Perio Tx 2 Flashcards
most severe inflammatory periodontal disorder caused by plaque bacteria
necrotising gingivitis/periodontitis
effect on pt of necrotising periodontitis/gingivitis
rapidly destructive and debilitating
pattern of ANUG/P
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.
is ANUG/P contagious
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.
4 main features of NPD
painful
bleeding gums
ulceration
necrosis of interdental papilla
type of infection in NPD
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
prevalance of NPD
less than 1% in developed countries
27% in developing countries
NPD is
only one type of periodontal disease
necrotising periodontal disease
severe symptoms - pain, discomfort
NPD can be divided into (5)
necrotising gingivitis NG
necrotising periodontitis NP
necrotising stomatitis NS
necrotising gingivitis
is restricted to gingiva tissue (soft tissue)
necrotising periodotitis NO
involves bone - clinical attachment loss
necrotising stomatitis
disease not restricted to peridontal tissue
oral mucosa is involved
acute and chronic
are descriptors of the disease
chronic periodontal disease
doesnt tend to give severe symptoms to pts - unfortunate because they can present late
(milkd discomfort, bleeding on brushing - present when teeth are mobile)
ANUG
acute necrotising ulcerative gingivitis
ANUP
acute necrotising ulcerative periodontits
old terms for NPD
fusospirochetosis - described bacterial flora involved, not infection
trench mouth - common in trenches in WW1
vincents gingivitis, gingivostomatitis, infection
classed as necrtosing periodontal disease
not vincents angina
vincents angina
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
NUG
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.
improper treatment of NUG
If improperly treated NUG may become chronic and/or recurrent.
usual course of NUG
acute
NUP
Necrotizing ulcerative periodontitis (or simply necrotizing periodontitis, NP) or acute necrotizing ulcerative periodontitis (ANUP) is where the infection leads to attachment loss.
NUP and NUG relation
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
necrotising stomatitis
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
most causes of necrotising stomatitis
in malnutrition and HIV infection
cancrum
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
diagnosis of NPD
based on symptoms no microbiological test
diagnosis checklist for NPDs (11)
- 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
ulcers in NUP
- 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
bone effect in NPD
Sequestrum formation necrosis of small or large parts of the alveolar bone
- not only interproximal bone but also adjacent oral and facial bone
why is NPD diagnosis not based on microbiological test
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)
specific bacteria that may be isolated in abundance from necrotic lesions
spirochetas and fusobacterias
not always evident in primary etiologic lesion
differential diagnosis with herpetic gingivostomatitis (early)
Similar in advanced stages
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
risk factors for NPD developed countries
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
risk factors NPD in developing countries
ANUG occurs mostly in malnourished children.
difference with HIV positive and seronegative pts with NPD
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
treatment of acute disease
debridement and antibiotics
- usually metronidazole
what needs to be first line of action for NPD treatment
poor OH and other predisposing factors needs to be corrected to prevent recurrence
what may be barrier to OH in acute stages
painful to perform - do slowly, commit, several appointments possible
debridement for NPD by
ultrasonic debridement (with LA)
reason for ultrasonic debridement
to facilitate healing
need to decrease plaque level
how to manage pain prevent OH in very acute stages
- 0.2% chlorhexidine mouth wash twice daily
how to manage pt with malaise, fever and lassitude, lack of response to mechanical therapy and with impaired immunity
- Fever – recommend ibuprofen
- antibiotics
- 200 mg Metronidazole TID (3 times daily) for 3 days
- 400 mg Metronidazole TID for 3 days
potential methods of managing factors that are influencing disease
smoking cessation
vitamin supplementation (malnourished)
dietary advice (malnourished)
what will the treatment be for necrotising periodontitis after carried out acute phase treatment
carry out hygiene phase therapy to treat periodontal disease
periodontal health is
the outcome of the balance between bacteria of the dental plaque and the host Immune system
2 possible adjuncts to treatment of periodontitis
systemic and topical antimicrobials
host modification therapies
periodontal disease is
imbalance between microbiome and host immune system
3 treatment strategies for periodontal disease
mechanical disruption
systemic or local antimirobials
host modulation therapy
accumulation of biofilm impact on bacteria presence
change in balance from aerobic to anaerobic
mechanical disruption as tx for perio
easiest most common
reducing the bacterial challenge
scaling and RSD
mechanial disruption for perio targets
biofilm
only method that fully works
systemic antibiotics or local antimicrobials as perio tx
only an adjunct
targets biofilm - once it has been disrupted
host modulation therapy for periodontal treatment
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
host modulation therapy for perio targets
functioning of immune system
means of mechanical disruption
- Oral hygiene instruction
- Tooth brushing technique
- Modified bass technique
- Flossing
- If papilla still intact
- Interdental brushes
- Black triangles present – papilla gone
- Tooth brushing technique
- Supra and subgingival plaque control (scaling, RSD)
use of systemic antiobiotics in perio tx
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
why is systemic antibiotic use alone ineffective
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
to use systemic antibiotics can be used for perio must have
Mechanical disruption of biofilm with systemic antibiotics
- never systemic antibiotics alone, and never first line of treatment
- decrease plaque levels, hygiene phase therapy first
what cases can we consider tx with systemic antibiotics with mechanical disruption of biofilm
cases of
- Aggressive periodontitis (old classification)
- Young people with grade B/C (fast progressing periodontitis) (new classification)
Treatment protocols for systemic antibiotic (specialist treatment) – only in patients after initial HPT and with excellent oral hygiene
- OH
- 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))
contraindication for amoxicillin
allergies
contraindications for metronidazole
- alcohol intake
- Increases anti-coagulant effect of Warfarin
- pregnancy
contraindications for doxycylcine
pregnancy – tetracycline staining of the teeth
antibiotic regime to start morning after intense full mouth RSD
- 500 mg amoxicillin 3 times a day for 7 days
200mg BSP (400 mg) metronidazole 3 times a day for 7 days
- 400mg metronidazole 3 times a day for 7 days (starting to become more popular than a))
antibiotics regime if pr allergic to amoxicillin or on warfarin
- 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
metronidazole effect on warafarin
increase anticoagulant effect
bleeding risk
contraindicated
advantages of local antimicrobials (7)
- 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
3 disadvantages of local antimicrobials for perio tx
- Expensive (depends on context)
- Still require RSD or biofilm disruption (same rules apply)
- Limited indications
example antimicrobial used in perio
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
4 indications for using local antiseptics (PerioChip) and Piscean, Chlo-site
- only persisting pockets > 5 mm
- always with RSD
- Only in isolated pockets/ restricted number (if many deep periodontal pockets in one area - OFD or systemic antibiotics combined with RSD is more beneficial)
- in case of periodontal abscesses – after evacuation of pus and RSD.
PerioChip
chlorohexidine local antimicrobial/septic
but
bovine origin gelatine based
Piscean
local antimicrobial
but
fish collagen based
chlo-site
chlorohexidine gel
local antimicrobial/septic
3 antibiotics that are local antimicrobials
- Arestin – 1 mg minocycline HCL microspheres
- Atridox – doxycycline hyclate 10 %
- Elyzol - 25 % metronidazole
how do antibiotics that are local antimicrobials work
constructed in microspheres – AB released in form where no fluctuation of concentration of AB, stable dosage in the tissue, protecting us against resistance development
2 alternative perio therapies
periostat
PerioWave
periostat
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.
PerioWave
-
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
- 1.Irrigate:
host modulation therapy for perio
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
periodontal disease is an overreaction
of self-microbiome immune system
with no self-resolution
an appropriate 5 day regime for periapcial abscess anitbiotics (adult)
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
