oral bacteria B Flashcards
endo disease progression
carious lesion can infect or inflame pulp leading to abcess or inflammed ligament
Dentoalveolar infections
Pyogenic infections associated with the teeth and surrounding supporting structures
Bacteriology of root canal infections
Endodontic infections are endogenous infections that are opportunistic
most frequent spp of root canals
bacteroids and prevotella
Presentation of dentoalveolar infections
- Abscess localized to tooth that initiated the infection
- Diffuse cellulitis which spreads along fascial planes
- Mixture of both
Dentoalveolar Abscess: routes of access to pulp/periapical tissue
- Spread from carious lesion (1)
- Tooth fracture/wear
- Through periodontal membrane and accessory root canals (2)
- Anachoresis (3) (via pulpal blood supply) during bacteremia from tooth extraction at different site
are dentoavleolar infections local or can they spread
Infection may remain localized or spread
O2 use of species commonly in abcesses
obligate or facultative anaerobes
spp commonly found at abcesses
Ludwigs Angina
spp involved?
risk?
A spreading, bilateral infection of the sublingual and submandibular spaces. Cellulitis of the fascial spaces rather than true abscess formation
Mixed endogenous infection: Porphyromonas spp. Prevotella spp. Fusobacteria Anaerobic streptococci
Airway obstruction - death by asphyxiation (without intervention)
Periodontal Abscess
species?
A localized collection of pus caused by acute or chronic destruction of the periodontium
Endogenous, subgingival plaque bacteria
Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci
Suppurative Osteomyelitis of the Jaws
species
like abcess but involves bone
polymicrobial Porphyromonas spp. Prevotella spp. Fusobacteria Anaerobic streptococci
Cervicofacial Actinomycosis
presentation?
speceis?
endogenous, granulomatous disease
65% in cervicofacial region
Actinomyces (oral commensal)
visible granules in pus called sulphur granules = collections of bacteria
Oral manifestations of bacterial infections: diseases we have learned
syphilis
leprosy
tuberculosis
Syphilis oral manifestations
congenital: Hutchinson’s incisors, mulberry molars
primary and secondary syphilis lesions
gummas (granulomatous lesions)
Tuberculosis oral manifestations
– oral lesions in up to 5% of primary and secondary tuberculosis cases ulcers on palate and gingiva
Leprosy oral manifestations
many
Bacterial infections of salivary glands involves what spp often?
– often Staphylococcus
Diseases or situations associated with
oral bacteria or their components:
Infective endocarditis Disseminated intravascular coagulation Nephritis Rheumatoid arthritis Behçets disease (chronic inflammatory disorder with oral ulcers) Atherosclerosis Low-birth-weight infants
how could oral bacteria cause infection elsewhere
altered metabolism/ gene expression when in a new environment, possible that a certain gene could be pathogenic elsewhere in body
Infective endocarditis
spp
streptococci from oral
damaged heart valves will have platelets bound
streptococci posses PAAP/ adhesins to bind these platelets
PAAP induces additional platelets to adhere via cross linking with fibrinogen
leukocytes may accumulate on the septic thrombus and induce an inflammatory response
Other possible associations between oral microbes and systemic disease
HSPs and Autorecognition induced by oral microorganisms
Heat shock proteins (HSPs) and systemic disease
Microbial HSPs are very similar to human HSPs that are normally shielded within cells.
Antibodies elicited by bacterial HSPs can cross-react with exposed human HSPs (e.g. present in damaged tissue).
If immune complexes are deposited in the arterial wall (atherosclerosis), joints(arthritis), or mucous membranes (Behçets disease), HSP mimicry can contribute to systemic disease.
Autorecognition induced by oral microorganisms and systemic disease
Streptococcus sanguinis express an epitope within PAAP which is similar to the arthritogenic epitope of type II collagen.
In a murine arthritis model, S. sanguinis infection exacerbates arthritis.
Interestingly, exposure of neonatal mice to PAAP+ S. sanguinis inhibited development of autoimmune arthritis in the adult (early exposure protective?).
how local inflammation with oral microbes can cause systemic pathology
gram - bac produce toxins to/LPS to diffuse into gingiva causing local response
Macrophages take up these toxin and produce TNF a and IL-1B, enter sys circulation
this induces the liver to produce acute-phase proteins (CRP)
TNF and IL-1B can also act on atherscerltoic lesions, exacerbating them
mucosal barrier for oral defense
Contains Toll-like receptors: TLRs recognize PAMPs
TLR of oral mucosa
TLR 2, 4, 6, 10
TLR2
peptidoglycan
TLR4
LPS, lipoteichoic acid
TLR6
LPS
TLR10
LPS
defensins of the oral surface (tooth/mucosa)
main one?
why bacteria would be susceptible?
Small peptides (proteins) that form pores in bacterial membranes, disrupting cells.
HBD-1 (human b-defensin 1) is the main defensin produced by epithelial cells.
Bacterial membranes are susceptibledue to their high phospholipid content.
Adherent mucin layer or oral surfaces
Mucins attached to mucosal surface form a selectively permeable layer (a mucus coat analogous to a bacterial capsule).
Mucins are glycoproteins and carbo-hydrates portion form a sticky slippery gel.
MG1 and MG2 are mucins in oral cavity
Commensal oral microbiota as a defense
tooth surfaces and mucosa
Endogenous bacteria keep out new bacteria, and the stimulate immune system. But
they can cause disease when the balance shifts.
fluid of oral defense
main components
Fluid phase: saliva=0.5 - 1.5 liters per day secreted into the mouth
Mucins: MG1 and MG2 aggregate and clear oral microbes via lectin-like interactions.
Lysozyme: Degrades peptidoglycan by cutting bond between NAG and NAM (muramidase)
Acquired specific immunity of oral cavity mediated by?
mediated by S-IgA
Mucosal lymphocytes
Lamina propria lymphocytes = resting memory cells awaiting reexposure; their role upon
reexposure is mainly cytokine production
Intraepithelial lymphocytes: surveillance for pathogens and removal of stressed and infected
epithelial cells
GCF
GCF flushes gingival crevice, removing microbes and products. Health vs inflammation: more
serum-like composition during inflammation (vs tissue-like composition)
IgG, IgA, and IgM
GCF is major source of leukocytes in oral cavity: 95% are neutrophils
