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BDS3 Perio > Perio Tx 2 > Flashcards

Perio Tx 2 Flashcards

1
Q

most severe inflammatory periodontal disorder caused by plaque bacteria

A

necrotising gingivitis/periodontitis

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2
Q

effect on pt of necrotising periodontitis/gingivitis

A

rapidly destructive and debilitating

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3
Q

pattern of ANUG/P

A

Due to shared predisposing factors in a population (e.g. students during a period of examinations, armed forces recruits) ANUG/P is known to occur in epidemic-type patterns.

This has led to the popular belief that ANUG/P is contagious, but this is not the case.

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4
Q

is ANUG/P contagious

A

NO

Due to shared predisposing factors in a population (e.g. students during a period of examinations, armed forces recruits) ANUG/P is known to occur in epidemic-type patterns. This has led to the popular belief that ANUG/P is contagious, but this is not the case.

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5
Q

4 main features of NPD

A

painful

bleeding gums

ulceration

necrosis of interdental papilla

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6
Q

type of infection in NPD

A

Opportunistic infection – caused by the bacteria inhabiting healthy oral cavity

  • not an infection that you can contract from someone else, only occurs in situation where there are supporting conditions for bacterial imbalance
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7
Q

prevalance of NPD

A

less than 1% in developed countries

27% in developing countries

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8
Q

NPD is

A

only one type of periodontal disease

necrotising periodontal disease

severe symptoms - pain, discomfort

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9
Q

NPD can be divided into (5)

A

necrotising gingivitis NG

necrotising periodontitis NP

necrotising stomatitis NS

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10
Q

necrotising gingivitis

A

is restricted to gingiva tissue (soft tissue)

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11
Q

necrotising periodotitis NO

A

involves bone - clinical attachment loss

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12
Q

necrotising stomatitis

A

disease not restricted to peridontal tissue

oral mucosa is involved

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13
Q

acute and chronic

A

are descriptors of the disease

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14
Q

chronic periodontal disease

A

doesnt tend to give severe symptoms to pts - unfortunate because they can present late

(milkd discomfort, bleeding on brushing - present when teeth are mobile)

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15
Q

ANUG

A

acute necrotising ulcerative gingivitis

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16
Q

ANUP

A

acute necrotising ulcerative periodontits

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17
Q

old terms for NPD

A

fusospirochetosis - described bacterial flora involved, not infection

trench mouth - common in trenches in WW1

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18
Q

vincents gingivitis, gingivostomatitis, infection

A

classed as necrtosing periodontal disease

not vincents angina

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19
Q

vincents angina

A

diseases of the throat not periodontium

  • Vincent for the first time described mixed spirochetal microbiota in necrotic areas in tonsils during sore throat infections

vincents gingivitis NPD and VA occur independently of each other

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20
Q

NUG

A

Necrotizing ulcerative gingivitis, or simply necrotizing gingivitis (NG), is a common, non-contagious infection of the gums.

  • Acute necrotizing ulcerative gingivitis (ANUG) is the acute presentation of NUG, which is the usual course the disease takes.

If improperly treated NUG may become chronic and/or recurrent.

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21
Q

improper treatment of NUG

A

If improperly treated NUG may become chronic and/or recurrent.

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22
Q

usual course of NUG

A

acute

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23
Q

NUP

A

Necrotizing ulcerative periodontitis (or simply necrotizing periodontitis, NP) or acute necrotizing ulcerative periodontitis (ANUP) is where the infection leads to attachment loss.

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24
Q

NUP and NUG relation

A

NUP may be an extension of NUG into the periodontal ligaments, although this is not completely proven.

  • Maybe both diseases develop without connection

In the meantime, NUG and NUP are classified together under the term necrotizing periodontal diseases NPDs

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25
Q

necrotising stomatitis

A

Progression of NUP into tissue beyond the mucogingival junction characterizes necrotizing stomatitis (infection of oral mucosa) mostly in malnutrition and HIV infection

  • may result in denudation of the bone leasing to osteitis and oro-antral fistulas
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26
Q

most causes of necrotising stomatitis

A

in malnutrition and HIV infection

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27
Q

cancrum

A

a.k.a noma

necrotizing and destructive infection of the mouth and face, and therefore not strictly speaking a periodontal disease (most severe)

In modern times, this condition usually occurs almost exclusively in malnourished children in developing countries.

  • Can be disfiguring and is frequently fatal.

suggested that all cases of cancrum oris develop from pre-existing NUG, but this is not confirmed.

  • Furthermore, the vast majority of cases of NUG and NUP will not progress to the more severe forms, even without treatment
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28
Q

diagnosis of NPD

A

based on symptoms no microbiological test

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29
Q

diagnosis checklist for NPDs (11)

A
  • Ulcerated and necrotic papillae and gingival margin resulting in a characteristic punched-out appearance
  • ulcers are covered by a yellowish, white or greyish slaim (sloughthing)
    • which has been termed pseudomembrane – misleading, should not be used
    • no coherence only slime made of fibrin, necrotic tissue, leucocytes, erythrocytes and mass of bacteria
  • Lesions develop quickly
  • painful – severe pain – unusual for periodontal disease – usually no severe pain
  • Bleeding readily provoked
  • first lesion tends to be interproximal in mandibular anteriors
  • hallitosis - severe due to necrotic tissue
  • ulcers
  • Sequestrum formation necrosis of small or large parts of the alveolar bone – not only interproximal bone but also adjacent oral and facial bone
  • Swelling of the lymph nodes
    • particularly in the advanced cases
  • Usually, no elevation of the body temperature
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30
Q

ulcers in NUP

A
  • ulcerations are often associated with deep pockets formation as gingival necrosis coincides with loss of crestal alveolar bone
  • Ulcers with central necrosis develop into craters
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31
Q

bone effect in NPD

A

Sequestrum formation necrosis of small or large parts of the alveolar bone

  • not only interproximal bone but also adjacent oral and facial bone
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32
Q

why is NPD diagnosis not based on microbiological test

A

Constant flora: Treponema sp., Selenomonas sp., Fusobacterium sp., Prevotella intermedia

  • Normal flora of the mouth - always there but heightened in NPD due to circumstance (not infectious)

It is opportunistic infection – caused by the bacteria inhabiting healthy oral cavity – need favourable environment (malnourished, poor OH etc)

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33
Q

specific bacteria that may be isolated in abundance from necrotic lesions

A

spirochetas and fusobacterias

not always evident in primary etiologic lesion

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34
Q

differential diagnosis with herpetic gingivostomatitis (early)

Similar in advanced stages

A

NPD – bacteria – number from biofilm increase

PHG – virus infection - VESICLES

NPD – developed, young people, students

In advanced stage – don’t see vesicles in PHG (already destroyed), misleading fibrin covered can be similar to ulcerations in NPD

  • PHG – 99% fever (rare in NPD)

PHG no bone loss as only gingival mucosa involved

35
Q

risk factors for NPD developed countries

A

occurs mostly in young adults with predisposing factors such as psychological stress, sleep deprivation, poor oral hygiene, smoking, immunosuppression (HIV infection and leukaemia) and/or malnutrition.

  • Student
  • systemic disease with impairment of immune function
36
Q

risk factors NPD in developing countries

A

ANUG occurs mostly in malnourished children.

37
Q

difference with HIV positive and seronegative pts with NPD

A

Clinical characteristics of HIV-positive patients don’t essentially differ from HIV- seronegative patients – but the lesion are not usually associated with a big amount of plaque and calculus immune system is weakened so only small number MO needed to trigger inflammation

38
Q

treatment of acute disease

A

debridement and antibiotics

  • usually metronidazole
39
Q

what needs to be first line of action for NPD treatment

A

poor OH and other predisposing factors needs to be corrected to prevent recurrence

40
Q

what may be barrier to OH in acute stages

A

painful to perform - do slowly, commit, several appointments possible

41
Q

debridement for NPD by

A

ultrasonic debridement (with LA)

42
Q

reason for ultrasonic debridement

A

to facilitate healing

need to decrease plaque level

43
Q

how to manage pain prevent OH in very acute stages

A
  • 0.2% chlorhexidine mouth wash twice daily
44
Q

how to manage pt with malaise, fever and lassitude, lack of response to mechanical therapy and with impaired immunity

A
  • Fever – recommend ibuprofen
  • antibiotics
    • 200 mg Metronidazole TID (3 times daily) for 3 days
    • 400 mg Metronidazole TID for 3 days
45
Q

potential methods of managing factors that are influencing disease

A

smoking cessation

vitamin supplementation (malnourished)

dietary advice (malnourished)

46
Q

what will the treatment be for necrotising periodontitis after carried out acute phase treatment

A

carry out hygiene phase therapy to treat periodontal disease

47
Q

periodontal health is

A

the outcome of the balance between bacteria of the dental plaque and the host Immune system

48
Q

2 possible adjuncts to treatment of periodontitis

A

systemic and topical antimicrobials

host modification therapies

49
Q

periodontal disease is

A

imbalance between microbiome and host immune system

50
Q

3 treatment strategies for periodontal disease

A

mechanical disruption

systemic or local antimirobials

host modulation therapy

51
Q

accumulation of biofilm impact on bacteria presence

A

change in balance from aerobic to anaerobic

52
Q

mechanical disruption as tx for perio

A

easiest most common

reducing the bacterial challenge

scaling and RSD

53
Q

mechanial disruption for perio targets

A

biofilm

only method that fully works

54
Q

systemic antibiotics or local antimicrobials as perio tx

A

only an adjunct

targets biofilm - once it has been disrupted

55
Q

host modulation therapy for periodontal treatment

A

newer therapy - very complex

  • Don’t need to address bacterial plaque exclusively if we can modulate immune response to not react to it – no inflammation

as inflammation = peridontal destruction

56
Q

host modulation therapy for perio targets

A

functioning of immune system

57
Q

means of mechanical disruption

A
  • Oral hygiene instruction
    • Tooth brushing technique
      • Modified bass technique
    • Flossing
      • If papilla still intact
    • Interdental brushes
      • Black triangles present – papilla gone
  • Supra and subgingival plaque control (scaling, RSD)
58
Q

use of systemic antiobiotics in perio tx

A

not the first line treatment and if used in selected cases are only allowed once combined with mechanical disruption of biofilm

  • Restricted

Used alone is inefficient and leads to resistance of antibiotics

59
Q

why is systemic antibiotic use alone ineffective

A

Because we are fighting with biofilm

Biofilm≠ planktonic bacteria

A biofilm is an aggregate of microorganisms in which cells adhere to each other on a surface.

  • These adherent cells are embedded within a self-produced matrix of extracellular polymeric substance (EPS) – DNA, proteins, polysacharyde.
    • All cells in biofilm are protected by the matrix
  • resistance to antibiotics, antibacterial agents, hidden from immune system of the host.

disrupt the biofilm and the bacteria are in the planktonic form for a few hours

  • vulnerable – unprotected by matrix – window of opportunity to additionally use antibiotics to kill vicious species of bacteria that are more responsible for inducing periodontal inflammation
60
Q

to use systemic antibiotics can be used for perio must have

A

Mechanical disruption of biofilm with systemic antibiotics

  • never systemic antibiotics alone, and never first line of treatment
    • decrease plaque levels, hygiene phase therapy first
61
Q

what cases can we consider tx with systemic antibiotics with mechanical disruption of biofilm

A

cases of

  • Aggressive periodontitis (old classification)
  • Young people with grade B/C (fast progressing periodontitis) (new classification)
62
Q

Treatment protocols for systemic antibiotic (specialist treatment) – only in patients after initial HPT and with excellent oral hygiene

A
  1. OH
  2. Supragingival scaling and RSD of all sites indicated in pocket chart (inflammation still present)
  • short time as possible within 1 week, in our Hospital within 1 day (morning and afternoon appointment)
    1. Start the antibiotic regiment on the morning of the first RSD visit
  • a) 500 mg amoxicillin 3 times a day for 7 days
  • 200mg (400 mg) metronidazole 3 times a day for 7 day
  • b) 400mg metronidazole 3 times a day for 7 days (starting to become more popular than a))
63
Q

contraindication for amoxicillin

A

allergies

64
Q

contraindications for metronidazole

A
  • alcohol intake
  • Increases anti-coagulant effect of Warfarin
  • pregnancy
65
Q

contraindications for doxycylcine

A

pregnancy – tetracycline staining of the teeth

66
Q

antibiotic regime to start morning after intense full mouth RSD

A
  1. 500 mg amoxicillin 3 times a day for 7 days

200mg BSP (400 mg) metronidazole 3 times a day for 7 days

  1. 400mg metronidazole 3 times a day for 7 days (starting to become more popular than a))
67
Q

antibiotics regime if pr allergic to amoxicillin or on warfarin

A
  • 100 mg doxycycline; once a day for 21 days with 200 mg loading dose during first day
  • 500 mg Azithromycin; one a day for 3 days
68
Q

metronidazole effect on warafarin

A

increase anticoagulant effect

bleeding risk

contraindicated

69
Q

advantages of local antimicrobials (7)

A
  • Reduced systemic dose
  • High local concentration
  • Superinfections, such as with Clostridium difficile, unlikely
  • Drug interaction unlikely
  • Site specific (deepest pockets)
  • Patient compliance not an issue as applied by HCP
  • Can utilise agents which can’t be utilised systemically e.g. chlorohexidine
70
Q

3 disadvantages of local antimicrobials for perio tx

A
  • Expensive (depends on context)
  • Still require RSD or biofilm disruption (same rules apply)
  • Limited indications
71
Q

example antimicrobial used in perio

A

chlorohexidine -

PerioChip- wait until most of the pockets heal after instrumentation during HPT and use it in persisting pockets only during targeted roof surface debridement and maintenance recalls – auxiliary aid

72
Q

4 indications for using local antiseptics (PerioChip) and Piscean, Chlo-site

A
  1. only persisting pockets > 5 mm
  2. always with RSD
  3. Only in isolated pockets/ restricted number (if many deep periodontal pockets in one area - OFD or systemic antibiotics combined with RSD is more beneficial)
  4. in case of periodontal abscesses – after evacuation of pus and RSD.
73
Q

PerioChip

A

chlorohexidine local antimicrobial/septic

but

bovine origin gelatine based

74
Q

Piscean

A

local antimicrobial

but

fish collagen based

75
Q

chlo-site

A

chlorohexidine gel

local antimicrobial/septic

76
Q

3 antibiotics that are local antimicrobials

A
  1. Arestin – 1 mg minocycline HCL microspheres
  2. Atridox – doxycycline hyclate 10 %
  3. Elyzol - 25 % metronidazole
77
Q

how do antibiotics that are local antimicrobials work

A

constructed in microspheres – AB released in form where no fluctuation of concentration of AB, stable dosage in the tissue, protecting us against resistance development

78
Q

2 alternative perio therapies

A

periostat

PerioWave

79
Q

periostat

A

20 mg of doxycycline - twice a day for 3 months, systemically, as an adjunct to supra-/sub-gingival instrumentation.

  • low dose of doxycycline is considered to be sub-antimicrobial, meaning that the dose is insufficient to inhibit the growth of bacteria, it is prescribed for its role as a collagenase inhibitor - an enzyme produced by both bacterial and human cells, is responsible for the breakdown of collagen and is implicated in periodontal tissue damage.
  • Sub-antimicrobial dose of doxycycline was unlikely to exert a significant evolutionary pressure and therefore less likely to accelerate the development of drug resistant bacteria.
80
Q

PerioWave

A
  • photodesinfection active and inactive in certain wavelengths – give control of the site they act on
    • 1.Irrigate:
      • photosensitizing solution is topically applied to the gums at the treatment site. It then preferentially attaches to the harmful bacteria and toxins associated with periodontal disease.
    • 2.Illuminate:
      • thin, plastic light diffusing tip is painlessly placed into the treatment site. The treatment site is illuminated with a specifically calibrated laser light, activating the photosensitizing solution and destroying the harmful bacteria and toxins
81
Q

host modulation therapy for perio

A

so far not very successful

tried use some therapies from autoimmune diseases

  • e..g. corticosteroids, NSAIDs, bisphosphonates, anit-TNF-alpha (infliximab), lipid mediators for resolution of inflammation

common issues: side effects (destroying own cells (healthy ones)) , no long-term outcomes

Need time and technology investment as need to be specific to periodontal tissue to reduce side effects

82
Q

periodontal disease is an overreaction

A

of self-microbiome immune system

with no self-resolution

83
Q

an appropriate 5 day regime for periapcial abscess anitbiotics (adult)

A

amoxicillin capsules 500mg

send: 15 capsule

1 capsule three times daily

if allergic - metronidazole tablets, 200mg, 15 tables, 1 tablet three times daily

if pt does not respons to first line tx or severe infection with spreading cellulitis

clindamycin capsules 150mg

send: 20 capsules

1 capsule four times daily, swallowed with water

BDS3 Perio (7 decks)

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