Acute Periodontal Disorders and their Management Flashcards
what is meant by acute periodontal disorders
these are perio disorders which present in acute phase and require emergency treatment OR alteration of original treatment plan
- NPDS
- perio abscesses
- primary herpetic gingivo stomatitis
acute periodontal conditions in the 1999 classification
gingival abscess
periodontal abscess
peri-coronal abscess
peri-apical abscess
why were the acute periodontal conditions in 1999 classification replaced
- cant distinguish between gingival and periodontal abscess easily
- abscess is by definition an ACUTE LESION thus chronic/ acute terms removed
- peri-coronal= when 3rd molars are trying to erupt but theres no space, we get formation of peri-coronal abscess. but this does not relate to periodontium tissues thus removed
acute periodontal conditions in the 2018 classification
- periodontal abscesses (in perio and non perio patients)
- necrotising periodontal diseases (in chronically, severely compromised patients and temporarily/ moderately compromised patients)
why might periodontal abscess present in a perio patient with a pre-existing perio pocket
acute exacerbation (untreated periodontitis, non-responsive to perio therapy, SPT) OR acute treatment (post-scaling, post-surgery, post-mediation such as anti-microbials or nifedipine)
why might periodontal abscess present in a NON-perio patient with no pre-existing perio pocket
impaction (from dental floss, orthodontic elastic, toothpick, rubber dam, popcorn hulls) OR harmful habits (wire/ nail biting, clenching) OR ortho forces (ortho forces, cross bite) OR gingival overgrowth OR alteration of root surface
why may there be alteration of root surface
severe anatomic alterations (invaginated tooth, odontodysplasia)
minor anatomic alterations (cementel tears, enamel pearls, developmental grooves)
latrogenic conditions ( perforations)
severe root damage (fissure, fracture, cracked tooth syndrome)
external root restoration
NPDs in chronically severely compromised CHILDREN may occur due to
severe malnourishment
extreme living conditions
severe viral infection
NPDs in chronically severely compromised ADULTS may occur due to
HIV/ AIDS with CD4 counts >200 and detectable viral load
OR other severe systemic condition (immuno suppression)
NPDS in all chronically severely compromised patients is likely to lead to which clinical conditions
NG NP NS noma possible progression
NPDs in temporarily/ moderatley compromised patients may occur in GINGIVITS patients due to
uncontrolled factors: stress, nutrition, smoking habits (lead to generalised NG , possible NP progression)
OR
previous NPD: residual craters (lead to generalised NG, possible NP progression)
OR
local factors: root proximity, tooth malposition(will lead to LOCALISED NG –> NP progression)
NPDs in temporarily/ moderatley compromised patients may occur in PERIODONTITIS patients due to
common pre-disposing factors for NPD
will lead to NG/ or NP with INFREQUENT progression
definition of periodontal abscess
a LOCALISED PURULENT infection within tissues ADJACENT to PERIO POCKET that MAY lead to destruction of periodontal ligament and alveolar bone
the perio breakdown occurs during a limited period of time
periodontal abscess can be further classified based on the SOURCE of infection. this includes..
- pulp necorsis (due to pulp tissues dying mostly bc of caries OR during crown prep an instrument that compromises the blood supply)
- periodontal infections
- peri-coronitis (3rd molar struggling to come out becomes infected)
- trauma or surgery
- microbes (mainly gram -ve anaerobes)
which microbes are linked with periodontal abscess
aerobes: s. viridans
anaerobes: p. gingivals, p. intermedia, f. nuceleatum, c.rectus, capnocytophag spp, tannerella forsythia, spirochaetes
what are the hypothesised periodontal abscess aetiological factors
- diabetes= increases the susceptibility to abscess formation if not managed
- systemic antibiotic therapy= can target ‘good bacteria; and lead to a superinfection with opportunistic org. here, you would prescribe antibiotics.
- furcation involvement= when theres an abscess between furcation it can be difficult to clean/ instrument
- occlusion of pocket orifice= can be due to many things:
- no clearance of bacteria
- accumulation of host cells
- some host cells will be damaged by neutrophils released lysosomal enzymes
- healing post scaling
when would occlusion of pocket orifice occur
when there is incomplete removal of calculus
impaction of food/ foreign body
bacterial invasion after instrumentation
what are the clinical features of periodontal abscess
- vital pulp response
- affected tooth will have deep pockets and CAL
- mobile tooth
- may be PAINFUL to bite on
- tooth extrusion (high height) thus patient may have sensation to grind on it
- ovoid elevation of gingiva on lateral apsect of ROOT
- gingiva are red, swollen, smooth, shiny
- suppuration from pocket
there are 2 different stages of developmental abscess what are they
early stage, acute= pus not yet draining (there will be swelling, redness etc)
if pus is draining, may become chronic
can periodontal abscess be seen on radiograph
NO
but, if its a perio related patient, then may seen bone loss/ furcation involvement if MOLAR
how do you distinguish from pulpal pain and pain from acute perio abscess
acute presentation of perio abscess= THROBBING pain
pulpal pain= SHARP pain
(this diagnosis will be based on clinical exam, pulp vitality test, radiograph)
what is the management of a perio abscess, PUS NOT draining
may be emergency so control infection, relief pain, assess prognosis
- check that there is no impacted material in pocket
- relieve occlusion e.g. affected tooth may be slightly extruded, may have to grind down opposing tooth?
- advise hot salt mouthwash to increase drainage
- advice painkillers (ibuprofen, paracetamol)
BUT IF severe pain, cant achieve drainage, AND risk of spread of infection then…. - prescribe systemic antibiotics (penicillin, metrandiazole)
- review patient after a few days
what is the management of a perio abscess, WITH PUS to drain
- achieve drainage first - local gentle debridement in pocket, remove impacted material, incision and drinage if indicated
- advise hot salt moutwashes
- relieve occlusion
- advise pain killers
- review in few days
indicators of perio abscess with SYSTEMIC INVOLVEMENT
EXTRA oral swelling lymphadenopathy rarely cellulitis malaise increased temperature
what is the management of a perio abscess, with SYSTEMIC INVOLVEMENT
same as pus to drain AND systemic antibiotics: - metranidazole -penicllin - very powerful combination of met. and amoxycillin for 1 week
then review
what is diffrential diagnosis
this is the other POSSIBLE DIAGNOSES from information in history, exams, signs, symptoms, special tests
in periodontal abscess, diffrential diagnosis may include…
periodontic-endodontic lesion
peri-apical abscess
it would NOT include gingival abscess or peri-CORNOAL absesses because dont exist in 2018 classification (will still cover all 4)
features of gingival abscess
localised purulent infection that involves marginal/ interdental papilla
localised
painful
rapidly expanding
red, shiny, smooth
flucant within 24-48hrs
points and discharges spontaneously
linked with acute inflammatory response to foreign agents
features of peri-coronal abscess
localised purulent infection WITHIN TISSUE surrounding crown of PARTIALLY erupted toooth
- mandibular 3rd molar is a common site
red, swollen gingival flap
infection may spread
possible systemic involvement
aetiology of periodontal-endodontic lesions
this lesion would be called ‘combined periodontal-endodontic’ lesion
aetiology may be
- primary periodontic, secondary endodontic (a necrotic pulp as a result of periodontal involvement) has a poor hopeless prognosis
- primary endodontic, secondary periodontic (periodontium is involved after pulpal necoris)
features of peri-apical abscess
pulpal necrosis (carious pulpal involvement on heavily restored tooth)
non-vital (confirm with pulp vitality test)
peri-apical tissues involved
periodontal tissues involvement is not a key feature
tooth tender to percussion (TTP) thus may be acutely painful
why are NG and NP collectively called NPDs (a type of acute perio abscess)
because they may be different stages of the SAME infection
NB. there is NO such thing as chronic NPDS, but they may ‘recur’
features of NPDS
RAPID onset PAINFUL!!! inter-dental necrosis bleeding gingivae necrotic ulcers affecting interdental papillae punched out papillae ulcers= painful, covered by grey slough gingival bleeding with little provocation possible hallitosis possible lymph nodes involvement tend to occur in young adults in 20s
what is the aetiology of NPDS
- fusiform- spirochaete bacterial infection
(selenomas spp, fusobacterium spp, p. intermedia, and spiroachaetes such as trepenoma sp) - 4 zones of gingival lesion: bacterial zone, necrotic zone, neutrophile rich zone, spircochaetal infection zone
- in young adults due to stress, immunosuppression, smoking, poor diet/ malnutrition, pre-existing gingivitis, poor OH, previous history of NPDs
what is the management of NPDS: local and systemic
local measures= remove gross deposit/ calculus (ultrasonic scaler) oxidising mouthwash (hydrogen peroxide) gentle alcohol +chlorohexidine rinse to preven a secondary infection
systemic measures= metrandizole 200/250 mg for 3 days
after this ‘acute’ phase would consider perio therapy including:OHI, smoking cessation, scale/ polish/ RSD, and focusing on other predisposing factors like stress
NPDS can become recurrent as NP and N. stomatitis. what is the difference between them
NP= necrosis of gingival tissues, periodontal ligament, alveolar bone
NS= necrotising process BELOW/ APICAL to the mucogingival junction
what causes herpetic gingivo stomatitis and how
caused by herpes simplex type ONE
- primary contact- is TRANMISSIBLE via saliva
- it is a disease of childhood, becoming more common in older ages. immunity to virus develops
- decreased resistance may lead to herpes LABIALIS= cold sore- in 30% of population. this IS transmissble
- defining feature = VESICLES
what is herpetic WHITLOW
when HG transmitted to dentist from infected patient
features of primary herpetic gingivo stomatitis
acute onset fever malaise cervical lymphadenopathy gingivae acutely inflammed- VERY red, swollen rising titre of ig to virus vesicles
what are the features of vesicles of primary HGS
found on ANY PART OF MUCOSA- often found on hard palate, dorsum of tongue, gingiva
PAINFUL
2-3 mm
dome shaped
rupture= leaves circular shallow ulcer with yellow/ grey floor and red margin
smears show ballooning degeneration of viral damaged cells
what is management of primary HGS
let it run its course for 7-18 days
NO antibiotics because virus
ACYCLOVIR=anti viral therapy, but needs to be used early to be effective
soft diet, lots of fluid
ANALGESICS= for pain/ fever
bed rest?
chlorohexidine/ gentle swab of it to relieve soreness, control secondary infection, increase healing possibly
