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Module 4 - perio > Systemic risk factors > Flashcards

Systemic risk factors Flashcards

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

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2
Q

what is a hyporesponsive immune system?

A

immunosuppressed: could be taking medication that is supressing immune system

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3
Q

How can immune response be modified?

A

diet
genetics
lifestyle

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4
Q

where is 90% serotonin made?

A

the gut

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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

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6
Q

what does adipose tissue produce?

A
  • Cytokines
  • TnF alpha IL6
  • Pro inflammatory mediators
  • Adipokines – leptin etc. (proinflammatory)
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7
Q

what are AGE products?

A

Advanced glycation end products
- fried food
- processed food
- meat
- cheese

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8
Q

cause of chronic hyperglycaemia?

A

immune system not working, impaired host defences through impaired chemotaxis (reduced migration)

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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.
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10
Q

what is vitamin C essential for?

A

collagen, immune functions, defends against oxidative stress and free radicles, promotes chemotaxis, iron absorption

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11
Q

what is a vitamin C deficiency value?

A

under 2mg/L

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12
Q

what disease results from lack of vit c?

A

scurvy

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13
Q

what is vitamin D essential for?

A

skeletal development, immune system, inflammatory modulator

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14
Q

how much vitamin D do you need per day?

A

100-125mg

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15
Q

how much vitamin D should you supplement?

A

50mg a day

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16
Q

what should a diet include to improve perio disease?

A
  • Omega 3
  • Cruciferous vegetables (cabbage, cauliflower, broccoli)
  • Pre and pro biotics
  • micronutrients
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17
Q

where do you find prebiotics?

A

soil, plant fibre

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18
Q

what are prebiotics needed for?

A

support gut bacteria

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19
Q

where do you find probiotics?

A

seeds, actual bacteria, fermented food

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20
Q

what do antioxidants do?

A

mop up free radicals and reduce oxidative stress on neutrophils

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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.

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22
Q

what are complications of DM?

A
  • Atherosclerosis
  • Retinopathy
  • Nephropathy
  • Impaired wound healing
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23
Q

what is the association between DM and chronic periodontitis?

A

degree of blood glucose (glycaemic) control

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24
Q

what are indicators of DM?

A
  • Recurrent perio abscesses
  • Exaggerated perio inflammation
    *Especially if OH and perio treatment is adequate
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25
Q

what would you find with prediabetes?

A

abnormally high blood sugar levels (hyperglycaemia) but below threshold for a diagnosis

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26
Q

what does undiagnosed DM lead to?

A

increased formation of AGE
altered immune cell function
altered fibroblast function
poor wound healing

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27
Q

how does DM alter immune function?

A

reduced neutrophil function
hyper-responsive monocytes
increased secretion of pro-inflammatory mediators (cytokines) and prostaglandins
chronic inflammatory response

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28
Q

what happens to fibroblasts in a patient with DM?

A

produce less matrix and collagen, and increased collagenase production (more breakdown, cell death of fibroblasts).
*Reduces tissue formation and healing potential

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29
Q

how does uncontrolled diabetes lead to exacerbation of periodontitis?

A

hyperglycaemia
elevated AGE/ RAGE
local immune dysfunction + elevation of pro-inflammatory cytokines
increased tissue breakdown/ reduced tissue repair

30
Q

give examples of pro-inflammatory cytokines?

A

IL-6
TNF
IL-1

31
Q

how may periodontitis lead to exacerbation of diabetes?

A

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
Q

what is normal glycaemic level?

A

less than 48mmol/mol
6.5%

33
Q

what are stages of an alcohol brief intervention?

A

raise the issue
screen and give feedback
listen for readiness to change
choose a suitable approach

34
Q

what are adverse effects of diabetes?

A
  • 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
Q

what are key points for grade C patients?

A

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
Q

what are types of stress?

A

emotional
physical
behavioural
psychosocial

37
Q

what models link psycho-social stress and chronic disease?

A

pyschoneurogenic model
behaviour-orientated model

38
Q

explain the pyschoneurogenic model

A

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
Q

explain the behaviour-orientated model?

A

stress results in changed behaviour which promotes chronic disease i.e., smoking, alcohol, poor diet, bad OH, sleep

40
Q

what type of stress is a risk factor for necrotising gingivitis?

A

emotional stress

41
Q

how may stress lead to plaque formation?

A

decrease saliva flow
increase glycoprotein content (viscocity)
increase saliva acidity

42
Q

what are the oral effects of chronic stress?

A

noradrenaline and adrenaline (catecholamines) reduce subgingival blood flow

43
Q

what is the genco study 1999?

A

financial strain and depression associated with increased periodontal breakdown

44
Q

what is classed as nicotine depedancy?

A

smoking at least 15-20 cigs a day
smoking within 30 minutes daily

45
Q

what is the half life of nicotine?

A

2 hours

46
Q

what questions should you ask a patient in relation to smoking?

A

how many cigs a day?
how long they have smoked for?
when they stopped?
how long they have stopped for?

47
Q

what does the prochaska and diclemente model cover?

A

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
Q

what is the 5 As approach?

A

ASK
ADVISE
ASSESS
ASSIST
ARRANGE

49
Q

what is the 5 Rs intervention?

A

RELEVANCE
RISKS
REWARDS
ROAD
REPITITION

50
Q

what carcinogens are in tobacco?

A

polycyclic aromatic hydrocarbons
N-nitroso compounds

51
Q

how does smoking affect the periodontium?

A

black/brown staining
rough surface
calculus build up
reduced inflammatory response
keratin lay down

52
Q

why does smoking allow calculus to build up?

A

particulates in smoke cause irritation which increases saliva flow (parotid), increasing pH, raising calcium carbonate which forms a precipitate of calcium phosphate

53
Q

why may smokers gums look healthy?

A

Keratin laid down

54
Q

what are the biological effects of smoking?

A
  • Reduced vascularity
  • Reduced inflammatory and immune response.
  • More pathogenic plaque biofilm
  • Direct toxic effects of cells like fibroblasts.
  • Thermal damage
55
Q

what vascularity change occurs in smokers gums?

A

fewer large vessels and more small vessels

56
Q

how does smoking affect immune cells?

A
  • reduced neutrophil function, impaired chemotaxis
  • phagocytosis and bacterial killing
  • reduced salivary IgA
  • reduced IgG
  • reduced T lymphocytes
  • more MMP and PGE2
57
Q

what does MMP and PGE2 cause?

A

tissue breakdown

58
Q

what does reduced GCF lead to?

A
  • reduced vascularity
  • immunoglobulin and other defence molecules cant reach perio pockets
  • reduced gingival crevice flushing
59
Q

how may perio bacteria reach the systemic bloodstream?

A

tissues very vascular
blood vessels within tissue are leaky

60
Q

what are the potential mechanisms linking CVD to perio disease?

A

direct bacterial effect on platelets
autoimmune responses
invasion/ uptake of bacteria into endothelial cells and macrophages
systemic inflammation

61
Q

what perio pathogens may trigger inappropriate blood clotting if reached the bloodstream?

A

Strep anguis
P gingivalis

62
Q

what is molecular mimicry?

A

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
Q

where is molecular mimicry most likely to occur?

A

arterial cells that have already been damaged

64
Q

how do perio pathogens contribute to plaque formation?

A

attracting macrophages

65
Q

what pathogen has been detected in all atherosclerotic plaque from carotid endarterectomy samples?

A

p.gingivalis

66
Q

how does systemic inflammation exacerbate CVD?

A

systemic release of IL-6, TNFa
leads to atherosclerosis
releases C-reactive protein from liver

67
Q

what is a non-modifiable risk factor of periodontitis?

A

genetics

68
Q

what is a strong indicator of genetic susceptibility of periodontitis?

A

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
Q

how do you assess genetic susceptibility?

A
  • Extent of previous perio disease (bone loss/ LOA or level of BOP).
  • Age
  • Level of oral hygiene (plaque score).
70
Q

what systemic disease genetic disorders result in periodontitis?

A

Ehlers-danlos syndrome
Papillion-LeFevre syndrome
Downs syndrome.
Chediak-higashi syndrome
Hypophosphatasia

71
Q

what is ehlers-danlos syndrome?

A

collagen defetcs

72
Q

what is papillion-lefevre syndrome?

A

young children, keratosis on hands and feet, severe perio disease.

Module 4 - perio (1 decks)

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