Case Conference Q’s Flashcards
What are some challenges in treatment
Identifying RF
Pt concerns / compliance
Benefits of LA
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
How do you explain periodontal disease / pocketing to pt?
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
Evidence of gum disease
Pocket > 4mm
Healthy gums
1-3mm pocketing + no BOP
Why is it important to explain why perio needed tx
Can be controlled however disease can relapse
What should we notice clinically as well as record when a pt smokes
How many for how long
Characteristics clinically
- fibrotic, tight gingiva
- decreased BOP
- xerostomia (challacombe scale)
- staining / tartare
What are pack years
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
How can polypharmacy affect pt lifestyle
- Xerostomia
- increased acidity in mouth (less saliva) = increased caries
- acidity - tooth surface loss - erosion
- fungal infections
- less saliva = inc decay - Anticoagulants
- inc risk of bleeding (blood thinner eg, warfarin)
- risk for LA - Statins
- for high cholesterol
How to manage NCTTL
Tooth surface loss due to process other than caries
Caused by attrition , erosion, abrasion
Define attrition
Flattening of occlusal surfaces
Do you agree with the diagnosi? Why ?
- Extent (assess by radiographs) + pattern of bone loss
Generalised / localised / MIP - Staging (use bone loss at worst site) to determine SEVERITY of disease
- Grading
(% bone loss / pt age) = rate of progression of disease
How do radiographs assist in treatment plan / diagnosis?
- Horizontal bone loss
- Loss of buccal / lingual cortices
- Loss of intervening trabecular bone - Vertical bone loss
- Discrepancy in degree of bone loss at 2 adjacent sites
- may indicate rapid bone loss
- angular bony defects - Furcation involvement
- local PRF
- radiolucency shows furcation
Therefore allowing you to stage and grade
+ identify extent
- can see calculus, PRF, occlusal trauma, sclerosis
Anatomy and chemistry of the tooth
Critical ph of dentine?
6.2-6.4
Root dentine vulnerable to acidic dissolution
Anatomy and chemistry of the tooth
Critical ph of enamel
5.5
Enamel structure
Highly organised, acellular tissue
- 95% inorganic material impure calcium HAP
- 5% fluid and organic protein
- mineral crystals organised into prisms / rods
Mineral crystals in enamel made up of
- Inorganic salt (calcium phosphate salt)
- Hydroxyapatite
What is the plaque biofilm? Why disrupt?
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
Periodontal indicies
Pocket probing depths
What do we use
Where do we probe
Pcp10 probe
6 point around each tooth
If lots of supra gingival calc present, periodontal charting should be postponed until after supra gingival scaling
What is true probing attachment level and why is it important
Probing depth measured from CEJ / other fixed point
Allows us to monitor periodontal progression
If considerable gingival hyperplasia, pocketing may be …, but attachment loss may be …
If considerable gingival hyperplasia, pocketing may be deep 5-7mm, but attachment loss may be small
In order to interpret pocket measurement, note…
- Position of gingival margin on tooth surface
- Position of the alveolar crest as seen on radiograph
- Factors affecting accuracy of periodontal probing
Why is it important to measure gingival recession?
So the total amount of measured attachment loss can be meaningfully compared with bone levels on radiographs
Periodontal screening - why is it important
- 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
Limitation of periodontal screening
- Not a replacement for perio indicies
- Not able to show extent of periodontal involvement
- Doesn’t not record plaque levels, attachment loss, recession
- Not suitable to monitor perio status / response to tx
Systemic risk factors / risk factors for periodontal disease
Smoking
Diabetes mellitus
Race / genetics / gender
Polymorphonuclear functional abnormalities PMN’s
Acquired systemic infections eg HIV
Mechanisms by which systemic risk factors apeoar to be operating
- Smoking
- increase inflammatory response
- direct toxic / thermal effects to cells
- increased staining / calculus
- decrease bone levels - 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 - 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 - Stress
- chronic stress / increased allostatic load =
- suppression of immune response
- increased susceptibility to infections
Periodontitis and diabetes
What’s usually happens to control BG
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
Insulin mode of action
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
Diabetes and periodontitis - bifunctional relationship
- Glucose in blood binds to haem in RBC.
- If BG levels remain high, other proteins will bind to excess glucose = AGE’s
- 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
Accumulation of AGE’s causes…
- 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
What is the effect of persistent chronic inflammation
Increased cytokines in saliva and GCF (in diabetics)
Dysregulated inflammatory environment
Increased insulin resistance
Why does poorly controlled diabates affect how perio tissues respond to local factors like plaque
- 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 - Monocytes macrophages release pro inflammatory cytokines but in diabetics..
- pro inflammatory cytokines in EXCESS = hyperactive cytokine release = perio breakdown
How are AGE’s produced
Glycation —> sugar molecules + protein mol = AGE’s
Periodontal tissues responses to healing and monitoring
- Acute inflammation 24-48hrs
- Decreased vasodilation / GCF / inflammatory cells
- Pocket ulceration heals
Periodontal tissues responses to healing and monitoring \
How does pocket ulceration heals
- Fibroblast proliferation = maturation of connective tissue
- collagen fibres
- ground substance - Formation of long junctional epithelium
- attaches gingiva to clean root surface - Bony remodelling (alveolar bone reattaches)
Response to tx - what is affected?
- 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 - 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
Monitoring - assessing to response to therapy
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
Why should probing be avoided in the first 6 weeks after treatment
Allows early healing / tissue maturation
When shoukd post tx indicies be done
8-12 weeks after tx
How do we know if tx is successful
Post tx indicies
Have probing pockets of 3mm or less with no BOP been achieved
If yes - supportive therapy
If no - corrective therapy
