Lecture 4 Flashcards
Bacteria and Oral Biofilms
bacterial infections
gingivitis and periodontitis
bacteria
replicate/adapt quickly to environmental changes
tough cell membrane
gram + or gram -
gram + periodontal microorganisms
facultative cocci: streptococcus sanguis, streptococcus mitis, streptococcus salivarius
facultative rods: actinomyces viscosus
obligate rods: eubacterium lentum
gram - periodontal microorganisms
facultative rods: aggregatibacter actinomycetemcomitans
obligate anaerobic rods and cocci: P. Gingivalis, P. Iintermedia, V. Alcalescens
anaerobic spirochetes: treponema denticola
intercellular matrix of dental plaque
organic: polysaccharides, proteins, glycoproteins, lipid material and DNA
inorganic materials: calcium and phosphorus with sodium, potassium and fluoride
supragingival dental plaque
gram positive cocci and rods
nutrients from saliva and diet
subgingival dental plaque
gram -, anaerobic, motile rods and spirochetes
nutrients from GCF and blood
subgingival bacterial attachment zones
tooth-associated: adhere to the tooth surface
tissue associated: adhere to the epithelium
free floating: unattached, not part of the biofilm
tooth associated plaque
densely packed and strongly adherent to the tooth surface
gram + rods, cocci and filamentous bacteria
facultative aerobic or facultative anaerobes
tissue associated plaque
loosely packed, loosely adherent to soft tissue wall
gram -, motile, anaerobic spirochetes
bacteria can invade the gingival CT and be found within the deeper perio tissues
unattached bacteria
free swimming in pocket
gram -, motile, anaerobic
spirochetes and others
what is the source of inorganic components of supragingival plaque
saliva
calculus is frequently found in areas of the dentition adjacent to
salivary ducts
the inorganic components of subgingival plaque are derived from
crevicular fluid
materia alba
white cheeselike accumulation
salivary proteins, bacteria, desquamated epithelial cells
lacks structure
displace with water
dental plaque
clear to yellow-grayish substance
bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides
a biofilm
impossible to remove by rinsing or water
calculus
hard deposit that forms via the mineralization of dental plaque
covered by a layer of unmineralized dental plaque
impossible to remove by rinsing or water
plaque biofilms
a matrix enclosed bacterial population adherent to each other and/or to surfaces or interfaces
structurally organized
life cycle of a biofilm
attachment: bacteria attach to a surface
growth: attract other bacteria, rapid multiplication, ECM for protection and maintain attachment
detachment: clumps break free to attach to new surfaces
phase 1
initial attachment
acquired pellicle formation
protein film forms within minutes after cleaning tooth surface
derived from salivary glycoproteins, antibodies, GCF
protect enamel from acid
gram + facultative bacteria
phase 2
irreversible attachment
additional bacteria colonization
coaggregation, gram negative colonizers adhere to bacteria
attract other free-floating bacteria
phase 3
maturation
formation of extracellular protective matrix
bacterial secretion
provides anchorage and protection for the attached bacteria from antimicrobials, antibiotics and immune system
phase 4
maturation phase II
bacteria microcolonies form mature biofilm
complex collection of different bacteria
increased numbers of gram neg/anaerobic bacteria
phase 5
dispersion
microbes disperse from the biofilm colony allowing biofilms to spread to new tooth surfaces
dental plaque - colonization
different bacteria species join the biofilm in a particular sequence
-early colonizers: nonpathogenic/gram +
-intermediated colonizers: specific cell-cell adhesion
-late colonizers: gram - bacteria join biofilm
why is physical/mechanical disruption so important for individuals with periodontitis
adequate disruption causes the entire process of bacterial succession to begin again
the cleaner the tooth surface, the less complex the bacterial formation
dental plaque biofilm development always begins _____ and progresses _______
supragingivally and progresses subgingivally
the clinical signs of inflammation may appear within
4-14 days
non-specific plaque hypothesis
accumulation of bacterial biofilms lead to periodontal destruction
specific plaque hypothesis
specific pathogenic bacteria lead to periodontal destruction
host response hypothesis
it is the host’s inflammatory and immune response, not the type of bacteria, which determines if periodontal destruction progresses
contemporary perspectives
despite plaque biofilm causing the initial inflammatory response, it is not sufficient for periodontal destruction to occur
it is the host inflammatory and immunes responses that determine whether gingivitis progresses to periodontitis
virulence factors
endotoxins
microbial invasion
enzyme production
endotoxins
in gram negative bacteria cell membranes are released when bacteria die or break apart
initiates inflammation
can kill pmns
microbial invasion
ability to penetrate tissue to avoid host defense cells
enzyme production
break down collagen and host proteins (basic structure of periodontium)
bacteria synthesize and release… and these do what
toxic by products (ammonia, hydrogen sulfide)
these increase the permeability of epithelium/toxic to cells and tissues
biochemical mediator in periodontitis include
cytokines
chemokines
prostoglandins
metalloproteinases
cytokines
initiate tissue destruction and bone loss
chemokines
attract additional immune cells
prostoglandins
cause bone destruction
metalloproteinases
cause collagen destruction of periodontal tissues
proteins, lipids, enzymes released by leukocytes activate
inflammatory response
attracts additional immune cells and increase vascular permeability
contributes to tissue destruction
4 histologic stages in development of periodontal disease
- initial lesion: healthy but mild inflammation
- early lesion: acute inflammation/gingivitis
- establish lesion: chronic gingivitis
- advanced lesion: transition to periodontitis
initial lesion
corresponds with clinically healthy gingival tissues/mild inflammation
develops 2-4 days after supragingival plaque accumulation
gram neg bacteria initiates immune response
pmns pass from blood vessels to CT into sulcus, cytokines destroy healthy tissue
tissue destruction easily repaired after infection fought
lesion is not seen clinically and is reversible with adequate OH
early lesion
corresponds with acute gingivitis, evident clinically
biofilm maturation continues 4-14 days
bacterial toxins penetrate junctional epithelium
JE cells release cytokines attracting larger # of PMNs
cytokines cause localized destruction of connective tissue
macrophages are recruited to the connective tissue (release biochemical mediators which recruit additional immune cells)
epithelial ridges appear in sulcular epithelium and adjacent CT
this lesion is reversible with adequate OH
established lesion
corresponds with chronic gingivitis
within 2-3 weeks of plaque accumulation
coronal portion of JE detaches from tooth surface
macrophages and lymphocytes are most numerous in tissue, PMNs most numerous in sulcus
lymphocytes produce large numbers of antibodies
macrophages produce cytokines with initiate collagen destruction
epithelial ridges extends deeper into the connective tissue
lesion is still reversible
periodontal instrumentation and patient education are helpful
advance lesion
transition from gingivitis to periodontitis
state of chronic inflammation
immune response is so strong it begins to harm the periodontium
biochemical mediators produced by PMNs/macrophages destroy CT and PDL fibers
apical migration of the JE occurs (periodontal pocket forms)
clinically- BOP, alveolar bone loss, furcation involvement, mobility
tissue destruction is not reversible
