ICS2/4: Acute Conditions in Periodontology Flashcards
(63 cards)
1
Q
what are the 4 main painful acute conditions in periodontology?
A
- ANUG
- acute herpetic gingivostomatitis
- periodontal abscess
- perio-endo lesion (combined lesion)
2
Q
ANUG: under which periodontal classification?
A
Class V: Necrotising periodontal diseases
3
Q
ANUG: age of onset? gender distribution?
A
- 16-30 years old
- same for females and males
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
5
Q
ANUG: describe the experience of pain
A
sudden onset
can be severe
may affect eating
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)
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
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)
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)
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
11
Q
name the principle bacteria of ANUG
A
- treponema vincentii & denticola
- fusobacterium nucleatum
- prevotella intermedia
- porphyromonas gingivalis
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
13
Q
predisposing factors for ANUG?
A
- poor OH
- stress
- immunodeficiency
- smoking
14
Q
how does smoking effect the immune system?
A
smoking alters
- serum IgG antibodies to subclinical bactria
- number of t-helper lymphocytes
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
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
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
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
19
Q
periodontal abscess: under which classification of perio diseases?
A
Class VI: abscesses of the periodontium
20
Q
periodontal abscess: possible causes?
A
- pocket obstruction
- post systemic antimicrobials
- local risk factors affecting morphology of the root
- manifestation of systemic disease
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
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
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
24
Q
multiple/recurrent periodontal disease: indicates what?
A
that patient is immunocompromised with possibly undiagnosed or poorly controlled diabetes
25
microbiology of periodontal abscess: 4 main GNABs?
- porphyromonas gingivalis
- prevotella intermedia
- tannerella forsythia
- fusobacterium nucleatum
26
describe the histopathology of a periodontal abscess
- bacterial invasion of soft tissue wall
| - leading to rapid periodontal destruction: polymorphonuclear lymphocytes + suppuration + osteoclasts (bone destruction)
27
diagnostic criteria for periodontal abscess? x6
- 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
differential diagnosis for periodontal abscess?
- periradicular abscess
- perio-endo lesion
- vertical root fracture
- gingval abscess
- pericoronal abscess
29
diagnosis of periodontal abscess: describe each component
- history
- lymphoadenopathy
- radiographs
- sensitivity tests? (what to take note?)
- 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
difference in sensitivity test for periodontal abscess and periradicular abscess?
periodontal abscess - tooth is vital
| periradicular abscess - tooth non vital
31
treatment of periodontal abscess? x3
- 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
primary herpetic gingivostomatitis: what is the primary infective agent?
usually herpes simplex 1 virus (HSV-1)
33
PHG: age group commonly infected? what is it usually mistaken for?
- children 1-10yrs old
| - mistaken for pre school children teething
34
PHG
- transmission?
- incubation period?
- diagnosis from?
- through infected saliva, or skin lesion contact
- 5 days
- from clinical symptoms
35
```
PHG
- onset?
- appearance of what in which oral tissues? this leads to?
what brings on a painful stomatitis?
how does gingivae appear?
```
- 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
other clinical features of PHG?
cervical lymphadenopathy
fever - mild to severe
malaise
painful mouth and throat (eating difficult)
37
PHG clinical features:
in young children?
course? subsides when?
healing?
- young children can be irritable, with profuse salivation and refusal to eat
- 10-21 days, subsides when antibody titre rises
- heals without scarring
38
treatment of PHG? x3
- 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
treatment of PHG? x3
| what to do for immunocompromised patients?
- chx mouth wash (aid healing and OH), only in those 8+ years
- difflam mouthwash (benzydamine hydrochloride)
- review in a week
- immunocompromised: systemic aciclovir
40
herpes labialis (cold sores)
- patients commonly at what stage of life?
- caused by?
- preceded by?
- 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
herpes labialis:
- lesions commonly on?
- initially appears as? that forms ___?
- heals in how long?
- mucocutaneous junction of upper lip, occasionally lower
- appears as blister which burst to form crust
- heals in about 10 days
42
herpes labialis: predisposing factors? x4
- systemic disease
- sunlight
- stress
- hormonal changes
43
herpes labialis: treatment?
start at initial/prodromal burning sensation
| - topical 5% aciclovir cream 5 times daily, every 4 hours for 5 days
44
what happens when oral lesion cracks and spreads to fingers?
herpetic whitlow (herpetic lesions on fingers)
45
perio-endo lesion:
infection involving which two components?
classified as?
- involves the periodontium and root canal system
| - classified as periodontal disease associated with endodontic lesions
46
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?
- between pulp and periodontal ligament, the routes are the accessory canals, lateral canals and the apex of the tooth
- aggressive periodontal treatment
47
perio-endo lesions: dentinal tubule exposure during? leads to?
pulp status?
what kind of changes?
- may be exposed during periodontal therapy, resulting in dentine hypersensitivity
- pulp is resilient, healthy
- mild inflammatory changes, but tooth still survives
48
accessory/lateral canal and exposure of apex allows infection to spread in which 2 possible ways?
ultimately leads to?
- 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
perio-endo lesions: other possible routes of communication?
- root fractures
- perforations during RCT
- caries
- resorption
- abnormal anatomy e.g. root groove
50
classification of perio-endo lesions x3
1 - primary endodontic disease
2 - primary periodontal disease
3 - true combined disease
51
primary periodontal disease:
| presence of? how does it expose canals? exposure leads to and causes what eventually?
- 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
primary perio disease: only significant evidence for perio pockets reaching where to cause pulp necrosis?
- 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
primary endo disease:
endodontic apical lesion extends laterally to create?
endodontic lesion spreads into periodontal tissues via?
- perio pocket, or joins with an existing perio pocket
- lateral/accessory canals
- dentinal tubules
- root fractures
- iatrogenic perforations
54
primary endo disease:
pulpal bacteria and toxins into perio tissues
explain the evidence that bacterial penetration through dentine is limited
- narrow dentinal tubules
- cementum present
- bacterial products/breakdown products may penetrate further
55
true combined lesion:
| regarded as?
independent endodontic and periodontal lesions that have merged
thought to be rare
56
diagnosis of perio-endo lesions:
history?
clinical exam?
radiographic findings?
- 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
diagnosis of perio-endo lesions:
| sensitivity tests?
- teeth non-vital
| beware of non-vital teeth
58
treatment of perio-endo lesion? if tooth is to be retained? why?
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
long term success of RCT depends on?
- dependent on elimination of bacteria from root canals and achieving good coronal seal
60
treatment of perio-endo lesion:
if tooth perforated?
if tooth fractured?
if unsure about prognosis?
- repair first
- extract first
- consider stabilizing by shaping and irrigating + leaving calcium hydroxide in canal for 6 weeks before reassessing and treating perio
61
treatment of perio-endo lesions: must consider what 2 factors? what are other treatment options? prognosis of true combined lesions?
- prognosis and usefulness of tooth
- root resection, extraction often indicated
- poor prognosis
62
perio-endo lesion prognosis: good indicators?
- single rooted teeth
- narrow pocket
- straightforward endo, good obturation, seal
- patient motivated
- primary endo lesion
63
perio-endo lesion prognosis: poor prognosis indicators?
- multi-rooted teeth (furcations, canals etc)
- re-root treatments
- unstable perio
- LOA
- complex lesion: root fractures, grooves, perforations
- true combined lesion
