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Restorative > periodontics > Flashcards

periodontics Flashcards

1
Q

2 types of acute gingivitis

A

ANUG

primary herpetic gingivostomatitis

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2
Q

why is GCF increased in gingivitis/PD?

A

delivers humoral + cellular defence factors to combat microbial insult

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3
Q

which bacteria dominates in health?

A

streptococci

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4
Q

which bacteria dominates in gingival disease?

A

anaerobic gram-negative bacteria - red

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5
Q

how does bone loss occur?

A

inflammation spreads to bone, bone resorbed by osteoclasts to create room for host defence cells

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6
Q

what epithelium is attached to tooth surface?

A

junctional

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7
Q

how many days for an established periodontal lesion to form?

A

21days+

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8
Q

3 clinical presentations of ANUG

A
  1. painful
  2. sloughing of gingival margin
  3. ulceration
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9
Q

causes of ANUG

A

poor OH
often immunocompromised
poor diet + general health
smoking

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10
Q

bacteria associated with ANUG

A

fuso-spirochaetal bacteria

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11
Q

treatment of ANUG

A
  1. OHI
  2. remove deposits
  3. if spreading infection - metronidazole (2nd line amoxicillin)
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12
Q

5 dermatological disease causing non-plaque induced gingivits

A
  1. lichen Planus
  2. pemphigoid
  3. pemphigus
  4. erythema multiforme
  5. lupus erythematous
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13
Q

4 main groups in 2017 classification of periodontal disease

A
  1. gingival health + gingivitis
  2. periodontitis
  3. other conditions affecting periodontist
  4. peri-implantitis
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14
Q

what is necrotising stomatitis

A

severe inflammation extending through peridontium + oral cavity - past gingiva

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15
Q

difference between localised + generalised gingivitis.PD

A

> 30% generalised

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16
Q

3 classifications our periodontal status of implants

A
  1. peri-implant health
  2. peri-implant mucositis
  3. peri-implantitis
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17
Q

how is a pocket created in periodontal disease?

A

junctional ep migrates apically to try and maintain ep barrier - anaerobic bacteria flourish

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18
Q

how to proceed if NPE code 4s or evidence of interdental recession?

A

radiographic assessment

full PPDs

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19
Q

how to proceed if any code 3 with no obvious sign of interdental recession?

A

radiographic assessment
initial therapy - OHI, risk factors, suprascale
localised PPDs in 3 months to review

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20
Q

grades of tooth mobility

A 
0 = physiological <0.2mm
1 = 0.2 - 1mm horizontal mouvement 
2 = >1mm horizontal but not vertical
3 = horizontal + vertical
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21
Q

classification of furcations

A 
1 = <3mm deep
2 = >3mm deep but not through
3 = through and through
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22
Q

how to measure recession + clinical attachment loss

A

recession = CEJ to gingival margin

clinical attachment loss = CEJ to base of pocket

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23
Q

what tooth brushing technique is used for spaces between teeth?

A

charter

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24
Q

how does chlorhexidine mouth was work?

A

bactericidal

disrupt negatively charged cell walls, disrupts osmotic barrier

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25
Q

disadvantages of chlorhexidine

A

taste disturbance + brown stain

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26
Q

difference between RSD + root planing?

A

RSD = no intentional removal of cementum

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27
Q

what is curettage?

A

instrumentation to remove soft tissue lining of periodontal socket

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28
Q

expected probing depth reduction + attachment gain following RSD if initial probing depth 4-6mm?

A

expected probing reduction = 1-1.5mm

expected attachment gain = 0-0.5mm

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29
Q

expected probing depth reduction + attachment gain following RSD if initial probing depth 7+mm?

A

expected probing reduction = 2-3mm

expected attachment gain = 1-2mm

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30
Q

why do probing depths reduce after RSD?

A

decreased gingival swelling, increase resisitance

formation of LJE

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31
Q

negatives of RSD

A

gingival recession
root sensitivity
aesthetic - black triangles

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32
Q

recall frequency for SPT?

A

2-4months

indices annually

33
Q

healing after RSD within a few hours

A

acute inflammatory reaction in pocket wall

34
Q

healing after RSD within 1-2days

A

epithelisation of pocket wall

35
Q

healing after RSD 1-2weeks

A

epithelial reattachment at base of pocket, gingival recession

36
Q

healing after RSD 3-6 weeks

A

formation of functionally oriented collagen replacing granulation tissue

37
Q

adjunctive treatments to RSD

A

local = periochip
chlorhexidine
antibiotics

38
Q

what is a periochip

A

2.5mg chlorhexidine in biosorbale gel - does not need to be removed

effective 7-10days

39
Q

2 bacterias typically associated with aggressive forms of PD

A

aggregatibacter actinomycemecomitans

porphyromonas ginigvalis infection

40
Q

what is rapidly progressing PD?

A

tissue destruction inconsistent with local + systemic factors

antibiotics may be indicated

41
Q

host response modulator used to treat PD?

A

doxycycline (periostat - 20mg twice daily)

inhibits MMP (colleganase) activity in periodontal tissue

42
Q

classification for traumatic incisor relationship?

A

akerly class II +III

43
Q

radiographic evidence of primary occlusal trauma

A

widened PMS but no loss in bone height

44
Q

difference between primary + secondary occlusal trauma

A

primary = excessive force to tooth/teeth with normal supporting structures

secondary = normal occlusal force becomes excessive because loss of attachment

45
Q

3 groups of acute gingival conditions

A
  1. infective
  2. traumatic
  3. systemic
46
Q

what is primary herpetic gingivostomatits

A

recurrent oral herpes effecting gingiva HSV1

47
Q

blood dycrasias causing acute gingivitis

A

leukaemia associated - acute myeloid leukaemia

neutropenia

48
Q

clinical appearance of ANUG

A

‘punched out’ ulcers covered with yellow/grey pseudomembranous slough

tips of interdental papilla affected first

linear erythema
bleeding
pain
halitosis 
lymphadenitis, fever, malaise
49
Q

clinical features of primary herpetic gingivostomatitis

A

fever, headaches, malaise, dysphagia, lymphadenopathy

aggressive marginal gingivitis
fluid filled vesicle tongue, palate, buccal, lips
burst to leave painful yellowf-grey ulcers, red inflamed margins
ulcers heal without scarring ~14 days

50
Q

7 riks factors for PD

A
  1. smoking
  2. diabetes
  3. genetics
    4, medications
  4. hormones + pregnancy
  5. Stress
  6. obesity
51
Q

how does diabetes effect PD

A

microvascular damage - affecting leukocyte/nutrient delivery

altered collagen turnover, increase PD breakdown, decreased PD healing

PMN dysfunction

more inflammatory mediators - more inflammation

52
Q

histology of drug induced gingival overgrowth

A

fibrous tissue forms bulk - proliferation of fibroblasts + increased collage content

highly vascularised tissue, increased inflammatory cells

53
Q

why is PD common in Ehlers dances

A

collagen deficient

54
Q

how does leukaemia cause gingival swelling

A

infiltration of gingiva with leukemic cells

55
Q

how does leukaemia cause gingival bleeding

A

thrombocytopenia

56
Q

oral manifestation of papillon lefevre syndrome

A

severe generalised periodontitis

57
Q

5 indications ofr periodontal surgery

A
  1. improved access for RSI
  2. excision of gingival hyperplasia
  3. correction of gingival recession
  4. access sub gingival caries
  5. increase sub gingival tissue for restorative procedures
58
Q

indications for open flap debridement

A

residual pockets of 5mm+
to response to convention management
motivated + optimised OH
accept risk of recession, sensitivity, aesthetics

59
Q

most common open flap debridement technique

A

modified Widman flap

60
Q

4 steps to flap debridement surgery

A
  1. raise buccal flap to visualise root surface/granulation tissue/calculus
  2. raise palatal flap
  3. debride + curettage of granulation tissue
  4. flap closure + apical repositioning for direct pocket reduction
61
Q

what is guided tissue regeneration

A

regenerate lost peridontium in localised vertical/infrabony defects

62
Q

4 steps of GTR

A
  1. direct vision - open surgically
  2. placement of stable biomaterial int well-constrained defect
  3. coverage with membrane - prevents ingrowth of ep
  4. primary closure
63
Q

2 options for healing of open flap debridemen?

A

new long junctional epithelium attachment

GTR

64
Q

what forms PDL in GTR

A

undifferentiated stem cells

65
Q

2 examples of GTR biomaterial

A

emdogain

bio-oss

66
Q

what dressing is used to promote secondary intention healing after gingivectomy

67
Q

miller classification of recession

A

1 = not extending beyond mucogingival junction + no loss of interdental soft tissue + bone

2 = extending beyond mucoginigval junction + no loss of interdental soft tissue + bone

  1. extending beyond mucoginigval junction + loss of interdental soft tissue + bone apical to CEJ but not coronal
  2. extending beyond mucogingival junction + loss of interdental soft tissue + bone apical + coronal
68
Q

cairo classification of recession

A

RT1 = no inter proximal tissue loss

RT2 = interproximal tissue loss not as significant as mid buccal

RT3 = interproximal tissue loss worse than mid buccal

69
Q

surgical options for gingival recession

A

soft tissue grafting - free gingival graft, connective tissue craft

if interproximal tissue lost = full root coverage not possible

70
Q

aim of gingival recession surgery

A

increase keratinised tissue or achieve root coverage

71
Q

where is free gingival graft taken from

72
Q

treatment indicated in extensive recession

A

not surgery- root coverage not possible

gingival veneer +/- composte augmentation

73
Q

3 indication for crown lengthening

A
  1. access subgingival caries
  2. increase surface area for restoration
  3. improve aesthetic - gummy/uneven
74
Q

how clear of alveolar crest must restorations be

A

3mm

prevent recession/bone loss by inflammatory response if encroaches on biologic width

75
Q

3 steps for crown lengthening surgery

A
  1. raise flap
  2. remove bone
  3. wait 3-6months for healing
76
Q

furcation surgery aim + disadvantages

A

improve OH - loss of tissue risking sensitivity/loss of vitality

77
Q

2 parts of furcationplasty in class 1 + 2 furcations

A

odontoplasty + osseoplasty

78
Q

treatment for class 3 furcations

A

tunnel preparation

Restorative (10 decks)

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