aetiology and pathogenesis Flashcards
diagram of clinical health gingivitis and periodontitis
just a reminder this is important to know well but there’s too much to make Qs from lol but look it up xoxox
what is plaque’s relationship to periodontal disease
plaque is necessary but not sufficient for periodontal disease
what helps plaque to build and progress to clinical disease / gingivitis
local plaque retention factors
- calculus
- restoration margins
- crowding
- mouth breathing
systemic modifying factors
- sex hormones
- medication
what is the clinical definition of gingival health
> 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
what can modify the gingival that isn’t gingivitis
- racial pigmentation
- smoking
- other factors / habits
why does it only take a few lips for a bited lip to heal
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
describe how the gingival sulcus fights infection in health
- 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
what happens in the gingival sulcus in gingivitis
- 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)
explain what is different between a healthy immune response and the immune response in early gingivitis
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
what is the difference between early gingivitis and established gingivitis
established gingivitis has a greatly increased leukocytic infiltration with plasma cells
whereas there are very few plasma cells in early gingivitis
how is gingivitis reversible
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)
what is a defining feature of periodontitis
irreversible loss of attachments (loss of bone)
how can you tell the difference between periodontitis and gingivitis
use a probe
cannot tell the difference without
what is a false pocket
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
what is a true pocket
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
what is in the process of periodonitis happening
- plaque formation
- immune cells move in
- gingivitis
- increase in pocket depth
does gingivitis always progress to periodontitis
not always
but it can
and in many patients it will
what is the progression of the attachment loss generally like
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
what is the biofilm
- one or more communities of microorganisms
- embedded in a glycocalyx
- attached to a solid surface
what are the properties of the biofilm
- 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
does a water pip useful as an interdental cleaning device
no
it squirts a little jet of water interdentally which will wash the biofilm but not actually remove it
explain bacterial virulence / how bacteria is tailored to cause periodontal disease
- 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)
what is Koch’s postulates
a set of criteria that an organism has to fulfil to cause a disease
what evidence is needed to prove specific bacterial causation
> 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
name bacteria which are very likely to play a role in periodontal disease
- P.gingivalis
- B.forsythus
- T.denticola
what do early colonisers in the biofilm allow for
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
what other than bacteria can modify the expression of disease
other host and environmental factors
what can be said about the bacteria that causes periodontal disease
its not one bacteria that causes this but a community shift
what mechanisms contribute to the host response
- saliva
- epithelium
> physical barrier
> shedding of cells
> production of inflammatory mediators - GCF
- inflammatory and immune responses
what are the 2 major functions of neutrophils in periodontal disease
- 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
What is a PMN cell?
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
what happens when the PMNs contain disease
gingivitis limited disease
ie the neutrophils are able to keep everything check without the gingivitis progressing into periodontal disease
what happens when the PMN’s do not contain the disease
evolution of pathogenic biofilm
what happens in the immune response during the evolution of pathogenic biofilm?
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
what does the initial periodontal lesion composed mainly of
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
is antibody protective?
probably
what are the protective functions of antibody
> 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
what problems can antibodies cause sometimes
inadvertent local tissue damage (bystander damage) combined with attempts at repair
immune response protects you but also causes bone damage
how does the immune response cause bone damage
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
what are MMPs
matrix metalloproteinases
family of zinc and calcium dependent protelytic enzymes (include collagenases) that break down connective tissues
secreted by host inflammatory cells
what do MMPs do in periodontitis
matrix degradation
break down the collagen matrix
what does the activation of osteoclasts do in periodontitis
breaks down bone
diagram on connective tissue bone metabolism / host immune response / microbial challenge / osteoblast / osteoclast
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
what is the normal bone level measured from the ACJ in health
between 1-2mm
what happens in horizontal bone loss
bone is resorbed in a straight line on both sides of the tooth
what happens in vertical (angular) bone loss
bone is lost on one side
kind of sloped
one area is more affected by bone loss than the other
what are the 2 patterns of bone loss
- horizontal
- vertical / angular
what pattern of bone loss is easier to regenerate bone in again
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)
how does vertical bone loss arise
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
what happens in furcation bone loss
bone lost at the furcation level of the bone
whole way through from buccal to lingual
name general risk factors that contribute to periodontitis disease
> smoking > diabetes (these first 2 are the easiest to define) > stress > drugs > systemic disease > nutrition
what are risk determinants of periodontitis disease
> genetics
socioeconomic status
gender
what are local risk factors
- anatomical risk factors
- tooth position
- iatrogenic risk factors
what are anatomical risk factors
- enamel pearls / projections
- grooves
- furcations
- gingival recession
how does the tooth position affect periodontitis disease
- malalignment
- crowding
- tipping
- migration
- occlusal forces
what are iatrogenic risk factors?
- restoration overhangs
- defective crown margins
- poorly designed partial dentures
- orthodontic appliances
how is smoking a risk factor of periodontal disease
- vasoconstriction of gingival vessels
- increased gingival keratinisation
- impaired antibody production
- depressed numbers of Th lymphocytes
- impaired PMN function
- increased production of pro-inflammatory cytokines
what is the primary aetiological agent in inflammatory periodontal disease
microbial plaque
what is the extent and severity of the disease dependent upon
the interaction between microbe and host
