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BDS2 - periodontitis > aetiology and pathogenesis > Flashcards

aetiology and pathogenesis Flashcards

1
Q

diagram of clinical health gingivitis and periodontitis

A

just a reminder this is important to know well but there’s too much to make Qs from lol but look it up xoxox

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2
Q

what is plaque’s relationship to periodontal disease

A

plaque is necessary but not sufficient for periodontal disease

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3
Q

what helps plaque to build and progress to clinical disease / gingivitis

A

local plaque retention factors

  • calculus
  • restoration margins
  • crowding
  • mouth breathing

systemic modifying factors

  • sex hormones
  • medication
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4
Q

what is the clinical definition of gingival health

A

> knife edge, scalloped gingival margin
- very well defined gingival margin

> stippling

  • only seen in about 30% of patients
  • just seen at the papilla of some of the sites

> pink
- healthy colour

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5
Q

what can modify the gingival that isn’t gingivitis

A
  • racial pigmentation
  • smoking
  • other factors / habits
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6
Q

why does it only take a few lips for a bited lip to heal

A

the epithelial barrier has a fairly quick turnover

only takes a few days for the cells at the basal layer to disappear into the oral cavity

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7
Q

describe how the gingival sulcus fights infection in health

A
  • originally there is an intact barrier provided by the junctional epithelium
  • bacteria invade and cause shedding of the oral epithelial cells
  • gingival crevice fluid (GCF) flows into where the bacteria are
  • there are antibodies present in the in GCF to fight the infection
  • phagocyte function and lymphocyte infiltrate
    (there is a cellular immune response even in health although it is relatively small ad controlled)
  • complement activity is also present
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8
Q

what happens in the gingival sulcus in gingivitis

A
  • altered microbial colonisation
    (increased accumulation in plaque)
  • gingival margins are red and inflamed, lose stippling
  • increased flow of GCF
  • influx of neutrophils, increased lymphocytes and monocytes
  • plasma cells infiltrate
  • proliferation and ulceration of the epithelium
  • bleeding upon probing (bleeds easily)
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9
Q

explain what is different between a healthy immune response and the immune response in early gingivitis

A

monocytes, macrophages, lymphocytes and neutrophils are present in both

in gingivitis there is

  • increased neutrophil emigration
  • proliferation of the junctional epithelium
  • increased infiltrate of the cells
  • dilated vessels
  • vascular proliferation
  • increased collagen loss
  • very few plasma cells
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10
Q

what is the difference between early gingivitis and established gingivitis

A

established gingivitis has a greatly increased leukocytic infiltration with plasma cells
whereas there are very few plasma cells in early gingivitis

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11
Q

how is gingivitis reversible

A

cleaning the teeth and maintaining good oral hygiene and the gingiva will return to the clinical definition of health (provided other factors are under control as well)

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12
Q

what is a defining feature of periodontitis

A

irreversible loss of attachments (loss of bone)

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13
Q

how can you tell the difference between periodontitis and gingivitis

A

use a probe

cannot tell the difference without

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14
Q

what is a false pocket

A

increased pocket depth but no loss of attachments
ie there is a pocket present in the gingival sulcus but the bone remains intact
junctional epithelium has not changed position but has become ulcerated
inflammation causes the pocket

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15
Q

what is a true pocket

A

apical migration of junctional epithelium
if the cause of the inflammation is not removed then there is a reasonable chance that the patient will progress from a false pocket to a true pocket

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16
Q

what is in the process of periodonitis happening

A
  • plaque formation
  • immune cells move in
  • gingivitis
  • increase in pocket depth
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17
Q

does gingivitis always progress to periodontitis

A

not always
but it can
and in many patients it will

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18
Q

what is the progression of the attachment loss generally like

A

generally very slow
between 0.05-0.1ml per year
this is highly variable

in some patients however the rate of attachment can be up to 2mm loss per year which will cause serious trouble = tooth loss

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19
Q

what is the biofilm

A
  • one or more communities of microorganisms
  • embedded in a glycocalyx
  • attached to a solid surface
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20
Q

what are the properties of the biofilm

A
  • provide protection for colonising species from competing organisms and environment (host defences, antibiotics)
  • facilitate uptake of nutrients and removal of metabolic products
  • development of appropriate physiochemical environment eg pH, oxygen concentration
  • communication between bacteria
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21
Q

does a water pip useful as an interdental cleaning device

A

no

it squirts a little jet of water interdentally which will wash the biofilm but not actually remove it

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22
Q

explain bacterial virulence / how bacteria is tailored to cause periodontal disease

A
  • degrade host immunoglobulin and complement
  • leukotoxin production (specifically kill certain cells)
  • tissue invasion
  • inhibition of antibody synthesis (or can change the synthesis so they are less effective)
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23
Q

what is Koch’s postulates

A

a set of criteria that an organism has to fulfil to cause a disease

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24
Q

what evidence is needed to prove specific bacterial causation

A

> presence in elevated numbers in diseased sites
reduced numbers following periodontal therapy
presence of an elevated specific immune response
production of virulence factors
evidence from animal models

25
Q

name bacteria which are very likely to play a role in periodontal disease

A
  • P.gingivalis
  • B.forsythus
  • T.denticola
26
Q

what do early colonisers in the biofilm allow for

A

other bacteria to come in and attach on top of the early colonisers
the biofilm accumulates and certain bacteria will turn up and put the whole thing to chaos

27
Q

what other than bacteria can modify the expression of disease

A

other host and environmental factors

28
Q

what can be said about the bacteria that causes periodontal disease

A

its not one bacteria that causes this but a community shift

29
Q

what mechanisms contribute to the host response

A
  • saliva
  • epithelium
    > physical barrier
    > shedding of cells
    > production of inflammatory mediators
  • GCF
  • inflammatory and immune responses
30
Q

what are the 2 major functions of neutrophils in periodontal disease

A
  • generates a trap
    = a web of sticky DNA and other molecules
    = traps bacteria so it is easier to kill
    = can also cause damage to the host
  • generates a reactive oxygen species to kill bacteria
    = causes by standing damage to the host
31
Q

What is a PMN cell?

A

A type of immune cell that has granules (small particles) with enzymes that are released during infections, allergic reactions, and asthma
Neutrophils, eosinophils, and basophils are PMNs.
A PMN is a type of white blood cell

32
Q

what happens when the PMNs contain disease

A

gingivitis limited disease

ie the neutrophils are able to keep everything check without the gingivitis progressing into periodontal disease

33
Q

what happens when the PMN’s do not contain the disease

A

evolution of pathogenic biofilm

34
Q

what happens in the immune response during the evolution of pathogenic biofilm?

A 
monocytes and lymphocytes infiltrate
they release cytokines / inflammatory mediators such as
- MMPs
- TNFs 
- prostaglandins 
- interleukins

these then cause connective bone metabolism, inflammation tissue destruction, pocketing bone loss and clinical disease
this then causes more evolution of pathogenic biofilm

35
Q

what does the initial periodontal lesion composed mainly of

A

T lymphocytes
these help other cells to do their job by secreting cytokines and influencing B cells

B cells and plasma cells predominate at a later stage

36
Q

is antibody protective?

A

probably

37
Q

what are the protective functions of antibody

A

> inhibition of adhesion / invasion
(if certain antibodies are stuck to the bacteria then it is more difficult for them to invade cells and it is more difficult for the virulence factors to work)

> complement activation

> neutralisation of toxins

> opsonisation and phagocytosis

> prevents progressive infection and therefore potentially serious systemic consequences

38
Q

what problems can antibodies cause sometimes

A

inadvertent local tissue damage (bystander damage) combined with attempts at repair

immune response protects you but also causes bone damage

39
Q

how does the immune response cause bone damage

A

this is an assumption
the body wants to keep pathogenic biofilm out of systemic circulation
can do this by having the body surfaces retreat away from the biofilm = resorption
ultimately the teeth will fall out as a result as well and this will get rid of the biofilm threat to the systemic circulation as well

40
Q

what are MMPs

A

matrix metalloproteinases
family of zinc and calcium dependent protelytic enzymes (include collagenases) that break down connective tissues

secreted by host inflammatory cells

41
Q

what do MMPs do in periodontitis

A

matrix degradation

break down the collagen matrix

42
Q

what does the activation of osteoclasts do in periodontitis

A

breaks down bone

43
Q

diagram on connective tissue bone metabolism / host immune response / microbial challenge / osteoblast / osteoclast

A

not even that complicated looking but the ‘+’ sign is confusing me lol and i dunno how to put this into a question but give it a little look xxx

44
Q

what is the normal bone level measured from the ACJ in health

A

between 1-2mm

45
Q

what happens in horizontal bone loss

A

bone is resorbed in a straight line on both sides of the tooth

46
Q

what happens in vertical (angular) bone loss

A

bone is lost on one side
kind of sloped
one area is more affected by bone loss than the other

47
Q

what are the 2 patterns of bone loss

A
  • horizontal

- vertical / angular

48
Q

what pattern of bone loss is easier to regenerate bone in again

A

vertical / angular bone loss
has a wall of bone on one side of the tooth which is beneficial to regeneration
can back material into the lost area to help with regeneration
(haven’t got this in horizontal bone loss)

49
Q

how does vertical bone loss arise

A

has something to do with the shape of the bone to begin with

if 2mm encompasses the whole bone (thinner bone) then it will probably be horizontal bone loss

if the bone is fatter than the loss might just nibble at one side of the tooth

50
Q

what happens in furcation bone loss

A

bone lost at the furcation level of the bone

whole way through from buccal to lingual

51
Q

name general risk factors that contribute to periodontitis disease

A 
> smoking
> diabetes
(these first 2 are the easiest to define)
> stress
> drugs
> systemic disease
> nutrition
52
Q

what are risk determinants of periodontitis disease

A

> genetics
socioeconomic status
gender

53
Q

what are local risk factors

A
  • anatomical risk factors
  • tooth position
  • iatrogenic risk factors
54
Q

what are anatomical risk factors

A
  • enamel pearls / projections
  • grooves
  • furcations
  • gingival recession
55
Q

how does the tooth position affect periodontitis disease

A
  • malalignment
  • crowding
  • tipping
  • migration
  • occlusal forces
56
Q

what are iatrogenic risk factors?

A
  • restoration overhangs
  • defective crown margins
  • poorly designed partial dentures
  • orthodontic appliances
57
Q

how is smoking a risk factor of periodontal disease

A
  • vasoconstriction of gingival vessels
  • increased gingival keratinisation
  • impaired antibody production
  • depressed numbers of Th lymphocytes
  • impaired PMN function
  • increased production of pro-inflammatory cytokines
58
Q

what is the primary aetiological agent in inflammatory periodontal disease

A

microbial plaque

59
Q

what is the extent and severity of the disease dependent upon

A

the interaction between microbe and host

BDS2 - periodontitis (4 decks)

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