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clinical practise 2 > Perio BSc > Flashcards

Perio BSc Flashcards

1
Q

what is reattachment?

A

the reunion of root and connective tissue serperated by incision/injury

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2
Q

is reattachment used in periodontal healing?

A

no. reattachment is not a term used in periodontal healing

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3
Q

what is new attachment?

A

union of connective tissue with previously pathogenically altered root surface

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4
Q

what is regeneration?

A

attachment of PDL cells and fibres to new cementum formation and coronal rewgrowth of alveolar bone

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5
Q

what happens following debridement within the following week?

A
  • acute inflammation begins to subside 24-48 hrs after
  • decrease vasodilation
  • decrease GCF
  • decrease PMN’s
  • decrease ulceration of pocket
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6
Q

pocket epithelium begins to attach to root surface via what?

A
  • via formation of basement membrane and hemidesmosome attachment
  • these hold keratinocytes to the cementum(forming long junctional epithelium)
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7
Q

what does long epithelium result in?

A

long epithelium results in the gradual closure of a pocket and may continue for moths after treatments

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8
Q

junctional epithelium acts like what?

A

junctional epithelium acts as a zip

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9
Q

what is regeneration?

A

regeneration means attachment of PDL cells and fibres to new cementum formation and coronal regrowth of alveolar bone

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10
Q

if epithelium is allowed to grow into the wound space. What will happen?

A
  • it will proliferate quickly

- it will prevent fibroblasts becoming attached to cementum and forming new attachment

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11
Q

what is guided tissue regeneration?

A
  • most successful method of new attachment formation

- it promotes repopulation of cells derived from PDL and bone

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12
Q

What are some clinical features of NUG?

A
  • sudden onset and very painful
  • necrotic ulcers
  • initially red swollen
  • ulceration starts on tips of ID papillae and spreads laterally along gingival margin
  • halitosis
  • spontaneous bleeding
  • metllic taste
  • localised or generalised
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13
Q

how long do symptoms of NUG usually last?

A

acute symptoms last around 2-3 weeks leaving chronic periodontitis to occur

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14
Q

what can NUG develop into?

A
  • cancrum oris

- orofacial necrosis

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15
Q

what bacteria are involved with NUG?

A
  • anaerobic fuso-spirochaetal complex
  • treponema vincentii&denticoli
  • fusobacterium nucleatum
  • prevotella intermedia
  • porphyromonas gingivalis
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16
Q

what are some predisposing factors of NUG?

A
  • smoking
  • poor OH
  • stress
  • Immunodeficiency
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17
Q

what is the tx of NUG?

A
  • OHI and explanation
  • gentle USS
  • antimicrobis (metronidazole 200mg for 3 days)
  • review in 48 hrs
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18
Q

what are non-plaue induced gingival lesions?

BIVFGTSTF

A
  • bacterial origin
  • viral origin
  • fungal
  • genetic
  • systemic
  • traumatic
  • foreign body
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19
Q

what are some examples of gingival diseases of viral origin?

A
  • herpes virus infections
  • primary herpatic gigivostomatitis
  • varicella zoster infections
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20
Q

give some examples of gingival diseases of fungal origin?

A
  • candida species infections
  • linear gingival erythema
  • hystoplasmosis
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21
Q

give an example of a gingival disease of genetic origin?

A

-hereditary gingival fibromatosis

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22
Q

what is recession?

A

-a seemingly inflammation free clinical condition characterised by the apical retreat of th periodontium

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23
Q

what is a fenestration?

A

window in bone

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24
Q

what is a dehiscence?

A

a lack of bone

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25
Q

what are some examples of recession?

A
  • ortho tx
  • frenum pulls
  • excessive perio scaling
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26
Q

what is stillmans cleft?

A

‘v’ shape in gums

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27
Q

what is mcCalls festoon?

A

gum has rolled margin

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28
Q

what is a furcation plasty?

A

-surgical procedure used to remove tooth substance to widen entrance to furcation

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29
Q

what is guided tissue regeneration?

A

-procedure which enables bone and tissue to regenerate in defects around periodontally compromised teeth

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30
Q

what are 3 dentine hypersensitivity theories?

A
  1. dentinal receptor mechanism
  2. hydrodynamic mechanism(branhstroms theory)
  3. modulation of nerve impulses by poly peptides
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31
Q

what is it in toothpaste that helps sensitivity?

A

-pottasium ions

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32
Q

what do anti-epileptic drugs cause oraly?

A

-gingival hyperplasia

33
Q

what anti-epileptic drug most commonly causes hyperplasia and where does it begin?

A
  • phenytoin

- hyperplasia is worse anteriorly and begins interdentally and then grows

34
Q

what type of drug is cyclosporin?

A

-immunosupressant

35
Q

what does cyclosporin do oraly?

A
  • gingival hyperplasia

- higher incidence in women and children

36
Q

what are some commonly used corticosteriods?

A

-prednisalone, betlamethason, hydrocortisone

37
Q

what do immunosupressants cause oraly?

A
  • reduced inflammatory response/reaction to plaque
  • decreased swelling/bleeding
  • impaired wound healing
  • increased susceptibility to infection
38
Q

how do NSAIDs work?

A

-inhibit synthesis and release of prostaglandins

39
Q

what oraly do NSAIDs cause?

A
  • decreased bleeding
  • decreased swelling
  • decreased bone loss
40
Q

how can oestrogen affect the periodontal tissues?

A

-oestrogen promotes keratinization and alters the composition of blood

41
Q

how can progesterone affect the periodontal tissues?

A

-progesterone increases the permeability of gingival blood vessels

42
Q

what is a pregnancy epulis?

A

soft, pedunculated granuloma arising from an inflammed gingival papilla

43
Q

does the OCP affect periodontium if there is no pre-existing condition?

A
  • No

- OCP only affect the periodontium if there is a pre existing condition

44
Q

is the percentage of female smokers increasing or decreasing?

A

% of female smokers is increasing

45
Q

smoking increases the prevelance of what?

A
  • lung cancer
  • cardiovascular disease
  • GI disease
  • low birth weight
46
Q

is smoking an important risk factor in the development and progression of periodontal disease?

A

Yes. Smoking is now seen to be one of the most significant risk factors in the development and progression of periodontal disease

47
Q

what are the constituents of a cigarette that cause the disease?

A
  • nicotine
  • napthalene
  • phenols
  • carboxylic acids
  • aromatic amines
  • tar
  • many more…
48
Q

what are some constituents of the gaseous phase?

A
  • ammonia
  • hydrogen sulphide
  • hydrocarbons
  • carboxylic acids
49
Q

where can low doses of nicotine be stored and released?

A

-low doses of nicotine cane be stored and released by the periodontal fibroblasts

50
Q

does nicotine act as a vasodilator or vasoconstrictor?

A

vasoconstrictor

51
Q

list things that smokers are more likely to have :

big list

A
  • spend less time brusing their teeth
  • have more calc. deposits
  • have more plaq. deposits
  • deeper pockets
  • greater alveolar bone loss
  • lose more teeth than smokers
  • gingivae have more keratinised cells
  • perio. tx often fails
52
Q

what are some things the perio tissued do in response to smoking?

A
  • promotes vasoconstriction
  • initial increase in GCF
  • PMNs are impaired by smoking
53
Q

is there any relationship between NUG and smoking?

A

yes. there is a clear relationship between NUG and smoking

54
Q

tobacco may play a significant role in the development of a ……….. response to perio tx?

A

refractory response

55
Q

there are clear links between smokeless tobacco products (snuff, betel nut) and what?

A

leukoplakia, and carcinoma

56
Q

the periodontal pockets of smokers are more …….. than non smokers

A

the periodontal pockets of somkers are more ANAEROBIC than non-smokers

57
Q

is smoking thought to alter the composition of plaque?

A

NO. smoking is not thought to alter the composition of plaque

58
Q

with regards to ‘the effects on the response to periodontal treatment’ what do smokers have:
(another list)

A
  • decreased salivary IgA antibodies to fusobacterium and P.intermedia
  • decreased serum IgG antibodies to fusobacterium and P.intermedia
  • decreased no. of T helper lymphocytes
  • decreased neutrophil function
  • tobacco smoke can impair the motility and chemotaxis of oral and peripheral PMNs
59
Q

what can downs syndrome cause orally?

A
  • class 3 occlusion
  • anterior open bite
  • large tongue
  • lack of lip seal
  • prone to infections
  • prone to destructive periodontitis
  • increased susceptiblity to NUG
  • impaired chemotaxis and phagocytosis of PMNs
60
Q

what can hypophosphatasia cause orally?

A
  • premature exfoliation of premature teeth
  • absence of gingival inflammation
  • loss of alveolar bone
  • prenament dentition does not appear infected
61
Q

what can papillon lefevre syndrome cause?

A
  • primary dentition prematurely lost and are shed in order of eruption
  • pernament dentition erupts early
  • aggressive periodontitis associated with permanent dentition
  • perio tx is usually unsucessful
  • accompanied with sever gingival inflammation
62
Q

what can ehlers danlos syndrom cause orally?

A
  • oral mucosa becomes fragile and susceptible to bruising
  • gingival tissues bleed easily
  • teeth become fragile and fracture easily
  • perio. tx should be as atraumatic as possible
63
Q

what are some features of hereditary gingival fibromatosis?

A
  • condition does not manifest till after eruption of the teeth
  • associated with pernament dentition
  • gingival tissues are enlarged
  • hyperplasia due to excessive production of collagen
  • may delay eruption of the teeth
64
Q

what is mucopolysacharidosis?

A
  • group of inherited disorders

- teeth are small and widely spaced

65
Q

what can a vitamin C deficiency cause?

A

scurvey

66
Q

chemical antimicrobials may cause?

A
  • sensitivity to the indvidual
  • resistance
  • super infections (mrsa, candidosis)
67
Q

what do quaternary ammonium compounds do?

A

-have moderate plaque inhibitory activity but is not retained in mouth for long

68
Q

give an example of a phenolic antiseptic?

A

listerine mouthwash

69
Q

what are some possible uses of antiseptic mouthwashes?

A
  • to replace mechanical toothbrushing when this is not possible
  • after oral surgery
  • during acute gingival conditions
  • for mentally/physically handicapped people
70
Q

can mouthwashes reach the subgingival area?

A

-no

71
Q

what are agents used systemically for subgingival plaque control?

A

antibiotics

72
Q

what are agents used topically/locally for subgingival plaque control?

A

antibiotics or antiseptics

73
Q

what is the ‘perio chip’?

A
  • contains 2.5mg chlorhexidine
  • prolonged chlorhexidine release from single chip
  • placed into pocket following RSD and arrest of haemorrhage
  • chips swells on contact with moisture this retains it in the pocket
74
Q

should antibiotics be the primary agent in the treatment of periodontal disease?

A

-No. Antibiotics should only be used as an adjunct in the tx of perio. disease

75
Q

the development of ……. can be caused by frequent misuse of antibiotics.

A

-hypersensitivity reaction

76
Q

what are the 5 phases of tx planning?

A
  1. initial examination and pain relief
  2. cause related therapy
  3. re-examination outcomes
  4. definitive tx
  5. maintenance
77
Q

what is the goal of cause related therapy?

A

to render the roots biologically compatible with soft tisue by eliminating calculus and altered cementum and reducing periodontal pathogenic micro-organisms.

78
Q

what is palliative care?

A
  • not the same as maintenance
  • palliative care recognises that the disease is not stable and it is not possible to achieve stability
  • sc&p every 2-3 months

clinical practise 2 (12 decks)

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