microbial etiology of perio disease Flashcards
what’s the etiology of perio disease?
a complex interaction between bacterial plaque and host response, modified by local anatomic factors of both natural and iatrogenic origin and by systemic factors
path of periodontitis
plaque (anatomical, iatrogenic, behavioral) + host response (smoking, systemic disease, genetics)=inflammation, connective tissue loss+ bone loss
non-specific plaque hypothesis
quantity or biomass of dental plaque
basis of conventional therapy–oral hygiene, mechanical removal of deposits by scaling and surgery
specific plaque hypothesis
association of specific bacteria with perio disease
dental plaque
soft deposits that form the biofilm adhering to the tooth and other oral surfaces
- supragingival
- subgingival
- composed predominantly of microorganisms
- intercellular matrix=0-25% of plaque mass subgingival, much more (80%) supragingival
- clinically cannot remove by water spray
formation of biofilm
starts clean/just in saliva
- molecular adsorption
- single organisms
- multiplication
- sequential adsorption of organisms
dental pellicle formation
- phase 1 of biofilm formation
- forms within minutes by selective adsorption
- glycoprotein (mucins) and antibodies
- origin: supragingival–saliva and subgingival–crevicular fluid
- coats enamel and other oral surfaces
- functions to prevent desiccation, lubrication
- provides substrate for bacterial colonization
- forms within minutes
what does dental pellicle contain?
- substrate for bacterial attachment
- fimbriae (adhesive)
- antibodies
initial bacterial colonization contains?
facultatively anaerobic G+ cocci and rods
secondary colonization & plaque maturation
takes days
co-aggregation
G - bacteria attach to pre-existing G+ bacteria
initial colonizer
streptococcus sanguis
24 hour plaque
some actinomyces
second phase colonizer
actinomyces viscosus dominates
third phase contents
G - bacteria attach to G +
- prevotella intermedia
- fusobacterium nucleatum
fourth phase contains
- increased heterogeneity and pathogenicity
- prevotella intermedia
- capnocytophaga species
- fusobacterium nucleatum
- **porphyromonas gingivalis
what is the developing plaque ecosystem influenced by?
- bacterial interactions:
- attachment/adherence
- exchange of nutrients
- bacteriocins - substrate characteristics
- smooth surface vs pit and fissure
- supra-gingival vs sub-gingival - bacteria–host interactions
- inflammation: blood and gingival crevicular fluid
layers of dental plaque
lower layer: dense microbes and matrix
loose intermediate layer
fluid superficial layer
how do nutrients penetrate plaque?
by molecular diffusion
how does the bacteria get O2
steep diffusion gradients
bacteria in deeper layers are protected from what?
antimicrobial agents
whats the advantage of biofilm formation vs planktonic growth?
- protects from competing organisms, host defense, and toxic environmental agents (antibiotics)
- processing and uptake of nutrients
- development of appropriate physico-chemical environment (pH, oxidation-reduction potential)
attachment of bacteria in biofilms
- fimbriae (actinomyces, strep, Pg)
- fibrils (strep, Pi)
structure of biofilms
- 20% bacteria and 80% matrix
- bacteria not randomly distributed
- water channels for passage of nutrients
- matrix=water + exopolysaccharides
what does the biofilm matrix do?
- maintains integrity of biofilm
- prevents dessication
- binds nutrients
- buffers
- reservoir of extracellular enzymes
physiological heterogeneity of biofilms
- bacteria in different physiological states in different locations within the biofilm
- increase respiratory activity and protein synthesis in outer layer of biofilm
- pH varies between microcolonies in biofilm
- bacteria in biofilms produce beta-lactamase, catalase, superoxide dismutase, elastase, cellulase
quorum sensing
- dependent on cell density
- involves regulation and expression of specific genes thru accumulation of signaling compounds
- signaling compounds detected for Pg, Pi, and Fn
- way the bacteria communicate
bacteria grown in biofilms are more resistant to what compared to plantonic suspension?
biofilm bacteria are more resistant to antibiotics
structure of supra-gingival dental plaque
- acquired pellicle
- G+ cocci bacteria
- G+ rods
- matrix–derived from microorganisms, saliva, and ging crevicular fluid; proteins and carbs like fructans/levans, glucans/dextrans, from dietary sucrose
structure of sub-gingival dental plaque
- cuticle–electron-dense layer, epithelial origin
- pellicle
- G+ cocci and G+ rods
- loosely-adherent superficial layer–spirochetes, motile bacteria
- no intermicrobial matrix
calculus
hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of non-mineralized plaque
calculus formation
- depends on presence of plaque and salivary gland secretions
- supra-ging correlates with salivary gland ducts
- subgingival contains products of blood and gingival crevicular fluid
- attaches to tooth surface via surface irregularities in enamel and cementum
supra-gingival calculus
- averages 37% mineral
- consists of different calcium phosphate crystals:
- -brushite (recent, 2 weeks old)
- -octa calcium phosphate (superficial layers of calc)
- -hydroxyapatite (inner layers of old calc)
- -whitlockite (small proportions)
subgingival calculus
- 58% mineral
- mostly whitlockite with some hydroxyapatite
calculus is a ______ for periodontitis?
secondary etiologic factor
provides a surface that facilitates plaque formation and compromises efficiency of plaque removal
what happens if calculus forms in germ-free animals?
-doesn’t result in periodontitis but when perio pathogen is added, periodontitis results
whats the primary etiology of periodontal disease?
dental plaque
how many different microorganisms can colonize the mouth?
500
how many different species can be in one individuals mouth?
150+
range of bacterial count
- 103 in health sulcus
- > 108 in deep perio pockets
- 109 in supra-gingival plaque on a single tooth
ecological relationship between plaque bacteria and host is usually _____
benign
the tooth as a feature of perio infection
- exposed to oral cavity
- enamel surface does not shed like epithelium
- bacteria in contact with tissues for long periods
- biofilm not accessible to host defense system
- surface irregularities are sanctuaries for bacteria
arguments against specific plaque hypothesis
- why is tissue destruction localized?
- why don’t all patients with heavy plaque have disease?
- why do some patients with good oral hygiene have disease?
koch’s postulates
- bacteria must be isolated from diseased tissues
- pure cultures must be obtained
- organisms must cause disease in animals
- same organisms must be obtained from experimental animals
modified koch’s postulates for periodontics
- putative pathogens in large numbers in diseased sites
- absence of pathogens in health
- demonstrated immune response to putative pathogens
- virulence factors can often be demonstrated
- animal models should simulate human disease
- elimination of organisms leads to clinical improvement
aggregatibacter actinomycetemcomitans
- formerly actinobacillus actinomycetemcomitans
- elevated in aggressive periodontitis, chronic perio and active sites
- elimination Aa results in successful therapy
- elevated host antibody in serum and saliva
- virulence factors: leukotoxin, collagenase, endotoxin, epitheliotoxin–invades epithelial cells
porphyromonas gingivalis
- elevated in chronic perio and active sites
- elimination of Pg results in successful therapy
- elevated host antibody in serum and saliva
- virulence factors: collagenase, proteolytic trypsin-like activity, gingipains (lysine and arginine), endotoxin (TLR2/TLR4), fibrinolysis and hemolysin, fimbriae invades epithelial cells, endothelial cells, dendritic cells
tannerella forsythia
- elevated in chronic periodontitis, active sites abscesses
- elimination of Tf results in successful therapy
- elevated host antibody in serum
- virulence factors: endotoxin, induces apoptotic cell death, induces production of inflammatory mediators by host, invades epithelial cells
treponema denticola
- spirochete
- elevated in necrotizing ulcerative periodontitis, deep pockets
- decrease numbers reported with successful therapy
- virulence factors: motile organism, invades epithelial cells
- difficult organism to culture and differentiate
- rare
prevotella intermedia
- elevated in necrotizing ulcerative gingivitis, chronic periodontitis and active sites
- decreased numbers with successful therapy
- virulence factors: collagenase, endotoxin, invades epithelial cells
association of bacteria in mixed biofilms is not what?
random
***six microbial complexes in periodontal disease
- actinomyces
- yellow complex (strep)
- green complex (capnocytophage, Aa-a, E corrodens, campylobacter concisus)
- purple complex (V parvula, actinomyces odontolyticus)
- orange complex (campylobacter gracilis, c rectus, eubacterium nodatum, F nucleatum, P intermedia)
- red complex (T forsythia, P gingivalis, T denticola)
top three microbes in etiology of perio disease
T forsythia
P gingivalis
t denticola
(red complex)
factors affecting composition of biofilm
- perio disease state
- local environment–supraging, subging, pocket depth
red complex at lower level in what?
supragingival
what has higher numbers of red complex?
in periodontitis and subgingival plaque
what is in deep pockets?
red complex bacteria (Pg, Tf)
orange complex bacteria (Fn, Pi)
what bacteria are not effected by pocket depth?
s. sanguis and actinomyces sp
requirements for perio disease initiation and progression
- host must be susceptible
- presence of bacterial pathogens
- pathogen must achieve sufficient numbers
- environment conducive to expression of virulence factors by the pathogen
host defenses against perio disease
- flow of saliva and gingival crevicular fluid
- mech displacement by chewing
- substances in saliva and GCF (antibodies, nonspecific blocking agents, lysozyme, lactoperoxidase, lactoferrin)
- desquamation of epithelial cells
- antibody
- PMNs
host susceptibility factors
- defects in PMN levels or function
- immunocompromised states
- diabetes
- smoking
S sanguis and actinomyces naeslundii inhibits ____
Aa while Aa produces bacteriocins against S sanguis and actinomyces naeslundii
bacterial factors that cause tissue damage
- substances that damage tissue cells
- LPS (gram - bacterial cell wall)
- causes host cell release of inflamm mediators (IL1, prostaglandin, TNF)
- substances that degrade intercellular matrix (collagenase, ARG-gingipain, LYS-gingipain)
- leukotoxins
most of the tissue destruction in perio is caused by what?
host-induced inflammation, rather than direct effect of bacterial products
-bacteria cause inflammation but host enzymes damage tissue
dysbiosis
commensoral organisms becoming accessory
