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Clinical Dentistry 4 > periodontal disease and systemic risk factors > Flashcards

periodontal disease and systemic risk factors Flashcards

1
Q

What BMI is considered obese and overweight?

A
  • greater than or equal to 30 is obese
  • 25 is overweight
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2
Q

what happens when we have over-nutrition?

A
  • higher circulating glucose
  • more adipose tissue
  • greater inflammatory drive
  • treatment becomes more complicated
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3
Q

Describe obesity and periodontitis

A
  • Obesity means a greater risk of dysbiosis
  • Obese patients have less diverse microbiomes, greater effect on females
  • dysbiosis results as aerobic pathways become fermentation
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4
Q

What happens if u reduce the amount of processed food and replace it with more wholesome food, and cut back on sugar

A

The biofilm changes, even if you have got a higher quantity of bacteria, the bacteria that are there both in the gut and orally become the more friendly type and the bleeding on probing will reduce in our patients and the pockets are reduced even without any oral hygiene

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5
Q

If u have poorly controlled diabetes and have refined food/sugar what occurs?

A
  • poorly controlled diabetes are 3x risk of periodontitis
  • high HbA1c affects the microbiome, loose good bacteria, destabilises immune system
  • oxidative stress, bacterial burden, low grade systemic inflammation IL6 significantly higher
  • advanced glycation end products (AGE) increase oxidative stress, these products are found in almost all ‘bad’ foods
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6
Q

What complications arise from obesity ?

A

More likely to suffer sleep apnoea
- stressful, 36% higher chance of severe periodontitis over control patients
- sleep regulates immune and inflammatory processes
- weight loss helps reset the oral microbiome
- complicates treatment
- more tissue makes surfaces harder to keep plaque free
- high cho diet favours plaque formation (and root caries)
- tissue and tongue spread make access difficult
- safety, comfort, and the dental chair
- comorbidity

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7
Q

what is diabetes mellitus?

A

is a chronic medical condition characterized by elevated levels of blood sugar (glucose). This happens either because the body cannot produce enough insulin or because the cells do not respond adequately to the insulin produced.

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8
Q

describe chronic hyperglycaemia

A
  • results in varying degrees of dysfunction of the carbohydrate, lipid and protein metabolism causing widespread cellular and molecular dysfunction
  • this causes significant disturbance of the immune response, angiogenesis and wound healing leading to microvascular and macrovascular systemic pathology
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9
Q

What are the 5 major complications that can arise from diabetes mellitus?

A
  • atherosclerosis
  • retinopathy
  • nephropathy
  • neuropathy
  • impaired wound healing
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10
Q

How is long term blood glucose control assessed?

A

By measuring the glycated haemoglobin (HbA1c) score from a blood sample

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11
Q

what is the recommended target level of glycaemic control?

A
  • HbA1c of less than 48mmol/mol (6.5%)
  • increased chance of preventing/delaying the complications of diabetes
  • the higher the HbA1 score above 48mmol/mol the higher the risk of developing the long term complications of diabetes
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12
Q

what should be aware of in terms of DM and periodontal disease ?

A
  • recurrent periodontal abscesses &/or exaggerated periodontal inflammation may indicate undiagnosed diabetes
    especially if the oral hygiene and periodontal treatment (debridement appears to have been adequate
    consider referral to GMP for investigation
  • periodontal disease in DM is associated with an exaggerated & prolonged inflammatory response to the periodontal microflora
  • diabetes has many complex negative effects on the host response to periodontal infection
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13
Q

What are problems with uncontrolled diabetes?

A
  • Increased formation of advanced glycation end-product (AGE)
  • altered immune cell function
  • altered fibroblast function
  • poor wound healing
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14
Q

what does chronic hyperglycaemia lead to?

A

non-enzymatic glycation (additional fructose or glucose) of proteins results in the formation of stable advanced glycation end products (AGE)

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15
Q

What is the link between AGE and DM

A

AGE formation is significantly increased in DM with greater levels of AGE formation being associated with poorer levels of glycaemic control

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16
Q

Describe AGE in relation to cells

A
  • Many cells throughout the body have specific cell surface receptors for AGE (RAGE)
  • therefore, AGE can negatively affect the cellular function of various cell types throughout the body
  • endothelial cells
  • fibroblasts
  • neurones
  • monocytes/macrophages
  • AGE products lead to oxidative stress
17
Q

Describe how chronic hyperglycaemia results in both up-regulation and impairment of various inflammatory cell types:

A

i) reduced neutrophil (PMN) function:
- impaired adherence. chemotaxis and phagocytosis
- postulated that this results in the persistent bacterial infection and tissue damage found in DM
ii) hyper-responsive monocytes & macrophages:
- AGE formation is thought to lead to this over activation leading to oxidative stress
- results in increased secretion of pro-inflammatory mediators such as cytokines (IL-1 & TNF(alpha)) & prostaglandins (PGE2):
- leads to the pronounced chronic inflammatory response found in DM:
- increased tissue damage
- contributes to the impaired wound healing
- pro-inflammatory mediators leak into the bloodstream leading to increased systemic inflammation:
causes liver to release acute phrase proteins (e.g. c-reactive protein CRP) which further amplifies systemic inflammation
- gingival fibroblasts produce less matrix & collagen, & increased collagenease production
- some evidence of increased fibroblast cell death
- results in reduced tissue formation & reduced healing potential
- results from the cumulative effect of the other changes:
- although patients with DM are susceptible to poor wound healing and infection, antimicrobial therapy is generally not needed

18
Q

How could periodontitis negatively affect glycaemic control?

A
  • The periodontal pocket is filled with a pathogenic anaerobic biofilm resulting in an inflammatory reaction in the adjacent gingival tissues resulting in the pocket wall being ulcerated & leaky
  • the surface area of the exposed ulcerated periodontal pockets can be extensive
  • the inflamed periodontal pocket contains large numbers of bacteria & host inflammatory cells (secreting pro-inflammatory mediators IL-1, TNF(alpha), PGE2)
  • the periodontal tissues are very vascular and the blood vessels within the inflamed tissue are very leaky allowing the inflammatory mediators to spill over the systemic bloodstream leading to systemic inflammation
19
Q

what short term conditions can excess alcohol intake cause?

A
  • dental trauma
  • facial injury
20
Q

what long term conditions can excess alcohol intake cause?

A
  • Oral cancer
  • periodontal disease
  • non-carious tooth surface loss
21
Q

what are the adverse effects of alcohol?

A
  • defective neutrophil function
  • altered clotting mechanism (defective prothrombin and vitamin k activity)
  • increased bone resorption & decreased bone formation
  • reduced healing (deficiency of vitamin B-complex and protein)
  • direct toxic effect on periodontal tissues
22
Q

Describe alcohol and periodontal disease

A

Alcohol is thought to have a similar influence on clinical attachment loss as moderate smoking

23
Q

what is the role of vitamin c?

A
  • essential for collagen
  • additionally important immune functions
  • defends against oxidative stress and free radicles promotes chemotaxis
  • also essential for iron absorption
24
Q

What is the role of vitamin D?

A
  • essential for skeletal development
  • modulation of immune system
  • deficiency of vitamin D associated with reduced immunity and increased autoimmunity
  • inflammatory modulator
  • links between low vitamin D and other chronic inflammatory diseases
25
Q

Describe undernutrition - message to patients

A
  • unless proven deficiency supplements most likely not that helpful
  • taking supplements does not necessarily translate into the nutrient being available (due to absorption and variations in GI microbiome)
  • most likely benefits to eating the whole fruit or vegetable rather than taking supplements, iron deficiency would be the exception however this is generally diagnosed by the GMP and monitored
  • eat a balanced diet
26
Q

Describe antioxidants

A
  • Neutrophils are best defence for periodontitis (phagocytose the pathogens)
    However,
  • When they are subject to oxidative stress (through high glucose) they go rogue and destroy tissues
  • Antioxidants can mop up the free radicles and reduce this
27
Q

What are key points for grade c patients?

A
  • Aim to reduce dysbiosis through controlling what is possible
    looking after the biome
    reducing inflammation drive
  • healthy diet
    cruciferous vegetables
    vitamins d, c, fresh fruit and vegetables
  • reduce carbohydrate especially sugar
  • be aware of AGE foods, reduce to minimal
  • achieve and maintain a healthy weight
  • advise patients on current guidelines on alcohol and risks
28
Q

What are the main types of stress?

A
  • emotional
    -physical
  • behavioural
  • psychosocial
29
Q

what are the 2 theories linking psycho-social stress and chronic disease?

A

1) psychoneurogenic model
2) behaviour-orientated model

30
Q

describe psychoneurogenic model

A
  • poor coping behaviour to chronic stress results in activation of the hypothalamus-pituitary-adrenal (HPA) axis and sympathetic nervous system
  • this activation leads to complex interactions between hormones, neurotransmitters and cytokines
  • this reduces the efficiency of the immune system (host response) resulting/ exacerbating in chronic disease
31
Q

describe behaviour-orientated model

A
  • poor coping behaviour to chronic stress results in changed behaviour
  • this changed behaviour may occur as:
    an adaptive response to the stress
    coping response to the stress
  • results in ‘at risk’ health behaviour which potentially promotes chronic disease:
  • increased smoking
  • increased alcohol intake
  • poor diet
  • decreased oral hygiene
  • disturbed sleeping patterns
  • poor compliance with health/dental care
32
Q

What are the oral effects of stress?

A
  • decreases salivary flow
  • increase glycoprotein content = increased salivary viscosity
  • increased salivary acidity
  • thus favours plaque formation
  • chronic stress induces increased levels of stress hormones (catecholamines):
  • noradrenaline (norepinephrine) and adrenaline (epinephrine) reduce gingival blood flow

Clinical Dentistry 4 (70 decks)

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