Oral Bacteria B Flashcards
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
Dentoalveolar Abscess (4)
• 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
bacteria commonly isolated from dentoalveolar abscesses Facultative anaerobes (2) Obligate anaerobes (4)
Streptococcus
Actinomyces spp.
Peptostreptococcus spp.
Porphyromonas gingivalis
Prevotella
Fusobacterium nucleatum
Ludwigs Angina (2)
A spreading, bilateral infection of the sublingual and submandibular spaces.
Cellulitis of the fascial spaces rather than true abscess formation.
Mixed endogenous infection: (4)
Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci
Airway obstruction -
death by asphyxiation
without intervention
Periodontal Abscess
Localized collection of pus caused by acute or chronic destruction of periodontium
Endogenous, subgingival plaque bacteria
polymicrobial
polymicrobial (4)
Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci
Suppurative Osteomyelitis of the Jaws
Same organisms as above but involves bone
Cervicofacial Actinomycosis
endogenous, granulomatous disease 65% in cervicofacial region Actinomyces (oral commensal) visible granules in pus sulphur granules = collections of bacteria
Syphilis –
congenital: Hutchinson’s incisors, mulberry molars
primary and secondary syphilis lesions
gummas (granulomatous lesions)
Tuberculosis –
oral lesions in up to 5% of primary and secondary tuberculosis cases
ulcers on palate and gingiva
Leprosy -
For leprosy just know there are
many oral manifestations
Bacterial infections of salivary glands – often
Staphylococcus
Diseases or situations associated with
oral bacteria or their components: (7)
Infective endocarditis Disseminated intravascular coagulation Nephritis Rheumatoid arthritis Behçets disease (chronic inflammatory disorder with oral ulcers) Atherosclerosis Low-birth-weight infants
Infective endocarditis
FIGURE 4 Platelet streptococcal interactions in infective endocarditis. Circulating
platelets adhere to collagen exposed on damaged heart valves. During polymicrobial
bacteremia, oral streptococci bind to the activated adherent platelets through expressed
adhesins and PAAP. PAP activates and induces additional platelers to aggregate on the
heart valve. Aggregation requires the cross-linking of platelets to one another by fibrin-
gen molecules. The fibrinogen molecules are polymerized into fibrin by thrombin,
forming an insoluble thrombus or platelet clot. Released plateler granules contain
innate antimicrobials, including platelet microbicidal protein, which may limit the
valvular infection by sensitive bacteria. Leukocytes accumulate on the exterior of the
septic thrombus as an inflammatory response is initiated.
PAP = platelet aggregation-associated protein = Streptococcal surface protein (adhesio)
Other possible associations between oral microbes
and systemic disease (2)
Heat shock proteins (HSPs)
Autorecognition induced by oral microorganisms
Heat shock proteins (HSPs)
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
Streptococcus sanguinis express an epitope within PAAP (plateletaggregation associated protein), 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?)
Inflammation -
a link between local
dental disease and
systemic pathology?
FIGURE 5 How oral microbes produce local inflammation to influence systemic
pathology. In the gingival sulcus, bacteria and their PA.MPs such as LPS affect under-
lying tissues, causing local inflammation. High levels of the inflammatory mediators
TNF-a and IL-1ß may enter the circulation and induce the liver to produce acure-
phase reactants, such as CRP. IL-1ß and TNF-a may also act on monocytes in exist-
ing atherosclerotic plaques, causing exacerbation of existing disease.
(PAMPs = pathogen associate molecular patterns)
Innate host defenses
Oral surfaces
The mucosal barrier
Contains Toll-like receptors
TLRs recognize
PAMPs (PathogenAssociated Molecular Patterns)
TLR2
peptidoglycan
TLR4
Lipopolysaccharide, lipoteichoic acid
TLR6
Lipopolysaccharide
TLR10
Lipopolysaccharide
Innate host defenses
Oral surfaces
Defensins
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 susceptible due to their high phospholipid content.
Innate host defenses: Oral surfaces
Adherent mucin layer
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.
Innate host defenses: Oral surfaces
Commensal oral microbiota (including on tooth surfaces)
Endogenous bacteria keep out new bacteria, and the stimulate immune system. But
they can cause disease when the balance shifts.
Innate host defenses
Fluid phase: saliva
0.5 - 1.5 liters per day secreted into the mouth
Innate host defenses
Fluid phase: saliva
Mucins
MG1 and MG2 aggregate and clear oral
microbes via lectin-like interactions.
Innate host defenses
Fluid phase: saliva (continued)
Lysozyme
Degrades peptidoglycan by cutting bond
between NAG and NAM (muramidase)
