There is a ton of literature, but I zoned in on just a few articles/studies
here. This is from an article by Larry Millikan, MD in 2003:

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http://www.medscape.com/viewarticle/448505_print

"Evidence supports the theory that patients with rosacea experience a
hypersensitivity reaction to Demodex mites or their products.[1]
Immunohistochemical findings suggest Demodex mites may trigger a
delayed hypersensitivity reaction in rosacea patients with mite
infestation.[17] An infiltration of lymphocytes has been documented in
rosacea patients with Demodex infestation.[1,17] These immunologic
reactions probably contribute to the formation of papules and pustules
(Figure 3).[1,2,5,9,12,17,18]"
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Demodex Hypersensitivity is actually implicated in Figure 6. "Proposed
inflammatory pathophysiology leading to symptoms of rosacea." aboout
2/3rds the way down in the article.

Anyway, as we know, a recent study through the NRS supports a
hypersensitivity reaction (below). I wonder if, for some, demodex
associated effects could be the initial triggering factor in this
process:

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"Allergy-like reaction may trigger inflammation in rosacea
Dr. Richard L. Gallo, associate professor of dermatology and
pediatrics at the University of California - San Diego, and Dr. Kenshi
Yamasaki, Veterans Medical Research Center (2006)

The bumps (papules) and pimples (pustules) of rosacea, a widespread
facial disorder affecting an estimated 14 million Americans, may be
the result of an allergy-like reaction to environmental and emotional
triggers, according to new study results presented at the National
Rosacea Society (NRS) research workshop during the annual meeting of
the Society for Investigative Dermatology in Philadelphia. The seventh
annual NRS workshop was attended by more than 130 medical scientists
from around the world.

"We are very excited about these findings because they may provide the
basis for improving the treatment and management of this condition,"
said Dr. Richard Gallo, chief of the division of dermatology at the
University of California-San Diego and lead investigator of the NRS-
funded study. "By defining the process leading to the inflammation,
new medications might be developed to block these effects."

Dr. Gallo explained that when the normal immune system is faced with
any of a broad range of potential dangers -- such as sun exposure,
emotional stress, heat and spicy foods, among many others -- receptors
recognize potential danger and protect the body by prompting the
production of protective substances that isolate and neutralize any
harmful effects. With rosacea, however, these protective substances,
like overzealous guards, turn the body on itself, leading to
inflammation.

Using advanced mass spectrometry technology to analyze the biochemical
composition of proteins in rosacea patients, the researchers
discovered an abnormality in the production of protective molecules
known as cathelicidins, Dr. Gallo said. In normal patients, the
cathelicidins are found in a form that is inactive and would not lead
to bumps and pimples. In rosacea patients, the forms of cathelicidins
are different and lead to skin inflammation. The cause of this
abnormality in cathelicidins seems to be due to an equally important
problem in rosacea -- an overabundance of yet another substance,
called kallikrein, which can spur dormant cathelicidins into action.

"It appears that the combination of these two substances at abnormally
high levels is a double whammy for rosacea patients," Dr. Gallo noted.

The researchers recently completed the picture when they were able to
demonstrate that this process is linked to the actual formation of
rosacea signs and symptoms. The skin of mice injected with the
cathelicidins found in rosacea patients showed a dramatic inflammatory
response -- including bumps and pimples -- while mice injected with
normal cathelicidins showed no inflammation, either visually or under
a microscope.

"The next step is to test these findings in human subjects through
various therapeutic interventions," Dr. Gallo said. "As we gain a
thorough understanding in humans, we can look for new medications that
block this process in order to treat or prevent the inflammation
associated with rosacea."
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..and then the chronic inflammation leads to vascular changes. I think
this article explains this part well:

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"From the Department of Pathology, University of Massachusetts Medical
School, Worcester, Massachusetts
-....The contribution of blood vessels to inflammation can be divided
into two phases. In the first phase, which lasts roughly 24 hours,
functional changes prevail: dilatation, increase in permeability,
activation of the endothelium, and diapedesis. In the second phase,
although some of the functional changes persist, structural changes
occur...
-.... Thurston et al find that the microcirculation responds to the
chronic stimulus either by producing more capillaries or by dilating
existing ones....
-... The observed capillary dilatation is more surprising than it may
seem because it has been known since Cohnheim (1867)5 that capillaries
in acute inflammation do not dilate significantly despite the
increased blood pressure. Something else must therefore be happening
to the capillary wall in chronic inflammation....
With time, the endothelial cells in the dilated capillaries of the
inflamed trachea multiply......At this point the dilated capillaries
acquire functional properties of venules and a sort of metaplasia
takes place.
For both new vessels and old ones made larger, Thurston et al report
that permeability to Evans blue appears to be in the normal range;
however, both types of vessels are more susceptible to a permeability-
increasing mediator, substance P. This finding is of interest for the
pathophysiology of chronic inflammation as it suggests that newly
formed or remodeled vessels could be maintained in an activated and/or
leaky condition with doses of chemical mediators too small to affect
normal vessels.."
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I wonder if, for some, the problem could be as simple as demodex and/
or bacteria it carries causing a chronic "allergic" reaction ("
neutrophilic dermatosis" as stated by Millikan) in those susceptible,
leading to chronic inflammation and resulting vessel changes.

Cheers!

Artist