Oral Microbiology Flashcards
Common microflora of oral cavity
– g+ cocci
..staph epidermidis
.. strept most predominant
.. St. Viridans important in infective endocarditis
.. capnocytophagia important in plaque and found in gum of posterior teeth
G+ bacilli
..actinomyces facultative anaerobes or anaerobes important in plaque
.. lactobacilli production of large amount of acid from carbohydrates
..diphtheroid aerobes
..nocardia aerobes
G- cocci
Neisseria facultative anaerobes
Vellonella anaerobes
Branhamella catarhalis aerobes
G - bacilli ..fusobacterium ..bacteroids Spirichetes .. treponema ..borrelia كلهم anaerobes strict
Fungi and viruses In oral cavity
B) Fungi:
Candida. the most commonly fungi present in oral cavity. . Present in small percentage of the total oral flora in normal healthy
mouth. Increase in number and may cause infections in diabetic patients, cancer, immune deficiency disorders as AIDS and after heavy doses of antibiotics & in pregnancy.
C Viruses:
Little is known about the role of virus in normal oral flora, but some varuses as herpes simplex. measles, mumps can be found in oral lesions during the course of the disease.
HIV virus and hepatitis viruses may be present in saliva during the
disease
Change in oral flora with age
Time during a lifetime
Oral cavity sterile. Soon colonised by facultative and
Newborn
aerobic organisms; esp S. salivarius Flora becomes more complex & includes anaerobic
orgs eg. Veillonella sp. & Fusobacteria
6 months
MAJOR COMPONENTS & CHANGES IN ORAL FLORA
Increase in complexity. S sanguis, S mutans and A viscosus appear. New habitats include hard surfaces
Tooth eruption
and gingival crevice. Various anaerobes frequently found inc. Members
Child to adult
of the Bacteroidaceae. Spirochaetes isolated more frequently
Loss of teeth
Disappearance of S mutan, S sanguis, spirochaetes and many anaerobes
Dentures etc
Reappearance of bacteria able to grow on hard
surfaces
Microbial flora at different parts of the mouth
: Many factors affect microbial flora at different sites due to conditions at
these sites vary with respect to: oxygen levels and anaerobiosis, availability of nutrients, exposure to salivary secretions or gingival crevicular fluid. mastication forces and other variables such as oral hygiene.
Strept salivarius: is the predominant on dorsal surface of the tongue.
Strept Sangius: colonize the smooth surface of teeth.
Strept Mitior: is the predominant on the buccal mucosa. Strept mutans: colonize the occlusal pits and fissures of crowns.
Bacteroides melaninogenicus and oral spirochetes: prefer the gingival
crevice.
Predisposing factors that lead to oral infections
: a) Normally there is balance between oral microflora and the host.
b) This balance can be disrupted in a number of ways that result in the
disease of the oral structure..
c) The oral flora together with other oral defense mechanisms plays an important role in protecting the oral cavity from infections by exogenous organisms.
These predisposing factors are:
- Physiological factor as old age- cause diminished antibody decrease in salivary flow→ lead to candidosis, root caries.
- Pregnancy: leading to gingivitis.
levels,
- Trauma: local leading to tissue integrity loss opportunistic infection, general trauma debilitation, dehydration leading to candidosis. 4. Malnutrition: deficiencies of iron, vitamin B12 leading to candidosis.
- AIDS: diminished cell mediated immunity- opportunistic infections, candidosis.
- Chemotherapy: disrupts the balance of the oral flora in cause selection of resistant microflora→ leading to opportunistic infectious, candidosis
and caries. 7. Oral malignancies: leading to candidosis & caries.
Disturbances to the oral cavity may allow one of 3 …
: 1) Selective overgrowth of certain endogenous species as Candida albicans, in patients with HIV infection or AIDS.
2) Displacement of certain endogenous species, for example actinomyces israelili with resulting actinomycosis after traumato the mucosa or jaws. 3) Introduction of exogenous microorganisms, such as Escherichia
coli that can cause osteomyelitis after radiotherapy.
E. Coli
Pericoronitis
:
Pericoronitis is inflammation around the crown (corona) of the tooth may spread into the surrounding tissues resulting in cellulitis or diffuse inflammation of the soft tissue. The involved bacteria produce large amounts of the enzymes hyaluronidase and fibrinolysins which are capable of breaking down
tissue cohesiveness leading to spread of infection.
Histology and pathogenesis of periodontal disease
Histologic and clinical changes:
Afler plaque accumulation & within 2 weeks gingivitis (gingiva show histologic changes called Established lesion with plasma cell infiltrate of sub-epithelial connective tissue) in some persons, the disease remains at this level
• Majority of cases progress with time- there is resorption of supporting alveolar bone formation of soft tissue pockets between the teeth and gingiva
Pathogenesis:
Pathogenesis is multifactorial and results from the interaction of the (body and its defense mechanisms with products from bacterial plaque
a Collagenase, Hyaluronidase,
h
Protease,
DNAse, and other enzymes Cytotoxic
agents as endotoxins,
Cell wall peptidoglycan
g Cell mediated immunity with lysozyme activation h. Complement activation by endotoxin or immune complex→ cell destruction
Formation of plaque
-pellicle
- first colonisers is s sanguise followed by mitis neisseria and veillonella
- after 14d
Colonised by g +bacilli like actino and nocardia fusobacteria
After 21d
Colonised by motile spirochetes with formation of dense layer of plaque at g margin
Dense confluent mass of plaque made of bac and matrix of salivary and bacterial polymers
3 factors of caries development
(1) A tooth susceptible to acid demineralization:
a) Susceptibility is related to low fluoridel content, surface irregularities) such as pits, fissure that can be colonized by S. mutans. b) The saliva normal saliva flow is essential for protection against caries &
there is dramatic increase in dental caries in diseases leading to 1 salivary flow. This is due to reduction of:
Mechanical cleansing and buffering capacity of saliva, Natural and acquired defense factors in saliva as lysozyme, lactoferrin (peroxidase and secretory IgA which have
antimicrobial activity and protect the teeth against caries.
(2) Dietary sucrose:
Sucrose is the major substrate for acid production by bacteria. S. mutans and other bacteria that use sucrose to produce adherent
polysaccharides this will prolong the maintenance of a low pH on the tooth surface with more caries production. (3) Bacteriologic basis:
S. mutans is the primary etiologic agent, also other acidogenic bacteria
especially lactobacillus species play a secondary role in the caries process.
Streptococcus mutans:
S. mutans produces lactic acid from sucrose and other carbohydrates, more rapidly than do other bacterial flora.
S. mutans cells have on their surfaces, surfaces protein antigen A which enable the organism to bind to tooth surface.
Also S. mutans can produce (high molecular weight insoluble glucans. S. mutans have receptor sites for glucans this promote aggregation of S. mutans to teeth surface and formation of insoluble plaque and in presence of sucrose- low pH- induce enamel deminalization, also the insoluble plaque acts as a barriers separating buffering agents in saliva from acids an tooth surface.
Other bacteria as lactobacilli is now considered as secondary agents in dental caries of particular importance in smooth surface caries and in carious leasios that have progresses into the dentin of the tooth. ⚫ Other acidogenic bacteria in the oral cavity include S. sanguis and S. mitis.
Assessment of caries risk
:
Oral Microbiology
The number of streptococcus mutans in saliva and lactobacilli correlate with the caries risk-↑ the number of S. mutans & lactobacilli - 1 caries risk.
Control and prevention of caries
Reduction of sucrose intake.
Use of systemic & topical fluorides: To reduce the acid solubility of the teeth and
⚫ for their potential anti-enzymatic and antibacterial effects.
. Regular oral hygiene: to reduce levels of dental plaque.
restoration of untreated carious cavities. Application of chlorohexidine as gels or rinse.
Vaccine: there are many trials by using varies antigen preparation for S. mutans including whole cell bacteria or cell wall.
Necrotizing ulcerative gingivitis (NUG)
Called trench mouth or vincent gingivitis.
This is sudden onset of painful inflammatory pseudomembranous conditions of the gingiva in young adults, usually patients under stress
and have deficient oral hygiene. Bacteria penetrate and infect the gingiva (there is Fusobacteria, Borrelia
vincenti). The interdental papilla is inflamed red, ulcerating.
There is bad odor of the mouth, due to H2S production by anaerobic bacteria.
Pyogenic orofacial infections
Pyogenic orofacial infections
May result from extension of plaque flora into tissues.
Bacteria may spread into tissues from periodontal pockets, infected dental pulps. from traumatic injuries, or during invasive dental treatments such as tooth extractions.
This may be serious due to extension to periocular tissues or to vital organs, may spread to cavernous sinus→ to brain.
Microbiology:
Many bacteria may cause pyogenic orofacial infections such as S. faecalis. S. sanguis, bacteriodes, veillonella, proprobacterium, and S. aureus.
Management:
II. Mycotic Infections
The fungal pathogens involve the oral cavity either in a superficial manner or as a consequence of systemic disease) The causative agents include: Candida albicans, Cryptococcus neoformans, and Geotrichum species.
Oral Candidiasis (Oral thrush): Risk factors:
a. Vitamin deficiencies. b. Iron deficiency anaemia. -
c. Pregnancy.
d. Diabetes.
e. AIDS
Pathogenesis:
Growth of Candida species appears to be restricted to the coexisting bacterial flora, but when this flora is suppressed by antibiotics. Candida grow without limitation. Thus oral Candida infections often follow heavy
dose of antibiotics.
2
Clinical presentation:
The oral lesions involve the tongue, palate, cheeks, and lips and may also extend to the tonsils, pharynx, and larynx. Candida species may enter tissues at time of tooth extractions.
Diagnosis: direct smear
Direct specimen examination.
Specimen cultivation.
Treatment:
Topical sodium caprylate.
Amphotericin B.
