A presentation with a view on how infection spreads through the focus of dental caries into a full cellulitis. Since dentists have to deal often with large space infections, this presentation helps to review your knowledge in this subject. - Dr. Abhishek John Samuel, MDS, Endodontics
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Spread of infection
1. Dr. Abhishek John Samuel
MDS
Endodontics & Conservative Dentistry
*SPREAD OF
INFECTION
2. *The healthy body usually lives in balance with
a number of resident normal flora. However,
pathogens can invade and initiate an
infectious process.
1. Dental infections involving the teeth or
associated tissues are caused by oral pathogens
that are predominantly anaerobic and usually of
more than one species.
2. These infections can be of dental origin or
from a non-odontogenic source.
3. *Those of dental origin - progressive dental
caries or extensive periodontal disease.
*Pathogens - introduced deeper into the oral
tissues – trauma, dental procedures, and
needle tracks during LA administration.
*Some dental infections are secondary
infections - tissues surrounding the oral cavity.
These nonodontogenic sources of infections
must be diagnosed and treated early.
4.
5.
6. Table TGJ-2. Causes of Dentoalveolar and Periodontal Abscesses, Ludwig’s angina, and
Osteomyelitis of the Jaw
Disease Causative Agents
Dentoalveolar abscess Strict anaerobes found in the oral mucosa
Periodontal abscess Gram-negative rods, Streptococcus viridans group,
anaerobic streptococci, spirochetes
Ludwig’s angina Streptococcus, Bacteroides, Fusobacterium,
Staphylococcus aureus
Osteomyelitis of the jaw Gram-negative rods, anaerobic streptococci,
Actinomyces israelii
Infectious Diseases Study, Fall 2013, Still University of Health Sciences/Kirksville College of Osteopathic Medicine.
7. *
*Kolmer viewed microbial pathogenicity as arising from two
microbial factors that he called toxicity and aggressiveness,
with the latter being a measure of invasive power (Kolmer
1924).
*Microbial poisons and toxins that damaged the host caused
toxicity, whereby aggressiveness was a complex trait that
included the ability of a microbe to survive and multiply in
tissue (Kolmer 1924)
8. *Bail (1880’s) proposed his aggressin theory -
aggressins that interfered with host defense
mechanisms and allowed the microbe to establish
itself.
*Virulence is a relative term
*An interaction between host response – bacteria
leading to a damage to the host.
9. *
* Exotoxins - interfering with cellular homeostasis. For toxigenic bacteria – disease is action of
the toxin
• inactivate calcium- and calmodulin-dependent adenylate cyclase and mitogen-activated protein
kinase,
• interfering with macrophage function and inhibiting an effective immune response
* Modulins - Microbial products that elicit detrimental cytokine responses, such as
lipopolysaccharide, have been called modulins
* Enzymes- Tissue damage makes the host permissive for microbial infection.
• Enzyme virulence factors that damage tissue include proteases, neurominidases and
phospholipases.
• These enzymes damage cells and provide nutrients by digesting substrates into smaller
components
* Adhesins- attach to host tissues. First Priority
• Flagellae, cell wall polysacc, proteins.
* Motility- Flagella, Actin-propulsion, ↑virulence,
* Capsules- protecting the microbe against host immune mechanisms, although for
• some the capsular structures can serve as adhesins
* Complement evasion- sialic acid, O-polysacc chains, altered receptor sites, c3b inhibition etc.
* Pigments- Melanin
* Biofilm formation - quorum sensing, attachement, signalling, host response evasion.
* Iron acquisition - necessary for Growth
10.
11. *Dental infections can result in different types of lesions,
depending on the location of the infection and the type of tissue
involved.
*An oral abscess - localized entrapment of pathogens, with
suppuration from a dental infection - closed tissue space.
*Periapical Abcess, Periodontal Abcess
*Formation of a Fistula (skin, oral mucosa or bone)
*The infectious process causes the overlying tissues to undergo
necrosis, forming a canal in the tissue, with a stoma – Path of
least resistance
14. *The position of the pustule is
largely determined by the
relationship between the
fistula and the overlying
muscle attachments.
The muscle attachments to the
bones serve as barriers to the
spread of infection, unlike the
other facial soft tissues.
33. *
*Base skull to diaphragm
*a subdivision of the retropharyngeal space, extending from the base of
the skull to the level of the diaphragm; it provides a route for the
spread of infection from the pharynx to the mediastinum.
*Contiguous spread from adjacent spaces
34. *
*Extensive venous communication (via the ophthalmic veins)
between the facial vein and the cavernous sinus.
*The cavernous sinus lies within the cranial cavity, between layers of
the meninges and is a major conduit of venous drainage from the
brain
*Inside cavernous sinus we can find constriction of the following
nerves: CN III (oculomotor nerve), CN IV (trochlear nerve), CN VI
(abducens nerve), CN V (trigeminal nerve), specifically V1
(ophthalmic nerve) and V2 (maxillary nerve) branches.
* Failure of each of the nerves – action of specific muscle, gland or a
parasympathetic innervations (from CN III).
* In addition, it is possible that inflammation of the cavernous sinus
will result in compression of the optic chiasm (resulting in vision
problems) and/or the pituitary gland
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50. *
*Pharyngeal swelling – difficulty swallowing
*Difficulty sleeping supine
*Sniffing position – Retropharyngeal space
*Head deviated to opposite side – Lateral pharyngeal space
*Muffled voice – Epiglottitis
*Distant quality to voice – Retropharyngeal / Lateral Pharyngeal
*Elevated tongue – Sublingual space
51.
52. *
*Caries
*Swellings of oral vestibule
*Periodontal disease
*Tooth mobility
*Pericoronitis
*Swellings
*Position of uvula