Diseases of the Oral Cavity

By Karisma Mancias
Periodontitis
Porphyromonas gingivalis, a Gram negative asaccharolytic rod, is the Herpes Simplex Virus-1
main contributor to periodontitis. Periodontitis is characterized by inflammation caused by Herpesviruses are large, enveloped, pleomorphic (they have several forms in on
a polymicrobial infection that leads to the destruction of bone and e life cycle) particles that include more than 30 virally encoded proteins. Herpes
support of the tooth. It can also cause atherosclerosis and aspiration pneumonia. simplex virus 1 causes oral lesions that are contagious when the person is
  symptomatic and occasionally when the patient is asymptomatic.
P. gingivalis has many virulence factors including cysteine proteinases called gingipains, hemagluttinins,  
lipopolysaccharides, and fimbriae. Saliva serves as a vector for its transmission and once it is in the host it attaches to HSV-1 needs to be transmitted through mucosal membranes because the membrane is so fragile. They contain linear
the film covering the tooth via its fimbriae which have an affinity for the bacteria that create the film. double stranded DNA in an icosahedral capsid. It enters its host through small breaks in the skin and establishes itself
  in the sensory ganglia. This is its preferred habitat because there are not many immune cells in this area which allows
It evades the immune system in various ways. It prevents apoptosis by secreting an ATP hydrolyzing enzyme that the virus to replicate without the threat of being eradicated. Another one of its virulence factors is its ability to infect
prevents ATP driven apoptosis. It also inhibits the ability of gingival epithelial cells to induce IL-8 chemoattractant and using many different receptors. The glycoproteins on the surface of HSV-1 interact with herpesvirus entry mediator
inhibits the activation of neutrophils. There are some catalase positive strains of P. gingivalis that allow it to survive (HVEM), nectin-1 and nectin-2, and heparan sulfate; each of these is located on the surface of the host membrane.
the harsh oxidative stress of the macrophage. The author of this paper implies that P. gingivalis is resistant to The gC glycoprotein on the virus that is used for entry binds to the C3b complement receptor making it more
complement because of its lipopolysaccharides and only suppresses complement (by way of gingipains) in order to resistant to the formation of the membrane attack complex. Finally, HSV has a protein, ICP47, that binds
prevent its scaffold of bacteria from being destroyed. to the transporter that allows for antigen presentation on MHC class 1. ICP47 prevents the transportation of the
viral proteins to the ER and the subsequent binding of viral peptides to MHC-1 and their presentation to
CD8 T cells. ICP47 works with virion host shutoff (vhs) located in the tegument which serves as an
Fig. 1 RNas that shuts off protein synthesis, degrades host RNA, and destroys ribosomes, as well as suppressing the
Model of P. gingivalis exploitation production of cytokines and chemokines.
of innate immune receptors for
undermining host defenses http://www.bio.davidson.edu/people/sosarafova/Assets/Bio307/jehodge/page05.html

The figure explains how P. gingivalis inhibits IL-12

Production to promote its survival

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704251/

Oral myiasis
Oral thrush Cochliomyia hominivorax is the causative agent of oral myiasis- the invasion of fly larvae in tissue. C. hominivorax
Candida albicans is a fungus that can accumulate on the lining of the mouth and cause oral thrush. It usually occurs in feeds on living tissue unlike the other similar parasites which only live on necrotic tissue and are usually found on
babies, people who wear dentures that do not fit correctly, people that use inhaled corticosteroids, and the corpses. C. hominivorax is an obligate parasite so it has to spend part of its life cycle on a living host. Because of its
immunocompromised. classification as an obligate parasite, it can also penetrate the skin, unlike others of its genus that usually just colonize
  open wounds. Oral myiasis is caused by the ingestion of the larvae and can also occur when the fly lays its eggs on an
The fungus has a capsule that prevents it from being phagocytosed and can vary its surface antigens. People that are open wound. When the larvae hatch, they dig into the flesh and feed on it. Maggots can invade the oral cavity
infected have a high enough concentration of the yeast in their mouth that it can be transmitted through kissing and through the periodontium (gums and bone surrounding the teeth) or the oral mucosa
saliva-saliva contact. C. albicans makes adhesins in order to bind to other yeast and to the host. It has a tropism for
salivary molecules that have been adsorbed into tooth enamel and tooth bacteria. It secretes aspartyl proteinases C. hominivorax, or the New World Screwworm, like to live in warm, tropical areas. Open wounds provide the perfect
that damage the host tissues and provide carbon and nitrogen that it needs to grow. habitat for the larvae because they are warm and provide the nutrients necessary for them to grow. After about a
  week in the living host, they no longer need to feed on the tissue and they leave the host in search for soil in which to
It colonizes through its adhesion to the host. This contact allows it to borrow and enter the pupal stage.
withstand salivary flow that flushes it out. Enzyme secretion and the formation of hyphae allow it to  
destruct and penetrate the host tissue. It binds to C3b in complement It can be treated noninvasively with nitrofurazone or surgery can be used to take out each individual worm.
and does not let the receptor recognize the C3b, therefore greatly reducing phagocytosis.
Like in most cases, most people that are infected with oral myiasis are immunocompromised

Figure 1. Adhesive interactions Fig. 1. Appearence of patient at presentation,

of C. albicans that overcome showing a indurated swelling of the upper lip.
saliva flow Fig. 2. A view of the upper lip showing the sockets
http://www.jdentaled.org/cgi/reprint/65/8/785.pdf after removal of the maggots and debridement of
http://www.nutritioninstitute.com/2.html necrotic tissue.
Fig. 3. A number of lavae removed from the
sockets.

http://www.ncbi.nlm.nih.gov/pubmed/16505789