Download Pathogenesis of Odongenic infections

Pathogenesis of O.I
Spreading of infection within the
tooth
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Note that infection usually follows the path of
least resistance,
Microbes ones have penetrated the pulp
stimulate the inflammation process within the
pulpal soft tissues,
Dental pulp is soft tissue enclosed by the
unyielding hard tissue structure (the dentine)
Inflammation process within pulp begins by
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Vasodilatation,
Spreading of infection within the
tooth cont…
Extravasation of tissue fluid and inflammatory cells,
 Causes edema,
 Because pulp is enclosed in unyielding tooth
structure,
 Rise of hydrostatic pressure within dental pulp
exceeds blood pressure,
 Circulation to soft tissues ceases,
 Resulting Ischemia,
 Eventually necrosis.
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Spreading of infection within the
tooth cont…
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What is resulted after necrosis?
Host’s defense access to pulpal tissues ceases (blood
flow supply cut off)
If give antibiotics –do not penetrate avascular areas
Dead tissues of dental pulp acts as culture medium for
invading bacteria to grow and multiply until beyond the
confines of tooth itself,
Seeding the surrounding tissues
Spreading of infection within the
bone
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Alveolar bone is like dental structures in terms of its
response to infection,
Alveolar bone consists of interconnecting marrow
spaces delimited by unyielding calcium tissue, all of
which circumferentially by a layer of cortical bone of
varying thickness,
Invasion of bacteria from pulp canal into these marrow
spaces triggers inflammation process,
Causes the same sequence of edema, ischemia, necrosis
and isolation from the systemic circulation and immune
system
Spreading of infection within the
bone cont…
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This is the process by which bacteria are able to
survive within the bone of the jaws,
Path of least resistance from this point is
medullary spaces – explain why O.I can spread
great distance along jaws before eroding through
cortical plates e.g in osteomyelitis,
Another factor in the spread of infection within
bone is the thickness of the cortical plate on
either side of the bone.
Spreading of infection within the
bone cont…
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In maxilla buccal plate os thinner, perforated
frequently by nutrient vessels from the
underlying periosteum,
Palatal bone is much thicker perforated much
less frequently.
Easier for infection from the maxillary teeth to
erode thorough the buccal plate of the maxilla
spreading into soft tissues of the face or into the
oral cavity.
Spreading of infection within the
bone cont…
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Posterior mandible the opposite is true,
Buccal plate of bone overlying the bicuspids and
molars is much thicker than the lingual,
Infection arising from the mandibular posterior
teeth is quite likely to erode inferiorly through
the thin lingual plate, spreading into the soft
tissues of the floor of mouth,
Spreading of infection within soft
tissues
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Muscles, fascial and bone function as barriers to
the spreading of infection within soft tissues,
They have a tight, dense capsule surrounding
them, and well vascularized,
Muscles are less susceptible to bacterial invasion
than are the surrounding loose fibrous
connective tissue,
Recall fascial spaces in anatomy
Spreading of infection within soft
tissues
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Ones infection spread beyond alveolar bone,
It enters the perialveolar soft tissues,
Direction from here differs depending site of
perforations;
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If point of bony perforation is on the oral side of the
muscles attached to the alveolar process such as
buccinator, may perforate alveolar mucosa and drain
into oral cavity,
Spreading of infection within soft
tissues cont…
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If infection does not perforate the oral mucosa it will
enter one of the fascial spaces of the face and neck
Bacterial growth without triggering an intense
inflammatory reaction,
Mild edema of the area,
 Swelling becomes sift and dough to palpation.
 Treatment here is removing dental source without
antibiotic.
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Stage II (Cellulitis)
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Occurs after bacteria have inoculated the soft
tissue space,
Multiply and elaborate toxins and metabolic by
products, and intense inflammatory process is
triggered,
Term cellulitis is from latin word “cellula”
means little room,
Thus it refers to inflammationon in one of the
fascial spaces of the body,
Stage II (Cellulitis) cont…
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Clinically presents as;
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It appears as diffuse reddened, indurated (hard)
exquisitely tender swelling,
Treatment – antibiotic is effective for a pure
cellulitis (because- no necrosis, blood circulation
is ok-access by antibiotic possible).
Stage III -Abscess
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As the cellular phase of the process of inflammation
progress,
Inflammatory cells consisting mainly of PMNL –drawn
to the area of infection,
Phagocytes engulfy bacteria and digest them,
Often themselves will die in the process,
There is necrosis of surrounding tissues due to
lymphokines,
Small pockets of necrotic tissue form within cullulitis,
coalesce and enlarge, compressing the surrounding
fibrous connective of deep tissue spaces,
Stage III –Abscess cont…
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Abscess is formed which is a collection of pus
surrounded by a wall of compressed fibrous
tissue,
Palpated clinically abscess is fluctuant.
Resolution (stage IV)
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One to two weeks after beginning of infection,
the specific immune system (T lymphocytes etc)
come into play,
Phagocytosis of bacteria and necrotic tissues,
Overtime -disposal of this materials
Resolution is speeded greatly by surgical
drainage of abscess cavity or by its rupture,
Repair of infected wounds leaves a palpable scar.
Treatment of infection (surgical)
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Primary treatment of acute infection and deep
space is by;
Establishment of dependent drainage of infection,
 Removal of the cause,
 BUT not antibiotic administration as treatment.
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Drainage established by I&D
Rubber drains
Steps in treatment
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Obtain culture,
Empirical antibiotic therapy,
Establish dependant drainage.
Cotton swab and transport media