Oral Bacteria B

Question 1

Dentoalveolar infections

Answer 1

Pyogenic infections associated with the
teeth and surrounding supporting
structures

Question 2

Bacteriology of root canal infections

Answer 2

Endodontic infections are endogenous infections

that are opportunistic

Question 3

Dentoalveolar Abscess (4)

Answer 3

• 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

Question 4

bacteria commonly isolated from dentoalveolar abscesses
Facultative anaerobes (2)
Obligate anaerobes (4)

Answer 4

Streptococcus
Actinomyces spp.

Peptostreptococcus spp.
Porphyromonas gingivalis
Prevotella
Fusobacterium nucleatum

Question 5

Ludwigs Angina (2)

Answer 5

A spreading, bilateral infection of the sublingual and submandibular spaces.
Cellulitis of the fascial spaces rather than true abscess formation.

Question 6

Mixed endogenous infection: (4)

Answer 6

Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

Question 7

Airway obstruction -

Answer 7

death by asphyxiation

without intervention

Question 8

Periodontal Abscess

Answer 8

Localized collection of pus caused by acute or chronic destruction of periodontium
Endogenous, subgingival plaque bacteria
polymicrobial

Question 9

polymicrobial (4)

Answer 9

Porphyromonas spp.
Prevotella spp.
Fusobacteria
Anaerobic streptococci

Question 10

Suppurative Osteomyelitis of the Jaws

Answer 10

Same organisms as above but involves bone

Question 11

Cervicofacial Actinomycosis

Answer 11

endogenous, granulomatous disease
65% in cervicofacial region
Actinomyces (oral commensal)
visible granules in pus
sulphur granules
= collections of bacteria

Question 12

Syphilis –

Answer 12

congenital: Hutchinson’s incisors, mulberry molars
primary and secondary syphilis lesions
gummas (granulomatous lesions)

Question 13

Tuberculosis –

Answer 13

oral lesions in up to 5% of primary and secondary tuberculosis cases
ulcers on palate and gingiva

Question 14

Leprosy -

Answer 14

For leprosy just know there are

many oral manifestations

Question 15

Bacterial infections of salivary glands – often

Answer 15

Staphylococcus

Question 16

Diseases or situations associated with

oral bacteria or their components: (7)

Answer 16

Infective endocarditis
Disseminated intravascular coagulation
Nephritis
Rheumatoid arthritis
Behçets disease (chronic
inflammatory disorder with oral
ulcers)
Atherosclerosis
Low-birth-weight infants

Question 17

Infective endocarditis

Answer 17

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)

Question 18

Other possible associations between oral microbes

and systemic disease (2)

Answer 18

Heat shock proteins (HSPs)

Autorecognition induced by oral microorganisms

Question 19

Heat shock proteins (HSPs)

Answer 19

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.

Question 20

Autorecognition induced by oral microorganisms

Answer 20

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?)

Question 21

Inflammation -
a link between local
dental disease and
systemic pathology?

Answer 21

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)

Question 22

Innate host defenses

Answer 22

Oral surfaces
The mucosal barrier
Contains Toll-like receptors

Question 23

TLRs recognize

Answer 23

PAMPs (PathogenAssociated Molecular Patterns)

Question 24

TLR2

Answer 24

peptidoglycan

Question 25

TLR4

Answer 25

Lipopolysaccharide, lipoteichoic acid

Question 26

TLR6

Answer 26

Lipopolysaccharide

Question 27

TLR10

Answer 27

Lipopolysaccharide

Question 28

Innate host defenses Oral surfaces Defensins

Answer 28

``` 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. ```

Question 29

Innate host defenses: Oral surfaces | Adherent mucin layer

Answer 29

``` 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. ```

Question 30

Innate host defenses: Oral surfaces | Commensal oral microbiota (including on tooth surfaces)

Answer 30

Endogenous bacteria keep out new bacteria, and the stimulate immune system. But they can cause disease when the balance shifts.

Question 31

Innate host defenses | Fluid phase: saliva

Answer 31

0.5 - 1.5 liters per day secreted into the mouth

Question 32

Innate host defenses Fluid phase: saliva Mucins

Answer 32

MG1 and MG2 aggregate and clear oral | microbes via lectin-like interactions.

Question 33

Innate host defenses Fluid phase: saliva (continued) Lysozyme

Answer 33

Degrades peptidoglycan by cutting bond | between NAG and NAM (muramidase)