Perio Tx 2 Flashcards
1
Q
most severe inflammatory periodontal disorder caused by plaque bacteria
A
necrotising gingivitis/periodontitis
2
Q
effect on pt of necrotising periodontitis/gingivitis
A
rapidly destructive and debilitating
3
Q
pattern of ANUG/P
A
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
Q
is ANUG/P contagious
A
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.
5
Q
4 main features of NPD
A
painful
bleeding gums
ulceration
necrosis of interdental papilla
6
Q
type of infection in NPD
A
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
7
Q
prevalance of NPD
A
less than 1% in developed countries
27% in developing countries
8
Q
NPD is
A
only one type of periodontal disease
necrotising periodontal disease
severe symptoms - pain, discomfort
9
Q
NPD can be divided into (5)
A
necrotising gingivitis NG
necrotising periodontitis NP
necrotising stomatitis NS
10
Q
necrotising gingivitis
A
is restricted to gingiva tissue (soft tissue)
11
Q
necrotising periodotitis NO
A
involves bone - clinical attachment loss
12
Q
necrotising stomatitis
A
disease not restricted to peridontal tissue
oral mucosa is involved
13
Q
acute and chronic
A
are descriptors of the disease
14
Q
chronic periodontal disease
A
doesnt tend to give severe symptoms to pts - unfortunate because they can present late
(milkd discomfort, bleeding on brushing - present when teeth are mobile)
15
Q
ANUG
A
acute necrotising ulcerative gingivitis
16
Q
ANUP
A
acute necrotising ulcerative periodontits
17
Q
old terms for NPD
A
fusospirochetosis - described bacterial flora involved, not infection
trench mouth - common in trenches in WW1
18
Q
vincents gingivitis, gingivostomatitis, infection
A
classed as necrtosing periodontal disease
not vincents angina
19
Q
vincents angina
A
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
20
Q
NUG
A
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.
21
Q
improper treatment of NUG
A
If improperly treated NUG may become chronic and/or recurrent.
22
Q
usual course of NUG
A
acute
23
Q
NUP
A
Necrotizing ulcerative periodontitis (or simply necrotizing periodontitis, NP) or acute necrotizing ulcerative periodontitis (ANUP) is where the infection leads to attachment loss.
24
Q
NUP and NUG relation
A
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
25
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
26
most causes of necrotising stomatitis
in malnutrition and HIV infection
27
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
28
diagnosis of NPD
based on symptoms *no microbiological test*
29
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
30
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
31
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
32
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)**
33
specific bacteria that may be isolated in abundance from necrotic lesions
spirochetas and fusobacterias
not always evident in primary etiologic lesion
34
differential diagnosis with herpetic gingivostomatitis (early)
## Footnote
*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
35
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
36
risk factors NPD in developing countries
ANUG occurs mostly in malnourished children.
37
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**
38
treatment of acute disease
debridement and antibiotics
* usually metronidazole
39
what needs to be first line of action for NPD treatment
poor OH and other predisposing factors needs to be corrected to prevent recurrence
40
what may be barrier to OH in acute stages
painful to perform - do slowly, commit, several appointments possible
41
debridement for NPD by
ultrasonic debridement (with LA)
42
reason for ultrasonic debridement
to facilitate healing
need to decrease plaque level
43
how to manage pain prevent OH in very acute stages
* 0.2% chlorhexidine mouth wash twice daily
44
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
45
potential methods of managing factors that are influencing disease
smoking cessation
vitamin supplementation (malnourished)
dietary advice (malnourished)
46
what will the treatment be for necrotising periodontitis after carried out acute phase treatment
carry out hygiene phase therapy to treat periodontal disease
47
periodontal health is
the outcome of the balance between bacteria of the dental plaque and the host Immune system
48
2 possible adjuncts to treatment of periodontitis
systemic and topical antimicrobials
host modification therapies
49
periodontal disease is
imbalance between microbiome and host immune system
50
3 treatment strategies for periodontal disease
mechanical disruption
systemic or local antimirobials
host modulation therapy
51
accumulation of biofilm impact on bacteria presence
change in balance from aerobic to anaerobic
52
mechanical disruption as tx for perio
easiest most common
reducing the bacterial challenge
scaling and RSD
53
mechanial disruption for perio targets
biofilm
only method that fully works
54
systemic antibiotics or local antimicrobials as perio tx
only an adjunct
targets biofilm - once it has been disrupted
55
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
56
host modulation therapy for perio targets
functioning of immune system
57
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
* Supra and subgingival plaque control (scaling, RSD)
58
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**
59
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
60
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
61
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)
62
Treatment protocols for systemic antibiotic (specialist treatment) – only in patients after initial HPT and with excellent oral hygiene
1. OH
2. 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))
63
contraindication for amoxicillin
allergies
64
contraindications for metronidazole
* alcohol intake
* Increases anti-coagulant effect of Warfarin
* pregnancy
65
contraindications for doxycylcine
pregnancy – tetracycline staining of the teeth
66
antibiotic regime to start morning after intense full mouth RSD
1. 500 mg amoxicillin 3 times a day for 7 days
200mg BSP (400 mg) metronidazole 3 times a day for 7 days
1. 400mg metronidazole 3 times a day for 7 days (starting to become more popular than a))
67
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
68
metronidazole effect on warafarin
increase anticoagulant effect
bleeding risk
contraindicated
69
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
70
3 disadvantages of local antimicrobials for perio tx
* Expensive (depends on context)
* Still require RSD or biofilm disruption (same rules apply)
* Limited indications
71
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
72
4 indications for using local antiseptics (PerioChip) and Piscean, Chlo-site
1. only persisting pockets \> 5 mm
2. always with RSD
3. Only in isolated pockets/ restricted number *(if many deep periodontal pockets in one area - OFD or systemic antibiotics combined with RSD is more beneficial)*
4. in case of periodontal abscesses – after evacuation of pus and RSD.
73
PerioChip
chlorohexidine local antimicrobial/septic
but
bovine origin gelatine based
74
Piscean
local antimicrobial
but
fish collagen based
75
chlo-site
chlorohexidine gel
local antimicrobial/septic
76
3 antibiotics that are local antimicrobials
1. Arestin – 1 mg minocycline HCL microspheres
2. Atridox – doxycycline hyclate 10 %
3. Elyzol - 25 % metronidazole
77
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
78
2 alternative perio therapies
periostat
PerioWave
79
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.**
80
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
81
host modulation therapy for perio
so far not very successful
tried use some therapies from autoimmune disease*s*
* 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
82
periodontal disease is an overreaction
of self-microbiome immune system
with no self-resolution
83
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
