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
neutrophils and perio
- can be protective and destructive
- LAD1 problem leads to NOT enough neutro so allow more perio destruction
- problems in MMP, ROS and pro inflam cytokines (IL1, TNF) when too much neutro
LAD1 and DEL1 problem
- problem with b2 integran so no transition to tissue
- leads to no release of il 17!
- DEL1 restrains b2 integrin (LFA1) transmigration of neutro
- problems in DEl1 leads to TOO much neutro
- aging leads to less DEL1
complement
- normal regulates pathogens
- bad complement can lead to hyperinflam
- activated comp is found in inflam gingiva of GCF
- activation of c3 in GCF increases with pocket depth
- perio leading to bone loss
- microbes exploit complement to do dysbiosis
- complement inhibitor, AMY101, stops perio inflam
inflam resolution
- neutrophils do apoptosis of the pathogen, then add it to macrophage
- pro resolving mediators are TGFb
- resolving macrophages restore tissue integrity and destroy bad cells
pro resolving lipid mediators
- arachidonic acid make lipoxins
- eicosapentaenoic acid (EPA) make resolvins
- docoshexaenoic acid (DHA) make resolvins
- lead to downreg of inflam mediators, stop neutro, efferocytosis (eating of neutro by macro), tissue repair
DEL 1
- promotes efferocytosis by binding phosphatidyk serine on apoptotic cells abd avb3 integrin on macrophage
- also increases the expression of resolvins
- bad DEl1 or resolvins leads to non resolving perio
osteoclastogenesis and bone resorption
- osteoblast and lymphocytes have RANK that binds to RANK on osteoclast
- osteoprotegrin
- RANKL is induced by inflam!! so high RANK/OPG ratio
B cells and perio
- B cells recruited to periodontium, then antibody diffuses into gingival sulcus to suppress bacterial challenge
- B and plasma cells make proinflam cytokines, MMP and rankl, so prob do perio
treg does
makes tgfb and immune suppression
- might stop perio
th17
innate immunity, inflammation = autoimmunity
- il 17 induces RANKL on fibroblasts and also stim TNF, Il1 and 6
- do osteoclastogenesis
- impaired dev (autosomal dom hyper IgE syndrome) means less perio BUT more susceptible to oral fungal infections
- makes antimicrobial peptides
th1
cell mediated/adaptive immunity = hypersensitivity
th2
humoral adaptive = allergy
systemic disease and perio
- bacteria can travel all over leading to sys inflam, alterations in bone marrow!!
- gingipains found in alzheimr patients
- atherosclerosis
- bac can translocate to gut and gause gut inflam!!! through th17 that do SPECIFICITY to the bac and have strong response
- memory cells in bone marrow react supar bad to perio bugs anywhere else in body
host modulation
- change host immune to stop tissue damage
- doxycyclince inhibits MMPS
- can block complement, DEL1 blocks LFA1
- RANKL antagonists
- block Il17
caries
- will find bac and fungi!! esp in kids with severe
- can treat it if you breakdown the EPS!
glucosyltransferases found where
- bac breaks down sucrose via glucosyltransferases into water-soluble glucans (GFTB and C) and C and D
- made by strep mutans to make glucan. has also a binding domain to help build a chain of polymers
- if inhibited, can stop cariogenic plaque. can also predict caries using this
- present in human whole saliva and pellicle AND bound to bac mem
- form glucans even at low pH on tooth surfaces
- these allow microbes to bind!!! using binding proteins (gbp a,b,c,d)
- also make EPS that is suppper sticky
- sucrose allows EPS and acid production, thus making biofilm!!
- has 1,3 linkages that can be broken by mutanase
acid production
- acidogenic bac transport fermentable carbs using sugar ABC transport system OR phosphotransferase system
- also effective in carrying out glycolysis and making acid from fermentable carbs = lactic acid that acidifies the eco
- survive at low pH by increasing ATPase, DNA repair at low pH, and changes in FA composition
- leads to demineralization of enamel BUT saliva is a buffer to remin
- acid pockets form, not hetero!!
EPS and acid
- can label EPS and see the glucans made
- shows that bac need EPS to grow
- eps needs sugar to grow
- EPS is like a diffusion barrier to stop saliva from neutralizing acid pockets
- also assists in demin!!
which xrays for which treatments
- bitewings for caries and interprox bone levels ALSO FOR PROXIMAL SMOOTH SURFACE CARIES
- periapical for interproximal caries and root
- pano for occlusal carries
- cbct shows tooth support structure
bitewing>PA.pano
*frequent radiograph exposure isn’t high caries risk
american dental association caries classification system
- e1 is invaded outerhalf enamel
- e2 is at dej
- d1 is outer dentin
d3 is innermost dentin
**restore past d2, d3 is endo/extract
types of caries
0 pit and fissure
- approximal/interprox
- cervical/smooth surface (buccal/lingual) **radiation caries!!
- root
international caries classification and management system (ICCMS)
- ra1 is lucent outer half enamel
- ra2 is inner enamel NO DEJ
- ra3 is outer dentin
- rb4 is outer third dentin extended
- rc5 is inner third
- rc6 is pulp
cervical burnout
- right by the crest, smooth edge
- shadow, not cavity!
crest cortication
- in anterior teeth, it is pointed and well corticated around the top btw 0.5-2 mm
perio and alveolar process changes
- resoroption
- vertical bone defect (big angle)
- buccal or lingual cortical plate loss (CBCT)
- horizontal bone loss
- interdental craters
- furcation of roots
other perio radio problems
- apical abcess is NOT same as perio abcess
- perio endo lesion
- calculus
- tooth alignment (MALOCCLUSION)
- overhanging restorations
- malignant lesion (looks like tooth is floating)
root canal system
- small cns btw teeth
- contains odontoblasts, t cells, fibroblast, nerves, blood, lymph, undiff stem cells
- should be sterile
- necrotic pulp is no vasculature, no inflam, and leads to bac infxn (no response to cold and leads to resorption at apex)
pulpal hyperemia
- result of caries, trauma, fracture, invasive restoration, bad response to dental materials, perio disease
- can also get in via root planing, root restoration
- extraradicular colonization:
- first cracket tooth, then ^^ leads to hyperaemiea (MORe blood flow) then pulpal ischaemia (no o2) to necrosis
apical perio
- bac invade perio tissues, resulting in invasion of necrotic pulp
- protective response to stop bac going into marrow
- inflammation has nowhere to go so bac just resorb bone
- can be symptomatic, dev into chronic abcess
- intraradicular biofilms in 80% even post treatment
- diff morph of biofilms, dentinal tubules often invaded
- more common in root canals of teeth with large apical peiro lesions (all teeth with endo infxns)
periapical abcess
- acute is inflam rxn to pulp infxn. fast onset and spontaneous pain, tender tooth to pressure. pulp forms and swelling
- usually necrotizing ulcerative gingivitis
- chronic is gradual, no discomfort, pus discharge, no symptom
*** extraradicular - have gram + anaerobes like actinomyces and PROPIONIBACTERIUM PROPIONICUM
how to ID endo infxn and ox tension
- 40% non cultivatable
- culture based, but for not, can use 16s ribosome sequencing
- corontal third is high o2, many nutrients
- apical third (lowest) is least o2, serum protein is food, many bac by products
** treatment requires full removal of bac, by products and pulpal debris from root canal system
endo infxn virulence factors
- colonization of root canal via adhesion
- evasion of host defenses using protease, capsule, complement
- tissue damage via proteases, lps endotoxin
- indirect damage by inflam response like cytokines
endo biofilms characteristics
- has channels, defense, more tolerate to antimicrobials (chlorhexidine and antibiotics, gene transfer), neutralize cell toxins using b lactamases, new gene expression, cell cell signalling, ph and o2 gradients, catabolism of host macromolec, more virulent
primary and secondary intraradicular biofilms
primary
- infxn of necrotic pulp
- less divers flora mainly from dental plaque, caries, saliva
- facultative then anaerobic, protein bac
- 40% can’t cultivate
secondary
- occur in previously treated!!! with persistent apical perio
- mostly gram +, facultative anaerobe INCLUDING strem, lacto and actinomyces
- enteric orgs like E facalis (EW)
extraradicular biofilm
- outside of pulp
- form on root surface adjacent to root apex of endo treated teeth
- most common in situations with sinus tract and no response to treatment
- found in teeth with asymptomatic apical perio, chronic apical and sinus tracts
- can be come calcified
- usually T forsynthesis, F nucleatum, P gingivalis
endo vs perio biofilm
- endo is less diverse, less nutrients
- perio is more diverse, more nutrients
e faecalis
- persistant following RCT
- very good at forming biofilms, attaching to denting via collagen binding protein
- small enough to colonize dentinal tubules
- can tolerate basic pH too so resistant to therapy
- can starve and use serum as nutrient source
- gram +
local aggressive perio is usually
in incisors and first molars
can radiographs be used to see if surface of a lesion is cavitated
no
do biofilms help bac survive better in a variety of Phs
NO!
subgingival eco vs supra
- higher temp, more iron, proteins, decreased ox, BUT NOT DECREASED PH
amount of attachment loss = disease for which condition
chronic perio!!
what happens in healthy mouth
f nucleatum DOESNT CAUSE gingivitis
- low GCF flow
- there can be a host immune response even in normal
** include the red bac tho
why does koch postulate not work for bac
- because bac might be a result of favourable conditions induced by perio disease
dentinal tubules
- dia is narrower near enamel, lined by collagen
** NOT a route for pulp infection
arrested lesions
- shiny, no sealant, more resistant to caries than uneffected enamel
***THEY AREN’T WHITE
is p gingivalis in mature supra gingival plaque
NO
adults and kids with perio
8.5% adults, 25% kids?
rampant caries =
early childhood caries
trauma leads to
widening of PDL (radiolucent)
- lamina dura is opaquw
perio vs malignant lesion
- radiolucent is malignant lesion and it looks like something is pushing it (flaoting teeth)
