fs2 mod 3 Flashcards
ox tension and f nuc and p ging
F nucleatum: anaerobe that binds to strep to help in ox
P gingivitis: sensitive anaerobe that aggregates when ox present
What changes in quorum sensing:
virulence, antibiotic production, motility, sporulation, biofilm formation
Determinants of microenvironment
host factors (what goes into mouth, including GCF), bacterial factors (adhesions, metabolic characteristics, congregation), local physicochemical factors (pH, redox, temp, nutrient availability)
- severity depends on these
acquired pellicle
albumin, lysozyme, amylase, cysteine phosphoproteins, IgA, proline rich proteins, statherin, mucins —> can be adhesions FOR BAC!
- minor levels of ded cells, GCF
Functions to lubricate against damage, regulation of mineral homeostasis
- takes 7 days to mature
strep spp
adhesion antigen 1 and 2, receptor is salivary agglutinin
S mutans
gulan binding protein and gluten
Actinomycete naeslundi
type 1 fimbriae and receptor is proline rich protein
Initial colonizers
strep oralis, Mitis, gordonii, sanguis, actinomyces naeslundii, actinomyces viscosus, veillonella spp, haemophilus parainfluenzae (gram -)** well tolerated by host
EPS
made of bacteria, saliva, GCF, DNA, inorganic molecules, mycoplasma, fungi, virus, protozoa, depends on the microbes in biofilm
helps in adhesion, aggregation (communication and quorum sensing), cohesion, protective barrier, sorption of organic compounds, enzymatic activity (biofilm di system), nutrient source
Coaggrecation
both are planktonic then can adhere to biofilm. CORNCOB STRUCTURE (changes from gram + to gram - over time)
- fusobac do this with early and late colonizer (BUT NOT ITSELF). Allows plaque comp to change
** coadhesion comes only after coaggregation
3 weeks plaque
** first gram + and rods, then gram - and rods. Then fusobac and filaments then spirochetes
mature. More = gram + and -, all shapes, both facultative and anaerobic, MOST causal of caries and gingivitis
NOT tolerated by host = inflame
- more filaments
Can be seeded to turn into calculus
health and red bacteria
p gingivitis, t forsythia, t denticola, aa bacteria —> all cause perio
Health bacteria is streptococci and actinomycete
Keystones!!
allo and autogenic succession
Allogenic succession: external factor change like smoking
Autogenic succession: interface and viral bac interactions (self factors)
subgingival plaque
- less organized!! mostly gram -, anaerobic, capnophilic** perio bac!
Inflammation helps, esp with increase in gingival fluid containing growth factors not present in saliva
Because of pocket, the gingival flow is removed so bacteria stick better
Less transport of new bac via saliva
Dentinal tubules are colonized!!
– shedding surface!!
- bac adhere using fimbriae and pili (made of polymeric fibrils that are composed of repeating subunits that can extend far from cell mem)
Specific plaque hypo:
specific bac cause diff forms of gingivitis and perio
acute necrotizing ulcerative gingivitis (ANUG) incudes spirochetes and fusobac
P gingivitis, aa bacteria
ID of bacteria
hard to cultivate like 40%. soln is gene sequencing
- tooth has 6 active sites
- disease classifications changing
- do longitudinal studies since disease isn’t linear
virulence factors
LPS, bacterial enzymes like collagenases, proteases (can inactivate antibodies), adhesions
- Result in indirect tissue damage (caused by immune response) or direct (caused by bac)
- Gram - LPS leads to inflammation stim, complement activation then immune cell stuff
P gingivitis and virulence 8
makes endotoxin for cytokine activity, vesicles (with toxic crap inside that can damage from a distance), cell toxic substances, specific cytotoxins like reducing gradient of PMN chemotaxis and phagocytosis,
- specific proteases, trypsin like proteases like gingipains (very aggressive and violent. food source. Also mess with host response)
- collagenase, invasins,
- capsule to protect against phago (increase pathogenic)
- FIMBRIAE TYPE A that can bind integrins or host cell stuff
aa bac and virulence 9
has leukotoxin (kills neutrophils), cytotoxins, chemotaxis inhibitors, collagenases, immunsuppress factors, fc binding protein (so no antibody made), invasion’s, bacteriocins, adhesions
- JP2A clone of AA causes SUPERPERIO or hyperleukotoxin
key determinants of biofilm formation
fluids like saliva and GCF, surfaces and bacteria
- what is available changes the comp of the biofilm
evading host immunity
Modulation of host responses by binding serum components on bacterial cell surface.
Invasion of gingival epi cells so can evade therapy!!
- capsule leads to more virulence
- proteolytic degredation
bacterial succession
early colonizers: gram +, aerobic/facultative, saliva
secondary: gram +/-, capnophilic and facultative anaerobic/anaerobic, saliva
late colonizers: gram -, motile rods, anaerobic, GCF
** perio has resorbed bone, severe inflam, subgingival biofilm
yellow bacteria
- c rectus, c gracilis, c showae
- s constellatus
- e nodatum
- p intermedia, nigrescens, micros
- f nuc vincentii, nucleatum, polymorphum, periodonticum
health vs disease bac
- strep and actino is health
- disease is prevotella fusobac, and red
nonspecific plaque hypo
- perio results from plaque accumulation regardless of species present within dental plaque
oral mucosa, gingivitis and perio
- gingival crevice btw free gingiva and tooth surface is where inflam rxn start, including complement activation
- gingivitis: confined in gingiva and CT
- perio is bad PDL, deep gingival pocket, alveolar bone loss
- can become systemic
- tissue damage by host does biggest problem!
- majority of virulence factors in perio come from not previously known species!!!
PSD
- perio is increased bad bac, less good bac = indigenous polymicrobial synergy and disbiosis
- group orgs do disease rather than 1
- involves accessory path (commensal but help pathogens colonize too) and pathobionts (commensals that take advantage of disbalance and promote inflam disease)
inflam and perio
- with no brushing, cause bac growth, leading to inflam
- inflam brings in GCF and stuff to heal, but the bac EAT IT TO GROW using proteases, heme (take out iron), blood derived peroxidase (stop h202) and potassium
p gingivalis and host responses
- messes up the TLR myD and activates MAL to block phago and promote inflam
- this benefits ALL dysbiotic bac
immune subversion
first poor hygeine leads to inflam then susceptible host leads to immune subversion by keystone path causing inflam and dysbiosis
- degredation of complement
- manipulate chemokine expression
- block TLR dependent killing of bacteria
** all red bac can do this
dysbiosis factors
- subversion of host, systemic disease like dia, obesity, smoking, aging, immune regulatory defects
- leads to inflam!!
- in gingivitis that moves to perio, there are certain factors that select for perio dysbiosis
genetics and perio
- chronic adult type is polygenic while monogenic is seen in young patients with b2 integrin problems
- LAD1 so no transition to tissue
- neutropenia (ELANE): not enough neutro
- WHIM syndrome: don’t release neutro from bone marrow
- Chedia higashi/ papillon lefevre also does perio
- aging
immune cells and perio
- neutrophils, APC and t lymphs
- if any are blocked, leads to perio