modulation of nerve impulses by polypeptides?

A

pulpal tissue has bradykinin etc which regualates neural transmission and can alter permeability of odontoblast cell membrane = increased sensitivity

140
Q

what is aplastic anaemia?

what is fanconis anaemia?

A
  • caused by drugs/chemotherapy/radiation - gingival bleeding and infections
  • rare form, associated with perio and premature tooth loss
141
Q

what is the PDL?

A

specialzed vascular tissue
derived from dental follicle
fibrous attachment of toth
cementum to bone attachment

142
Q

if pt has kidney failure, caution with what antibiotics?

A

acyclovir
amoxicillin
erythromycin

143
Q

what is pemphigus vulgaris?

A

oral lesions before skin lesions
bullae anywhere on OM
corticosteroid tx

144
Q

when would you use anti plaque mouthwashes?

A

after surgery
acute mucosal infections/gingival infections
disabled pts
primary herpetic gingivostomatitis

145
Q

what are clinical signs of NUG?

A 
necrotic ulcers starting ID and spreading laterally
grey pseudomembranous slough
halitosis
spont bleeding
metallic taste
local or generalised
146
Q

how do cytokines regulate healing?

A

attract fibroblasts

147
Q

what do haematological conditions do to the gingivae?

A

conditions cant cause gingivitis but tissue changes cause an altered tissue response to plaque

148
Q

how is formaldehyde used in sensitivity tx?

A

formalin in toothpaste

precipitates protein in tubules

149
Q

what is hereditary gingival fibromatosis?

A

autosmal dominant
gen g enlargement
can be associated with epilepsy and mental retardation

150
Q

what is the hydrodynamic mechanism?

A

tubules have more fluid and stimuli causes rapid movement in the tubules = deformation in process and pain
explains why LA does not block sensitivity

151
Q

why does a furcation cause loss of vitality?

A

hard to clean

loss of vitality bc accessory canals

152
Q

describe the oral gingival epithelium?

A

stratified sqaumous orthokeratinised
junction with underlying gingivae
tissue is wavy - connective tissue papila rete pegs

153
Q

describe the advanced lesion?

A

fibrosis in ct
ulceration and migration of JE
pdl fibres breakdown
bone loss and osteoclasts present

154
Q

how does the junctional epitherlium form?

A

fusion of REE with oral ep on tooth eruption

as tooth reaches occlusal attachment, moves apically down the crown and stabilises near ACJ

155
Q

what does short use of systemic and topical tetracycline and metronidazole cause?

A

reduced gm negative, anaerobes, spirochates, improved clinical condition,
reduced pocket depth, reduced bop

156
Q

how does perio destruction progress?

A

site specific episodic manner and bursts of destructive activity alternating with periods of quiesence and poss repair = socransky burst theory

157
Q

what is the histopathology of NUG?

A 
bac zone - surface slough
pmn rich zone - superficial ct
necrotic zone
deeper tissues
bact infiltrate
158
Q

what is benign mucous membrane pemphigoid?

A

disease of mucous membranes caused by an immunological disorder
lesion = bula = ulcer = heals with scarring
diffuse erythema and areas of desquamation

159
Q

describe the ealry lesion?

A

after 1 week of plaque accumulation
antibody/cytokine release
increased size of CT = gingival inflammation
loss of fibroblasts/collagen = loss of stippling
increased gcf and pmns
swelling = deeper crevice = false pocket
bac = gm -ve, anaerobic, endotoxins produced

160
Q

what is the aim of NS tx?

A

create an environment biollogically compatible with healing = decon of root surface, disruption and elimination of plaque biofilm
removal of bulk of subg calc

161
Q

what is secondary dentine?

A

forms slowly throughout life and deposited at floor and roof of pulp chamber

162
Q

describe gingival connective tissue?

A

highly vascular CT - collagen fibres and extracellular matrix
fibroblasts, macrophage, polymorphs, lymphocytes

163
Q

oral signs of aneamia?

A

om pallor
smooth tongue
with or without apthous ulceration

164
Q

how can enzymes be involved in perio disease?

A
  • break down plaque structure
  • interfere with plaque attachment
    D - resistant strains develop, sensitivity, superinfection
165
Q

what is actisite?

A

25% tetracycline
active for 10 days
left in situ for 10 days

166
Q

what are MCG’s?

A

formed in prickle and granular layers
contain lipids that are discharged into intercellular layers
barrier to permeability of water

167
Q

what is papillon leverfe syndrome?

A

rare autosmal recessive disorder
palmer planter keratosis
premature loss of both dentitions
skin lesions - diffuse erythematous keratotic areas on palms and soles of feet
primary lost early in order of eruption
secondary erupts early with aggressive perio
edentulous by 16 years

168
Q

what are the 2 types of gingival disease?

A

plaque induced

non plaque induced

169
Q

what would you see on a radiograph in an area of a furcation?

A

arrow head lesion

170
Q

what kind of reponse to perio tx do smokers have?

A

refractory response despite good oh and peristant bop

171
Q

how does limited remodelling of the alveolar crest happen?

A

collagen laid down by migration of fibroblasts

172
Q

why is dentine highly sensitive?

A

richly innervated

173
Q

what is regeneration?

A

attachment of pdl cells and fibres to new cementum and coronal regrowth of the alveolar bone

174
Q

what are the layers of non keratinised epithelium?

A

basal
prickle
intermediate
surface

175
Q

how does calc contribute to perio disease?

A

coating of plaque
impedes cleaning
absorbs endotoxins
false ppd/impedes

176
Q

what do chemotheraputic agents do to the gums?

A

reduced WBC count = increased susceptibility to perio

177
Q

smokes have what things?

A
  • more calc
  • more plaque
  • deeper pockets
  • brush for less time
  • increased bone loss
  • loose more teeth
  • increased keratinisation
  • tx often fails
178
Q

what is a perio pocket?

A

pathogenically altered gingiva crevice

pocket = ulcerated epithelial lining of pocket wall, JE, diseased root surface - pathogenic and sub calc

179
Q

what is periodontitis associated with endodontic lesions?

A

combined perio endo lesions

180
Q

what is the ideal aim of perio tx?

A

regeneration

attachment of pdl cells and fibres to new cementum and coronal regrowth of the alveolar bone

181
Q

what bacteria are present in chronic perio disease?

A

p ging
f nucelatum
p intermedia

182
Q

what are gingivae?

A

fibrous tissue covered by epithelium

183
Q

what is the area covered by odontoblasts at ADJ/pulp?

A

20 000mm squared

65 000mm squared

184
Q

how does the PDL breakdown?

A

loss of collagen fibres in cementum

fibroblast damage

185
Q

what is the components of the periodontium and what is its function?

A

gingiva, pdl, alveolar bone, cementum

attachment of teeth to jaws, effective support during masticatory function

186
Q

what are types of non plaque induced gingival diseases?

A 
vira
fungal
specific bacteria
genetic
systemic - mucotaneous/alergic
traumatic lesions
187
Q

how do you manage/review a furcation?

A

regrade - 6/12

vitality test - 12/12

188
Q

what is cervitec?

A

1% chx, 1% thymol
reduced bacterial levels
mechanical blockage

189
Q

how do oxygenating agents work?

A

inhibit obligate anaerobes

190
Q

how do sex hormones affect the gums?

A

oestrogen - increased keratinisation, altered CT composition

prgesterone - increased gingival vessel permeability

191
Q

what is gcf and what does it contain?

A

produced by dentogingival plexus post capillary cells
blood cells
various plasma proteins
defence cells/proteins - pmns, abs, complement

192
Q

what changes in tissue response happen when smoking?

A

vasoconstriction
transient increase in gingival crevicular fluid
passes through OM and causes >50% inhibition of function of neutrophils - motility and chemotaxis

193
Q

what happens 1 week post RSD?

A

reduced vasodilation, gcf, pmns, ulceration

194
Q

what are systemic perio risk factors?

A 
genetic
environmental
behavioural
lifestyle
metabolic
haematological
195
Q

what are the advantages of local administration?

A

higher conc in pocket
lower total dose of antibiotic
lower systemic spillover

196
Q

what is a root resection/hemisection?

A

removal of one or more roots

retained root - RCT

197
Q

what are types of necrotizing periodontal diseases?

A

NUG

NUP

198
Q

what is hypersensitivity?

A

pain with thermal, chemical or osmotic stimuli or pathology

199
Q

what is reattachment?

A

union of root and CT after incision or injury

200
Q

what should you tell pts to avoid when using chx?

A

avoid smoking, tea,coffee, red wine

201
Q

sensitive dentine has how many more x tubules of what x the diameter?

A

8x no of tubules

2x diameter

202
Q

what happens during healing?

A

long JE
shrinkage
tightening and formation of g cuff

203
Q

what bacteria are present in gingival health?

A

strep and actinomyces

204
Q

deep pockets should see what after RSD?

A

reduced ppd 2mm

+1mm attachment

205
Q

what are the layers of keratinised epithelium>?

A

basal cell
prickle cell
granular cell
keratinized

206
Q

why are downs syndrome pts more at risk of perio disease and in what part of the mouth is it more common in? what is there an extra increased risk of having?

A

related to immune system abnormalities - impaired chemotaxis and phagocytosis of pmns
- lower ants, NUG

207
Q

why does tooth mobility happen?

A

trauma
periapical disease
periodontal disease

208
Q

how do corticosteroids affect the gums?

A

reduced response to plaque
reduced swelling
increased infection susceptibility

1st year (8 decks)

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