Systemic risk factors Flashcards
(72 cards)
1
Q
what is a hyperresponsive immune system?
A
too busy: starts reacting to things we don’t need it to react to, over triggered, several allergies
2
Q
what is a hyporesponsive immune system?
A
immunosuppressed: could be taking medication that is supressing immune system
3
Q
How can immune response be modified?
A
diet
genetics
lifestyle
4
Q
where is 90% serotonin made?
A
the gut
5
Q
how does being obese affect your hunger hormones?
A
more adipose tissue
insulin doesnt work normally
inhibits hormones that make you feel full
6
Q
what does adipose tissue produce?
A
- Cytokines
- TnF alpha IL6
- Pro inflammatory mediators
- Adipokines – leptin etc. (proinflammatory)
7
Q
what are AGE products?
A
Advanced glycation end products
- fried food
- processed food
- meat
- cheese
8
Q
cause of chronic hyperglycaemia?
A
immune system not working, impaired host defences through impaired chemotaxis (reduced migration)
9
Q
what are complications of obesity?
A
- Sleep apnoea: higher chance of severe periodontitis due to stress, sleep regulates immune and inflammatory response.
- Uncomfortable to sit in dental chair.
- Can’t treat molars if cheek fat in the way.
- More tissue makes surfaces harder to keep plaque free.
- High carb diet favours plaque formation (and root caries).
- Tissue and tongue spread make access difficult.
10
Q
what is vitamin C essential for?
A
collagen, immune functions, defends against oxidative stress and free radicles, promotes chemotaxis, iron absorption
11
Q
what is a vitamin C deficiency value?
A
under 2mg/L
12
Q
what disease results from lack of vit c?
A
scurvy
13
Q
what is vitamin D essential for?
A
skeletal development, immune system, inflammatory modulator
14
Q
how much vitamin D do you need per day?
A
100-125mg
15
Q
how much vitamin D should you supplement?
A
50mg a day
16
Q
what should a diet include to improve perio disease?
A
- Omega 3
- Cruciferous vegetables (cabbage, cauliflower, broccoli)
- Pre and pro biotics
- micronutrients
17
Q
where do you find prebiotics?
A
soil, plant fibre
18
Q
what are prebiotics needed for?
A
support gut bacteria
19
Q
where do you find probiotics?
A
seeds, actual bacteria, fermented food
20
Q
what do antioxidants do?
A
mop up free radicals and reduce oxidative stress on neutrophils
21
Q
what is DM?
A
Chronic hyperglycaemia results in varying degrees of dysfunction of the carbohydrate, lipid and protein metabolism causing widespread cellular and molecular dysfunction.
22
Q
what are complications of DM?
A
- Atherosclerosis
- Retinopathy
- Nephropathy
- Impaired wound healing
23
Q
what is the association between DM and chronic periodontitis?
A
degree of blood glucose (glycaemic) control
24
Q
what are indicators of DM?
A
- Recurrent perio abscesses
- Exaggerated perio inflammation
*Especially if OH and perio treatment is adequate
25
what would you find with prediabetes?
abnormally high blood sugar levels (hyperglycaemia) but below threshold for a diagnosis
26
what does undiagnosed DM lead to?
increased formation of AGE
altered immune cell function
altered fibroblast function
poor wound healing
27
how does DM alter immune function?
reduced neutrophil function
hyper-responsive monocytes
increased secretion of pro-inflammatory mediators (cytokines) and prostaglandins
chronic inflammatory response
28
what happens to fibroblasts in a patient with DM?
produce less matrix and collagen, and increased collagenase production (more breakdown, cell death of fibroblasts).
*Reduces tissue formation and healing potential
29
how does uncontrolled diabetes lead to exacerbation of periodontitis?
hyperglycaemia
elevated AGE/ RAGE
local immune dysfunction + elevation of pro-inflammatory cytokines
increased tissue breakdown/ reduced tissue repair
30
give examples of pro-inflammatory cytokines?
IL-6
TNF
IL-1
31
how may periodontitis lead to exacerbation of diabetes?
bacteria and bacteria antigens in bloodstream -> increased systemic inflammatory state (increased insulin resistance)
OR
elevated IL-6, TNFa, c-reactive protein and oxygen radicals in bloodstream -> increased systemic inflammatory state
32
what is normal glycaemic level?
less than 48mmol/mol
6.5%
33
what are stages of an alcohol brief intervention?
raise the issue
screen and give feedback
listen for readiness to change
choose a suitable approach
34
what are adverse effects of diabetes?
- Defective neutrophil function
- Altered clotting mechanism (defective prothrombin and vitamin K activity)
- Increased bone resorption and decreased bone formation.
- Reduced healing (deficiency of vitamin B-complex and protein)
- Direct toxic effect on periodontal tissues.
35
what are key points for grade C patients?
reduce dysbiosis by reducing inflammatory drive
healthy diet (cruciferous veg, vit D, C)
reduce carbs especially sugar
be aware of AGE foods
healthy weight
advise on current alcohol guidelines and risks
36
what are types of stress?
emotional
physical
behavioural
psychosocial
37
what models link psycho-social stress and chronic disease?
pyschoneurogenic model
behaviour-orientated model
38
explain the pyschoneurogenic model
stress results in activation of the hypothalamus-pituitary-adrenal (HPA) axis and sympathetic nervous system. This leads to complex interactions between hormones, neurotransmitters, and cytokines. This reduces efficiency of immune system = chronic disease
39
explain the behaviour-orientated model?
stress results in changed behaviour which promotes chronic disease i.e., smoking, alcohol, poor diet, bad OH, sleep
40
what type of stress is a risk factor for necrotising gingivitis?
emotional stress
41
how may stress lead to plaque formation?
decrease saliva flow
increase glycoprotein content (viscocity)
increase saliva acidity
42
what are the oral effects of chronic stress?
noradrenaline and adrenaline (catecholamines) reduce subgingival blood flow
43
what is the genco study 1999?
financial strain and depression associated with increased periodontal breakdown
44
what is classed as nicotine depedancy?
smoking at least 15-20 cigs a day
smoking within 30 minutes daily
45
what is the half life of nicotine?
2 hours
46
what questions should you ask a patient in relation to smoking?
how many cigs a day?
how long they have smoked for?
when they stopped?
how long they have stopped for?
47
what does the prochaska and diclemente model cover?
Pre-contemplators – not interested.
Contemplators – interested unready (use brief interventions/ discussions that may push them into the next group).
Active quitters – making an attempt.
48
what is the 5 As approach?
ASK
ADVISE
ASSESS
ASSIST
ARRANGE
49
what is the 5 Rs intervention?
RELEVANCE
RISKS
REWARDS
ROAD
REPITITION
50
what carcinogens are in tobacco?
polycyclic aromatic hydrocarbons
N-nitroso compounds
51
how does smoking affect the periodontium?
black/brown staining
rough surface
calculus build up
reduced inflammatory response
keratin lay down
52
why does smoking allow calculus to build up?
particulates in smoke cause irritation which increases saliva flow (parotid), increasing pH, raising calcium carbonate which forms a precipitate of calcium phosphate
53
why may smokers gums look healthy?
Keratin laid down
54
what are the biological effects of smoking?
- Reduced vascularity
- Reduced inflammatory and immune response.
- More pathogenic plaque biofilm
- Direct toxic effects of cells like fibroblasts.
- Thermal damage
55
what vascularity change occurs in smokers gums?
fewer large vessels and more small vessels
56
how does smoking affect immune cells?
- reduced neutrophil function, impaired chemotaxis
- phagocytosis and bacterial killing
- reduced salivary IgA
- reduced IgG
- reduced T lymphocytes
- more MMP and PGE2
57
what does MMP and PGE2 cause?
tissue breakdown
58
what does reduced GCF lead to?
- reduced vascularity
- immunoglobulin and other defence molecules cant reach perio pockets
- reduced gingival crevice flushing
59
how may perio bacteria reach the systemic bloodstream?
tissues very vascular
blood vessels within tissue are leaky
60
what are the potential mechanisms linking CVD to perio disease?
direct bacterial effect on platelets
autoimmune responses
invasion/ uptake of bacteria into endothelial cells and macrophages
systemic inflammation
61
what perio pathogens may trigger inappropriate blood clotting if reached the bloodstream?
Strep anguis
P gingivalis
62
what is molecular mimicry?
Perio pathogens enter the bloodstream and cause a cross reaction which causes the host to produce antibodies against itself leading to damage to the host cells
63
where is molecular mimicry most likely to occur?
arterial cells that have already been damaged
64
how do perio pathogens contribute to plaque formation?
attracting macrophages
65
what pathogen has been detected in all atherosclerotic plaque from carotid endarterectomy samples?
p.gingivalis
66
how does systemic inflammation exacerbate CVD?
systemic release of IL-6, TNFa
leads to atherosclerosis
releases C-reactive protein from liver
67
what is a non-modifiable risk factor of periodontitis?
genetics
68
what is a strong indicator of genetic susceptibility of periodontitis?
Periodontitis stage 3 / 4 grade C – rapid perio destruction (more than expected for their age), strong family history of periodontal disease/ early tooth loss).
69
how do you assess genetic susceptibility?
- Extent of previous perio disease (bone loss/ LOA or level of BOP).
- Age
- Level of oral hygiene (plaque score).
70
what systemic disease genetic disorders result in periodontitis?
Ehlers-danlos syndrome
Papillion-LeFevre syndrome
Downs syndrome.
Chediak-higashi syndrome
Hypophosphatasia
71
what is ehlers-danlos syndrome?
collagen defetcs
72
what is papillion-lefevre syndrome?
young children, keratosis on hands and feet, severe perio disease.
