host bacterial interactions in periodontal disease Flashcards
what is included in the term periodontal diseases
- gingivitis
- periodontitis
what is gingivitis
- inflammation localised to gingival tissues
- acute inflammation = normal, physiological response, if successful will repair to homeostasis
- normal, physiological response to infection or injury
what is periodontitis
- inflammation of the gingival tissues and supporting periodontal structures
- chronic inflammation
- pathological inflammatory response associated with tissue destruction
what do gums look like in health
- pink gums
- knife edge gingival margins
what do gums look like in gingivitis
- gingival swelling/inflammation
- triggered by plaque
what do gums look like in periodontitis
- accumulated plaque and calculus, more severe
- very red and inflamed gums
what does the amount of plaque relate to
- amount of plaque correlates to the amount of swelling
is plaque the only factor that affects the disease
- no
- it does affect the disease, but it is not the only factor
is poor oral hygiene an aetiological factor in periodontitis
- yes, but it’s not the whole picture
how many species have been identified in oral biofilm
- there have been 1,000 different species identified in oral cavities
- every person will have around 150
what species did late colonisers typically have in oral biofilm
gram-negative anaerobes
what species did early colonisers typically have in oral biofilm
commensal species
how many complexes are in sub-gingival plaque
- 6
- blue
- yellow
- orange
- green
- red
- purple
- within each complex were microbes that were found together
what is the red complex in sub-gingival plaque
- bacterial species most commonly isolated form diseased sites = numbers correlated with pocket depth and bleeding on probing
- these are the PERIODONTAL PATHOGENS
what is the orange complex
- also correlated with periodontal disease but to a lesser extent than red
- significantly associated with disease parameters but less than red
how does the presence of these complexes not necessarily mean disease
- some of these complexes were isolated from healthy sites in the mouth as well so don’t mean disease
do specific bacterial species cause periodontal disease
- periodontitis cannot occur int he absence of bacteria
- it is difficult to establish role of specific microbes
where are periodontal pathogens present
- present at low levels in the mouth
- increased numbers in diseased sites
- can be absent from disease sites
what is the difference between colonisation and infection
- colonisation does not mean disease whereas in infection they invade tissues and cause inflammation
what is colonisation
- microbial pressure on a body surface without clinical signs of inflammation or disease
- commensal
what is infection
- microbial invasion of host tissues
- pathogens
- 1st stage of infection
can commensal organisms become pathogenic
- yes
- if conditions favour expression of virulence
- if opportunity arises
can pathogens behave like commensals
- yes
- if conditions do not favour expression of virulence
what is the outcome of host-bacterial interactions
- microbial pathogenicity
what is the microbial challenges
- antigens
- virulence factors
what is the host response
- adaptive
- innate
what do microbes do
- microbes actively suppress virulence factors
- some microbes are more virulent than others so it can be easier to overcome the body’s immune system
what are the virulence factors for P gingivalis
- immune evasion and subversion
- asacharolytic
- gingipans
- atypical LPS
- inflammaphobic
what are asacharolytic
- nutrients from breakdown of proteins and peptides
- means can’t use carbs as an energy source
what are gingipans
- proteases with broad-specificity
- degrade host proteins = to make them available as nutrients for bacteria
- activate MMP’s to clear up tissue damage
what is the atypical LPS
TLR4 antagonist
what are inflammaphobic’s
- inflammatory environment favours expression of virulence
- these like inflammation as can express all factors in this environment
are virulence factors present in a healthy mouth
- yes
- but these will not do anything until there is inflammation
what can modify the host response
- genetic risk factors
- environmental risk factors
what factors trigger gingival inflammation
- changes in orla biofilm
= accumulation
= composition
= expression of virulence
what factors determine whether inflammation resolves or progresses
- period tonal pathogenesis is determined by host-bacterial interactions
what makes teeth ideal for biofilm accumulation
- they are the only hard non-shedding site exposed to the environment
what makes saliva an important defence
- S-IgA
- lysozyme
- perioxidase
- lactoferrin
- muffins
- agglutinins
- cystatins
- histatins
what do neutrophils do during periodontal disease
- travel through the tissues to the gingival margin and then degranulate and release all components into the gingival margin
what makes the oral mucosa an important defence
- AMPs
- cytokines
- chemokine
what does gingival crevicular fluid contain
- AMPs
- cytokines
- chemokines
- lactoferrin
- IgG
what type of biofilm exists in health
- symbiotic biofilm
- exists along with the host immune response
what occurs during gingivitis
- altered microbial colonisation
- increased flow of GCF
- influx of neutrophils, increased lymphocytes and monocytes
what is the process of gingivitis
- any changes can trigger inflammation
- increased TLR stimulation
- increased production of pro-inflammatory mediators
- trigger acute inflammatory response = redness, swelling, bleeding, increased vasodilation, cell migration
- neutrophils number increased = remain predominant cell
- monocytes activated by cytokine and bacterial components there = recruited, activated and differentiate into macrophages
- lymphocytes are recruited to fine-tune the immune response
what can happen after gingivitis
- ca resolve back to health or progress into periodontitis
- if disease eliminated then return back to health
- if disease not eliminated then inflammation allows the inflammaphobics more of an advantage to survive than commensal
what type of biofilm is formed in disease
- dysbiotic biofilm
- works against the host
what are the environmental and genetic risk factors that can alter the ecological pressure exerted on the oral biofilm
- disease
- genetic differences
- activity of salivary gland
- salivary flow
- innate/adaptive immune factors
- oral hygiene
- diet
- smoking
- antimicrobial agents
what pressure can alter the competitiveness of bacteria within biofilm
- ecological pressure
what species are more susceptible to inflammatory response
- symbiotic (avirulent)
- have a competitive advantage
what type of pocket is in gingivitis
- bigger pocket but there is not a true pocket
what type of pocket is in periodontitis
- attachment loss and formation of a true pocket allowing bacteria and biofilm to descend deeper into pocket
- host immune response to the biofilm causes destruction
how does the host immune reason change as disease progresses
- changes drom protective to destructive
what is the role of neutrophils in periodontal tissue destruction
- crucial for maintaining healthy periodontium
- in these patients the neutrophils are trapped and can’t enter the tissues so can have periodontitis from a young age
- number of neutrophils increase during gingivitis = if it can contain the infection then will return to health, if not then periodontitis
what is aggressive periodontitis associated with
- leukocyte-adhesion deficiency
- immune under reaction
what is excessive infiltration of neutrophils associated with
- chronic inflammation
- degradative enzyme
- inflammatory cytokines and oxygen radicals contribute to hypoxic environment
what does connective tissue destruction manifest as clinically
- attachment loss
what can adult chronic periodontitis be caused by
- an immune over reaction
- the neutrophils are ineffective in controlling
what can happen if you don’t get the balance of neutrophils right
- if there is not enough then it can contribute to disease
- if there is too many neutrophils then it can contribute to tissue destruction and attachment loss
what is the role of adaptive immunity in periodontal destruction
- T and B lymphocytes are present in early lesion = present in gingivitis and help eliminate pathogen
- aggregates rich in CD4 T cells, B cells and dendritic cells evident as lesion progresses
- goes from innate to adaptive
- unable to regulate dysbiotic biofilm
- B cell preodominate advanced lesions
- IgG fills to regulate dysbiotic biofilm
- protective = prevents systemic infection
- destructive = inflammation induced alveolar bone loss
what are osteoblasts
- synthesises and secretes bone tissue
- boen formation
what are osteoclasts
- resorbs bone
- derived from monocyte/macrophage lineage
what happens in health for bone
- bone formation and resorption are coupled
- regulated by RANKL/RANK/OPG triad
what is RANKL
it is a cytokine and RANK is expressed on cytokines and OPG regulates
what are the stages leading to bone loss
activated T and B cells in periodontal lesion secrete RANKL into the environment t
- RANKL binds to RANK to induce osteoclast differentiation = RANKL binds to RANK on pre-osteoclasts which then become osteoclasts by differentiation
- OPG prevents RANKL binding to RANK = OPG is a decoy receptor
- OPG inhibits osteoclast differentiation
how inflammation leads to bone loss
- high levels of RANKL
- low levels of OPG
- inflammation induced bone resorption
- pathological bone destruction
what are the cellular and molecular events linking bacterial-induced inflammation with pathological tissue destruction
- bacterial products bind TLR’s on epithelium, stimulating secretion of cytokines, chemokine and AMPs= perio pathogens
- vasodilation and selective recruitment of leukocytes mainly neutrophils = swelling
- bacterial products activate neutrophils, further release of pro-inflammatory mediators = amplification loop of neutrophil
- activated lymphocytes express RANKL = RANKL/OPG balance disrupted
- RANKL binds to RANK on osteoclast precursors = activate osteoclastogeneis (bone resorption)
- pre inflammatory cytokines contribute to bone resorption by inhibiting bone formation
- elevated and dysregulated MMP activation contributes to connective tissue destruction
interaction between what determines the pathogenesis and severity of the disease
- interaction between the host and microbes
what governs patient susceptibility of the disease
- regulation of immune-inflammatory mechanisms governs patient susceptibility
- modified by environmental factors
what is the aetiology of periodontal disease
- bacteria
