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ICS - PERIODONTOLOGY > ICS2/4: Acute Conditions in Periodontology > Flashcards

ICS2/4: Acute Conditions in Periodontology Flashcards

1
Q

what are the 4 main painful acute conditions in periodontology?

A
  • ANUG
  • acute herpetic gingivostomatitis
  • periodontal abscess
  • perio-endo lesion (combined lesion)
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2
Q

ANUG: under which periodontal classification?

A

Class V: Necrotising periodontal diseases

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3
Q

ANUG: age of onset? gender distribution?

A
  • 16-30 years old

- same for females and males

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4
Q

ANUG: prevalence higher in which type of countries and what type of conditions?

A

prevalence higher in developing countries, associated with malnutrition and infection, especially in children

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5
Q

ANUG: describe the experience of pain

A

sudden onset
can be severe
may affect eating

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6
Q

clinical feature of ANUG?

A
  • grey pseudomembraneous slough: easily removed leaving raw bleeding surface
  • necrotic ulcers
  • halitosis
  • spontaneous bleeding
  • metallic taste: anaerobes in mouth (try to locate where it’s coming from)
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7
Q

describe the necrotic ulcers in ANUG and how they progress

A
  • initially: red swollen interdental papillae
  • punched out ulceration starts on tips of interdental papillae
  • ulceration spreads laterally along gingival margin
  • results in loss of the interdental papillae leading to “punched out” appearance
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8
Q

ANUG: distribution?

systemic symptoms?

A
  • localised/generalised
  • generally no systemic symptoms, there may be mild/moderate fever, malaise and lymphadenopathy (cervical and submandibular)
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9
Q

what is the course if ANUG is not treated?

A
  • acute symptoms: 2-3weeks
  • healing leaves a chronic gingivitis
  • recurrence of disease: further interdental papillae damage
  • areas of stagnation promote disease progression (of underlying chronic periodontitis)
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10
Q

if ANUG not treated: what will happen to those in developing countries (with malnourished/diseased children)?

A

Cancrum oris/ NOMA

  • in malnourished/diseased children, can progress to affect facial tissues
  • causes massive oro-facial necrosis: can be disfiguring or fatal
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11
Q

name the principle bacteria of ANUG

A
  • treponema vincentii & denticola
  • fusobacterium nucleatum
  • prevotella intermedia
  • porphyromonas gingivalis
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12
Q

what proves the important role of bacteria in ANUG?

A
  • the fact that patients with ANUG respond quicky to bacteria
  • ANUG rarely occurs in a clean mouth
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13
Q

predisposing factors for ANUG?

A
  • poor OH
  • stress
  • immunodeficiency
  • smoking
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14
Q

how does smoking effect the immune system?

A

smoking alters

  • serum IgG antibodies to subclinical bactria
  • number of t-helper lymphocytes
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15
Q

SDCEP recommendations for ANUG management

A
  • oral hygiene TIPPS behaviour change; emphasize importance of plaque removal
  • remove supragingival plaque, calculus and subgingival stain deposits
  • 6% hydrogen peroxide or 0.2% Chx mouthwash
  • metronidazole if there is spreading infection or systemic involvement
  • review within 10 days, carry out further supra/sub gingival instrumentation
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16
Q

management of ANUG: aim of initial visit?

A
  • relief of pain
    1. OHI
    2. explanation of cause
    3. USS
    4. antimicrobial therapy?
    5. see pt again in 48 hours
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17
Q

management of ANUG: aim of subsequent visits? further visits will access which 3 things?

A
  • majority of cases would have sufficiently reduced to allow a full periodontal examination
  • explanation of cause
  • carry out further cause related therapy: OHI, smoking cessation, sub/supragingival debridement
  • further visits will access: patient compliance with OHI, smoking cessation, tissue response to treatment
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18
Q

periodontal abscess: define

may cause damage to which periodontal tissues specifically?

A
  • localised purulent infection within the tissues adjacent to the periodontal pocket
  • PDL & alveolar bone
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19
Q

periodontal abscess: under which classification of perio diseases?

A

Class VI: abscesses of the periodontium

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20
Q

periodontal abscess: possible causes?

A
  • pocket obstruction
  • post systemic antimicrobials
  • local risk factors affecting morphology of the root
  • manifestation of systemic disease
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21
Q

periodontal abscess aetiology: pocket blockage caused by?

A
  • untreated periodontal disease: accumulation of calculus
  • inadequate periodontal treatment: leaving calculus at pocket base after debridement, pushing calculus fragments into tissues during scaling
  • foreign body impaction into gingival sulcus or perio pocket: e.g. fish bone
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22
Q

pocket blockage leads to?

lysosomal enzymes contribute to?

A
  • reduced clearance of GCF, leading to accumulation of bacteria and host cells
  • infection spreads to surrounding gingival/periodontal tissue
  • much of tissue damage is due to release of lysosomal enzymes from the host neutrophils
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23
Q

local risk factors affecting morphology of root: perio abscesses can occur more readily in relation to?

A
  • furcations
  • defects in root morphology:
    1. root fissures
    2. enamel pearls
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24
Q

multiple/recurrent periodontal disease: indicates what?

A

that patient is immunocompromised with possibly undiagnosed or poorly controlled diabetes

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25
Q

microbiology of periodontal abscess: 4 main GNABs?

A
  • porphyromonas gingivalis
  • prevotella intermedia
  • tannerella forsythia
  • fusobacterium nucleatum
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26
Q

describe the histopathology of a periodontal abscess

A
  • bacterial invasion of soft tissue wall

- leading to rapid periodontal destruction: polymorphonuclear lymphocytes + suppuration + osteoclasts (bone destruction)

27
Q

diagnostic criteria for periodontal abscess? x6

A
  • sudden throbbing pain (mild-severe)
  • patient can localize pain
  • tooth may be high on occlusion
  • increased mobility
  • tooth may be ttp
  • localized gingival swelling + tenderness
28
Q

differential diagnosis for periodontal abscess?

A
  • periradicular abscess
  • perio-endo lesion
  • vertical root fracture
  • gingval abscess
  • pericoronal abscess
29
Q

diagnosis of periodontal abscess: describe each component

  • history
  • lymphoadenopathy
  • radiographs
  • sensitivity tests? (what to take note?)
A
  • patient’s history
  • disease of the lymph nodes, sometimes localized
  • may show no change or some bone loss.
  • vital response: tooth is vital in periodontal abscess. beware of interpretation because teeth can be multi rooted and heavily restored
30
Q

difference in sensitivity test for periodontal abscess and periradicular abscess?

A

periodontal abscess - tooth is vital

periradicular abscess - tooth non vital

31
Q

treatment of periodontal abscess? x3

A
  • root surface debridement: removal of calculus/foreign object under LA
  • drainage: crossed incision to allow prolonged drainage
  • antibiotics: last resort option where drainage not possible (oral amoxicillin 250mg capsules x3 a day for 5 days OR metronidazole 200mg x3 a day for 5 days)
32
Q

primary herpetic gingivostomatitis: what is the primary infective agent?

A

usually herpes simplex 1 virus (HSV-1)

33
Q

PHG: age group commonly infected? what is it usually mistaken for?

A
  • children 1-10yrs old

- mistaken for pre school children teething

34
Q

PHG

  • transmission?
  • incubation period?
  • diagnosis from?
A
  • through infected saliva, or skin lesion contact
  • 5 days
  • from clinical symptoms
35
Q 
PHG
- onset?
- appearance of what in which oral tissues? this leads to?
what brings on a painful stomatitis?
how does gingivae appear?
A
  • sudden onset
  • vesicles develop in gingivae, tongue, buccal mucosa, lips
  • vesicles burst, leaving superficial ulcers (yellow-greyish) with red halo
  • ulcers coalesce, develop fibrous coating -> painful stomatitis
  • gingivae appears inflamed, swollen, tender often with fiery red appearance
36
Q

other clinical features of PHG?

A

cervical lymphadenopathy
fever - mild to severe
malaise
painful mouth and throat (eating difficult)

37
Q

PHG clinical features:
in young children?
course? subsides when?
healing?

A
  • young children can be irritable, with profuse salivation and refusal to eat
  • 10-21 days, subsides when antibody titre rises
  • heals without scarring
38
Q

treatment of PHG? x3

A
  • reassure patient: explain disease and inform that will resovle in 1-2 weeks
  • dietary advice: bland soft food, plenty of fluids
  • paracetamol: aspirin for >12 y/o, reduces pain and temperature
39
Q

treatment of PHG? x3

what to do for immunocompromised patients?

A
  • chx mouth wash (aid healing and OH), only in those 8+ years
  • difflam mouthwash (benzydamine hydrochloride)
  • review in a week
  • immunocompromised: systemic aciclovir
40
Q

herpes labialis (cold sores)

  • patients commonly at what stage of life?
  • caused by?
  • preceded by?
A
  • 30% patients at later stage of life
  • caused by reactivation of latent HSV in trigeminal ganglion
  • preceded by itching/burning sensation prior to lesions
41
Q

herpes labialis:

  • lesions commonly on?
  • initially appears as? that forms ___?
  • heals in how long?
A
  • mucocutaneous junction of upper lip, occasionally lower
  • appears as blister which burst to form crust
  • heals in about 10 days
42
Q

herpes labialis: predisposing factors? x4

A
  • systemic disease
  • sunlight
  • stress
  • hormonal changes
43
Q

herpes labialis: treatment?

A

start at initial/prodromal burning sensation

- topical 5% aciclovir cream 5 times daily, every 4 hours for 5 days

44
Q

what happens when oral lesion cracks and spreads to fingers?

A

herpetic whitlow (herpetic lesions on fingers)

45
Q

perio-endo lesion:
infection involving which two components?
classified as?

A
  • involves the periodontium and root canal system

- classified as periodontal disease associated with endodontic lesions

46
Q

perio-endo lesions:

  • through which routes of communication between what can potentially allow microorganisms to exchange?
  • what kind of treatment may remove cementum which usually covers the lateral/accessory canals?
A
  • between pulp and periodontal ligament, the routes are the accessory canals, lateral canals and the apex of the tooth
  • aggressive periodontal treatment
47
Q

perio-endo lesions: dentinal tubule exposure during? leads to?
pulp status?
what kind of changes?

A
  • may be exposed during periodontal therapy, resulting in dentine hypersensitivity
  • pulp is resilient, healthy
  • mild inflammatory changes, but tooth still survives
48
Q

accessory/lateral canal and exposure of apex allows infection to spread in which 2 possible ways?
ultimately leads to?

A
  • pulp into PDL: primary endodontic disease with secondary periodontal involvement
  • PDL into pulp: primary periodontal disease with secondary endodontic involvement
  • leads to disease of both the pulp and periodontal tissues
49
Q

perio-endo lesions: other possible routes of communication?

A
  • root fractures
  • perforations during RCT
  • caries
  • resorption
  • abnormal anatomy e.g. root groove
50
Q

classification of perio-endo lesions x3

A

1 - primary endodontic disease
2 - primary periodontal disease
3 - true combined disease

51
Q

primary periodontal disease:

presence of? how does it expose canals? exposure leads to and causes what eventually?

A
  • deep periodontal pockets that extend close to apex, and expose the lateral/accessory canals
  • exposure leads to bacteria/toxins accessing the pulp, causing endodontic symptoms/pulpal necrosis (amy be silent)
52
Q

primary perio disease: only significant evidence for perio pockets reaching where to cause pulp necrosis?

A
  • significant evidence that perio pockets reaching root apex to cause pulp necrosis
  • little evidence that perio pockets exposing lateral/accessory canals result in pulpal necrosis - outward flow of dentinal fluid likely to be protective
53
Q

primary endo disease:
endodontic apical lesion extends laterally to create?
endodontic lesion spreads into periodontal tissues via?

A
  • perio pocket, or joins with an existing perio pocket
  • lateral/accessory canals
  • dentinal tubules
  • root fractures
  • iatrogenic perforations
54
Q

primary endo disease:
pulpal bacteria and toxins into perio tissues
explain the evidence that bacterial penetration through dentine is limited

A
  • narrow dentinal tubules
  • cementum present
  • bacterial products/breakdown products may penetrate further
55
Q

true combined lesion:

regarded as?

A

independent endodontic and periodontal lesions that have merged
thought to be rare

56
Q

diagnosis of perio-endo lesions:
history?
clinical exam?
radiographic findings?

A
  • pt’s history
  • deep pocketing,
    BOP,
    suppuration from pockets,
    inflammatory response (redness and swelling of tissue)
    sinus formation
    increased mobility
    TTP/painful tooth
  • possible furcation involvement, bone loss (angular bone loss around the apex), periradicular pathology
57
Q

diagnosis of perio-endo lesions:

sensitivity tests?

A
  • teeth non-vital

beware of non-vital teeth

58
Q

treatment of perio-endo lesion? if tooth is to be retained? why?

A

always treat the endodontic problem first (RCT) before any periodontal treatment
- necrotic pulp acts as reservoir of infection and must be adequately treated prior to perio treatment

59
Q

long term success of RCT depends on?

A
  • dependent on elimination of bacteria from root canals and achieving good coronal seal
60
Q

treatment of perio-endo lesion:
if tooth perforated?
if tooth fractured?
if unsure about prognosis?

A
  • repair first
  • extract first
  • consider stabilizing by shaping and irrigating + leaving calcium hydroxide in canal for 6 weeks before reassessing and treating perio
61
Q

treatment of perio-endo lesions: must consider what 2 factors? what are other treatment options? prognosis of true combined lesions?

A
  • prognosis and usefulness of tooth
  • root resection, extraction often indicated
  • poor prognosis
62
Q

perio-endo lesion prognosis: good indicators?

A
  • single rooted teeth
  • narrow pocket
  • straightforward endo, good obturation, seal
  • patient motivated
  • primary endo lesion
63
Q

perio-endo lesion prognosis: poor prognosis indicators?

A
  • multi-rooted teeth (furcations, canals etc)
  • re-root treatments
  • unstable perio
  • LOA
  • complex lesion: root fractures, grooves, perforations
  • true combined lesion

ICS - PERIODONTOLOGY (10 decks)

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