INFECTIONS OF THE ORAL CAVITY

OBJECTIVES
Know the microbiologic consideration of oral cavity
infection
Describe the pathogenetic mechanism
Describe the mucosal immunity of the oral cavity
Know the clinical manifestation and management
Describe the diagnostic approaches and therapeutic
consideration

SKDI 2012
Daftar Masalah Kesehatan

SKDI 2012-Daftar Penyakit

Infections of the oral cavity >> odontogenic

Odontogenic: dental caries, pulpitis, periapical abcess, ginggivitis, periodontal
disease, infection deep facial abcess

Nonodontogenic: ulcerative mucositis, noma, parotitis

Hematogenous
dissemination
to heart valves,
prosthetic devices,
and other metastatic
foci

Intracranial,
retropharyngeal,
or pleuropulmonary
extension

Potentially
serious
nature

MICROBIOLOGIC CONSIDERATION

The microbiota associated with odontogenic

infections are complex:
Typically polymicrobial
More than 700 bacterial species from the oral cavity have
been identified
Invasiveness is often influenced by synergistic interactions of
multiple microbial species

Certain species or combinations may be:

more invasive or
more resistant to therapy than others

UNIQUE NICHES OF THE INDIGENOUS ORAL FLORA

The total cultivatable bacteria:

anaerobic bacteria averaged 1.8 x

1011 microorganisms/gr
facultative bacteria averaged 2.2 x
1010 microorganisms/gr

Streptococcus, Peptostreptococcus,
Veillonella, Lactobacillus,
Corynebacterium, and Actinomyces
>80% of the total cultivable oral flora

UNIQUE NICHES OF THE INDIGENOUS ORAL FLORA

Factors that govern localization patterns
Selective adherence characteristics certain bacteria for various types of cells
Local environmental conditions (oxygen tension, oxidation-reduction
potential, pH
Interbacterial coaggregation
Microbial inhibition

Factors influence composition of the oral flora

age
pregnancy
diet and nutrition
eruption of deciduous dentition
oral hygiene
smoking habits
the presence of dental caries or periodontal disease
antimicrobial therapy, hospitalization
genetic or racial factors

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

Normal commensal microflora are adapted to

their unique ecologic niches known as biofilm

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

Healthy periodontium
consists mainly of Gram-positive organisms such
as Streptococcus oralis, S. sanguis, and
Actinomyces spp

Dental caries
An etiologic association of S. mutans in dental
caries has been firmly established
S.mutans is hemolytic streptococcus, mutans
(changing) cocci that may appear rodlike,
particularly when initially isolated in culture

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

Gingivitis
anaerobic gram-negative rods, Prevotella
intermedia, Capnocytophaga spp., and
Peptostreptococcus spp

Establish periodontitis (adults)

anaerobic gram negative and motile organisms
and spirochetes
Porphyromonas gingivalis, P. intermedia,
Actinobacillus actinomycetemcomitans, Tannerella
forsythensis and Treponema denticola

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

Early onset periodontitis (juvenile)

Prevotella intermedia, Capnocytophaga spp.

Suppurative odontogenic infections, periapical

abscesses, deep fascial space infections
Fusobacterium nucleatum, Bacteroides spp.,
Peptostreptococcus spp., Actinomyces spp.,
Streptococcus spp.,
facultative gram-negative bacilli and
Staphylococcus aureus (only in patients with
serious underlying illness)

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MICROBIAL SPECIFICITY IN ODONTOGENIC INFECTIONS

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PATHOGENETIC MECHANISMS

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1. CARIES
Host protection
cleaning (tongue)
buffering (saliva)
acquired pellicle

Fermentation
of sucrose

Low pH

Low hygiene

Pathogenic bacteria
Adhere
Resist
Compete
Evade
Penetrates

Demineralization

Caries

Utilize
sucrose

Produce
glucans

Stick to
tooth
surface

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Development of Caries
S. sanguis and S. parasanguis a fimbrial protein
binding to hydroxyapatite on the tooth surface
P. Gingivalis protease, collagenase, hyaluronidase
binding to fibroblasts and matrix proteins by
degrading host proteins
S. mutans and S. sobrinus, reside within the
supragingival plaque acidogenic (produce acid)
and aciduric (able to grow at low pH)

2. PERIODONTAL
DISEASE
Virulence factors
lipopolysaccharide
proteolytic enzymes,
leukotoxin (A.
actinomycetemcomitans)
Predisposing factors
Poor oral hygiene
Increasing age
Smoking
Malnutrition
DM
Neutrophil defects
Hormonal (puberty,
menstruation,
pregnancy)

19

Periodonthopathic microorganisms
within subgingival dental plague
penetrate the gingival epithelium

Elicit an inflammatory host

response
Destruction of the
periodontium

Gingival recession, loss of

periodontal attach

Periodontal disease

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MUCOSAL IMMUNITY OF THE ORAL CAVITY

21

Three Types of Immunity

Physical
barrier

Nonspesific

Adaaptive,
MALT

Basal membrane

22

Keratinocytes
Constantly undergoes cellular renewal and turnover
Activating TLR regulate pro- and antiinflammatory
mediators
Producing antimicrobial peptides : histatin, -defensin

Lamina Propia
Phagocytic cells (leukocytes, macrophages)
Mucosa-associated lymphoreticular tissue (MALT)
Lymphocytes, macrophages, dendritic cells, NK cells, eosinophils

The dendritic cells (Langerhans cells)

process foreign antigens for presentation to and activation of T
cells, and differentiation of B cells into immunoglobulin-secreting
plasma cells

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sIgA
Function : bacterial agglutination, inhibition of
bacterial adherence, toxin neutralization, antigen
exclusion at the mucosal surface
Downregulates the proinflammatory cytokine
response
Oral microorganisms implicated in periodontitis :
including P. gingivalis, P. intermedia, Prevotella
melaninogenica, Capnocytophaga spp., S. sanguis,
and S. mitis, are able to secrete IgA proteases

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Saliva
coats the teeth and contribute to the protective
pellicle
flushes the oral cavity, clearing away bacteria and
their by-products,food debris
maintains salivary pH
contains lysozyme, lactoferrin, defensins, and
peroxidase that inhibit bacterial growth

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Lysozyme
Lyse bacteria by catalyzing breakdown of the bacterial
cell wall
Disrupts the lipopolysaccharide coat in the cell wall of
Gram-negative bacteria

Lactoferrin
Sequesters iron from the environment, thus inhibiting
the growth of bacteria

Lactoperoxidase and myeloperoxidase

generates a hypothiocyanate (HOSCN) molecule that is
toxic to bacteria

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CLINICAL MANIFESTATIONS
AND MANAGEMENT

OROFACIAL ODONTOGENIC INFECTIONS

27

DENTOALVEOLAR INFECTIONS
Etiology: S.mutans
Mostly are results from carious exposure in
pits and fissures
Demineralizationdiscoloration
destruction of enamel and dentin pulpal
necrosisperiapical abscess
Clinical signs : sensitive to percussion,
heat, cold (early), a hot stimulus (late)
Treatment: elimination of infected pulp,
extraction, drainage
May complicate to
osteomyelitis

GINGIVITIS AND PERIODONTAL

INFECTIONS
Ginggivitis
Simple gingivitis:
Etiology: Prevotella intermedius
Bluish-red discoloration, swelling and thickening free
gingival margin
Gums bleeding after eating or tooth brushing

28

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Ginggivitis (contd)
Acute necrotizing ulcerative gingivitis (ANUG):

Etiology: Prevotella intermedia, Fusobacteria, Treponema

= Vincents angina, trench mouth
Necrosis in the interdental papila
Superficial grayish pseudomembrane, halitosis, fever,
malaise
Treatment: local debridement, penicillin or metronidazole

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Periodontitis
is a severe gum infection that can
lead to tooth loss and other serious
health complications.
Etiology: P.intermedia, Actinobacillus
actinomycetemcomitans
Gingiva is inflamed and discolored,
bleeds readily, periodontal pockets
(+), pus (+)
Treatment: systemic antibiotic
(tetracyclin, metronidazole), root
debridement, surgical resection

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Periodontal Abscess
red, fluctuant swelling of the gingiva, extremely
tender to palpation
in communication with a periodontal pocket, pus (+)
Etiology:
P.intermedia
Actinobacillus actinomycetemcomitans

Treatment: surgical

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Pericoronitis

acute localized infection

associated with gum flaps
overlying a partially erupted
or impacted wisdom tooth
The pericoronal tissues are
erythematous and swollen,
pus (+), trismus (+)
Etiology: Staphylococcus,
Streptococcus
Treatment: incision and
irrigation, systemic antibiotics
(if cellulitis occurs), excision
of the operculum or
extraction

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DEEP FASCIAL SPACE INFECTIONS

Ludwigs Angina
Etiology: Fusobacterium nucleatum,
Bacteroides spp., Peptostreptococcus
spp., Actinomyces spp., and Streptococcus
spp.
Infection is always bilateral
Both the submandibular and sublingual
spaces are involved
Infection begin in the floor of the mouth
rapidly spreading cellulitis without
abscess formation
Treatment: high dose parenteral
antibiotic (ampicillin-sulbactam/penicillin
G+metronidazole), airway monitoring,
surgical intervention

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OROFACIAL NONODONTOGENIC INFECTIONS

INFECTIONS OF THE ORAL MUCOSA
Noma (Gangrenous Stomatitis)

Journal of Pakistan Association of Dermatologists 2008; 18: 110-112.

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Noma (Gangrenous Stomatitis)

Etiology: Borrelia vincentii, F.nucleatum, P. melaninogenica
F.nucleatum is a key organism in the maturation of pathogenic
biofilms in periodontal pockets, and spreading odontogenic
infection
Is similar to acute necrotizing ulcerative gingivitis (ANUG), but
more focal and destructive, involving deeper tissues beyond
the gingiva
Treatment : high doses of intravenous antibiotics

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Aphthous Stomatitis
Etiology: uncertain, virus (CMV), autoimmune (elevated
cytotoxicity for epithelium)
Clinical variants:
minor aphthous ulcers
major aphthous ulcers
herpetiform aphthous ulcers

Treatment primarily symptomatic

 Mucositis and Stomatitis in the Severely

Immunocompromised Patient
Etiology: complication after irradiation or during chemotherapy for
acute leukemia, solid organ transplantation, AIDS, autoimmune
diseases associated with xerostomia and systemic immunosuppression
Breakdown of the mucosal epitheliummucositissecondary
bacterial/fungal (candidiasis)/reactivation or latent viral infection
Clinical manifestation quite variable
Treatment: symptomatic, secondary infection

37

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Herpes Ulcer
HSV types 1 and 2
primary or recurrent
oral ulcers
Small,single or multiple,
painful, smooth ulcers
on an erythematous
base on the lips, buccal
mucosa, hard palate,
gums
Episodes may last
several weeks
Treatment: acyclovir

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Oral Hairy Leukoplakia

A raised white lesion of the oral mucosa that is
usually seen on the lateral margin of the tongue
Caused by the replication of Epstein-Barr Virus in
the epithelium of keratinized cells on the surface
of the tongue and buccal mucosa
Frequency >> if CD4 << (HIV)
Large lession may impair taste
Treatment:
Sistemic : acyclovir, gancyclovir, foscarnet
Topical : podophyllin, isotretinoin

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Oral Candidiasis
Candida infection of the hard and soft palates,
buccal mucosa, tongue, pharynx, and
hypopharynx.
Candida albicans >> (others: C.tropicalis,
C.glabrata, C.krusei)
Caused by impair cellular immunity

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Oral Candidiasis
Diagnosis: physical examination, KOH preparation,
Gram staining

Treatment: nystatin suspension, fluconazole

antifungi (C.glabrata, C.krusei are resistant)

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Thrush
pseudomembrane
candidiasis
Cottage cheese plaque,
can be removed easily

Atrophic candidiasis
Flat erythematous
plaque without white
exudate

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Hyperthropic
candidiasis
Nonscrapeable white
plaque, smooth

Angular cheilitis
Candida of the lateral lip
Causing pain, fissures,
erythema, difficulty
opening the mouth

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INFECTIONS OF THE SALIVARY GLAND

Viral Parotitis
Rapid painful swelling of one/ both
parotid glands
Etiology: paramyxovirus, influenza,
enterovirus
Transmitted by saliva or aerosol via
oral cavity/ respiratory tract
invades oropharynx replicate in
upper respiratory tract
hematogen to salivary gland
Treatment: symptomatic
Prevention: vaccine (MMR)

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Suppurative Parotitis, Acute Bacterial Parotitis

Etiology: Staphylococci, enterobacteriaceae, other
Gram-negative bacilli, anaerobes
Sudden onset of pain and swelling, pus from the duct
Management: antibiotics, gland massage, hydration,
warm compress, oral hygiene, sialogogues

AAFP Volume 89, Number 11 June 1, 2014

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Chronic Bacterial Parotitis

Etiology: staphylococci or mixed oral aerobes and
anaerobes
Recurrent parotitis
Therapy: systemic antibiotics, ductal saline or
antibiotic irrigations

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MICROBIOLOGIC INVESTIGATION

DIAGNOSTIC APPROACHES

48

Major challenge: distinguish true pathogens from commensals

low virulence bacteria (coagulase-negative staphylococci,
diphtheroids, enterococci) are harmless in healthy hosts, but may
cause invasive disease in immunocompromised patients
Surface cultures from mucosal sites : generally not recommended
mostly show colonization rather than infection
Important !! :
proper specimen collection : proper disinfection, needle
aspiration of loculated pus (extraoral approach is desirable)
correlate laboratory data with clinical information
Transport specimen immediately to the laboratory under
anaerobic conditions.
Aerobic and anaerobic cultures should always be obtained

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Gram, acid-fast stains, KOH should routinely be done

Chronic osteomyelitis (soft tissue swelling and draining fistulas (+))
aspirates from adjacent soft tissue swellings may be valuable
cultures from sinus tracts may be misleading because of
colonization (do not reflect the bone infection)
Cultures from bone biopsies are necessary for definitive
diagnosis.

Many pathogens are not cultivable immunofluorescence

staining and DNA probes or PCR are increasingly used
BANA (benzoyl-dl-arginine naphthylamide) test : detects a
trypsin-like enzyme (BANA) produced by periodontopathic
anaerobic bacteria, including P. gingivalis, T. denticola,
Tannerella forsytheusis.

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Substrat + BANA

Hidrolysis

Formation of
chromophore

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THERAPEUTIC CONSIDERATIONS

52

DENTAL CARIES AND PERICORONITIS

Control supragingival and subgingival plaques
Antiseptic and antimicrobial regimens
Fluoride exerts bacteriostatic effect
Chlorhexidine 0.12% has bactericidal effect
Not for long term promote the emergence of
resistant microorganisms

Combination of both synergistic

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Acute simple gingivitis penicillin+ metronidazole,

clindamycin, ampicillin-sulbactam
ANUG metronidazole
Severe periodontitis systemic AB
(metronidazole, doxycycline) 1- 2 weeks+
mechanical debridement
Adult/ established periodontitis topical
antibiotics (minocycline, doxycycline)

 No routine use of systemic antimicrobial

prophylactic in healthy host
Vaccine for S. mutans explored, not yet
applicable

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SUPPURATIVE SOFT TISSUE INFECTIONS

Surgical drainage and the removal of necrotic tissue!!
Antimicrobial therapy halts the local spread of
infection and prevents hematogenous dissemination
Resistance to penicillin increasing (-Lactamase
producing anaerobic Gram-negative bacteria) use
combination with -Lactamase inhibitor
The initial selection of antimicrobial agents
guided by knowledge of the most likely causative
organisms and predicted antibacterial spectrum
bioavailability in oral or parenteral formulations

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For normal host

Agent of choice:
Metronidazole + penicillin
-Lactam + -Lactamase inhibitor
Clindamycin

Alternative agents:
Cefoxitin
Cefotetan
Moxifloxacin

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For Severely Immunocompromised

Are at risk for unhalted and rapidly spreading infection
AB regimen should be broad-spectrum, bactericidal,
and cover nosocomial pathogens, including facultative
Gram-negative bacilli / MRSA as local data supports
Agent of choice:
ciprofloxacin + metronidazole
3rd or 4th gen.cephalosporin + metronidazole
Alternative agents:
ticarcillin-sulbactam, piperacillin-tazobactam
carbapenem (i.e., imipenem-cilastatin, meropenem)
tigecycline

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