Sore Joints and Bad Breath: What Is Going On | Felipe Andrade, M.D., Ph.D.

Sore Joints and Bad Breath: What Is Going On | Felipe Andrade, M.D., Ph.D.

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I’ll introduce the next speaker,
my long-standing colleague at Johns Hopkins and
friend, Felipe Andrade who is an expert in autoimmune
disease at Hopkins. He’ll be talking about
Sore Joints and Bad Breath, What is Going on? Felipe?>>[INAUDIBLE]
Can I can use this one?>>Sure.>>Yeah, this is easier for
me to see the slides. Okay, good morning everybody,
thanks so much for being here. And the division of
Methodology at Hopkins is focused on understanding
the cause of and the specific group of
auto immune diseases. And today I’m going to talk
about my work on this area. So this way, this way, okay. How can I move it forward? Whoops, it wasn’t me, okay. Thank you. So the function of the immune
system is to protect against environmental factors,
such as bacteria, virus. Also against malignant tumors. And some of this function is, oops, is driven by
the production of antibodies. So the antibodies
have proteins that recognize the foreign invaders,
the bacteria, the viruses. And they help the clearance
of these pathogens. And then the antibodies stay
to give a second protection if the individual is exposed
again to the same pathogen. In autoimmune diseases, antibodies are made against
normal proteins of the body. So these antibodies
can reduce damage and destruction of the different
organs in the body. So autoimmune diseases can
have different phenotypes, depending on the antibody
that is made and depending on the organs
that are being damaged. So today I’m going to talk about
my work on rheumatoid arthritis. This is a disease that
affects the joints. It causes inflammation and
destruction of the joints. It is present in about 1%
of the general population. About 1.3 million Americans
are affected by this disease which can be very
debilitating and also associated with
high mortality. So autoimmune diseases
are the consequence of the interaction of
different factors. You need to have a genetic
susceptibility, some defect in the immune system, and also
something in the environment. These are complex diseases, which they need to have all
three components to be present. So by modifying at least one of
these, it might be possible to prevent the disease or
even to cure the disease. Although there are major
advances in genetics and also in the way to
the immune system. Environmental factors are still
a major site in which we can intervene and modify and
prevent disease. Something that is interesting
is observation that it appears existing and maybe the disease
was introduced from America. This idea has brought
the hypothesis that maybe the disease has been
driven by a pathogen. Some interesting observations, which are observations from
the late 1800s and early 1900s. Is the association between
rheumatoid arthritis and periodontal disease. Periodontic disease, a chronic
inflammatory process of the gums,
which are driven by bacteria. And they have [INAUDIBLE]
diseases, not only [INAUDIBLE]. There is about. More on that, 1000 bacteria, different bacteria
that are in the mouth. Some bacteria are good. Some bacteria are bad. And identifying those that are arthritis has
been a big challenge. Something that is
a unique feature in and in fact is part of the. Is they find in the patients
have antibodies against proteins that are citrullinated. So in normal conditions, proteins can diversify their
function by being modified. These modifications look
a costume, as are shown here, in which a single protein can
make different functions by adding something,
here represented by hats. Or a mustache or glasses. So when you add this little
modification a protein can have different functions. And one of these modifications
that is called citrullination is a target for the antibodies in patients
with rheumatoid arthritis. So a part of a major focus on my lab is to understand what drives
this process of citrullination. That is important for the activation of the new
response [INAUDIBLE]. So if you analyze
the joint of a patient, something that is striking is
that all this black here but you can see are proteins are. If you compare with the second
lane in which we have a sample from a patient that doesn’t have
rheumatoid arthritis or have a different disease, you don’t
see all these black components. In fact,
from now everything that you see that is black
means striation. When we analyze the gums of
patients with periodontal disease, we found a striking
similarity between the striation that you find in the joints with
striation that is happening in the gums of patients
with periodontal disease. Meaning that maybe
there’s a connection and periodontal disease might be
a source of the protein that activates in your system. As I mentioned before,
the proline is a complexity of all the bacteria
that are in the mouth. So the easiest question
was to identify, among all the bacteria,
what are the worst that are associated with
periodontal disease. If there’s any one of these
bacteria that may be able to produce a citrullination
process, that we identify in the joints,
and also we found in the mouth. And in fact we
identify one bacteria. The name is aggregatibacter
actinomycetemcomitans. The name is complicated, took me
a month just to remember it and to pronounce the name, so
don’t worry about the name. You can just call it A A,
that is what we do. So, here in this experiment
is just to clarify these. There’s three different
strains of these bacteria, all bacteria that are known
to be pathogens to. And again, it’s a very easy
experiment you only need to be a big scientist,
you realize that it’s a huge of citullination
that this bacteria. So to understand the
significance of these finding, We develop an acid that
allows to identify by testing serum in the blood of patients, which patient has been
exposed to these bacteria. And we identified that almost
half the patients with rheumatoid arthritis have
been infected with AA. Something that was even more
exciting was that the majority of these individuals,
more than 90%, have evidence of having a genetic predisposition
for the disease, in addition of producing antibodies against
proteins that are citrullinated. Which brings together this
hypothesis of the interaction between genetics, environmental
factors, and the immune system. So the hypothesis that we are
working on is that at some time, some individuals get
infected with this bacteria. Some of these patients are going
to develop periodontal disease. Not everybody that is exposed
to AA are going to develop periodontal disease. Some are going to do it. And if you don’t have
the genetic predisposition to develop the disease, you may stay just with
the periodontal process. And only in those individuals
that have the genetics to have rheumatoid arthritis,
which are the minority. Are going to move on to
develop antibodies and to develop the disease. So identifying a pathogen is
an incredible opportunity in which we can intervene with
therapies that can either prevent the disease or modify
the course of the disease. So at this time what
we are doing is trying to define what is
the significance of the bacteria in rheumatoid arthritis. And we might be able to
target the bacteria to modify the evolution
of the resistance. Before I do the
acknowledgements, I would like to mention that this is
an incredible time for science. It’s just amazing. We have the tools. We have everything. Trouble is, almost any disease that has caused problems
to humanity for centuries. This is the perfect
time to do it, and we have the tools to do it. However, we need to have
the financial support to do it. Not only to do our research, but we need to train people that are
going to continue with our work when we might not be able to. And we need young people that
are aware that they will invest 10 or 15 years or
20 years of their life. And they will find the sources
to continue working otherwise nobody smart is
going to do the search. About acknowledgements,
some information just to people because they’re the youngest
one of the group. And many people were involved
in this work that had many situations in America and
outside of America. One is Maximilian who
is a young scientist, a young physician in fact
that came from Germany and I have the privilege
that he joined my lab. And Loreto Abusleme, that she’s
a grad student at NIH that is working with an incredible
investigator, Niki Moutsopoulos. So they are the youngest ones,
and they are the ones that are being
trained to continue with work. I also want to mention Tony who
is the leader in our division. And I won’t go in detail
because I don’t want to use too much of your time and
take some time for questions. So, thank you very much.>>[APPLAUSE]
>>Is there any question? [INAUDIBLE] Yes.>>[INAUDIBLE]
>>Say it again.>>Go to one of the mics please.>>[LAUGH]>>So in juvenile
rheumatoid arthritis, do you see the same prevalence
of antibodies against AA?>>Excellent question. We don’t know yet. We are exploring
different populations. We need to expand this to
other group of patients. We don’t know yet, but
we will know soon. And I hope that we will
may find something, yes. Excellent question.>>And what exactly
is rheumatoid factor?>>Rheumatoid factor
is an antibody. That is targeting
another antibody. That is something that is
quite interesting in fact. It is that this is the first
antibody that was discovered in autoimmune diseases in
the middle of the 1900s, around 1945. And I will say that we don’t
know which antibody it is. We don’t know how it’s
driving the disease. It’s an antibody that the
proteins that is not specific for rheumatoid arthritis. It can be present
in other diseases. However, if you have it and
you have rheumatoid arthritis, your disease can be very bad. And in our story, we find
association with both in the, with antibodies against proteins
that are citrullinated and also factors. So it appears that
rheumatoid factors and AA may also be linked somehow to
induce these antibodies, yeah.>>Hi, thank you. Is there a time connection
between when someone’s infected with a periodontal disease and
rheumatoid arthritis?>>We don’t know it yet, we will
know it in three months maybe.>>[LAUGH]
>>So we have access to samples from
individuals in which the samples of serum has been
collected just before the. So we will have an idea of the
timing in which the individual is exposed and the disease
is clinically evident. So we don’t know yet
but we will know.>>I’ll check back.>>[LAUGH]
>>Yes.>>Yeah, I was curious, some of
the news articles have connected oral hygiene with
rheumatoid arthritis. Does any of that come from this?>>Yeah we had a big
media cover for this. I think that newspapers
everywhere here and UK and other places. This is the papers-
>>Do you think supports the idea that mouth hygiene is
>>But you know mouth hygiene is
important for anything. So independent of
whether you may or not have rheumatoid arthritis,
mouth hygiene has been linked to even cancer or
cardiovascular disease. So yes, it is critical. I think that the hygiene
is something that needs to be done carefully, and you
need to be checked by a dentist. I think just doing it by
yourself is not enough. So someone needs to
keep the teeth clean. And yes, I think that a good
hygiene is important. But having a good one, and
a good follow up by a dentist, I think, is critical.>>How could these findings
with the interaction between periodontal disease and
bacterial response potentially affect the
sex specificity of RA symptoms?>>So can you say it again,
it wasn’t fully clear to me.>>So we know that rheumatoid
arthritis affects more women than men, how do
the findings relate to that?>>I don’t think that the
bacteria is going to make a big difference on that. I think that the gender
differences, the sex differences are,
which is quite interesting. Might be linked
to other factors. The immune system is quite
different in woman and in men. And woman may have a slow,
in fact, it’s known that the immune
system is more active in woman. So maybe that, and there
are some recent papers about it, which are quite interesting. So it is possible that women
are just more predisposed to autoimmunity. Because it’s not only
rheumatoid arthritis. It’s also lupus and
other diseases. It’s that women has an immune
system that is more active and therefore is more susceptible to
develop an autoimmune process. I don’t think that
the bacteria will be able to address that point. The difference of
periodontal disease is not major between men and
women, in my knowledge. So I think a correlation
to women may be explained by other factors. Yes?>>I was wondering if there’s
any evidence or any thoughts on whether susceptibility to RA
makes you more susceptible to other autoimmune diseases,
if there’s any connection there?>>What has been found is that
in families, you can have more than one patient with
rheumatoid arthritis. Or even there are patients that
have other autoimmune diseases. For example, the grandmother
have Lupus and the daughter has arthritis and somebody else
has a thyroid disease. So in autoimmune disease
it is likely that there are common genes, common autoimmune genes that may
predispose to have autoimmunity. So the addition of
external factors and other things, gender and sex, may also define which disease
you are going to develop. But this aggregation of
different diseases in families was something that we have seen. And maybe it’s driven by some
genetic common defect, yeah. Okay, thanks so much.>>[APPLAUSE]

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