ICS2/4: Acute Conditions in Periodontology Flashcards
what are the 4 main painful acute conditions in periodontology?
- ANUG
- acute herpetic gingivostomatitis
- periodontal abscess
- perio-endo lesion (combined lesion)
ANUG: under which periodontal classification?
Class V: Necrotising periodontal diseases
ANUG: age of onset? gender distribution?
- 16-30 years old
- same for females and males
ANUG: prevalence higher in which type of countries and what type of conditions?
prevalence higher in developing countries, associated with malnutrition and infection, especially in children
ANUG: describe the experience of pain
sudden onset
can be severe
may affect eating
clinical feature of ANUG?
- 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)
describe the necrotic ulcers in ANUG and how they progress
- 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
ANUG: distribution?
systemic symptoms?
- localised/generalised
- generally no systemic symptoms, there may be mild/moderate fever, malaise and lymphadenopathy (cervical and submandibular)
what is the course if ANUG is not treated?
- 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)
if ANUG not treated: what will happen to those in developing countries (with malnourished/diseased children)?
Cancrum oris/ NOMA
- in malnourished/diseased children, can progress to affect facial tissues
- causes massive oro-facial necrosis: can be disfiguring or fatal
name the principle bacteria of ANUG
- treponema vincentii & denticola
- fusobacterium nucleatum
- prevotella intermedia
- porphyromonas gingivalis
what proves the important role of bacteria in ANUG?
- the fact that patients with ANUG respond quicky to bacteria
- ANUG rarely occurs in a clean mouth
predisposing factors for ANUG?
- poor OH
- stress
- immunodeficiency
- smoking
how does smoking effect the immune system?
smoking alters
- serum IgG antibodies to subclinical bactria
- number of t-helper lymphocytes
SDCEP recommendations for ANUG management
- 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
management of ANUG: aim of initial visit?
- relief of pain
1. OHI
2. explanation of cause
3. USS
4. antimicrobial therapy?
5. see pt again in 48 hours
management of ANUG: aim of subsequent visits? further visits will access which 3 things?
- 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
periodontal abscess: define
may cause damage to which periodontal tissues specifically?
- localised purulent infection within the tissues adjacent to the periodontal pocket
- PDL & alveolar bone
periodontal abscess: under which classification of perio diseases?
Class VI: abscesses of the periodontium
periodontal abscess: possible causes?
- pocket obstruction
- post systemic antimicrobials
- local risk factors affecting morphology of the root
- manifestation of systemic disease
periodontal abscess aetiology: pocket blockage caused by?
- 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
pocket blockage leads to?
lysosomal enzymes contribute to?
- 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
local risk factors affecting morphology of root: perio abscesses can occur more readily in relation to?
- furcations
- defects in root morphology:
1. root fissures
2. enamel pearls
multiple/recurrent periodontal disease: indicates what?
that patient is immunocompromised with possibly undiagnosed or poorly controlled diabetes
microbiology of periodontal abscess: 4 main GNABs?
- porphyromonas gingivalis
- prevotella intermedia
- tannerella forsythia
- fusobacterium nucleatum
describe the histopathology of a periodontal abscess
- bacterial invasion of soft tissue wall
- leading to rapid periodontal destruction: polymorphonuclear lymphocytes + suppuration + osteoclasts (bone destruction)
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
differential diagnosis for periodontal abscess?
- periradicular abscess
- perio-endo lesion
- vertical root fracture
- gingval abscess
- pericoronal abscess
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
difference in sensitivity test for periodontal abscess and periradicular abscess?
periodontal abscess - tooth is vital
periradicular abscess - tooth non vital
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)
primary herpetic gingivostomatitis: what is the primary infective agent?
usually herpes simplex 1 virus (HSV-1)
PHG: age group commonly infected? what is it usually mistaken for?
- children 1-10yrs old
- mistaken for pre school children teething
PHG
- transmission?
- incubation period?
- diagnosis from?
- through infected saliva, or skin lesion contact
- 5 days
- from clinical symptoms
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
other clinical features of PHG?
cervical lymphadenopathy
fever - mild to severe
malaise
painful mouth and throat (eating difficult)
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
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
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
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
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
herpes labialis: predisposing factors? x4
- systemic disease
- sunlight
- stress
- hormonal changes
herpes labialis: treatment?
start at initial/prodromal burning sensation
- topical 5% aciclovir cream 5 times daily, every 4 hours for 5 days
what happens when oral lesion cracks and spreads to fingers?
herpetic whitlow (herpetic lesions on fingers)
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
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
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
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
perio-endo lesions: other possible routes of communication?
- root fractures
- perforations during RCT
- caries
- resorption
- abnormal anatomy e.g. root groove
classification of perio-endo lesions x3
1 - primary endodontic disease
2 - primary periodontal disease
3 - true combined disease
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)
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
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
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
true combined lesion:
regarded as?
independent endodontic and periodontal lesions that have merged
thought to be rare
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
diagnosis of perio-endo lesions:
sensitivity tests?
- teeth non-vital
beware of non-vital teeth
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
long term success of RCT depends on?
- dependent on elimination of bacteria from root canals and achieving good coronal seal
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
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
perio-endo lesion prognosis: good indicators?
- single rooted teeth
- narrow pocket
- straightforward endo, good obturation, seal
- patient motivated
- primary endo lesion
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
