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DCP2 > Case Conference Q’s > Flashcards

Case Conference Q’s Flashcards

1
Q

What are some challenges in treatment

A

Identifying RF

Pt concerns / compliance

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2
Q

Benefits of LA

A

Pt / operator comfort

Pt conscious and alert

Analgesic use of vasoconstrictor
- decrease haemorrhaging/bleeding
- extended duration of pulpal analgesia
- more effective / deeper analgesia level
- decrease systemic toxicity

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3
Q

How do you explain periodontal disease / pocketing to pt?

A

If bacteria sits on gums for toot long enough= irritation
Gums start to pull away from tooth

Pocketing = plaque accumulation beneath gums = hard to clean = plaque mineralisation = tartare /calculus

Increases disease process = deeper pocketing = bone dissolving = irreversible bone loss = mobility = tooth loss

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4
Q

Evidence of gum disease

A

Pocket > 4mm

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5
Q

Healthy gums

A

1-3mm pocketing + no BOP

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6
Q

Why is it important to explain why perio needed tx

A

Can be controlled however disease can relapse

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7
Q

What should we notice clinically as well as record when a pt smokes

A

How many for how long

Characteristics clinically
- fibrotic, tight gingiva
- decreased BOP
- xerostomia (challacombe scale)
- staining / tartare

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8
Q

What are pack years

A

Describes how may cigs smoked in lifetime

A pack has 20

Multiply number of packs smoked per day by number of years they’ve smoked

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9
Q

How can polypharmacy affect pt lifestyle

A
  1. Xerostomia
    - increased acidity in mouth (less saliva) = increased caries
    - acidity - tooth surface loss - erosion
    - fungal infections
    - less saliva = inc decay
  2. Anticoagulants
    - inc risk of bleeding (blood thinner eg, warfarin)
    - risk for LA
  3. Statins
    - for high cholesterol
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10
Q

How to manage NCTTL

A

Tooth surface loss due to process other than caries

Caused by attrition , erosion, abrasion

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11
Q

Define attrition

A

Flattening of occlusal surfaces

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12
Q

Do you agree with the diagnosi? Why ?

A
  1. Extent (assess by radiographs) + pattern of bone loss
    Generalised / localised / MIP
  2. Staging (use bone loss at worst site) to determine SEVERITY of disease
  3. Grading
    (% bone loss / pt age) = rate of progression of disease
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13
Q

How do radiographs assist in treatment plan / diagnosis?

A
  1. Horizontal bone loss
    - Loss of buccal / lingual cortices
    - Loss of intervening trabecular bone
  2. Vertical bone loss
    - Discrepancy in degree of bone loss at 2 adjacent sites
    - may indicate rapid bone loss
    - angular bony defects
  3. Furcation involvement
    - local PRF
    - radiolucency shows furcation

Therefore allowing you to stage and grade
+ identify extent
- can see calculus, PRF, occlusal trauma, sclerosis

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14
Q

Anatomy and chemistry of the tooth

Critical ph of dentine?

A

6.2-6.4

Root dentine vulnerable to acidic dissolution

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15
Q

Anatomy and chemistry of the tooth

Critical ph of enamel

A

5.5

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16
Q

Enamel structure

A

Highly organised, acellular tissue

  • 95% inorganic material impure calcium HAP
  • 5% fluid and organic protein
  • mineral crystals organised into prisms / rods
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17
Q

Mineral crystals in enamel made up of

A
  1. Inorganic salt (calcium phosphate salt)
  2. Hydroxyapatite
18
Q

What is the plaque biofilm? Why disrupt?

A

Community of ,microorganisms - spatial organisation into a 3D structure, enclosed in a matrix of extracellular material

Remove plaque before 48hrs when it hardens to tartare / calculus

Disrupt biofilm by mechanical TB - stop colonies

19
Q

Periodontal indicies
Pocket probing depths

What do we use
Where do we probe

A

Pcp10 probe
6 point around each tooth

If lots of supra gingival calc present, periodontal charting should be postponed until after supra gingival scaling

20
Q

What is true probing attachment level and why is it important

A

Probing depth measured from CEJ / other fixed point

Allows us to monitor periodontal progression

21
Q

If considerable gingival hyperplasia, pocketing may be …, but attachment loss may be …

A

If considerable gingival hyperplasia, pocketing may be deep 5-7mm, but attachment loss may be small

22
Q

In order to interpret pocket measurement, note…

A
  1. Position of gingival margin on tooth surface
  2. Position of the alveolar crest as seen on radiograph
  3. Factors affecting accuracy of periodontal probing
23
Q

Why is it important to measure gingival recession?

A

So the total amount of measured attachment loss can be meaningfully compared with bone levels on radiographs

24
Q

Periodontal screening - why is it important

A
  • to detect disease so tx can be carried out (Screening BPE) - helps detect who would benefit for further perio indicies
  • to diagnose
  • to educate pt
25
Q

Limitation of periodontal screening

A
  1. Not a replacement for perio indicies
  2. Not able to show extent of periodontal involvement
  3. Doesn’t not record plaque levels, attachment loss, recession
  4. Not suitable to monitor perio status / response to tx
26
Q

Systemic risk factors / risk factors for periodontal disease

A

Smoking
Diabetes mellitus
Race / genetics / gender
Polymorphonuclear functional abnormalities PMN’s
Acquired systemic infections eg HIV

27
Q

Mechanisms by which systemic risk factors apeoar to be operating

A
  1. Smoking
    - increase inflammatory response
    - direct toxic / thermal effects to cells
    - increased staining / calculus
    - decrease bone levels
  2. Diabetes
    - increased infections
    - impairs immune response - interferes with wound healing
    - induces hyper inflammatory state (activated protein kinase C + advanced glycation of proteins)
    - = increased tissue destruction / infection
  3. Obesity
    - adverse effects associated with adipokines and cytokines by macrophages in adipose tissue (pro inflammatory mol)
    - = hyper inflamed state = periodontal tissue destruction
    - inflammatory mediators produced by adipose tissue (TNF-a) = insulin resistance = diabates = increased risk of periodontal disease
  4. Stress
    - chronic stress / increased allostatic load =
    - suppression of immune response
    - increased susceptibility to infections
28
Q

Periodontitis and diabetes

What’s usually happens to control BG

A

Bifunctional relationship
General inflammatory response triggered by perio also affects regulation of blood sugar/glucose

Usually…
Increased sugar = increased insulin = decreased BG

In the presence of gen inflammation, substances are formed that interfere with this mechanisms
- inhibit binding of insulin
- decreased glucose uptake from blood by cells
- BG remains elevated

In severe perio, BG elevated even in absence of diabetes = insulin resistance

29
Q

Insulin mode of action

A

Insulin binds to membrane bound insulin receptors which activates glucose transporters
Therefore glucose in cells
Glucose is absorbed from blood by cells
= BG levels decreased

30
Q

Diabetes and periodontitis - bifunctional relationship

A
  1. Glucose in blood binds to haem in RBC.
  2. If BG levels remain high, other proteins will bind to excess glucose = AGE’s
  3. AGE’s increase inflammation
    - they crosslink fibres in connective tissue
    - therefore interfering with wound healing in the oral cavity
    - WBC recognise AGE’s = increased inflammation
    = increased inflammatory cells, decrease healing = periodontal destruction
31
Q

Accumulation of AGE’s causes…

A
  • forms cross links in collages = production of bad collagen
  • bad collagen is easily broken down + poor healing
  • alters immuno-inflammatory response
  • receptor on monocytes / macrophages for AGE’s
  • increase WBC / inflammation
  • increased free radical species
  • increased pro inflammatory cytokines
    ===== periodontal disease

Chronic inflammation = insulin resistance
Insulin resistance = hard for cells to uptake glucose
= elevated BG levels

32
Q

What is the effect of persistent chronic inflammation

A

Increased cytokines in saliva and GCF (in diabetics)
Dysregulated inflammatory environment
Increased insulin resistance

33
Q

Why does poorly controlled diabates affect how perio tissues respond to local factors like plaque

A
  1. Neutrophils (first line of defence)
    - defective chemotaxis by chemokines (inflammatory mediators that help neutrophil to site)
    - therefore decrease phagocytosis
    - therefore microorg can survive and proliferate = periodontal breakdown
  2. Monocytes macrophages release pro inflammatory cytokines but in diabetics..
    - pro inflammatory cytokines in EXCESS = hyperactive cytokine release = perio breakdown
34
Q

How are AGE’s produced

A

Glycation —> sugar molecules + protein mol = AGE’s

35
Q

Periodontal tissues responses to healing and monitoring

A
  1. Acute inflammation 24-48hrs
  2. Decreased vasodilation / GCF / inflammatory cells
  3. Pocket ulceration heals
36
Q

Periodontal tissues responses to healing and monitoring \

How does pocket ulceration heals

A
  1. Fibroblast proliferation = maturation of connective tissue
    - collagen fibres
    - ground substance
  2. Formation of long junctional epithelium
    - attaches gingiva to clean root surface
  3. Bony remodelling (alveolar bone reattaches)
37
Q

Response to tx - what is affected?

A
  1. Bacterial flora
    - decrease in total amount of microorganisms in perio pockets
    - residual microorganisms shifts from gram - anaerobes to gram + aerobes (associated with perio health)
    - decreased plaque = increased oxygen in residual plaque
  2. Periodontal tissue
    - perio tissue heals (may show recession)
    - decrease in pocket depths
    - decreased inflammation / redness / BOP / suppuration
    - increased pink / firm tissue / fibrous
    - ging cuff tightens as collagen fibre bundles reform
    - attachment may occur at base of pocket
38
Q

Monitoring - assessing to response to therapy

A

Post tx indicies
- healing indicted by decreased pockets / BOP
- pt ability to remove plaque at home by PFS
- decrease mobility / furcation maybe
- may increase recession

39
Q

Why should probing be avoided in the first 6 weeks after treatment

A

Allows early healing / tissue maturation

40
Q

When shoukd post tx indicies be done

A

8-12 weeks after tx

41
Q

How do we know if tx is successful

A

Post tx indicies

Have probing pockets of 3mm or less with no BOP been achieved

If yes - supportive therapy

If no - corrective therapy

DCP2 (5 decks)

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