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Chronic Periodontitis: Geographic Differences in the Oral Biofilm

Media: The Inside Scoop

January 2005

It has long been assumed that all chronic periodontitis is the same no matter where one lives in the world.  But some scientists have wondered whether the bacterial composition of the oral biofilm - the sticky, mat-like microbial communities that form on our teeth and cause chronic periodontitis - might vary geographically.  In the November issue of the Journal of Clinical Periodontology, NIDCR grantees and their colleagues report for the first time that this is indeed the case.  In a study of more than 300 patients with chronic periodontitis from Sweden, the United States, Brazil, and Chile, they found clear geographical differences in the bacterial content of dental plaque obtained from the periodontal lesions.  To hear more about this important paper, the Inside Scoop recently talked with lead author Anne Haffajee, B.D.S., and Sigmund Socransky, D.D.S., the senior author. Both are scientists at The Forsyth Institute in Boston.

Why did you decide to pursue the question of geographic variations in the oral biofilm?

Haffajee:  We got the idea about five years ago while conducting a study of chronic periodontitis with our collaborators at the University of Goteborg in Sweden.  What happened was we were reviewing the preliminary data and noticed differences in the composition of the biofilms obtained from Sweden and the U.S.  We said, "Oh my goodness, what’s wrong?  Why are we seeing these differences?"  It made no sense because standardized techniques were used to collect the samples, and we analyzed all of them in a very reproducible, standardized fashion here in Boston.  This eventually seeded the idea of collecting samples from other parts of the world to see whether the differences that we noticed were a Swedish-U.S. phenomenon?  Or whether there also are differences in other countries?

Is that when you started placing telephone calls to South America?

Haffajee:  Right.  We have collaborators in Chile and Brazil, and we were able to get samples from many people with chronic periodontitis in these countries.  In total, we obtained 28 plaque samples in each of 26 people from Chile, 58 from Brazil, 101 people from Sweden, and 115 from the U. S.

Socransky:  One of the study’s real strengths is all of the analyses were performed in Boston using standardized techniques.  The exception was in Brazil, but the work there was  performed by Magda Feres, who trained with us.  In fact, she spent four years learning the techniques used in this study and was running them with the same DNA probes that we used in Boston.  So, the standardization was very good in this study.

What did you discover?

Socransky:   Comparing the subgingival plaque obtained from patients with chronic periodontitis, we found marked variations in the microbial profiles from country to country.  After adjusting for age, gender, smoking status, and other factors, these differences held up.  There’s no doubt now in my mind that there are differences.  Absolutely none.

What do you mean by "differences?"

Haffajee:  What we mean is the proportions of the pathogens are different in people with chronic periodontitis from these countries.  It’s not a case, for example, that the Brazilians have a whole different set of bacterial species in their mouths compared to the Americans.  What we found was one pathogen might be very high in Brazil, somewhat lower in the Swedes - or vice versa.  So, it’s the pattern of colonization that is not the same geographically.

In this study, you looked at the colonization patterns of 40 different species in the biofilms. Why these 40 species?

Haffajee:  For most of the last 20 years, we worked strictly with the bacteria in culture.  Based on this work, we consistently found 40 species were dominant in the oral biofilm.  These species include, just to name a few:  Porphyromonas gingivalis, Tannerella fosythia, Treponema denticola, Prevotella intermedia, and Capnocytophaga gingivalis

Some people would say, "but there are 600 or 700 species in the oral biofilm."

Socransky:  That’s an important point.  Sure, there are perhaps 600 species, but they aren’t uniformly distributed.  It’s sort of like saying that in New England forests, there are a large number of mammals.  But the number of wolves and bears is far less than the number of, say, foxes and rodents.  They are absolutely not uniformly distributed.  This is true in any ecosystem.  Some species are extremely high in number in that ecosystem, others in moderate numbers, and others are very low in numbers.  And, that’s true of bacterial species in the mouth.  Based on our many years of experience, we are quite confident these 40 species represent about 60 percent of the bacteria in the microscopic world of the mouth, which we call the oral microbiota.  They are clearly the dominant species.

If it’s the proportions of pathogens that matter, what does this mean for treating chronic periodontitis?

Haffajee:  Our findings suggest that because different microbial profiles are found in oral biofilms throughout the world, treatment responses with a given therapy might be different geographically.  What we want to know now is:  Which treatment works best for a given microbial profile?  We want to find the right treatment for a given infection, instead of what we do at the moment, which is to give everybody the same therapy.  Our goal is to be in the position one day to say, "Well, no, this patient will do very well with Treatment X, but this other patient will not.  That patient needs Treatment Y."   We’re not there yet, but we’re headed in the right direction and can start to ask more insightful questions.

What are some of these questions?

Socransky:  We need to know, for example, if a person moved from Stockholm to Boston, how long would it take until the microbiota changed to what we typically see here at Forsyth?  Or, would it change at all?  Another question is:  If you visited a remote, isolated community, would the microbiota be similar in each person?  What about people who live in cities, which often are  melting pots of race and ethnicity?  And, what’s the role of diet on the biofilm?  Do people from fish-eating cultures have a different oral biofilm than their counterparts in a meat-eating society?  In a nutshell, what are the differences?  How do these differences occur?  Why do they occur?  And, can one explain them?    
Haffajee:  A different but related question is:  What is the baseline composition of the oral biofilm in healthy people throughout the world?  Our group has a paper in press in which we compare the oral biofilms of healthy individuals in Sweden and the USA.  Interestingly, we found microbiologically marked differences.  The populations examined were primarily Caucasian whites in both cohorts.  But, what’s interesting is the difference between the two populations was substantial.  The bottom line is:  The microbial differences are NOT confined to disease.  You see them in healthy individuals as well. 

How much was known previously about these geographic differences in the oral biofilm?

Haffajee:  Not a great deal.  A few small studies in Asia and Europe had suggested possible geographic differences.  The problem was these studies were not particularly comprehensive.  They looked at maybe a handful of bacteria present in the oral biofilm.  As a result, it was tough to draw any fast conclusions from their data.  What’s different about our study is it is far more comprehensive in that we studied 40 bacteria.

What enabled you to look more comprehensively?

Socransky:   A lot of it has to with the DNA-based techniques that we employed.  These tools, which only have emerged over the past decade, greatly enable these types of comparative multinational studies.

Why’s that?

Haffajee:  If we had attempted this study using culture techniques, we would have had to plate the samples almost immediately or risk losing a lot of the species in the biofilm.  This would have made a comprehensive analysis extremely difficult, both scientifically and logistically.  With the DNA-based techniques, an investigator can collect a sample in Chile, for example, place it in a tube with buffer, stabilize it with sodium hydroxide, then send it to us in Boston for analysis many weeks or months later.  That helps tremendously in standardizing the methodology and, because these DNA-based techniques are performed rapidly, we can greatly expand our scope of study to include multiple samples collected from the same mouth or to detect a wider array of microorganisms.  To give you an idea, a few years ago using culture methods, we might look at a couple hundred samples a year.  Now, with these DNA-techniques, we look at tens of thousands of samples every year. 

In this study, you used a technique called "checkerboard dna-dna hybridization" to measure the presence or absence of the 40 bacteria in question. Tell me about this technique? 

Socransky:  We actually have just published a paper on this technique in the December 2004 issue of the journal Oral Microbiology and Immunology [insert link].  This particular technique is automated and very, very rapid, or as we say "high throughput."  It allows us to look at very large numbers of samples from different clinical conditions, both before and after therapy.  As far as I know, we have a throughput that’s really not matched in studying microbial infections anywhere.

Socransky:  Well, in terms of the numbers of samples that we can process.  We can look at so many more samples to than we could using culture, immunofluorescence, or by real-time PCR  detect microorganisms.  The throughput is at least an order of magnitude beyond those for the same labor and cost.

So, although the periodontal diseases have been studied for many years, it’s an exciting time in the field right now.

Socransky:  Absolutely.  I think in the last 10 years, there has been far more accomplished in understanding etiology, pathogenesis, ecology, and therapy of periodontal disease than in the previous 100 years.  That’s by a long shot.  It’s not even subtle.  And, a lot of that has to do with the better techniques now available to us. 

And now researchers are in the process of delivering those molecular discoveries to the clinic?

Socransky:  That’s our hope, and I think there is good reason to be optimistic.

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This page last updated: February 26, 2014