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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

  • 1st trimester - Premature labour
  • 3rd trimester – difficulty lying down

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 signs

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

gingival health measurements

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 - Nifedipine
immunosuppressants - cyclosporin

action - gingival hyperplasia by

  • interact with fibroblast - increase con tis deposition in gums
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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 - vit C
  • 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

Necrotiotising stomatitis

A

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

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40
Q

systemic diseases/conditions affecting the periodontal tissues

A 
- Squamous cell carcinoma
 - Langerhans cell histocytosis
  • 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

cancer cell tissues can invade and destroy PD attachment

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41
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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42
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 - leucocyte adhesion deficiency
hypophosphatasia
(Down syndrome)
EDS
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43
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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44
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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45
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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46
Q

mucogingival deformities and conditions

A

gingival recession

- lack of keratinised gingiva
- aberrant frenal attachment
- pregnancy epulis
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47
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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48
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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49
Q

IP LOA

A

measured from IP CEJ to depth of IP sulcus/pocket

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50
Q

buccal LOA

A

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

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51
Q

RT3

A

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

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52
Q

gingival abscess

A

localised to gingival margin

- often caused by trauma

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53
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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54
Q

pericoronal abscess

A

associated with PE tooth most commonly 8s

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55
Q

perioendo lesions

A

tooth is suffering from various degrees of endo and perio disease

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56
Q

most prevalent infection demanding emergency tx

A
  • dentoalveolar abscess
  • pericoronitis
  • periodontal abscess
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57
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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58
Q

periapical infection in perioendo lesions

A

infection via carious cavity or traumatised crown

infection via PDL

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59
Q

Communication btw pulp and periodontium

A
  • apical foramen - main route
  • exposed dentinal tubules
  • lateral & accessory canals
  • furcal canals
  • perforation
    • extensive caries
    • resorption
    • iatrogenic
  • developmental groove (infrabony pocket）
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60
Q

dentinal tubules as a communication

A

dentine porous so pathogens can pass down

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61
Q

lateral canals as a communication

A

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

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62
Q

furcal canals as a communication

A

between roots and furcation area

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63
Q

necrotic pulp can lead to perio endo lesions

A
  • pulpal inflammatory by-products out apex, lateral, accessory canals and dentinal tubules - trigger inflammatory response in periodontium
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64
Q

primary perio with secondary endo mechanism

A 
- infection entering via lateral canals/apical foramen
- accessory canal exposed to oral micro biofilm
  • if blood supply circulating through the apex is intact - pulp good prospects for survival
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65
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

  • cementum has a protective effect
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66
Q

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

A

a vertically fractured tooth

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67
Q

if what remains intact will the pulp maintain vitality?

A

if the microvasculature of the apical foramen remains intact

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68
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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69
Q

primary endo lesion characteristics

A

non-vital

local perio only

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70
Q

primary perio lesion characteristics

A

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

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71
Q

what does combined lesions prognosis depend on?

A

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

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72
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
73
Q

what is PD health the outcome of?

A

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

74
Q

primordial prevention

A

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

75
Q

primary prevention

A

identify groups with risk factors and prevent development of disease

76
Q

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

A

specific inherited, behavioural and env factors

77
Q

risk determinants

A

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

78
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
79
Q

risk/modifying factors - broad groups

A

can change them
1 - general
2 - local risk factors

80
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

81
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
82
Q

smoking

A
  • effect on palque microbiome more anaerobic
  • increases activation of immune system
  • vasoconstrictor of gingival vessel - recue healing and mask severity of disease

risky if >10 cig a day

83
Q

nutrition

A

severe vit C deficiency - scurvy - scorbutic gingivitis

lack of nutrients decreases function of the immune system

84
Q

obesity

A

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

85
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

86
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

87
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
88
Q

diabetic control and questions to ask

A

For diabetic pt - good control (no more than)
- HbA1c test
- 48-58mmol/mol
- 6.5-7.5%

should do blood test every 3 months
- RBC turnover every 3 months

* degree of control
* age of onset
* duration of disease

89
Q

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

A

Papillon-Lefevre syndrome
Chediak-Higashi syndrome
Lazy leukocyte syndrome
Luekocyte adhesion deficiency LAD syndrome
EDS
chronic granulomatous disease
Down Syndrome
hypohosphatasia

90
Q

drugs that can lead to gingival enlargement

A 
anticonvulsant - phenytoin
immunosuppressant - cyclosporin
 = rarer
Ca channel blockers - nifedipine, amlodipine
 = common
91
Q

why can drugs lead to gingival enlargement?

A

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

92
Q

gingival enlargement / hyperplasia

A

more fibroblasts

often have inflammation also as enlargement is making OH difficult

93
Q

gingival swelling

A
  • more intercellular fluid,
  • increased permeabilisation of the vessels

softer as full of water - press with probe

94
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

95
Q

PDD as a risk factor for systemic diseases

A

systemic activation of the immune system

  • RA
  • diabetes
  • pre-eclampsia and adverse pregnancy outcomes
  • atherosclerosis and hypertension
  • Alzheimers disease
  • neoplasms
96
Q

acquired systemic diseases and syndromes - HIV

A

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

97
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

98
Q

acquired systemic diseases and syndromes - scurvy

A

vit C deficiency causing abnormal collagen turnover

increased risk of PD attachment loss

99
Q

acquired systemic diseases and syndromes - pregnancy

A
  • increased risk of pregnancy gingivitis
  • immune system in pregnancy is reduced
  • risk of adverse pregnancy
    • oral bacteria entering feto-placental unit
100
Q

osteoporosis and osteopenia

A
  • low bone mineral density in max and mand
  • oestrogen
  • RANKL/ OPG ratio dysregulaiton
101
Q

psychological stress

A

increased cortisol - stimulates immune system

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

102
Q

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

A

NPDs

103
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

104
Q

main features of NPDs

A
  • painful bleeding gums
  • ulceration and necrosis of the ID papilla
  • gingival margin “punched out” appearance,
  • craters
  • sloughing - yellow/white/grey
  • lesions develop quickly
  • 1st lesions often seen IP in mandibular anteriors
  • halitosis
  • sequestrum formation necrosis of parts of alv bone
  • lymphadenopathy
105
Q

what type of infection is NPDs?

A

opportunistic - caused by bacteria inhabiting healthy oral cavity

106
Q

epidemiology of NPDs

A

more common in developing countries

107
Q

what may happen if NG is improperly txed?

A

become chronic and/or recurrent

108
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

109
Q

NG and bone loss

A

no bone loss or attachment loss

inflammation confined to STs

110
Q

NP and bone loss

A

attachment loss

111
Q

NS and bone loss

A

more extensive mucosal and bone loss beyond gums

112
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

113
Q

NP

A

where the infection leads to AL

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

114
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

115
Q

what is the diagnosis of NPDs based on?

A

symptoms

116
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)

117
Q

risk factors

A 
developed countries - mostly young adults
 - stress
 - sleep deprivation
 - poor OH
 - smoking
 - immunosuppression (HIV and leukaemia)
 - malnutrition
developing countries - malnourishes children
118
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
119
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

120
Q

NPDs indications for ABs

A
  • pts with malaise, fever, lassitude,
  • lack of response to mechanical therapy,
  • impaired immunity
  • unable to complete local measures upon initial presentation
121
Q

NPDs antibiotics

A

400mg metronidazole x3 daily for 3 days

122
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
123
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 C

124
Q

amoxicillin contraindication

A

allergies

125
Q

metronidazole contraindications

A

alcohol intake
increases anticoagulant effect of warfarin
pregnancy

126
Q

doxycycline contraindications

A

pregnancy
(tetracycline shown staining of teeth)

127
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

128
Q

advantages of local antimicrobials

A

reduce systemic dose -
reduce GI upset ( intestinal microbiome)
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

129
Q

disadvantages of local antimicrobials

A

£££
still require RSD or biofilm disruption
limited indications

130
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

131
Q

Piscean

A

fish collagen based

local antimicrobial/antiseptic

132
Q

Chlosite

A

CHX gel

local antimicrobial/antiseptic

133
Q

local antimicrobials - antibiotics

A

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

134
Q

Periostat dosage

A

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

135
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
136
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

137
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

138
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

139
Q

function of the periodontium

A
  • attach the teeth to the jaws
  • dissipate occlusal forces
140
Q

dissipating occlusal forces - periodontium

A

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

141
Q

horizontal forces

A

constant - ortho

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

142
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

143
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

144
Q

occlusal interferences

A

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

145
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

146
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
147
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

148
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

149
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

150
Q

occlusal trauma

A

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

151
Q

occlusion and periodontitis

A

an association with vertical bone defects? NO

increased rate of disease progression? MAYBE

152
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

153
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

154
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

155
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

156
Q

why can tooth mobility be improved by NSHPT?

A

long JE

general maturation of tissue, improved tissue tone

157
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

158
Q

when can’t tooth mobility be accepted?

A

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

159
Q

therapy to reduce tooth mobility

A

control plaque-induced inflammation
correction of occlusal relations
splinting

160
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

161
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

162
Q

what splint is most commonly used?

A

composite and wire

163
Q

indications for splinting

A

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

164
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

165
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

166
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

167
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
168
Q

why can poor margins cause recession?

A

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

169
Q

overhangs and bone loss

A

larger the overhang = greater bone loss

- development of pathogenic flora

170
Q

contour

A

contour - shape of Rxs same shape as teeth

inadequate tooth prep = over contoured crowns

171
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
172
Q

biological width

A

base of sulcus to alveolar bone approx 2mm

JE 1mm, CT 1mm

173
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

174
Q

if margin enroaches on BW: possible outcomes

A

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

175
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

176
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
177
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
178
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

179
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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