Biofilm and Capsular Contracture

Hey everybody, um, just getting started. Everybody hop on, we'll get going promptly here in a few moments. Just getting loaded up on all the platforms. Get a little delay seemingly on, um, hi Danielle, on, uh, TikTok for whatever. Reason I don't know what's going on. We'll see. We shall see what's going on on TikTok. I don't know. All right, here we go. Everybody get loaded up. Gonna talk about biofilm and capsular contracture tonight. Oh, can read my own talk for a moment. All right, biofilm and capsular contracture. We did this as a follow-up to my talk last week about genes and capsular contracture. See if I can misspeak here a couple times about capsular contracture. All right, share this around if you know somebody who has a problem with capsular contracture. So that's firmness, hardening of scar tissue around an implant. It's very important that you have a working understanding of that. All right, share it around. Capsular contracture, biofilm, that's what we're going to talk about tonight. You can watch us live on Instagram, TikTok, YouTube. Facebook, LinkedIn, X, Substack. My Rumble feel, uh, feed failed, so can't see it on Rumble tonight. And, um, yeah, let me know if you have any audio, you know, problems. I can do, um, a couple setups where we're getting good or better audio. Um, Let me know if there's any trouble hearing me. I'm gonna put on an extra mic tonight so we can do a little bit, uh, more recording. Or I'll just take over the sound so it sounds better. Oh boy, sorry about that. I'm gonna put in an extra mic on Instagram. Oh, come on now. There we go. All right, should have better sound on Instagram. How do I sound on Instagram now? Probably better. Hi everybody on TikTok. Thanks, Anna B. Thanks, Susan, for joining. Share this with a friend. Everybody can learn a bit more about capture contracture, potential options and causes and We'll try to discuss as many things as I can. We'll give a talk and then go into my private circle. Circle is easy to join. You got to go to drrobscircle.com. It's free to sign up. It's not as loud. Okay, that's weird. Huh. How about now, Danielle? It's good. Somebody tell me if it's loud or no. Okay, I have an air filter running. Let me turn that off. Should be better now. I forgot I had my air filter running. I like my clean air. Okay, yeah, everybody who wants to go to the circle, I'm live streaming in my community. Hello Diana, hello Joan. Um, why is the broadcast not playing in my Oh, there it is. Yeah. Okay. Yeah, I'm live in the circle as well. So I'll give the talk and then we'll take a couple questions off of the platforms and then we'll go into the circle. So you go to drrobscircle.com, D-R-R-O-B-S-C-I-R-C-L-E dot com. Every time I type that, I mess it up. So I rely on somebody way, way Smarter. Oh good, on TikTok somebody said, I need a doctor. That's always helpful. All right, let's get going. All right, so the talk tonight is about biofilm and capsular contracture. So biofilm does not explain every single problem. So the more useful question is, what are the microbial signals we detected in the samples of the patients we took care of, and how do we interpret those results, and how do we understand them, and what can we learn from them and help our patients? So we will separate, obviously, samples from patients, and we want to separate detection from an infection and association from causation. There's a lot made about direct implications that I find on implants and I think obviously I like to follow the evidence and see where it leads us. So the distinctions are where we really need to, you know, make strides and try to close out gaps. So I'm Dr. Whitfield. I'm in Austin, Texas. I want to thank you all for joining me tonight. You know, our paper looked at 694 samples. So we looked at what biofilm, how it showed up in our practice, because I had this frustrating experience in 2018 where I took care of somebody and did a conventional culture and it showed nothing. But I was a little bit taken aback because I know better than that. I've been in practice a long period of time. I knew there was something else wrong. So Although biofilm doesn't directly implicate a cause and effect relationship with capsular contracture, it certainly can be a contributor. So obviously, I'm the first author of that paper, and I was the physician who collected all the samples in that study. So we did those all sterilely, implants on the back table, case was done. And we're going to try to go through the data and try to make sense of it for you and try to help you better understand, you know, capsular contracture. And this is educational only. It's not, you know, me giving you specific medical advice on your situation. Always try to help everybody, but you got to have in-person consultations or calls and visits to get your specific case analyzed. The testing discussed tonight is obviously, like I said, a prevention. By itself, it doesn't diagnose anybody. If you have more symptoms or questions— so, uh, oh, somebody's already asking about my paper. Yeah, my paper's listed in my bibliography on my website, drrobertwhitfield.com. It is, um, if you just type in, um, my Google Scholar ID, which is also listed on my website, um, but I have a whole list of my publications on my website. The paper's there, you can click on it. It's in PubMed, it's open access. Okay. Um, but once again, take specific symptoms, uh, Questions about those implants, laboratory results, or treatment options to your provider. And if you want to work with us, obviously we'll help get you connected. We have a team that helps vet and takes calls, does discovery calls for me. So if you go to drrobertwhitfield.com, they'll help you get a complimentary call set up. And so when I do these tests, I get asked a lot, what do we do afterwards? Well, we don't use oral antibiotics. And I don't in particular have a specific regimen for supplementation or anything afterwards. We have a curated set of tests and supplements and guidance on nutrition that we use pre-op and post-op and That's how we just help patients move through the process more simply and clearly. So let's let's talk about a capsule, right? So the body normally forms a capsule or layer of scar tissue around any implant. Now we're talking about just and focusing on breast implants, and that's the expected response. Capsular contracture is different. The capsule can become unusually firm, and in some instances almost, you know, what I find in the operating room is tight, and it may become painful to the patient. It may change shape or position of the breast. It can be a real problem for patients both in How it feels, how their clothing fits. Capsular contracture is, as we talk about today, considered to be a multifactorial problem. The patient's individual biology, of course, inflammation, of course. At the time of surgery, was there bleeding or problems in the pocket? Other surgical factors or implant-based factors. And of course, any microbial processes are relevant depending on the circumstances of the patient. So biofilm is one plausible contributor, and it's not a universal explanation. So that distinction matters for patients who are trying to make sense of their symptoms. 2 people can have similar implants, very different clinical experiences. One person may develop A firm capsule. Another may have pain without a severe contracture. Another may have local symptoms or simply have nothing at all. So any of the findings may be relevant in one clinical picture or another. The study that we designed—it wasn't designed in a way to. Sort through symptoms or categorize them. It was designed to describe the findings of any microbes on the devices. So that's that was my like intent in trying to set the true incidence of bacterial contamination on implants. So a biofilm is simply an organized community of those Microbes associated with— basically think of like a layer of goo, and it just helps protect them. It makes it harder for your body to deal with them. In medicine, biofilms are not new. They can behave differently from free-floating bacteria, though. They may be unevenly distributed and difficult to characterize in a single type of sampling method. But here is a critical distinction: detecting bacteria through genetic material by itself, it doesn't really demonstrate a mature biofilm. It does not prove that there is an active infection. So, in my paper, it certainly does not do that, and that's, you know, why the language I use refers back to that all the time. So, there have been a number of papers published about biofilm. I reviewed one of them recently by Dr. Mathun Sina and colleagues about biofilm and oxylococci I've been Tinham. I also reviewed a paper about the transcriptome. So I think it's important. You know, my paper was published in Microorganisms in 2024, the title of which is Clinical Evaluation of Microbial Communities and Associated Biofilms with Breast Augmentation Failures. So. The IRB-approved study was my surgical experience and— excuse me— it covered really a sample from February of '19 to September of '22. Total of 694 explant samples were examined through next-gen sequencing for microbial profiling. So, you know, that's a large number of samples. Also, this was a specific set of samples. Obviously, people are coming to me for explant surgery. The specimens came from that particular population who were removing their implants, and so that's the selection of the patient population that I'm taking care of. So the study can describe findings that are submitted obviously by those specimens I took. It cannot establish the prevalence of these findings among all people with implants. It cannot tell us what we'd find in general screening population. Because the review is retrospective, it cannot identify any patterns and associations outside the limitations of the study. Those Those are the limits, right? I was looking specifically at like, all right, how many of these explants have bacterial contamination that are existing within this? Like, what's the true incidence? How do we figure that out? And so the literature was really confusing to me. It ranged all over the place and the sample sizes were relatively small. So We used next-gen sequencing. So the testing used this NGS, next-gen sequencing, including bacterial 16S ribosomal RNA profiling. In plain language, this approach looks for bacterial genetic material and compares the detected sequences with the reference information that already exists in the database to estimate Which organisms may be present. This can identify bacterial DNA that routine growth-based methods may not be able to identify. That includes genetic material from organisms that are difficult to grow, organisms that are no longer viable, or very small amounts of material. That is key. All right, so in culture medium, the thing has to be alive, it has to grow, so there has to be enough of it. That's an important distinction. The strength of this other method is about Finding it, is it there? And it can be in small amounts, and that makes it still relevant. A 16S result tells us that a bacterial genetic signal was detected under the assay's condition. It does not tell us by itself that the organism was alive at the time of testing. If everybody remembers from my livestream previously, I talked about the transcriptome, which is basically the RNA signatures. Of live organisms or cell types. And that's, that's like the next step in this, if I were to be like perfectly blunt about it. So once again, it doesn't prove that there was structure of a biofilm present or anything like that. So obviously results can be affected by how I, you know, collected the sample, how it was handled, how it was transported, all those things. So I think it's important that, you know, in a culture-based setting, as we go back to traditional cultures, if something didn't grow in the culture-based setting, you know, they send us this, you know, no growth at 24 hours, no growth 72 hours final, or they'll show you culture results bacteria placed on a Petri dish and it'll say normal flora. So, that's skin flora, Staph epi, Cutibacterium, Propionibacterium, all these normal Campylobacter, all these skin bacteria. But, they don't end up showing up in high enough amounts, so they don't actually consider those to be Pathogens. They're, they're not a problem. So I'm very cognizant that those are problems. And so although no single microbiology result should be interpreted outside, you know, the clinical picture— so I have all these, um, examples of patients with chronic inflammatory symptoms, of which I explant, and then 29% in my study had bacterial contamination. So that's a contributor to inflammation. You know, think of the methods as just different windows in the same room. A culture asks whether an organism can grow under laboratory conditions provided. Next-gen sequencing asks whether the targeted genetic material can be detected and classified. So using the microscope, you can see the structure of organisms and tissue, while pathology evaluates the tissue changes. One window may reveal something Another does not, but no single window shows the entire room. So interpretation asks, you know, whether or not these findings agree with one another and whether they fit the history, exam, operative findings, symptoms. It also asks whether contamination during collection or processing is reasonable alternative explanation. I've done so many of these thoroughly, so you all know, um, and if, if there's a contamination, then typically both samples have the same contaminants, which is not the case. We would always identify that as a pattern and concern. So sensitivity can reveal information that older methods miss, and that's why I switched to PCR, but clinical meaning still has to be established. The correct response to a molecular result like the ones we get is it's another piece of the puzzle. I don't over-respond to it, and I don't just be dismissive if there's nothing there. And I think probably I had to hedge a little bit. I would like to see something there that would reassure me that that's another signal the patient was dealing with. So of the 694 samples submitted, 203 returned positive findings. So that's 29%. And again, this is a sample-level result. It is not correct to say that 29% of patients had infection. It is not correct to say that 29% of all the people breast implants have biofilm. The accuracy, I mean, this, you know, of the specimens that I took care of, 29% were positive. And across these positive samples, the analysis detected 103 unique types of bacterial species. The median was 3 per positive sample. 72% of the positive samples had fewer than 5. These results suggest that the detected signals were often not limited to a single species. They also show Variation across specimens. What they do not establish is equally important. More detected species does not automatically mean more severe disease. Fewer species does not automatically mean less severe disease. Descriptive counts do not provide a validated diagnostic threshold, severity score, or treatment guide, or anything like that. They are measurements from my dataset. They are not, you know, the end-all be-all of every Analysis, so it always needs further work. The three names that showed up the most were Cutibacterium acnes, Staph epidermidis, and Corynebacterium. So the dominant organisms included those, and there was also Pseudomonas that was relatively prominent. Some of these names they kind of sound wild, but. Many of them are just skin bacteria. Organisms commonly associated in our skin are and have been relevant to surgery for a long period of time and device placement. But finding their genetic material in a tissue sample still does not tell us on its own whether they were viable, whether they formed a mature biofilm, or whether they caused that person's symptoms. So the microbial findings, so what we found, You have to take it in larger context. I did this very purposefully to help create a better idea and incidence in patients with symptoms and bacterial contamination on devices. So the study gives us a more detailed picture of what microbial signals appeared in those specimens I took. It does not convert any one species into the the culprit specifically. That is important when results list several organisms. A long list can look. A little bit more daunting. Scientifically, it is still just a molecular profile that requires interpretation. So I think it adds another piece to an already interesting, you know, puzzle. The paper also examines species richness. Richness means the number of different species detected in a sample. It does not mean the amount of live bacteria, the strength of biofilm. Or establishing the biofilm. It's an initial comparison. Implant filling appeared related to richness, but age and implant filling were also related to— I'm sorry, were also related in the dataset. So after the analysis controlled for age, implant filling was no longer significantly associated with the species richness, but age remained significant. So that's why, you know, I didn't do this analysis. The company that we work with for the examination of the samples did the scientific analysis, and it is, you know, it's important not to like overinterpret results. I think These findings, like they don't prove that aging causes a greater microbial richness. I know that's not true. It does not tell us the specific pathways. It does not show that changing implant fill types would change a result. It should not be obviously used to predict an individual's symptoms or outcomes or anything like that. So the responsible. Like thing that I concluded from it is a bit narrower. In, you know, in my set, in my study, we had this 29%, implant fill really didn't matter. And that's kind of where I stopped, you know, trying to make stronger and stronger conclusions about the data. So really, what does the data support? The data supports When you target and profile these bacteria, obviously you can get in a large sample size a pretty good example of what's going on at the microbial signal level. It describes the diversity of species detected in these positive samples. It identifies several commonly detected organisms, and it does offer us You know, options for further research into these microbial communities, acute and chronic inflammation, implant failures, capsular contractures. You know, what does it establish? Well, for a long time, you know, I always kind of thought anybody who had fluid around an implant, anybody who had a capsular contracture, basically I'm always worried about an infection. And I was worried that we didn't have as sensitive a technique To examine it, I think this is a much more sensitive and specific technique. So if we had a lot of studies that looked at biofilm relative to the capsule contracture, we may have a lot more answers. It does not establish the prevalence among all implant patients. Of course, it does not prove that a positive sequencing result represents an active infection. It doesn't obviously show that this is correlated with capsule contracture. I didn't look at that. It does not prove that a detected organism caused capture contracture, local symptoms, systemic symptoms, or implant failure. It does not establish that a negative result rules out microbial contribution. And it does not show that antibiotic supplement surgery or another treatment improves outcomes based on these findings. This is not— and once again, it's not a weakness of the study. It's basically— this study is a retrospective sample analysis. of my series to help, like, clarify to me personally, like, this is the incidence I see in my practice. And for those who, you know, for instance, have a very similar practice, this— if they reported similarly, this would be great. Scientific restraint, you know, is not the same as saying the finding does not matter. It means matching, you know, the strength of our statements to the strength of the evidence. And I think this is a great start in terms of evidence. It's the largest published series in the world. And we can say we detected the signal. We can report how often it appeared in these samples. We can describe which organisms. So we've added quite a bit to the literature in terms of evidence. But, you know, I don't jump to any conclusions or make any broader claims about it. I think biofilm does matter. I think we're going to learn more and more about it. One of the reasons I was really excited about the transcriptome paper is because if you took my technical paper about incidence and then added RNA analysis to it, then you would really have something combined and powerful, uh, from the same, uh, patients. And if you paired that with an age-matched cohort, that would be a powerful tool. So can we— and I just basically gave the end of the talk— so we, we want to Create research protocols, obviously, that compare groups and have control groups. And what I just said is that's my favorite thing would be to you know have a group of patients probably just undergoing another breast procedure, and you're you're checking their PCR and you're checking their RNA analysis, and then you're comparing that to a sample like I have. Of an implant-based situation, or you can do it on exchanges if patients are getting exchanges and compare those age-matched cohorts. I'm getting a little long in the tooth to run that kind of study, but maybe some young folks want to do that. Other things to look at are, do these specific patterns dictate specific outcomes? Meaning, do the bacteria of certain patterns we find have different outcomes? I haven't seen that yet, but that would be good to study. And then, obviously, can independent teams reproduce the data? We also need studies designed specifically to evaluate these diagnostic testing and treatment outcomes because there's not good tools right now, you know, that we can utilize for that. We have a very specific curated prep and recovery protocol, so it's not a fair fight to run my patients against others typically. But I think trying to get more ideas about outcomes Helps patients. I know that's an optimistic message, but I think that helps patients the most. I would like to see that. And patients really deserve more and better research that respects obviously their experiences and also protects them from conclusions that the data doesn't yet support. And I think we can do both. We can obviously— I always take symptoms very seriously. These symptoms are are sometimes very hard for providers to understand and for patients to convey. I want to give you some takeaways tonight. One, the sample size, right? 694 samples. It's a good sample size. So I'm glad our clinic could produce that with our co-authors from MicrogenDX. And 2, 29%. I believe that number. I believe that's a real number in my patient population. I don't think it's a vague general number at all. I think the sequencing method is great for detecting bacterial genetic material, but once again, it doesn't establish that they're alive or dead, right? That's an RNA function, not a DNA function. It doesn't dictate active infection. 4. We still think In my study, even though I wasn't looking specifically at capture contracture, the biofilm plays a role. We just don't know the level of the role in each patient. Testing is informational, obviously. It's not diagnostic by itself. We don't prescribe antimicrobial therapy or supplementation based on findings. That would be something you have to pursue with your provider. I will say I recently got a call and took care of a patient who had a rapidly evolving breast process— breast rest process pre-surgery, and I, you know, had to take care of it, but it increased in size. It was drained, ruled out for ALCL. We'll get the final analysis on that. But if you have signs of increased urethral warmth, swelling, drainage, fever, any kind of severe pain, you don't feel well, obviously with a device in place, you need to seek attention. Reach out, go get examined. If you don't feel like you're being heard, obviously we've we've put out a lot of data. We have a book out about breast implants, explant surgery, and breast implant illness, and then my short method. There's a book out about that. We have all sorts of free podcasts and educational material. Things that we put out are for education only. Doesn't replace working with a provider. And, um, for Q&A, I'm going to take some off of Instagram and TikTok and then shut those down and go to the, uh, private community, Dr. Rob's Circle. So that is it for my talk. All right, let me get some— let me see if there's a question here. There's a question. It says, how many bacteria do you actually test for? Also funguses? Yes, it tests for over 150 bacteria, mycobacterium, and fungus. Okay. Oh, hi, Miss Danny Williams. Williamson. Oh my gosh, I said Williams. Hi, Danny. It's been a long day, Danny. I have to tell you, tired. I'm looking on Ignite the Fight. So is asking me, do I still do implants? Now, I haven't placed implants in the last six years. All right, Aphrodite two nine eight five. Yes, we do. My team will do them complimentary. All right, Brittany, we will see you. All right, um. Somebody's getting an MRI of their hips tomorrow. I'm a little confused about, uh, some of these comments on TikTok. It's a confusing thing. All right, I'm gonna shut down TikTok. All right. Can everybody go over to Dr. Rob's Circle? I'm going to take the rest of the questions there. So Jamie, Tony, Lisa, go to Dr. Rob's Circle. And Aphrodite, Mary, TS, Jesse, Sherry, go to drrobscircle.com. I'm going to type it in the chat. Thank you, Miss Danny. Yes, back in the day, I thought we'd open an office in Franklin for you, but that didn't come to fruition. But we do have our surgery center open now in Austin, Texas, and, um, we'll see what the next steps take. So everybody go over to drrobscircle.com and, um, uh, Lisa, I can do that in the circle. Why don't you hop over to the circle and I can talk about that? Lisa Thomas, uh, Cox has a great question on Facebook. Okay, I'm tired. I'm just dropping off all of the stuff, uh, off of, um, the live