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perio > 3rd year > Flashcards

3rd year Flashcards

1
Q

aims of supportive PD care (maintenance)

A

maintain PD health
detect and tx recurrence
maintain accepted level of disease
manage tooth loss

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2
Q

supportive PD care (maintenance) - who

A

pts who have had PD tx

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3
Q

supportive PD care (maintenance) - consequence of not returning

A

txed pts who do not return for regular recall are x5.6 greater risk for tooth loss than compliant pts

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4
Q

what does supportive PD care (maintenance) involve?

A

exam
tx
report and scheduling

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5
Q

other causes for recurrence other than inadequate OH/compliance?

A

inadequate/insufficient tx that has failed to remove all of the potential factors favouring plaque accumulation

incomplete calculus removal in areas of difficult access

inadequate Rxs placed after PD tx was completed

failure of pt to return for check-ups

health changes - systemic disease that may affect host resistance to prev acceptable levels of plaque

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6
Q

how long are pts at risk of disease recurrence for?

A

the rest of their lives

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7
Q

PD tx in pregnancy

A 
tx before if possible
provide non-surgical tx in 2nd trimester
avoid 'traumatic' procedures
 - PD surgery
 - full mouth debridement??
discuss w pt
as a minimum provide supportive care
 - supra gingival without LA and regular OHI
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8
Q

2017 PDDs classification - main overall groups

A

health, gingival diseases and conditions
periodontitis
other conditions

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9
Q

2017 PDDs classification - parts

A

PD health
Gingivitis - dental-biofilm induced
Gingival diseases and conditions: non-dental-biofilm induced
Necrotising periodontal diseases
Periodontitis
Periodontitis as a manifestation of systemic disease
Systemic diseases/conditions affecting the periodontal tissues
Periodontal abscesses and perio-eondo lesions
Mucogingival deformities and conditions
Traumatic occlusal forces
Tooth and prostheses related factors

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10
Q

2017 PDDs classification - mneumonic

A 
Please
Give
Greg
Nine
Percy
Pigs
Straight
Past
Meal
Time
Tonight
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11
Q

2017 PDDs classification - PD health subcategories

A

intact periodontium

reduced periodontium

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12
Q

2017 PDDs classification - gingivitis dental-biofilm induced subcategories

A

intact periodontium

reduced periodontium

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13
Q

2017 PDDs classification - periodontitis subcategories

A

localised ≤30%
generalised >30%
MI pattern

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14
Q

problems with 1999 system

A

aggressive vs chronic
- more likely to be genetic
- often in young pts
- “usually affecting persons <30yrs but pts may be older”
- v woolly - room for interpretation
diagnosis of gingival health
- if pt has one bleeding site - gingivitis
- diagnosing everyone with a disease whether or not they have one
diagnosis of prev periodontitis?

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15
Q

2017 classification aims

A

capture extent and severity
- amount of PD tissue loss
pt susceptibility
- estimated by historical rate of progression
current PD state
- pocket depths/BOP
a system that can be future-proofed for update with new biomarker info e.g. if start to get salivary biomarkers

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16
Q

extent

A 
captures distribution
localised <30% teeth
generalised >30% teeth
MI pattern
 - tends to occur in younger pts
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17
Q

what does grading tell you?

A

disease susceptibility

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18
Q

what does staging tell you?

A

severity

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19
Q

what stage is a pt if they are known to have lost teeth due to perio?

A

stage 4

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20
Q

potential consequence of stage 3

A

potential for additional tooth loss

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21
Q

potential consequence of stage 4

A

potential for loss of dentition

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22
Q

what does currently in remission mean?

A

pt who had periodontitis who now has gingivitis

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23
Q

what does BPE guide?

A

need for further diagnostic measures prior to establishing a definitive PD diagnosis and appropriate tx planning

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24
Q

4mm threshold

A

critical as determines PDD stability at non-bleeding sites following successful PD therapy
5/6mm in absence of bleeding may not always represent active disease - in particular soon after PD tx
- need clinical judgement

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25
Q

health

A

intact periodontium
reduced periodontium due to causes other than periodontitis
reduced periodontium due to periodontitis
- but pt will always be a perio pt

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26
Q

plaque-induced gingivitis

A

associated w dental biofilm alone
mediated by systemic/local risk factors
drug influenced gingival enlargement

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27
Q

gingival health on an intact periodontium

A 
no BOP
no erythema and oedema
no pt symptoms
no attachment and bone loss
physiological bone levels range from 1-3mm apical to CEJ
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28
Q

classification of gingival health

A

for an intact periodontium and a reduced and stable periodontium, gingival health is <10% bleeding sites with probing depths ≤3mm

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29
Q

plaque-induced gingivitis: intact periodontium

A 
no ID recession - papilla intact
no probing AL
pocket depths ≤3mm
BOP ≥10%
no radiological bone loss
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30
Q

plaque-induced gingivitis: reduced periodontium (non-perio pt)

A 
e.g. on distal of 7 where 8 has been extracted may be a bony defect
probing AL
pocket depths ≤3mm
BOP ≥10%
radiological bone loss possible
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31
Q

plaque-induced gingivitis: successfully txed perio pt (gingival inflammation in pt with history of perio - remission)

A 
probing AL
pocket depths ≤4mm
 - no site ≥4mm with BOP
BOP ≥10%
radiological bone loss
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32
Q

plaque-induced gingivitis - modifying factors

A

A - associated with bacterial dental biofilm only
B - potential modifying factors
C - drug-induced gingival enlargements

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33
Q

plaque-induced gingivitis: potential modifying factors

A 
1 - systemic conditions
 - sex steroid hormones: puberty, menstrual cycle, pregnancy, OCP
 - hyperglycaemia
 - leukaemia
 - smoking
 - malnutrition
2 - oral factors enhancing plaque accumulation
 - prominent subgingival Rx margins
 - hyposalivation
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34
Q

plaque-induced gingivitis: drug-induced gingival enlargements

A

anticonvulsants - phenytoin
Ca channel blockers - amlodipine
immunosuppressants - cyclosporin

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35
Q

pregnancy epulis

A 
considered a mucogingival deformity
may decide to biopsy
often resolve after baby born
no radiological bone loss
no ID recession
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36
Q

Rx margins 1/2 mm into sulcus

A

pt needs to be aware of risk of recession

- 80% have recession after 5yrs

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37
Q

non-plaque induced gingival diseases and conditions

A

genetic/developmental disorders
- e.g. hereditary gingival fibromatosis - if you resect it often it resolves and doesn’t recur
specific infections e.g. herpetic gingival stomatitis, c albicans
inflammatory and immune conditions e.g. LP, pemphigoid
reactive processes
neoplasms
endocrine, nutritional and metabolic diseases
traumatic lesions
gingival pigmentation

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38
Q

necrotising PDDs in chronically severely compromised pts

A 
adults
 - HIV+/AIDS with CD4 <200
 - other severe systemic conditions (immunosuppression)
children
 - severely malnourished
 - extreme living conditions
 - severe (viral) infections
clinical conditions
 - NG, NP, NS, Norma possible progression
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39
Q

NG S+S

A 
necrosis and ulcer in interdental papilla
gingival bleeding
pain
pseudomembrane formation
 - white/yellow coating over gingivae
halitosis
EO - regional lymphadenopathy/fever

in children, pain and halitosis less freq, whereas fever, lymphadenopathy and sialorrhea were more freq

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40
Q

NP

A

in addition to S+S of NG
periodontal attachment and bone destruction
freq EO signs
in severely immunocompromised pts, bone sequestrum may occur

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41
Q

NS

A

serious, unlikely in UK
bone denudation extended through the alveolar mucosa
larger areas of osteitis and bone sequestrum

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42
Q

NPDs in temp/mod compromised pts

A

gingivitis pts
- uncontrolled factors: stress, nutrition, smoking
- prev NPD - residual craters
- generalised NG, possible progression to NP
- local factors: root proximity, tooth malposition
- localised NG, possibly to NP
need to find out why they have it - may need to investigate systemic diseases
if common predisposing factors in gingivitis and periodontitis pts (temp/mod)
- NG infreq progression
- NP infreq progression

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43
Q

systemic diseases/conditions affecting the periodontal tissues

A

mainly rare conditions affecting the PD tissues independently of dental-biofilm induced inflammation
- disease process itself is destroying the tissues
A more heterogeneous group of conditions which result in breakdown of PD tissues and some of which may mimic the clinical presentation of periodontitis
- SCC
- Langerhans cell histocytosis

cancer cell tissues can invade and destroy PD attachment

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44
Q

PD abscesses in non-perio pts

A

impaction: floss, ortho elastic, dam, popcorn hulls
harmful habits: nail biting and clenching
ortho factors: forces or a X bite
gingival overgrowth
alteration of root surface

= need to understand why they have the abscess

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45
Q

periodontitis as a manifestation of systemic disease

A

classification based on primary systemic disease
mainly rare diseases that affect the course of periodontitis resulting in the early presentation of severe perio
- much more pronounced than e.g. diabetes
Papillon Lefevre Syndrome
- defect in immune system
LAD
hypophosphatasia
(Down syndrome)
EDS

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46
Q

risk factors

A

e.g. diabetes - variable effects that modify the course of periodontitis
- part of multifactorial
in clinical classification
e.g. diabetes could be well-controlled and not really affect perio

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47
Q

PD abscesses in a perio pt (in a pre-existing pocket)

A 
acute exacerbation
 - un-txed perio
 - non-responsive to therapy perio
 - supportive PD therapy
after tx
 - post-scaling
 - post-surgery
 - post-medication
    - systemic antimicrobials
    - other drugs: nifedipine
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48
Q

perio-endo lesions classification

A 
with root damage
 - root fracture/cracking
 - RC or pulp chamber perforation
 - external RR
without root damage
 - perio pts
 - non-perio pts
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49
Q

mucogingival deformities and conditions

A

gingival recession

- lack of keratinised gingiva/aberrant frenal attachment

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50
Q

RT1

A

no loss of IP attachment
IP CEJ not clinically detectable at both M+D aspects of the tooth
might be amenable to grafting surgery

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51
Q

RT2

A

loss of IP attachment
some papilla left
amount of IP LOA ≤ buccal LOA
may??? be able to graft surgery

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52
Q

IP LOA

A

measured from IP CEJ to depth of IP sulcus/pocket

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53
Q

buccal LOA

A

measured from buccal CEJ to apical end of buccal sulcus/pocket

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54
Q

RT3

A

loss of IP attachment
amount of IP LOA > buccal LOA
papilla destroyed
can’t graft with surgery

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55
Q

gingival abscess

A

localised to gingival margin

- often caused by trauma

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56
Q

periodontal abscess

A

usually related to pre-existing deep pocket also associated with food packing and tightening of the gingival margin post-HPT

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57
Q

pericoronal abscess

A

associated with PE tooth most commonly 8s

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58
Q

perioendo lesions

A

tooth is suffering from various degrees of endo and perio disease

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59
Q

SDCEP definition of PD abscess

A

infection in a PD pocket which can be acute or chronic and asymptomatic if freely draining

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60
Q

S+S of PD abscess

A 
swelling 
pain
tooth may be TTP in lateral direction (rather than apically)
deep PD pocket
bleeding
suppuration (neutrophils)
systemic in severe
 - enlarged regional LNs
 - fever
tooth usually vital
commonly pre-existing PDD
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61
Q

SDCEP tx of a PD abscess

A

1 - careful subgingival instrumentation short of the base of the PD pocket to avoid iatrogenic damage (inflamed and friable tissue)
- LA may be required
2 - if pus present - drain by incision or through the PD pocket
3 - recommend optimal analgesia
4 - do not prescribe ABs unless there are signs of spreading infection or systemic involvement
5 - recommend use of 0.2% CHX MW until acute symptoms subside
6 - following acute management, review and carry out definitive PD instrumentation and arrange an appropriate recall interval

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62
Q

systemic antibiotics for a PD abscess

A

only if signs of spread and systemic effects or if symptoms do not resolve with local measures
careful RSD
amoxicillin 500mg x3 5 days
metronidazole 400mg x3 5 days

MUST only be used in conjunction with mechanical therapy in order to disrupt the biofilm and reduce the bacterial load
- don’t just give ABs and do nothing

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63
Q

periapical infection in perioendo lesions

A

infection via carious cavity or traumatised crown

infection via PDL

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64
Q

perioendo lesions - comminications

A 
dentinal tubules
apical foramen
lateral canals
furcal canals
fractures
resorption
iatrogenic perforation
dentine exposure at CEJ - direct communication
 - 18% of teeth, 25% of anterior teeth

lesions can coalesce

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65
Q

dentinal tubules as a communication

A

dentine porous so pathogens can pass down

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66
Q

lateral canals as a communication

A

up whole length of tooth but most common in apical 1/3

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67
Q

furcal canals as a communication

A

between roots and furcation area

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68
Q

number of dentinal tubules

A

varies from approx 8000 at DCJ to 57000 per mm2 at pulpal end

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69
Q

apical foramen

A

direct route of communication between pulp and periodontium
exit - to cause PA pathosis - pulp inflammation/necrosis extends into the PA tissues causing a local inflammatory response accompanied with bone and root resorption
entry - from deep PD pockets to pulp

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70
Q

can endo pathology affect PD progression?

A

endo infection promotes PD pocket formation on an instrumented marginal root surface
- so risk factor in periodontitis progression
RC infection is associated with poorer PD healing
PA pathology has significant correlation with increased picket depth
approx x3 rate of marginal proximal radiographic bone loss by endo infection in perio prone pts
endo infection in L molars found to be associated with additional AL in furcation area
- presence of furcal communications

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71
Q

necrotic pulp can lead to perio endo lesions

A

direct inflammatory response by the PDL at the apical foramen/opening of the accessory canals
pulpal inflammatory by-products out apex, lateral, accessory canals and dentinal tubules - trigger inflammatory response in periodontium
living and non-living pathogens - many are similar pathogens encountered in PD infections

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72
Q

primary endo with secondary perio tx

A

both endo and perio txs required
if endo tx adequate, prognosis depends on severity of plaque induced periodontitis and efficacy of PD tx

with endo tx alone, only part of the lesions will heal to the level of the secondary PD lesion
in general, healing of the tissues damaged by suppuration from the pulp space can be anticipated
- as long as not super infected with plaque and calculus

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73
Q

primary perio with secondary endo mechanism

A

apical progression of a PD pocket may continue until the apical tissues are involved
pulp may become necrotic - infection entering via lateral canals/apical foramen
effect of progression of chronic perio on vitality of pulp is controversial
- if blood supply circulating through the apex is intact - pulp good prospects for survival
- pulpal changes from perio more likely to occur when apical foramen involved?
- in these cases, bacteria originating from the PD pocket are the most likely source of RC infection

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74
Q

primary perio with secondary endo prognosis

A

in single rooted teeth the prognosis is usually poor
- only one root to hold it in
molar teeth prognosis may be better

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75
Q

perio endo lesions - when does PDD usually directly affect the pulp?

A

when recession has opened up an accessory canal to the oral env
- an accessory canal quite high up could lead to infection
- pathogens may cause a chronic inflammatory reaction and (pulp necrosis)
if accessory canals are protected by sound cementum, necrosis doesn’t usually occur
- cementum has a protective effect

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76
Q

when do combined perio endo lesions usually occur?

A

usually formed when endo disease progressing coronally joins with an infected PD pocket progressing apically - 2 separate lesions happening simultaneously
tooth non-vital
perio detected in other parts of mouth
PA bone loss
PD/alveolar bone loss
true combined diseases occur less often
- need to exclude perforation or root fracture, root anomalies

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77
Q

what may the radiographic appearance of combined endo perio disease be similar to?

A

a vertically fractured tooth

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78
Q

combined lesions prognosis

A

AL large
guarded esp for single rooted teeth
in most cases the PA healing may be anticipated following successful endo tx
PD tissues may not respond well to tx, and healing will depend on severity of condition
fracture that has invaded pulp space causing pulp necrosis may also be considered a true combined lesion but may not be amenable to successful tx
often necessary to perform surgical exploration of the affected site to confirm the diagnosis
- OFD

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79
Q

if what remains intact will the pulp maintain vitality?

A

if the microvasculature of the apical foramen remains intact

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80
Q

effect of PD tx on the pulp

A

similar during scaling and RSI or PD surgery if accessory canals are severed/opened to oral env
microbial invasion and secondary pulp necrosis can occur

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81
Q

perio endo lesions presentation

A

generalised periodontitis may be present with localised pain
swelling +/- suppuration on palpation
deep pocketing to root apex with BOP

82
Q

primary endo lesion characteristics

A

non-vital

local perio only

83
Q

primary perio lesion characteristics

A

generalised perio
minimally/unrestored tooth
non-vital, possibly vital if apex has managed to remain intact

84
Q

true combined lesion characteristics

A

generalised perio and endo disease coexisting until coalescing into one lesion

85
Q

what does combined lesions prognosis depend on?

A

primarily upon severity of PDD and PD tissues response to tx, and PA tissues

86
Q

SDCEP tx of a perio endo lesion

A

1 - endo tx of affected tooth
2 - recommend optimal analgesia
3 - do not prescribe ABs unless there are signs of spreading infection or systemic involvement
4 - recommend use of 0.2% CHX MW until the acute symptoms subside
5 - following acute management of the lesion review within 10 days and carry out supra and subgingival instrumentation if necessary and arrange an appropriate recall interval

87
Q

primary endo with secondary perio

A

if suppurating primary endo disease remains untied, may become secondarily involved with PD breakdown
plaque forms at gingival margin of sinus tract and leads to plaque induced periodontitis in the area
when plaque/calculus are detected, the tx and prognosis of the tooth are different than those of teeth only involved with primary endo disease

88
Q

PDDs

A

group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque

  • gingivitis - inflammation of STs of gingiva
  • doesn’t always progress…
  • periodontitis - disease of entire periodontium inc bone
89
Q

what is PD health the outcome of?

A

the balance between bacteria of the dental plaque and the host immune system

90
Q

risk factor

A

something that increases a persons chances of developing a disease

91
Q

why is it important to know about risk factors?

A

for prevention

92
Q

primordial prevention

A

prevention in whole of society without particular risk factors, prevent development of risk factors

93
Q

primary prevention

A

identify groups with risk factors and prevent development of disease

94
Q

what does the development of risk factors appear to be dependent on?

A

specific inherited, behavioural and env factors

95
Q

risk determinants

A

genes
gender - M
systemic diseases which are genetic disorders and syndromes (periodontitis as manifestation of systemic diseases)
SE status

96
Q

multifactorial disease - complex aetiopathogenesis

A 
microbial biofilm - type of bacteria present
fct of the immune system (genetics)
genetics
general health
 - stress
 - fatigue
 - smoking
 - diet
 - medications
 - hygienic habits
additional pathological conditions
 - viral/bacterial infections
 - diabetes mellitus
 - hypoxia
 - liver diseases
97
Q

risk/modifying factors - broad groups

A

can change them
1 - general
2 - local risk factors

98
Q

general risk/modifying factors

A

smoking
systemic diseases: diabetes mellitus, leukaemia, HIV, osteoporosis, osteopenia
stress
drugs: Ca channel blockers, immunosuppressants, anticonvulsant, OCP (in past)
nutrition
obesity
pregnancy

99
Q

local risk factors

A

PRFs (dentists can contribute to development of PDD in pts)
- calculus, Rxs, carious cavities, RPDs, ortho appliances, malpositioned teeth

others

  • trauma from occlusion
  • insufficient OH - microbial factor
100
Q

smoking

A

effect on oral microbiota
- alters composition of plaque - more anaerobic
increases activation of immune system
- chemicals in cigarettes increase activity
reduces healing capacity (reduction in blood flow)
- bleeding in smokers with PDD isn’t indicative of the severity of their disease
- vessels are constricted - v little blood flow in PD tissues

101
Q

nutrition

A

severe vit C deficiency - scurvy - scorbutic gingivitis

lack of nutrients decreases function of the immune system

102
Q

obesity

A

contributes to systemic inflammation - pro inflammatory effect
adipose tissue produces lots of inflammatory cytokines
adipokines secreted by adipocytes

103
Q

genes

A

genetic polymorphism can affect expression levels of genetic products
IL-1 most important
possible polymorphisms of genes encoding TNF-a, IL-1, vit D receptor, IgG receptor

104
Q

occlusal trauma

A

may lead to production of IL-1 and bone loss but doesn’t cause periodontitis
may be a co-factor in destructive PDD - enhance rate

105
Q

suboptimally controlled diabetes mellitus

A

hyperglycaemia

  • may modulate RANKL/OPG ratio and so contribute to alveolar bone destruction
  • production of AGE (advanced glycation end products) increases inflammation
  • production of pro-inflammatory cytokines and destructive MMPs
106
Q

important factors in diabetes contributing to PDD severity

A 
degree of diabetic control
 - non-fasting HbA1c below 53 mol/mol, below 7%
 - fasting plasma glucose level 7mmol/L
age of onset
duration of disease
107
Q

why is HbA1c better for monitoring degree of diabetic control?

A

tells you more about their stability over last 3m (lifespan of an erythrocyte)

108
Q

systemic genetic conditions/diseases where periodontitis is one of the symptoms

A 
Papillon-Lefevre syndrome
Chediak-Higashi syndrome
Lazy leukocyte syndrome
LAD syndrome
EDS
chronic granulomatous disease
Down Syndrome
hypohosphatasia
109
Q

drugs that can lead to gingival enlargement

A 
anticonvulsant - phenytoin
immunosuppressant - cyclosporin
 = rarer
Ca channel blockers - nifedipine, amlodipine
 = common
110
Q

why can drugs lead to gingival enlargement?

A

interaction between the drug and host fibroblasts - increased deposition of CT supporting a hyperproliferative epithelium

111
Q

gingival enlargement

A

more fibroblasts

often have inflammation also as enlargement is making OH difficult

112
Q

gingival swelling

A

more ICF, increased permeabilisation of the vessels

softer as full of water - press with probe

113
Q

managing drug related gingival enlargement

A

need professional scaling
v intensive pt training - plaque control at v high level
surgical tx to remove excess - but need some plaque control before you go down surgical route
change meds? speak to doc

114
Q

PDD as a risk factor for systemic diseases

A

systemic activation of the immune system

  • RA
  • pre-eclampsia and adverse pregnancy outcomes
  • atherosclerosis and hypertension
  • Alzheimers disease
  • neoplasms
115
Q

acquired systemic diseases and syndromes - HIV

A

increased risk of necrotising conditions but no evidence of increased progression of periodontitis

116
Q

acquired systemic diseases and syndromes - blood dyscrasias e.g. neutropenia, agranulocytosis, leukaemia

A

reduced numbers/fct of neutrophils and macrophages

increased risk of NG and progressive periodontitis

117
Q

acquired systemic diseases and syndromes - scurvy

A

vit C deficiency causing abnormal collagen turnover

increased risk of PD attachment loss

118
Q

acquired systemic diseases and syndromes - pregnancy

A

increased risk of pregnancy gingivitis

119
Q

osteoporosis and osteopenia

A

research - speculative at present
low bone mineral density - accelerates alveolar bone resorption that is initiated by the PD infection
factors affecting systemic bone remodelling (e.g. hereditary, oestrogen, vit D, RANKL, OPG) may modify local tissue response to PD infection, increase release of pro-inflammatory mediators and lead to enhanced destruction of PD tissues

120
Q

psychological stress

A

increased cortisol - stimulates immune system

ANS stimulated - catecholamine and substance P - regulates immune response, affect bacterial adhesion and growth

121
Q

what is the most severe inflammatory PDD disorder caused by plaque bacteria?

A

NPDs

122
Q

why are NPDs known to occur in epidemic-like patterns?

A

due to shared predisposing factors in a pop (e.g. students during exams, armed forces recruits)
not contagious

123
Q

main features of NPDs

A

painful bleeding gums
ulceration and necrosis of the ID papilla and gingival margin “punched out” appearance, ulcers with central necrosis - craters
ulcers covered by sloughing - yellow/white/grey
lesions develop quickly
1st lesions often seen IP in mandibular anteriors
bad breath
sequestrum formation necrosis of parts of alv bone
LN swelling
usually no elevation of body temp (compare to PHG)

124
Q

what type of infection is NPDs?

A

opportunistic - caused by bacteria inhabiting healthy oral cavity

125
Q

epidemiology of NPDs

A

more common in developing countries

126
Q

what may happen if NG is improperly txed?

A

become chronic and/or recurrent

127
Q

NS

A

progression of NP into tissue beyond the mucogingival jct
mostly malnutrition and HIV
may result in denudation of the bone - osteitis and OAFs

128
Q

NG and bone loss

A

no bone loss or attachment loss

inflammation confined to STs

129
Q

NP and bone loss

A

attachment loss

130
Q

NS and bone loss

A

more extensive mucosal and bone loss beyond gums

131
Q

Vincent’s angina

A

different disease - of the throat not the periodontium
mixed spirochetal microbiota in necrotic areas in tonsils during sore throat infections
NPDs and VA occur independently of each other

132
Q

NP

A

where the infection leads to AL

may be an extension of NG into the PDL but not completely proven

133
Q

cancrum oris (noma)

A

necrotising and destructive infection of the mouth and face
not a PDD
usually in malnourished children in developing countries
may be disfiguring, often fatal
been suggested that all cases develop from pre-existing NG - not confirmed
- most NPDs won’t progress to the more severe forms, even without tx

134
Q

what is the diagnosis of NPDs based on?

A

symptoms

135
Q

why is the diagnosis of NPDs not based on any test?

A

biopsy - histopathology is not pathognomic (characteristic) for NPD
microbiology - not characteristic
- constant flora: treponema sp, selenomonas sp, fusobacterium sp, prevotella intermedia
- variable flora: heterogeneous array of bacterial types
spirochetes and fusobacterias are isolated from large numbers of necrotic lesions, their presence is not evidence of a primary etiologic importance (they are not always found in the primary lesion)

136
Q

risk factors

A 
developed countries - mostly young adults
 - stress
 - sleep deprivation
 - poor OH
 - smoking
 - immunosuppression (HIV and leukaemia)
 - malnutrition
developing countries - malnourishes children
137
Q

NPDs in HIV pts

A

clinical characteristics don’t essentially differ

but the lesions are not usually associated with a big amount of plaque and calculus

138
Q

NPD vs PHG

A 
NPD
 - bacteria
 - age freq 15-30yrs
 - site: ID papilla, rarely outside gingiva
 - symptoms: ulceration and necrotic tissue, yellowish plaque, bad breath, may have mod fever
 - lasts 1-2 days if tx
 - not contagious - no immunity
 - healing: destruction of PD tissue remains
PHG
 - HSV
 - freq children
 - site: gingiva and entire oral mucosa
 - symptoms: multiple vesicles which disrupt - small round fibrin covered ulcerations, bad breath, fever
 - lasts 1-2 weeks
 - contagious, get partial immunity 
 - no permanent destruction
139
Q

NPDs tx

A

US debridement
if pain preventing pt from brushing - 0.2% CHX MW x2 daily
only ABs if indicated
recall for review
smoking cessation, OH, vit supplementation, dietary advice
- prevent recurrence

140
Q

NPDs indications for ABs

A

pts with malaise, fever, lassitude, lack of response to mechanical therapy, impaired immunity

141
Q

NPDs antibiotics

A

200mg metronidazole x3 daily for 3 days

400mg metronidazole x3 daily for 3 days if severe

142
Q

adjuncts to tx of periodontitis - tx strategies

A 
mechanical disruption
 - reducing the bacterial challenge
 - scaling and RSD
systemic ABs or local antimicrobials
host modulation therapy
143
Q

PD tx with use of systemic ABs

A

not first line tx, if used in selected cases are only allowed once combined with mechanical disruption of biofilm
cases to consider
- aggressive perio
- young pts with grade B/C - young pts with fast progression of bone loss

144
Q

systemic ABs as tx - tx protocols

A

OHI
supragingival scaling and RSD of all sites indicated in pocket chart - short time as possible
start ABs on morn of last RSD visit
- 500mg amoxicillin x3 daily 7 days
- 400mg metronidazole x3 daily 7 days
- pts allergic to amoxicillin or on warfarin - 100mg doxycycline once per day for 21 days
- 500mg azithromycin x1 day for 3 days

145
Q

amoxicillin contraindication

A

allergies

146
Q

metronidazole contraindications

A

alcohol intake
increases anticoagulant effect of warfarin
pregnancy

147
Q

doxycycline contraindications

A

pregnancy (tetracycline shown staining of teeth)

148
Q

biofilm formation

A

pedicle - proteins and glycoproteins of saliva - a few mins to form
association adhesion - trailblazing bacteria - streptococcus, actinomyces - poses adhesion molecules
growth - micro colonies - production of polysaccharides matrix
mature biofilm - microcolonies transition into metabolic complexes

aerobic to anaerobic bacteria

149
Q

advantages of local antimicrobials

A

reduce systemic dose - not damaging intestinal microbiome and biofilm
high local conc
superinfection e.g. c dificile unlikely
drug interactions unlikely
site specific
pt compliance not an issue as applied by HCP
can utilise agents which can’t be utilised systemically e.g. CHX

150
Q

disadvantages of local antimicrobials

A

£££
still require RSD or biofilm disruption
limited indications

151
Q

Periochip

A

local antimicrobial/antiseptic
bovine origin gelatine based
evidence shows benefits
only good for certain clinical conditions
use during HPT or maintenance or both? - wait until pockets heal after instrumentation and use it in persisting pockets only during review visit and maintenance recalls

152
Q

Piscean

A

fish collagen based

local antimicrobial/antiseptic

153
Q

Chlosite

A

CHX gel

local antimicrobial/antiseptic

154
Q

local antimicrobials - antibiotics

A

Arestin - 1mg minocycline HCl microspheres
Atridox - doxycycline hyelate 10%
Elyzol - 25% metronidazole

155
Q

Periostat dosage

A

20mg doxycycline x2 daily for 3m systemically, as an adjunct to supra/subgingival instrumentation

156
Q

Periostat mechanism of action

A

dose sub-antimicrobial - insufficient to inhibit the growth of bacteria
prescribed for role as collagenase inhibitor
- breaks down collagen, implicated in PD tissue damage
- produced by bacterial and human cells
dose unlikely to exert a significant evolutionary pressure so less likely to accelerate the development of drug resistant bacteria

157
Q

indications for local antiseptics

A

only persisting pockets >5mm (review visit, maintenance visit)
always with RSD
not many of them as if a lot of persisting pockets in the quadrant OFD is more beneficial or systemic antibiotics with RSD within 24hrs from starting ABs
in cases of PD abscesses
- after evacuation of pus and RSD

158
Q

Periowave - photodisinfection

A

irrigate
- photosensitising solution topically applied to the gums at the tx site
- preferentially attaches to the harmful bacteria and toxins associated with PDD
illuminate
- thin plastic light diffusing tip is painlessly placed at the tx site
- specifically calibrated laser light, activating the photosensitising solution and destroying the harmful bacteria and toxins

159
Q

host modulation therapy

A

corticosteroids
- suppress immune response they don’t modulate it
NSAIDs
anti-cytokine and biological therapies
biological-disease-modifying anti-rheumatic drug
- e.g. infliximab, TNF-a
lipid mediators of resolution of inflammation
- derived from omega-3 fatty acids resolvins, protectins, maresins
small molecule compounds
- target specific cytokine-mediated processes - inhibition of RANKL - induced OC
bisphosphonates
- disrupt OC activity and inhibit bone resorption

160
Q

function of the periodontium

A

attach the teeth to the jaws

dissipate occlusal forces

161
Q

dissipating occlusal forces - periodontium

A

living tissue - viscoelastic fct
interradicular tissues filled with a fluid which absorbs forces
tension, compression, viscous forces

162
Q

horizontal forces

A

constant - ortho

intermittent - occlusal (jiggling) e.g. denture clasp too tight

163
Q

tipping movement

A

selective deposition and resorption of bone due to horizontal forces
areas of pressure result in bone resorption
areas of tension - bone deposition

tooth tips due to bone remodelling

164
Q

protective occlusion

A

ideal
posterior teeth meet first
anterior teeth just touch in ICP
when mandible slides forward anterior teeth take all of the load - posteriors disocclude
lateral excursion - all molars disocclude, canines guide

165
Q

occlusal interferences

A

often no effects
but eccentric occlusal contacts can mean come teeth are taking excessive loading - jiggling
- discomfort
- excessive mobility

166
Q

the effect of “abnormal” occlusal forces on:

A

the healthy periodontium
the healthy but reduced periodontium
- previous PDD, shortened teeth, surgery
the diseased periodontium
- presence of plaque-induced inflammation

167
Q

effect on healthy periodontium

A

non-axial occlusal load - PDL well-designed to take axial vertical loading
areas of intermittent pressure and tension
- needs more shock absorber so excessive load is dissipated
areas of widened PDL
hyper-mobile tooth - attachment unaffected
gingival margin remains normal and intact - no LOA
gingival inflammation is not initiated by occlusal forces
- in the absence of bacteria occlusal trauma doesn’t cause perio disease - need a biofilm

168
Q

effect on a reduced but healthy PDL

A

less PDL to dissipate load - higher forces per mm2 of ligament
same will happen but to a greater extent
excessive mobility
widening of PDL
no further LOA in absence of biofilm inducing inflammatory action

169
Q

response of the healthy periodontium: physiological

A

PDL width increases until forces can be adequately dissipated, the PDL width should then stabilise
increased tooth mobility
successful adaptation to increased demand - physiological
if demand is subsequently reduced (e.g. remove high spot, stop Bruxism etc) PDL width should return to normal

170
Q

response of the healthy periodontium: pathological

A

if demand of occlusal forces is too great or the adaptive capacity of the PDL reduced, PDL width may continue to increase
PDL width and tooth mobility fail to reach a stable phase
failure of adaptation - pathological

171
Q

occlusal trauma

A

tooth mobility which is progressively increasing and/or tooth mobility associated with symptoms
with radiographic evidence of increased PDL width

172
Q

occlusion and periodontitis

A

an association with vertical bone defects? NO

increased rate of disease progression? MAYBE

173
Q

vertical bone defects

A

for a given amount of biofilm you get a certain amount of bone loss - 2mm
narrow bone spicule - all within circle so all lost - horizontal bone loss
wider alveolar bone spicule - same circle of destruction but because bone is wider you retain the medial aspect of the bone
not directly related to occlusal trauma - vertical bony defect are a factor of how wide bone is at beginning - zone of destruction the same regardless of the cause of periodontitits

174
Q

occlusal trauma and periodontitis - increased rate of disease progression - maybe?

A

two processes
- pathological resorption due to inflammation
- physiological resorption (remodelling) due to excessive occlusal forces
happening at same time
if coalesce - additive effect - zone of co-destruction - see more PDL and attachment loss than if you had only one process
1 - plaque-induced inflammation
2 - trauma-induced inflammation

175
Q

occlusal forces and periodontitis

A

alone cannot initiate or exacerbate gingival inflammation
alone cannot initiate or sustain loss of CT attachment
can result in widening of PDL and increasing tooth mobility
in combination with plaque-induced inflammation may exacerbate LOA

176
Q

what does tooth mobility depend on?

A

width of PDL
height of PDL
inflammation - flaccid tissue tone due to inflammatory infiltrate
number, shape and length of roots

177
Q

why can tooth mobility be improved by NSHPT?

A

long JE

general maturation of tissue, improved tissue tone

178
Q

why doesn’t tooth mobility necessarily show pathology?

A

may indicate successful adaptation of the periodontium to functional demands
and/or
may reflect the nature of the remaining attachment

179
Q

when can’t tooth mobility be accepted?

A

it is progressively increasing
it is causing symptoms
it creates difficulty with restorative tx

180
Q

therapy to reduce tooth mobility

A

control plaque-induced inflammation
correction of occlusal relations
splinting

181
Q

correcting occlusal relations

A 
don't adjust very often
occlusal adjustment (selective grinding)
restorations
orthodontics

= occlusal therapy may be indicated for the management of tooth mobility and migration
BUT it isn’t a tx for periodontitis

182
Q

management of tooth migration

A

tx the periodontitis
correct occlusal relations
either
- accept position of teeth and stabilise
- move the teeth orthodontically and stabilise

183
Q

what splint is most commonly used?

A

composite and wire

184
Q

indications for splinting

A

mobility due to advanced LOA
mobility causing discomfort or difficulty in chewing
teeth need to be stabilised for debridement

185
Q

disadvantages of splinting

A

doesn’t influence the rate of periodontal destruction
may create hygiene difficulties - PRF
“last resort” - palliation tx
- won’t save the tooth will just save the fct

186
Q

deep traumatic overbite

A

trauma from the bite - not occlusal trauma it is trauma from the occlusion
treat plaque-related inflammation
relieve trauma
- occlusal slint - palliative
- orthodontic/orthognathic tx
- restorative - must inc occlusal stops for anterior teeth

187
Q

PD therapy as an aid to Rx dentistry

A

improves soft tissue management
- impressions, placing restorations, moisture control
establishes stable gingival margin position
contributes to aesthetics
reduces tooth mobility
informs prognosis

188
Q

signs of an inflamed gingival margin

A 
linear band of inflammation
lost stippling
abundant soft plaque
bleeds during operative procedures
unstable in its apico-coronal location
189
Q

why can poor margins cause recession?

A

gingivae will recede away from the irritant e.g. cement

190
Q

overhangs and bone loss

A

larger the overhang = greater bone loss

- development of pathogenic flora

191
Q

contour

A

contour - shape of Rxs same shape as teeth

inadequate tooth prep = over contoured crowns

192
Q

keys to periodontally successful indirect Rxs

A 
start with healthy tissue
adequate tooth prep
precise margin location
excellent provisional Rxs
careful tissue handling and impression technique
 - prevent damage to tissues
193
Q

biological width

A

base of sulcus to alveolar bone approx 2mm

JE 1mm, CT 1mm

194
Q

biological width and Rxs

A

if you place a crown margin in this space you will cause inflammation
Rx margins need to be within the gingival sulcus - don’t place >0.5mm subgingivally
in non-aesthetic areas - supra gingival as more cleansable
margins need to follow the interdental col - otherwise will be way too subgingival interproximally
need to be at least 3mm from alveolar crest

195
Q

if margin enroaches on BW: possible outcomes

A

persistent inflammation
LOA
- pocketing or recession
later - exposure of Rx margin

196
Q

gingival veneer/masks/flange prostheses/removable gingival prostheses

A

restore gingival contour and improve aesthetics even after successful PDD tx
acrylic/silicone
can be removed for OH

197
Q

indications for gingival veneer

A

post-PD therapy
- aesthetics
- speech (spitting when talking - IP bone loss)
- foaming of saliva
- interference of lip and tongue
- dentine hypersensitivity (cover exposed roots)
- lack of lip support
local drug administration
- could apply a topical steroid underneath it

198
Q

gingival veneer contraindications

A 
poor OH
uncontrolled PDD
incomplete PD therapy
allergy to acrylic/silicone
high caries susceptibility
poor manual dexterity
risk of inhalation (epilepsy)
prominent labial frenum - may be too weak in midline
199
Q

Ante’s law

A

combined PD area of the abutment teeth should be equal to or greater than the PD area of the tooth/teeth to be replaced

200
Q

what prostheses are usually preferable from a PD perspective?

A

fixed - in a compliant pt with good OH

perio (8 decks)

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