For too long, “a little bleeding” has been minimized or accepted as normal—but Dr. Mia Geisinger makes it clear: bleeding is a sign of inflammation, and inflammation matters. With dozens of systemic illnesses linked to or exacerbated by periodontal inflammation, dental professionals have a critical opportunity to help patients understand that periodontal health is not just about saving teeth—it is about supporting whole-body health.

In this episode, Dr. Geisinger breaks down the science, the responsibility, and the opportunity we have as clinicians to collaborate with our patients, improve periodontal outcomes, and reduce the oral inflammatory burden that may contribute to systemic disease. If you have ever struggled to get patients to take bleeding gums seriously, this conversation will give you the language, confidence, and clinical perspective to change the way they see their oral health.Tune in for a compelling episode that reminds us why periodontal health is no longer optional—it is foundational.

Episode transcript:

Brian Novy: 
So speaking of perio, Dr. Mia Geisinger, some people don't know who you are. They don't know that you're the past president of the American Academy of Periodontology. But Pam and I know who you are. And now you have a new position. So do you want to tell our audience who you are? 

Mia Geisinger: 
Sure. My name is Mia Geisinger. I am a board-certified periodontist. I am the chair of the Department of Periodontology here at the University of Alabama at Birmingham. I'm the Kent and Phoebe Pugh Canizaro Endowed Chair in Periodontics. I am the immediate past president of the AAP, which is the best job in show business because I can sit back and kind of watch the show and watch other people in the limelight, which is very nice. 

I've recently been tapped by the American Academy of Periodontology Foundation to chair a new initiative that they have coming up that's really focusing on research and education in the oral-systemic space. It is the Levi Richmond Initiative through the AAPF, and so I'm very excited about that. It gives you an opportunity to talk about one of my favorite things, which is the oral-systemic connection. 

Pamela Maragliano: 
And it's such an important thing to be talking about. And it's something that I think we, as practicing dentists, should be talking about day in and day out with our patients. The fact of the matter is, Americans aren't periodontally healthy. We're just not. 

Can you share some stats that are out there that I think should hit home for most of us that are driving to work right now? 

Mia Geisinger: 
Yeah. So if we look at adults in the US—individuals over the age of 30—about 42.5% of US adults have some form of destructive periodontitis. It's about 65 million Americans. It's about twice as common as diabetes mellitus and three-and-a-half times as common as coronary artery disease. 

We all know someone who has diabetes. We all know someone who's had maybe a heart stent or is on medication for coronary artery disease. But we often don't either know or acknowledge that we know people who have periodontitis, and it is extremely common. 

On a global scale, it affects an even larger percentage of the population than just that 42%. And severe periodontal disease—the type of periodontal disease where individuals are at significant risk of losing teeth or even their entire dentition—affects about 15% of the population globally. 

Pamela Maragliano: 
And it's not just about teeth. I feel like you'd have to be kind of under a rock if you didn't know that oral inflammation ties to the rest of the body. But for those who could use a refresher, can we talk about, I don't know, just a few of the 57 systemic illnesses that are exacerbated by poor oral hygiene and oral inflammation?

Mia Geisinger: 
If you have a bingo card, I may be in trouble if I miss one or two. But, Pam, you're absolutely right. When we think about this interconnection between periodontal disease and systemic disease, there is significant data to link periodontal disease to at least 57 systemic diseases and conditions. 

Really, the two mechanisms that we see are a common inflammatory burden. Inflammation in your mouth affects inflammation throughout your body, and chronic inflammation in particular is really deleterious to many, many of these chronic conditions. But also through the microbiome. 

There are diseases that have maybe a heavier emphasis on one of those two mechanisms than the other. So, for example, dementia has been linked to periodontal disease through both the inflammatory pathway, but also because a really landmark study out of the University of California, San Francisco demonstrated that virulence factors and proteins from Porphyromonas gingivalis are found in brain tissue and cerebrospinal fluid from individuals with Alzheimer's across the board. 

Similarly, research in rheumatoid arthritis has shown that P. gingivalis, again, is the one organism other than humans that can take an arginine amino acid residue and replace it with citrulline. These citrullinated proteins are, in fact, a huge autoimmune target that triggers rheumatoid arthritis. So in susceptible individuals, when there is P. gingivalis present and these citrullinated proteins, it can tip the scales into frank RA. 

Of course, many of us learned in dental school or in CE courses about things like osteoporosis, pregnancy outcomes, diabetes mellitus. But now we're learning about things like oral cancer, esophageal cancer, pancreatic and gastric cancers, all linked to specific periodontal organisms and periodontal inflammation.

Things like Crohn's disease and ulcerative colitis are tied to oral inflammation and oral microbiome changes, and there are other, maybe more obscure or less well-recognized conditions. 

There isn't evidence that periodontal disease has a mechanism to be a causative agent for things like kidney disease. But in individuals with kidney disease, when they have periodontitis, they are much more likely to have serious morbidity and mortality—to actually die at a more frequent rate. 

During the COVID pandemic, we found that having a history of periodontitis was linked to up to a ninefold increase in hospitalization and death versus individuals who are periodontally healthy. 

So this body-on-fire mechanism—this common inflammatory burden, the thought that your mouth is connected to the rest of your body and that it's not Las Vegas. What happens in your mouth doesn't stay in your mouth. It travels from your mouth throughout your whole body, and it impacts all of these other systems that we really have been treating in isolation and treating the mouth as sort of its separate, hermetically sealed, encapsulated thing, when it is part and parcel of overall health and overall wellness. 

Brian Novy: 
Mia. As I'm listening to you talk, I can't help but think about the red complex and the colored complexes. Are we still thinking in terms of colored complexes, or what are we thinking? 

I know we just got this new periodontal staging system, which I'm still trying to wrap my mind around. And to our listeners, I'm with you all going, bad things happen to general dentists who start tangling with periodontists on these issues. 

I feel like the odd man at the party wanting to say, "But what about caries?" And I'm not going to do that.

But I do want to know, from an etiology perspective in perio—because I haven't sat in a perio class—where are they thinking in terms of etiology? 

Because I remember learning about Porphyromonas gingivalis in dental school and the complexes. But you're talking specifically about Porphyromonas gingivalis and its constituents being found in the brain, and this is fascinating. I mean, this is really, really, really cool.

But how do I put this in the context of my old thinking system of these colored complexes? 

Mia Geisinger: 
So you're right to think about those colored complexes, but it's part of the story, not the whole story. So it sort of builds across the spectrum, and you think about it like how plaque builds in the mouth. The initial colonizers are going to be your green complex—your early colonizers, your least pathogenic bacteria. 

Then you get secondary and tertiary colonization with your yellow and your orange complex. And when we have those deep probing depths, those sites where we see disease progression, we are much more likely to see those red complex bacteria, which is Tannerella forsythia, Porphyromonas gingivalis, and Treponema denticola. There will not be a quiz. I will not make you spell them. 

Brian Novy: 
Where is Fusobacterium nucleatum in there?

Mia Geisinger: 
Ah, such a good question. So we circle back. Fusobacterium is in the orange complex. 

One of the things that we are learning is because dysbiosis is really the crux that we focus on now—not just the presence of individual bad-guy bacteria. It's that shift from health to disease. 

So that orange complex, those quaternary colonizers where you have bridging organisms that can allow for the late facultative and strict anaerobes in the red complex to then populate those deep probing depths, are probably the best predictors and the best harbingers of a patient moving from severe gingival inflammation, gingivitis, to destructive periodontitis. 

So if we were looking at it now, it's really that shift toward a more and more anaerobic, more and more dysbiotic biofilm rather than any one individual bacterium within that biofilm.

Once you have established periodontitis and you have niches for these facultative and strict anaerobes in the red complex—and some of them in the orange complex as well—to take a foothold and really be in a protective environment, then there's that ulcerated epithelium inside the periodontal pocket that allows them to translocate and induce bacteremias throughout the whole body. 

And that's how those bacteria get to places like your synovial capsules for rheumatoid arthritis or your cerebrospinal fluid and brain tissue, particularly in the presence of inflammation, where we have leakier barriers—both the blood-brain barrier and some of these other protective barriers that protect those organs and spaces within the body.

Pamela Maragliano: 
I still have to ask, though. I know we're not talking specific bacteria, but I do have to check in with our friend Actinobacillus actinomycetemcomitans. 

I'm so glad you're talking about AA anymore. I know PG is the nasty one, but AA was always something that used to come up all the time in classes. 

Mia Geisinger: 
So AA actually lives outside the complexes, particularly AA serotype B. It's its own non-complex bacterium, and it is highly associated with a very rapidly progressing form of periodontitis, particularly one that affects people circumpubertally and affects the first teeth to erupt in the mouth.  
So, in teenagers—13 to 15—and it affects the first teeth to erupt in the mouth, so first molars and incisors preferentially. 

In the updated classification system—it's nine years old now—this is captured as a Grade C, so a rapidly progressing periodontal disease, and the distribution is captured as molar-incisor distribution.

But because AA is so highly associated with that one form of disease in that particular patient population, we also know that we have an advantage of being able to use antibiotic therapy adjunctively with some of the nonsurgical and surgical treatments and improve our outcomes for those patients, because AA is very responsive to a combination of amoxicillin and metronidazole. 

Brian Novy: 
Is it? Well, that's lucky. 

I didn't mean to say that flippantly. Thank goodness we're not saying, "It doesn't respond to amoxicillin or clindamycin or metronidazole. This stuff is just nasty." 

At least we're not saying that, right?

Mia Geisinger: 
Yeah. There's been some work done by Daniel Fine in large cohort populations in Newark, New Jersey, looking at kids who are eight years old. 

Before we actually see the destruction, if eight-year-olds have five-millimeter pockets on their molar teeth—even without bone loss—and the presence of AA, and you treat them with nonsurgical therapy and antibiotic therapy with amoxicillin and metronidazole, you can significantly decrease the risk if they develop that molar-incisor pattern disease. 

Brian Novy: 
An eight-year-old with a five-millimeter pocket on a first permanent molar.  
Just hearing you say that, I'm more worried about what hygienists are pocket probing eight-year-olds. 

Mia Geisinger: 
Well, that's one of the things that I always think about. 

We really probably should, at least for eight- and nine-year-olds before they get to that onset of puberty, be doing one comprehensive periodontal exam. 

Of course, for adults, the American Academy of Periodontology recommends that we do an annual comprehensive periodontal exam.

But at least we should have baseline data in kids to be able to identify those higher-risk individuals, particularly if they have a family history of aggressive periodontal disease on those particular teeth or early tooth loss of first molars or incisor teeth in first-degree relatives.

Brian Novy: 
So how can you identify these patients early? 

Can you identify them with something like a BANA test or some other test that starts predicting? 

It sounds like it'd be great to do a—I don't know—a Bristle test and find out, do they have AA in their mouth, period? 

I guess there are tests that are available for that right now. 

Mia Geisinger: 
Yeah. There's been some studies on salivary testing, particularly in higher-risk patient populations. 

That particular form of disease has a significantly higher prevalence in African American populations and Asian/Pacific Islander populations versus other ethnic and racial groups. 

So in those patient populations, and in patients who may have other risk factors, doing salivary testing is one of the things that's being examined as a screening tool for patients who may be developing that type of more aggressive or rapidly progressing periodontitis. 

Pamela Maragliano: 
So we're in practice, and we're probing an eight-year-old and we find a five-millimeter pocket. You tell the parents that there's an increased risk for this child developing periodontal disease when, honestly, I would say from a consumer standpoint, they're wondering if they have any cavities. 

And you say, "Okay, if I put them on an antibiotic"—and, I mean, amoxicillin and metronidazole is really no joke as far as antibiotics. 

How do you get parents behind that? What's the conversation that you have to have to get them to say, "I know they're at an increased risk," because increased risk doesn't necessarily mean you have it. We like to keep things at arm's length, right? Just because we're at risk doesn't mean we're going to get it. And, you know, "Not my child." 

I feel like, how do we have that conversation?

Mia Geisinger: 
So my first step wouldn't be to move to an antibiotic prescription. 

My first step would be to move to testing the bacteria because it's really the combination—at least in Dr. Fine's work—the combination of that five-millimeter pocket and the presence of AA that increases the risk. 

So it's not a five-millimeter pocket alone, but it's those two things together that have an increased risk. 

So if you saw those two things together, then thinking about: Are these patients that we should be monitoring more closely? Are these patients that should have more frequent maintenance and recall visits?

For me, as a periodontist, one of the most heartbreaking things that I see in my practice is a 16-, 17-, or 18-year-old individual who is referred for a periodontal defect on a first molar tooth. 

When I request the bitewings, I can see the bone loss for four, five, and six years going back. It was present, much less severe, and much easier to arrest and treat at an earlier time point. 

So if we're aware that there's that increased risk, we can surveil in different ways. We can make sure we're doing annual comprehensive periodontal exams. And at the earliest signs of attachment loss, we can do scaling and root planing, nonsurgical therapy, with the adjunctive advantage of antibiotic or antimicrobial therapy to hopefully arrest disease before we have these big defects that can jeopardize the longevity of those teeth. 

Pamela Maragliano: 
So I'm going to say something that's going to sound a little crazy. 

We recommend three- to four-month recalls on probably 95% of our patients in the practice because biofilm—specifically periodontal pathogens—takes about 90 days for that biofilm to mature. 

And so we, as a profession, are constantly chasing this inflammation. 

Even when I was a hygienist, I just kind of accepted that everybody, even my healthy patients, bled a little bit somewhere. At least there was a little blood on a two-by-two by the end of that appointment somewhere. 

And it really doesn't have to be the case. 

So I think when we find these susceptible populations, or these children who are presenting with these gross amounts of biofilm and inflammation, or our orthodontic patients that we've accepted are going to have gingival hypertrophy around their orthodontic brackets, we don't have to accept that. 

We can have them come in more frequently, and we're not going to get struck down by lightning. 

Mia Geisinger: 
And that twice-a-year number is really from a toothpaste advertisement from the 1930s. So that is not an evidence-based way to make decisions, both from a profession standpoint but also from those payers, where the insurance companies have basically said, "Well, twice a year is the right amount of time to see your dentist." 

Of course, there's no other chronic disease where we would say, "Everybody gets the same schedule." Whether it's diabetes or heart disease or whatever, we would base it on the patient's disease severity and symptomatology. 

One of the things that I often talk about with our medical colleagues is this: 

If you have a patient with moderate periodontitis—a patient with five- and six-millimeter probing depths at, let's say, 30% to 50% of the sites in their mouth—and those probing depths bleed, the surface area of that bleeding, ulcerated, non-healing chronic wound is about the size of the palm of your hand. 

Well, if I'm diabetic and I have a non-healing diabetic ulcer the size of the palm of my hand anywhere else on my body, I'm being seen weekly. I'm having wound care at home. I'm being told to change my dressings. I'm going in regularly. I may have adjunctive PRF applied to the wound to improve wound healing. I'm having debridement performed on a regular basis. 

And yet we're okay saying, "Actually, you get two cleanings a year, and if you want to meet the standard of care for at least four cleanings a year, you have to pay out of pocket." 

Because that's the way the rules were written years and years ago. 

And it's not an effective way to manage chronic conditions. 

Brian Novy: 
So managing the chronic condition—let's talk about that because not all our patients can actually reach us, right?

When we see 40% to 50% of the population that actually sees an oral healthcare provider, 50% of the population is living out there. 

I'm going to assume I'm going to go differently than the payers do, because the payers say, "Well, if they're not seeing a dentist, they must not need care." 

And I would say, "No. If they're not seeing a dentist, it's because they're terrified, and you need to do a better job of getting them routed to a provider who will." 

Mia Geisinger: 
Or they don't have coverage, or they don't have access, or their life has gotten in the way. 

Brian Novy: 
But even the patients who do have coverage, we know that only about 50% of those patients actually go and receive care. 

The majority—that's why insurance companies make money—is because most patients aren't getting the care. 

But you're managing a chronic disease, and we all agree these are preventable diseases that can be managed at home. 

I want to put you on the spot, and I want you to go back to the '70s. 

How did you feel about Paul Keyes and the Keyes technique? 

Mia Geisinger: 
This is a blast from the past. So for anyone who was not alive in the late 1900s, let me give you a little Cliff Notes version of what the Keyes technique was. 

The reason why you can walk into CVS or Walgreens or Walmart and buy a baking soda-flavored toothpaste is because there was a particular dentist-periodontist in the 1970s who promoted this intensive form of oral hygiene called the Keyes technique. 

He used a slurry that was made of both baking soda and salt. Patients were instructed to brush for 20 minutes twice a day.

They also came in every two to three months for professional debridement in his office, and he used dark-field microscopy—a type of subgingival sampling where he would go in, take plaque from underneath the gumline, look at it under a particular filter on a microscope, and if he saw things moving—and the moving ones are the Treponema, the spirochetes, the real bad guys underneath the microscope—he would put those patients through either another round of nonsurgical therapy or surgical therapy to try to eliminate those bacteria. 

As it turns out, if you spend 40 minutes a day delivering oral hygiene, it probably doesn't matter what you put on your toothbrush, whether it is baking soda or an inert sugar-free paste. 

If you spend 40 minutes a day mechanically debriding your own teeth, you will have better oral health than someone who spends, on average—as the average patient does—about 1 minute 56 seconds total daily on oral hygiene. 

The recommendations are two minutes twice a day. If you add another minute for flossing, that's five minutes a day. 

The average patient spends less than two minutes, and on average about 4% to 8% of the overall population flosses on a daily basis. 

Probably most of them are listening to this podcast. 

Brian Novy: 
Yeah, 4% to 8% of the population. Wow. 

So...you can brush your teeth with baking soda 40 minutes a day. 

Mia Geisinger: 
You could, or you could use a fluoride dentifrice, which is what I recommend—particularly stannous fluoride because it has an antigingivitis effect and an antisensitivity effect, too. 

I think you kind of get a triple whammy for your bang for your buck. 

From our perspective, I agree with you. 

When we talk about the two most common dental diseases—dental caries and periodontal diseases—the treatment is not a filling. The treatment is not scaling and root planing. 

The treatment is disrupting oral dysbiosis. 

It is removing that oral biofilm. 

That can't be done every three months or every two months or every month. It has to be done on a regular basis through effective home care. 

Then we as professionals can support that through biofilm control in our offices, through debridement of subgingival areas. 

But effective home care is really critical to managing both of those diseases. 

Pamela Maragliano: 
So with the last few minutes that we have here, I have to say that I don't want to say we were doom and gloomy about periodontal disease and caries. 

Because I think right now is a pretty exciting time to be an oral healthcare professional. 

We do know there's this oral-systemic link, and there's a lot of education that we can provide our patients. 

Back in the day, we'd see bleeding and we'd tell them to brush more, floss more, something like that. Now we see patients wearing monitoring devices—Oura Rings, watches, all of the things. There is more engagement with patients and them owning their own health conditions. 

So how do you increase value with patients to get them to do what they need to be doing at home and see us as a partner in health as opposed to somebody who's just going to slap them around because they're not flossing? 

Mia Geisinger: 
This is such a great question because I never want to guilt anyone when we're diagnosing them with periodontal disease. 

I want to talk about what we can do moving forward. Like I said, some of the hardest conversations I have are, "Why now?" Why am I just being diagnosed now? What I like to say is: 

"We've been monitoring your..."—and then insert whatever we're monitoring. 

Because of those changes, or because we haven't seen resolution, we're now making additional recommendations. 

One of the really interesting things about what we're learning regarding the oral-systemic connection, particularly with periodontal disease and chronic systemic health conditions, is that this is a big motivator. 

Patients want to be healthy. They want to live longer, more active, healthier lives. If we can take the time as oral healthcare professionals and dental teams to educate them about the importance and impact that oral health can have on their overall health—and their ability to control things like glycemic control, reduce vascular inflammation, reduce the risk of heart attack and stroke, and reduce their risk of developing dementia over time by maintaining good oral health throughout life—it becomes a very worthwhile investment. 

It's worthwhile to come in and get the biofilm therapy that you offer in your office, Pam, or to come in more frequently and see the periodontist for regular periodontal maintenance visits because it's an investment not just in maintaining your teeth, but in maintaining your overall health. 

Brian Novy: 
It's everything I know to be true.

I'm sitting here thinking, what's the future? Do you ever listen to This Week in Microbiology, by any chance? They absolutely drive me nuts because they get dental biofilm, plaque, and oral microbiology wrong. 

I feel like they need to have you on their show, Dr. Geisinger, because I think you could set them straight. 

I want to facilitate an introduction to you and the folks at This Week in Microbiology because I scream at the podcast when they're talking, and I think you have a lot to offer them. 

I still can't help but wonder: What do you see as the future of perio? I've heard them mention phage mouthwash. What do you know about phage mouthwash?

Mia Geisinger: 
There's a whole host of chemical agents that are promoted to improve or reduce oral dysbiosis. 

One of the things that we currently understand is that because it's a biofilm—and not individual planktonic bacteria—mechanical disruption and mechanical removal are still critically important. 

It's interesting because when I talk to my medical colleagues—and my husband is a physician—I sometimes ask him, "What did they teach you about teeth in medical school?" 

He'll say, "They're the white things you look past to see the tonsils." 

I remember taking every medical class—every physiology and anatomy class—with my medical colleagues in dental school. 

It's sort of a foreign concept to them. They'll ask, "If it's a bacterially mediated disease, why can't you just give antibiotics to clear it up?" Sometimes they ask the same thing about caries. I have to explain that because it's a biofilm disease, you would need about 7,000 times the concentration of antibiotic, and that would kill the human taking it. 

I think we have some tremendous opportunities in dentistry. I mentioned the Levi Richmond Initiative.It really has two prongs. One is education, where we're spreading the word to both the general public and our medical colleagues about oral-systemic interactions. 

We're tying those efforts to disease awareness days. 

There was recently one focused on smoking and periodontal disease and how smoking affects oral health, but also how oral bacteria can increase the carcinogenicity of components in cigarettes and nicotine. Many oral bacteria can transform nicotine into certain nitrosamines. 

Those are much more highly carcinogenic and increase the risk for oropharyngeal and esophageal cancers. 

We'll also have upcoming educational initiatives related to endocrine disorders, metabolic syndrome, obesity, diabetes mellitus, cardiovascular disease, and pregnancy outcomes. 

The second part is partnering with industry—specifically PDS—to look at big data within the medical-dental integration space. 

We're looking at AI-driven deep-learning analyses on the interaction between periodontal disease and systemic disease, and what happens when we treat periodontal disease. 

Finally, the initiative is sponsoring research into the underlying mechanisms so that we can eventually make definitive statements about causation for some of these diseases that are currently linked to periodontitis. 

We also want to expand the evidence base so we can go to our medical colleagues—and even insurance carriers—and demonstrate that for some patients with lifelong chronic diseases, paying for oral healthcare may actually save money. 

Pamela Maragliano:

Where can people follow you? You're always doing so many things that it's hard to keep up. 

Mia Geisinger: 
If you're interested in learning more about the Levi Richmond Initiative, you can go to periofoundation.org. 

If you're super interested and want to talk nerdy about perio with me, you can follow me on Instagram at @MiaGDDS. 

My next CE speaking engagement is at the Florida Dental Convention, so I'll be in Orlando in a few weeks. 

Brian Novy: 
Thank you, Dr. Geisinger. I appreciate it. 

Pamela Maragliano: 
Yeah, this was amazing. All right, Mia, thank you so much for joining us. 

Everybody out there, thank you for joining us this week on Dentistry Unmasked, and we'll see you all next week. 

Brian Novy: 
Go put your masks back on.