This is another long one. I think it is worth reading if you are researching BII. The goal is to take an impartial, critical view of the current literature. Depending on your perspective, and what you have been told elsewhere, some of this may challenge your ideas of what BII is. That's good. But as always, happy to discuss if you think I've got this wrong.
As this article is quite lengthy, I have decided to put a bit of an index here with links to different sections - will make it easier to read in digestible chunks and come back to it.
As things stand currently, we have no definition of what breast implant illness IS. We know a bit about what it is NOT. This poses a few challenges.
Breast implant illness is a"self-diagnosed" condition. There is no test, no form of imaging which can diagnose BII. There is no objective diagnostic feature that allows a clinician to diagnose the patient. Indeed, it is impossible to currently define BII: a list of over 100 symptoms have various been ascribed to BII, but there is no single symptom that is unique to BII.
BII is a diagnosis of exclusion - which is to say, it is the diagnosis that can only be arrived at following the exclusion of all others - but that is rarely how patients attain the label of BII. Essentially, any patient with BII arrives at a diagnosis based on their own perceptions of symptoms and an attribution of those symptoms to the presence of their breast implants.
This is a tricky problem then, because BII, and the veracity or otherwise of that diagnosis, becomes a matter of faith.Which really bothers surgeons (admittedly, some more than others).
But that isn't to say that we haven't tried to find a better way of determining the underlying cause, and as a corollary, a way of impartially diagnosing this increasingly prevalent condition.
So where are we at?
Over the years, numerous culprits have been assessed (and eventually discarded) in the pursuit of understanding how some patients with breast implants develop symptoms that might be considered auto-immune in certain contexts, or simply inflammatory in others.
Way back in the 1980s when the Americans decided to ban silicone-filled breast implants (they were only allowed to use them again in 2006!), the concern was for auto-immune conditions that were lumped together as "connective tissue" disorders. Many attempts were made to determine whether, like patients with conditions like rheumatoid arthritis or lupus, patients with breast implant-related symptoms showed elevations in classical auto-immune markers like ANA (anti-nuclear antibody) or anti-phospholipid antibodies for example. That all came to nought. And in the absence of clear findings to account for patients' symptoms, surgeons fell back on the old trope of blaming symptoms on anxiety and depression.
Once the FDA in America re-approved silicone-filled breast implants for use, this was hailed by some surgeons as vindication - proof, if you will that there was no possible immune-mediated response to breast implants that might lead to systemic symptoms.
But, patients' concerns have never really been completely addressed. We have certainly been shielded from this here in Australia. Interestingly, we continued using silicone-filled implants all the way through the moratorium in the USA, and consequently, Australia has the highest per-capita use of silicone breast implants in the world (at least I think that is still true).
In fact (and this is certainly interesting), the question of BII (as we now call it) has only become really significant in Australia in the last 10 years, with big spikes in interest in the wake of implant recalls in 2018 in response to the BIA-ALCL (breast implant associated lymphoma) issue which build up a head of steam around 2016. With the attention suddenly on the safety of breast implants due to concerns about who could be at risk of BIA-ALCL, and the fact that Australia seemed to be demonstrating the highest rates of that rare condition in the world (due to the overwhelming prevalence of macro-textured implants in the Australian market), there was a sudden shift in popular sentiment attached to breast implants. And with that shift, we have seen a large change in the type of surgery being performed.
Statistics over the last 10 years have been quite interesting. We have three main sources of data available.
If we look at the Medicare data since 2010,the use of the item number 45551 (which is indicated for capsulectomy - although this may only indicate that a small portion of the capsule was removed - NOT associated with another breast implant being put in) was quite low until a dramatic spike in the 2018 data, with a peak attained in 2021 and essentially maintained in recent years. The application of that number has been highest in women aged 35-44 years old.
Very few women are actually having explant procedures due to ALCL. Some women are having explant procedures because they are scared of ALCL. But most women are having explant procedures because of two things: BII concerns, and a change in aesthetic attitudes.
Now, we are seeing sustained elevation of explant procedures here and internationally.
Interestingly, in the same time period, the rates of implant revision appears to have dropped (presumably because women are choosing explant rather than implant replacement), and the data from the ABDR would suggest that the number of primary cosmetic breast augmentations has also decreased significantly. This is really interesting. Between 2017 and 2022, the average (even accounting for COVID) number of cosmetic breast implant procedures sat around 9500 per year logged in the ABDR. In the 2023 data, that number dropped to just over 7800, which appears significant. ABDR data demonstrates a capture rate of around 80% of cosmetic breast procedures performed.
One of the useful aspects of the ABDR is that it is tracking implant revision procedures including explant surgery. This aspect of the registry is only likely to become relevant with time. Given the average time from implant to explant could be anywhere from 9-14 years (based on my own data), and given that the ABDR really only kicked off in 2016-17, I would expect that for us to start to achieve meaningful data based on women whose cosmetic breast augmentation was included in the ABDR data, we will need to wait until somewhere between 2026 and 2030 to start seeing those women coming back for explant surgery. At that point, we will potentially have a large population (there are well over 100 000 patients currently logged in the ABDR) from whom we can start draw data. But of course, the ABDR remains incomplete as it's use is at the discretion of the surgeon involved, and my own research (not yet published) has shown that not all surgeons who perform explant surgery are contributing the explant procedure data to the ABDR. And even once we achieve a necessary threshold for the data in the ABDR to become useful, it does not capture any specific BII information.
The other publicly available data source is the Australian Institute of Health and Welfare. If we consider the ACHI code for bilateral augmentation mammaplasty (445528-00), this allows us to isolate the purely cosmetic breast augmentations whilst excluding things like unilateral cosmetic procedures for symmetry etc. That shows, for the financial year 2022-23, there were 8328 cosmetic bilateral breast augmentations performed.
If we compare that to the number of explants, the AIHW data which tells us that there were 7050 breast prostheses removed in 2022-23. Because the relevant codes are unilatera, if we halve that, we have 3525 patients (assuming bilateral removal in each case, which we know isn't the case but it gives us a rough number to work with).
In any case, the change over the last 10 years in the ratio of explants to cosmetic implants is significant - 1:2.36 in 2022-23, compared to 1:13.6 in 2012.
In other words, from 2013-2023, while the available data suggests that breast augmentation has increased by less than 10%, explant procedures have surged with a greater than 5-fold increase! American data by comparison shows 255000 augmentations performed in 2022 against 65000 implant removals - an explant:implant ratio of 1:3.9.
...between 2012-13 and 2022-23, breast augmentation has increased by less than 10%, whereas explant procedures have surged with a greater than 5-fold increase!
So we are seeing a pretty substantial reversal of historic aesthetic trends and the rate of explant surgery has absolutely exploded, which comes with risks (and we've already talked about that in another article here).
Explant data becomes even more interesting when we consider these numbers on a state-by-state basis (this data, from Medicare, is presented on a per-capita basis).
In 2015, the rate of 45551 application per 100 000 people was 3/100 000 in SA and in Victoria, but double that at 6/100 000 in QLD and WA. Fast forward to now, and the per capita rate of 45551 use is ~25/100 000 in WA and QLD (a >4 fold increase) and 15/100 000 in SA (a 5 fold increase!). But in Victoria, that number has stayed much lower at 9/100 000. What does that mean? Is it because of prevailing surgeon attitudes? Or is there a true difference in patient demand?
Victoria has shown dramatically lower increases in explant procedures compared to other states. There is no immediately obvious explanation for this. My own data (not published) indicates that NO surgeons in Victoria are performing explant procedures regularly, with all respondents in a recent survey performing explant on a monthly basis at most (and 44% performing explant surgery only 'rarely'). Contrast this to QLD surgeons, where 50% of respondents are performing explant surgery weekly. Is this simply a reflection of demand, or are surgeons' attitudes/preferences throttling the frequency of explant procedures being offered in some states?
One would have thought that with such data, there would be a strong push to increase our understanding of what is driving these trends, a push to understand the conditions or concerns that are leading women to explant, and a push to critically assess the best way of managing patients who want to have their implants removed. I find it very curious that none of these things have occurred.
If we consider the main question I want to address in this article - what is the underlying cause of BII - then there is a very limited research base currently available.
I think that for many surgeons, it is still much more comfortable for them to say that BII isn't real, or at the very least, patients' symptoms are arising from factors unrelated to the implants.
One of the challenges we do seem to confront here is the desire that I see from plastic surgeons to turn this into a non-issue. I think that for many surgeons, it is still much more comfortable for them to say that BII isn't real, or at the very least, whatever symptoms patients have are arising from factors unrelated to the implants. Whether the finger is being pointed at comorbidities (things like thyroid disorders, hormonal fluctuations, menopause, stress, anxiety or depression), many surgeons are comfortable being inappropriately definitive in saying that, because there is a symptom overlap between BII and many other conditions, then BII can't be a real condition and it is just a case of patients trying to blame their implants for other problems in their lives. And that is manifesting to some extent in the literature, where we continue to see statements along the lines of: there is no evidence that BII exists. This then extends into discussions of the surgical approach to explant surgery, with the repeated claim that capsulectomy is not necessary (which I have addressed AT LENGTH previously).
But, based on the research that has been done, let's consider what we can say.
Throughout this article, I will try to include the DOI to any referenced research - you can search the DOI, and you'll at least be able to read an abstract if the full paper is behind a paywall (which most will be).
4 ASERF papers have been published. These papers are important, but also deficient in some respects. Most importantly, I can't help but wonder whether the ASERF studies are affected by some degree of bias, given some public statements made by one of the lead authors (Dr Pat McGuire).
Dr McGuire has previously written, in response to comments about the science behind BII and capsulectomy on a public forum for members of the American Society of Plastic Surgery (of which I am an international member):
"There is a Facebook group with 11,000 members with “explant regret”. These are women who thought they had BII, had an explant with an aggressive capsulectomy, some of whom are left with devastating results and had no or incomplete symptom improvement...They are kicked out of the BII groups if they tell their story of no improvement or if they report complications from a recommended surgeon...I get messages from these women...(who) want recommendations for surgeons in their area who can help with their post explant deformities or reimplantation. I don’t know what percentage of BII patients replace their implants. I have had a few. I don’t know that we will ever be able to get a good number because most surgeons who promote themselves as “explant experts”, don’t replace implants...
Now, I mentioned this particular comment in another article I wrote recently about "explant regret". But the fact that she has made these comments suggests that a) she is potentially biased against the idea of total capsulectomy, and b) she has publicly expressed doubt and disdain for the idea of explant surgery being a procedure that demands specific expertise which is distinct from that required for other breast procedures.
Anyway, onto the papers.
These 4 studies looked at (the same) 150 women in 3 cohorts: 50 women with breast implants and BII symptoms; 50 women with breast implants and NO BII symptoms having either implant replacement or removal; and 50 women without breast implants having other breast surgery (the women in cohort 3 all had mastopexy procedures).
The first study considered whether there was any difference between these groups based on a range of blood tests, and then more importantly, whether there was any difference in outcomes for those women with BII symptoms who underwent implant removal, on the basis of the capsulectomy performed - total-intact/en-bloc vs. total vs. partial.
Important differences between groups 1 and 2 included that women with BII symptoms used more pain medications, used more marijuana/THC, had more tattoos and more allergies. The other interesting difference was that 58% of group 1 nominated social media as their primary source of medical information compared to 3% in group 2 and 2% in group 3.
Now where this study looks a little sketchy to me is that in group 1 (the ladies with BII symptoms) 64% were saline implants and 90% of implants were smooth surface - this is absolutely NOT reflective of women in Australia, and maybe that is relevant. In group B, with NO BII symptoms, 78% were silicone gel and 57% of implants were textured. So, at the outset, we have two groups who differ in fundamental characteristics, which potentially renders subsequent comparisons problematic. If this study were repeated in Australia, I would think that both of these groups would have a preponderance of textured silicone implants. A few would have smooth silicone, a few would have polyurethane. Almost none would have saline filled devices. Does this matter? Well, we certainly won't be able to tell based on the outcome of this study.
In terms of outcomes, for women with BII symptoms, 94% had at least partial improvement at 6 month follow-up, but only 10% (5 patients) had TOTAL resolution of their symptoms. Most importantly, this is the study that demonstrated that the degree of symptom improvement showed no statistical correlation with the type of capsulectomy performed. That is, en-bloc and total capsulectomy DID NOT confer a greater chance of symptom resolution compared to partial capsulectomy.
Now, the other thing about this first study is that 70% of women in group 2 and 50% of women in group 3 still reported pre-operative symptoms (most commonly fatigue, headache and anxiety). There were far fewer symptoms in these groups compared to group 1 (women with BII), but it does speak to the issue of BII symptoms being common and having overlap with other conditions, and somewhat like the question of breast implant-related pain, it also raises the point of whether the right questions are being asked.
I guess the main strength of this first study is that there really haven't been other attempts to follow and assess outcomes for women with BII undergoing implant removal. So, whilst imperfect, and with a number of glaring issues, this first study sets an important precedent.
DOI: 10.1093/asj/sjab417
The second study considered specifically the presence of "heavy metals" in breast implant capsules - a frequent claim made online, especially by so-called wellness influencers who have undergone explant procedures and claim that patients need to "detox" from the effects of these supposedly toxic heavy metals.
This is an important paper in that it helps us to solidly refute some of the claims made about breast implants and their health effects - and I think this is really vital so that we can actually talk about stuff that matters, and biologically plausible theories of BII, instead of constantly having to convince patients that the crap they hear on social media isn't actually true.
In this study, from the same groups as in study 1, the capsules were assessed for 22 different heavy metals. There were no statistically significant differences between the groups when considering 20 of the 22 heavy metals observed. The 2 metals in which differences existed were arsenic and zinc. The really interesting thing though is that the level of arsenic the breast tissue of group 3 (women without implants) was higher than group 1 (women with BII symptoms); however women with BII symptoms demonstrated a higher level of arsenic in the capsular tissue compared to those women without BII symptoms.
2 major confounders may account for some differences. The first is that a significant proportion of women with BII reported a gluten-free diet (18%) whereas only 2% of women without BII reported gluten / wheat allergies. This is relevant as rice absorbs arsenic more readily than wheat. The other confounder is the increased prevalence of tattoos in women with BII, with some tattoo inks containing arsenic. We also have to consider arsenic sources including cigarette smoke, drinking water, and food sources which may have geographical variations in arsenic content.
It is also important to understand that the estimated average daily exposure of adults in the USA to arsenic is 11-14 micrograms per day. The measured amount of arsenic in implant capsules was about 7.8 micrograms in total. Given that arsenic is readily absorbed from the environment, it is hard to conclude that this represents a meaningful potential BII trigger.
With regards to zinc, there was a higher level of zinc found in breast implant capsules compared to breast tissue in women without breast implants. However, the total estimated zinc content in breast implant capsules was 826 micrograms, versus an acceptable daily intake of 6400 micrograms per day. So again, not really plausible.
So it is quite easy to say, based on this data, that there is absolutely no evidence of heavy metal toxicity being a cause of breast implant illness. Let's put that one to bed.
...there is absolutely no evidence of heavy metal toxicity being a cause of breast implant illness.
Whilst this isn't the first study to address the question of heavy metals in silicone breast implants, it is the first to look at the presence of a broad range of heavy metals, and it is the first to do so with consideration for whether patients present with breast implant illness. Previous studies have most commonly considered platinum (because of its role in the manufacture of silicone breast implants) which is used in cross linking reactions to form specific silicone polymers. Whilst the weight of evidence has NOT supported any potential toxicity of the tiny amount of platinum which is residual in breast implants, that hasn't stopped a range of dissenting opinions being published.
Some patients will have heard about so-called "hair analysis" which is commonly promoted by naturopaths and others to determine exposure to heavy metals. Whilst this technique is valid for environmental exposures in some cases (given that heavy metals, levels of which drop rapidly in urine and blood after exposures, accumulate in human hair), it has also been shown that platinum levels do not demonstrate any differences between women with BII and those without (admittedly based on a small study).
I am sure the heavy metal thing won't go away, and I am equally sure that some opportunistic alternative practitioners will continue to push this line, but the data from this second ASERF study is robust, and certainly far more robust than any previous data we have had to combat these rather pernicious claims.
DOI: 10.1093/asj/sjac106
The third study considered specifically whether there were any microscopic findings from the breast implant capsules, including the presence of microbes (based on next-generation sequencing, as compared to traditional culture techniques), to account for breast implant illness. The study also considered various cytokines (signalling molecules), immunological evidence of activity against certain bacteria toxins, and a standard panel of blood tests in women with breast implants.
NGS (next-generation sequencing - an evolution of the technique of PCR) allows for the detection of microbial DNA even when organisms cannot be cultured using traditional methods. This typically involves targeting the 16s rRNA gene which is highly conserved across all bacterial species, with sufficient variability between species to allow identification. This technique is not without some questions however.
...shoving a large implant in through a 5cm incision means there is a lot of skin contact with the implant, which will result in some skin cells, and any commensal bacteria going along for the ride.
The bacteria within the implant pocket have generally been considered to exist in biofilm, representing a sub-clinical, non-infective bacterial population, which can however present an ongoing inflammatory stimulus.
The question of WHY we are trying to identify these organisms has been historically relevant in trying to understand the aetiology of capsular contracture, and more recently BIA-ALCL. However it has never offered us any form of clinically relevant, therapeutic target. Just because we can more readily identify certain bugs with NGS, does NOT imply in any way that smashing someone with targeted antibiotics against those bacteria will alter the patient's clinical recovery after explant surgery. Not least because if the capsule has been removed, then those bacteria no longer exist within the breast. Furthermore, NGS can identify bacteria which exist in tiny, possibly irrelevant numbers, as well as bacteria that may not actually be alive. So questions on the validity of findings based on NGS identification remain.
Anyway, back to the study findings. Essentially, they found that there was no correlation between any identified bacteria using NGS (from capsule tissue, implant swabs and capsule swabs) and the likelihood of experiencing BII. The presence of bacteria (of any type) was not statistically different between women with BII and women (with implants) without BII.
What was interesting was that in this study, they found that there was less capsular contracture in the BII cohort compared to the non-BII cohort. If you recall, the strange things about these studies was that the BII cohort was predominantly made up of women with smooth, saline-filled implants (which is nothing like the Australian population with BII), whereas the non-BII cohort was predominantly silicone-filled implants and the majority were textured.
Now, this does two things. Firstly, it pokes a curious hole in the long-standing claims from most surgeons that surface texturing of implants is protective against capsular contracture. But it also runs counter to the idea that capsular contracture (which is an inflammatory process) is intrinsically linked to the experience of BII symptoms. Not sure what to make of that. I am planning to go back to my own data to consider which of my patients presented with BII and capsular contracture, vs those with BII without capsular contracture - should be interesting.
The final interesting bit of data from this study was that there was no difference in the types of bacteria present in implant capsules between women with textured and women with smooth implants.
DOI: 10.1093/asj/sjac225
What about other microscopic findings? As I tell all of my patients, I always send capsules for routine pathology assessment, but what does that actually mean? And perhaps just as importantly, given the findings above, why don't I request microbiology testing to determine what bacteria are present in the capsule?
So routinely I send the implant capsules for histopathology. Histopathology involves the processing of the capsules into very fine slices to allow examination under a microscope. The purpose of this assessment is to ensure that a) there are no atypical cells - in particular, we are looking to exclude any sort of malignancy including BIA-ALCL; b) I ask the pathologist to comment on the presence of acute or chronic inflammatory cells within the capsule; and c) I ask the pathologist to comment on the presence of silicone within the capsule tissue.
Now, of those 3 questions, only the first one is essential. The other two questions (about inflammatory cells and silicone) are more a matter of curiosity (for now), because we don't have any data to support their association with patients' symptoms. What we suspect however is that inflammation is the most likely explanation for BII, and inflammation is the root cause of capsular contracture. We have data to suggest that the infiltration of inflammatory cells into capsules is significantly associated with capsular contracture. But inflammation in response to what? Bacteria? Silicone? Something else? Multiple somethings? Well, that's the million dollar question.
Silicone, and its presence in the implant capsule, is an interesting one. Over the years there have been a lot of concerns about whether silicone itself is the cause of BII. There is some nuance to this part of the discussion, so let's take some time to think about it.
Question 1 is: how does silicone get from an implant into your body? And no, that isn't an obvious question.
So, we can say that in every case, the silicone comes from the implant (duh). But there's more to it.
Silicone can get from an implant into your body by 3 fundamentally different (although somewhat related) processes. And this matters, because each different process varies with time, implant style and generation, and depending on what else is happening.
RUPTURE
The first process leading to silicone escape from an implant is the obvious one: rupture.
Before we really get into that, you need to remember that silicone implants are typically comprised of two discrete elements, both of which are made of silicone (but silicone polymers in different configurations).
It is also vital to understand that the shell is the design feature of breast implants that has undergone the most profound change over time; we are currently in what is commonly referred to as the "6th generation" of implant design.
The first generation devices in the 70's were comprised of a very thick shell and a silicone gel filling. These devices were prone to rupture as the thick shell tended to crack. The second generation devices in the late 70's and early 80's were a response to this with a thinner shell which was much more elastic (so thought to result in less risk of rupture) and a softer gel filling (for a more "natural" feel). These were plagued by gel bleed (we'll get onto that) and still had a high rupture rate. The third generation in the 80's changed the shell again back to a thicker layer, with a more cohesive gel.
We then saw the 4th and 5th generation devices introduced in the 90's and these were the first "modern" breast implants, many of which are still with their original "owners" to this day. These implants introduced surface texturing (thinking that this would reduce capsular contracture; spoiler - it didn't) and with the 5th generation, we saw the tear-drop/anatomical devices with highly cohesive gels giving rise to the popular moniker of "gummy bear" implants. The 5th generation were the devices largely caught up in the BIA-ALCL issue and many were subsequently recalled.
The current 6th generation devices (which really refers to the Motiva breast implants) are those with specifically engineered surfaces designed to reduce the contractile activity of fibroblasts (scar cells), with further evolution of the silicone gel polymers used for fill.
Now the relevance of those generations I have already alluded to above - the rupture risk is intrinsically linked to the mechanical properties of the "shell", and the cohesivity of the gel filling. Stiff shells will tend to crack when they fold; thin shells may have less resistance to mechanical stresses at the time of insertion and may also be at risk due to contact with surgical instruments. Thin gels will leak out of the implant easily resulting in a "puddle of goo" in the implant scar capsule (not fun to remove); more cohesive gels will tend to hold together even when the implant shell ruptures
A rupture simply implies that the outer shell of the implant has been disrupted in some fashion, allowing the gel filling to escape from the implant (to a variable extent). Implant rupture implies NOTHING about whether the silicone is contained within the implant capsule or not per se. We typically use additional descriptors for that purpose. An "intracaspular" implant rupture implies that the rupture remains contained within the implant scar capsule that the body has formed. This is how the vast majority of ruptures present. On the other hand, an "extracapsular" rupture implies that there has been a breach in the implant scar capsule, allowing silicone to escape. In most circumstances, this is limited, forming a kind of appendage attached the implant capsule, however in rare circumstances the silicone can migrate more extensively.
The presence of a rupture influences the findings in the pathology report. A rupture will be associated with a more significant amount of silicone deposition within the scar capsule. Having said that, the silicone from a rupture doesn't necessarily elicit any sort of "response" from the body (at least, no more than the response we'd see to an implant that was unruptured).
There have been a couple of interesting studies on this recently.
DOI: 10.1097/PRS.0000000000011780
DOI: 10.1093/asj/sjae244
A group in Chicago recently published their findings demonstrating that the simple presence of a breast implant alters the immune response to several proteins found in normal breast tissue. They also demonstrated that the presence of an implant lead to upregulation of genes associated with immune cells (in particular, Th-17 cells which have been identified in abundance in implant capsules, and are considered possible drivers of abnormal inflammatory responses to breast implants). Whilst the characterisation of the implant capsule has been clarified previously, this study demonstrated that the presence of an implant altered genetic expression in breast tissue beyond the capsule, and they also demonstrated elevated levels of antibodies to breast tissue proteins in peripheral blood samples, indicating that there is a systemic inflammatory process elicited by the presence of breast implants.
This same group then published a further study demonstrating that whilst there is a difference in antibody expression and gene expression when comparing ladies with and without implants, they found NO difference when comparing ladies with intact implants vs. rupture implants, and also no differences between implant surfaces or placement.
So the summary of these findings is that it appears that whilst the body does react to the presence of an implant, the presence of rupture on top of that doesn't appear to change that inflammatory response.
Now, having said that, we also have studies suggesting that the amount of silicone in the capsule may be associated with the presence of contracture.
DOI: 10.1093/asj/sjaf012
So, a Danish group who have be researching the importance of silicone found within the capsule tissue, have previously found that the degree of silicone deposition in the capsule is higher with low-cohesivity silicone gels, and this is true both when comparing intact and ruptured implants. More recently, they have reported that with higher silicone deposition in the capsule, there is a correlation with capsular contracture, noting a 12% increased risk of capsular contracture when comparing patients with low silicone deposition to those with moderate deposition, and then a big spike in contracture with high silicone deposition.
Now, confounding these findings are a couple of important points: 1) the ladies with more silicone in their capsules had their implants in for longer, 2) the ladies with more silicone demonstrated higher rates of rupture, and 3) ladies with more silicone tended to have less cohesive silicone gels. The problem then is that we come back to the perennial chicken & egg scenario: what comes first? The contracture, or the rupture?
The issue with this study then is that whilst we have (yet again) seen an association between the presence of silicone in the capsule and capsular contracture, this is NOT a demonstration of causality. This is something of an eternal problem when considering this issue, and short of a new way of continuous implant monitoring to determine EXACTLY when a rupture occurs, there is no way to know which event causes which outcome.
Does the rupture cause the contracture, or does the contracture cause the rupture?
SILICONE PARTICULATES
The second process by which silicone enters the body is the shedding of silicone "particulates" from the surface of the implant. This is fundamentally linked to surface texturing. Most people are aware of the implant recalls that took place in 2018/9 and many women with textured Allergan branded implants received notices that their implants had been withdrawn from market, but "don't panic" they were told, it wasn't really a big deal.
Whilst causality is not clearly defined (at this stage), the association between implant surface texturing and BIA-ALCL is clear. There is no case of BIA-ALCL described without exposure to a textured breast implant.
So, the implant recall was due to BIA-ALCL, but surface texturing is a much bigger overall story. There are two parts to that bigger story. One part relates to the formation of silicone particulates. The other part relates to the pro-inflammatory effects of those surface textures, and what that means in the context of BII.
That seems like a reasonable excuse for us to take a detour to consider surface treatments of breast implants.
Surface texturing has been a feature of implants since the 4th and 5th generation devices, and it was sold by the implant companies as two things: a way of preventing capsular contracture (it doesn't) and a way of keeping implants still (it does, sort of - essential for the teardrop shaped devices which needed to maintain a certain orientation).
Texturing can be grouped into 5 categories according to the size of the surface irregularities - smooth, nanotextured, microtextured, macrotextured and polyurethane coated. Most people are familiar with the idea of a rough surface texture if they have implants - normally surgeons will have a few sample implants in their office so patients can feel them. But, there is a bit more to it.
Smooth implants demonstrate no evidence of contouring to the naked eye and microscopically there is no defined pore structure. These implants will typically look quite translucent.
Nanotextured implants (Motiva) are the newest category of surface treatment, and the first to have been engineered with a specific purpose that is actually evidence-based. The have a silky texture to the touch, and microscopically there are distinct surface "spikes". The engineering here is at a cellular scale - the purpose of the surface contour on these implants is to provide multiple points of contact (ie. multiple spikes) for the individual cells (fibroblasts) that form the implant scar capsule. In doing so, this inhibits the tendency these cells have to want to contract over time - in other words, Motiva implants truly do decrease the risk of capsular contracture, and they truly do have evidence to support that assertion.
Now, the more traditionally textured implants made a bunch of claims when introduced, but in reality, there was never an evidence base for them being able to decrease contracture. The argument that was put forward though went a little like this: if we make a rough surface texture, then the surface area of the implant will be greater than a smooth implant (due to the irregular surface outline). Therefore, if a scar capsule forms, it will also have a greater surface area than the scar capsule for a smooth implant, and thus, it will need to shrink more before it becomes contracted. Which, as it turns out, was complete rubbish, with no science to support it. In reality, as mentioned above, the main reason for the introduction of surface texturing was to facilitate the use of anatomical/teardrop shaped implants. For those devices, the surface texture was meant to act like "velcro", with scar tissue growing into the texture and thus keeping the implant still (ie. preventing the implant from rotating - because if the projected part of an anatomical implant ended up at the top of the breast, that looked very weird).
These traditional textures were manufactured in two distinct ways (the technicalities don't matter here) but this lead to two different "pore" sizes in the texturing, giving rise to the terms microtextured (seen on Mentor branded implants) and macrotextured (seen on Allergan branded implants). Both had a similar goal, both were introduced at the same time, but only one is still available on the market today (although with a dramatically reduced market share compared to 10 years ago). The texturing of implants came under enormous scrutiny in the context of BIA-ALCL, with the realisation that ONLY textured implants could induce the cellular changes of ALCL. The risk of ALCL was far higher after exposure to Allergan (and other) macrotextured devices (with a risk of around 1:2400), leading to their recall. The risk associated with Mentor microtextured devices was substantially lower (around 1:18000), allowing these implants to remain in use. Having said that, most surgeons have switched to smooth or nanotextured implants since 2020 in response to this issue.
Polyurethane coated devices (so-called "furry Brazilians") are basically silicone implants with a sponge like polyurethane coating, which forms the most aggresive type of surface treatment. They correspondingly have the highest risk of ALCL (1:1500) and have largely been withdrawn from market. This category is less relevant when discussing silicone particulates (becuase the surface is not made of slicone), so we won't dwell on this further.
Now, that was all a rather long (but hopefully still useful) tangent to get to talk about silicone particulates.
Particulates are a distinct form of silicone microparticles which arise from implant surface texturing (micro and macrotextures) and are generally considered to be a consequence of some sort of friction which "rubs" off small fragments of those textured surfaces. It has been shown that the more aggressively textured the implant, the greater the friction arising from the implant rubbing on itself when it forms folds, and the greater the number of silicone particles generated.
The fact that the implant has to fold on itself is important - implant folds only form when there is a capsular contracture. So the question is whether silicone particulates are cause, or consquence, of capsular contracture? But the other mechanism by which friction may be generated is the movement of the implant in a sub-pectoral pocket. The constant shifting of an implant under the influence of muscle contracture, and the constant agitation of an implant which has an adherent capsule, are like to result in the formation of particulates.
Silicone particulates (as compared to silicone arising from gel bleed - see below) result in larger, albeit fewer silicone deposits in breast implant capsules, typically in association with enlarged macrophages, resulting in so-called "foam cells".
SILICONE GEL BLEED
The third process is a feature predominantly of older generation devices, called silicone "bleed". This is the process by which silicone can leach across the implant shell in the absence of a rupture, and historically is a feature of 2nd generation implants. I've mentioned silicone bleed in other articles as well.
Whilst silicone bleed remains a relevant pathway for silicone to enter the body, it is a feature most ascribed to older fashioned low-cohesivity silicone gels, and in more recent times, it has been seen with cheap, low quality implants such as those implicated in the PolyImplant Prosthese (PIP) debacle.
Silicone gel “bleed” occurs when low molecular weight silicone polymer migrates through molecular pores in the more highly cross-linked elastomer shell. Whilst this is characteristic of the thin-shelled, 2nd generation devices, it remains a feature of implants which have been in-situ for extended periods of time - length of implantation time is closely related to increased molecular mobility across the implant shell.
...and Question 2 (which is not asked enough) is: what changes with different implant types/styles? Perhaps just as importantly, what changes with different implant placement?
Microscopic silicone is observed within capsules of all silicone filled and saline-filled macrotextured devices, but not with saline-filled smooth surface devices. This is an absolutely vital piece of information, for one very clear reason.
BII is seen in patients with all forms of implant and with all surface treatments, and this includes women whose only implant exposure has been to smooth-shelled saline-filled implants. Given that ladies with smooth saline implants demonstrate NO silicone within their implant capsules or within their breast tissue, but they can still experience BII, the conclusion therefore is that silicone, in isolation, cannot be cause of BII.
...silicone, in isolation, cannot be the cause of BII.
Whether silicone is a trigger for some ladies to develop BII in response to other exposures remains undetermined.
The question of whether there is a greater degree of silicone deposition for women with textured implants, versus modern nanotextured implants, or versus smooth implants is unclear. There are suggestions that surface texturing results in a high silicone dose due to silicone particulates (as mentioned above), especially if we consider implants using a more cohesive gel filling, but the findings are poorly reproduced.
A rather interesting recent study from a Danish group looked at the influence of gel cohesiveness, surface treatment, and position to determine whether these factors influence silicone leakage from implants. This study population is relevant to us in Australia due to the demographic similarities (in strong contrast to the ASERF studies, which don't reflect Australian women at all!). The implant characteristics and placement were similar to what we see here (mostly textured, mostly under the muscle).
In terms of silicone leakage from INTACT implants, they considered a comparison of implants with low cohesiveness vs. those with high cohesiveness and found that whilst there was silicone leakage from BOTH groups, the degree of leakage was greater in the low cohesiveness group. They then did something rather useful which was a sub-analysis of a single brand (in this case, Mentor) to compare the low-cohesiveness implant styles and the highly cohesive styles from a single manufacturer - this matters because each manufacturer has proprietry formulas of silicone polymer that are used in the shells, and the gel filling, so comparisons between manufacturers are not always relevant - and this confirmed their initial findings regarding the importance of cohesiveness in silicone leakage.
The next part of the study considered surface treatment and the plane of implant insertion. Comparing silicone leakage between different surfaces wasn't especially helpful, but there was a signficant difference when comparing sub-pectoral and pre-pectoral implant position. Here, they found that implants under the muscle showed significantly greater leakage when adjusted for time and cohesiveness.
Under the muscle implants showed a higher volume of silicone leakage when compared to over the muscle implants.
DOI: 10.1097/PRS.0000000000011395
Whilst the above study is interesting, most studies looking at this question are limited by confounding variables. Because implants have evolved, because the degree of silicone deposition is related to the age of the implants, and because there is very limited data available from large populations (most data is limited to single institutions), our ability to draw conclusions is limited.
A related consideration is the presence of silicone in lymph nodes (so-called siliconoma). This is a relatively common finding which doesn't appear to have a significant clinical correlate - silicone in lymph nodes is often identified on ultrasound, but is not associated with specific symptoms relating to that silicone deposition. An interesting recent study (again this is single institution data) has shown that, among other things, there is a significantly higher risk of siliconoma for patients with implants in a dual-plane/under-the-muscle position. This intuitively makes sense, given the constant activation of the pec muscle is almost certainly going to be responsible for some degree of agitation/friction resulting in silicone particulates.
DOI: 10.1093/asj/sjae113
Ok, so back to the fourth and final ASERF study, which considered the longevity of outcomes for women with BII after implant removal. This paper presented data on a range of typical BII symptoms, with particular focus on fatigue, cognitive function and anxiety levels. The paper made a couple of really important points: 1) patients with BII reported an average of 13 different symptoms! 2) patients without BII still reported symptoms that are seen in BII, but they typically reported no more than 2-3 individual symptoms, and 3) BII symptoms substantially improved in a sustained fashion after explant (irrespective of whether capsulectomy was performed) but patients with BII still experienced on average 5 distinct individual symptoms 12 months after explant vs. the 2-3 symptoms reported by non-BII patients.
This paper does then fall back on the typical discussion about anxiety and somatisation as an underlying cause for many symptoms attribtued to BII. It isn't to say that this isn't an important part of the discussion, and yes, many women with BII will also have features consistent with an underlying anxiety condition. It will be impossible to ever discount psychology as a contributor to the experience of women with BII. But I think there has to be a degree of caution in the constant tendency of researchers to fall back on this in the absence of other findings. Sometimes it is enough to just say "we don't know". This has been the prevailing issue over the last 40 years - attributing everything to "anxiety" is not a way forward.
Ultimately, the conclusions from these important studies are that based on a wide range of diagnostic testing, there is no evidence of statistically significant differences between patients with breast implant illness, and those without.
DOI: 10.1093/asj/sjad098
So whilst we perhaps have a greater ability to refute certain unscientific claims (like heavy metal toxicity), we do not have any clear answers, or even any hints, as to the true cause of BII from these studies. That is of course assuming that the "cause" is the same in all patients who experience BII - and that is a big assumption!
Most of the data we have discussed above comes from very reputable journals. And that matters, because in this space there is quite a bit of dodgy research appearing in dodgy (read predatory) journals and open-access online only publications. The issue there relates to the quality of peer-review, and the integrity of the data that is presented.
Now, that being said, there is some interesting stuff floating around that is specifically relevant to certain BII symptoms. This stuff sometimes appears what we might kindly refer to as less reputable journals. But hey, given the issue the "establishment" has with BII perhaps we need to keep an open mind.
There are 3 further topic that are worth thinking about here.
1 - Antibodies to autonomic nervous system receptors - there are some studies which are suggesting that women with breast implants and a history of palpitations (and other cardiovascular symptoms broadly grouped together as "dysautonomia") may have specific changes in circulating auto-antibodies to autonomic nervous system receptors (G-protein coupled receptors). The findings here may be suggestive of a link between symptoms like palpitations, and even POTS (postural orthostatic tachycardia syndrome) and breast implants. Whilst an association has been suggested in several papers, the actual mechanism of a possible cause remains unclear.
2 - A rather interesting recent paper has also suggested a link between oxylipins and breast implant illness, raising the prospect that these molecules may represent a mechanistic link between the local breast response to a breast implant, and systemic symptoms. Oxylipins are compounds that are formed by the oxidation of lipids in an inflammatory environment stimulated by the placement of a breast implant. They arise due to the activation of enzymes including cyclooxygenase (which is the main target of non-steroidal anti-inflammatory drugs like nurofen or celebrex).
I think this is an interesting finding and one that hopefully we'll see some more data on in the near future. This study looked at 3 groups: women with implants and BII symptoms, those with implants without BII symptoms, and a control group of women without implants. They found that in the BII group (compared to the non BII and control groups) there were significant elevations in 5 specific oxylipins. Further, they found that there were elevations in different oxylipins in the women with breast implants (whether BII or no BII symptoms were present) when compared to women without implants.
The implication of these findings is that some oxylipins appear to be simply a response to the presence of an implant, whereas other specific oxylipins appear to be present only in women with BII, and the manifestation of BII symptoms was significantly associated with elevated oxylipin levels.
DOI: 10.1093/asj/sjae128
We'll want to see this data replicated in other studies before we draw too many conclusions, but it is both plausible and interesting - watch this space?
3 - And finally, we can't ignore mast cells, because "Mast Cell Activation Syndrome" is such a common "co-diagnosis" that I am now seeing in patients with BII. The question of what role mast cells play in capsular contracture, and more recently in BII has been around for years. There have been a reasonable number of studies indicating that mast cells (these are the cells that release histamine in allergic responses amongst other things) are present in breast implant capsules and that mast cell derived mediators can activate the fibroblasts (the scar cells that produce collagen) in capsules, representing a possible link to capsular contracture.
In the last few years however, we've seen an explosion in so-called Mast Cell Activation Syndrome diagnoses, mostly coming from naturopaths and "integrative" GPs, and typically without any actual diagnostic criteria having been met. So this is worth thinking about for a second.
A recent review paper (DOI: 10.1016.j.jaip.2021.06.011) from a panel of eminent immunologists and allergists makes a few statements that I would point patients (and practitioners) to:
That second statement is a big issue - because you can see that MCAS has become a diagnosis that is now subject to the same quandary as BII - when the symptoms of a condition are so manifest as to have no specificity, it becomes impossible not only to accurately diagnose, but to refute a diagnosis once made.
..when the symptoms of a condition are so manifest as to have no specificity, it becomes impossible not only to accurately diagnose, but to refute a diagnosis once made.
Suffice it to say (in a very summary fashion), MCAS is rarely an appropriate or accurate diagnosis in BII patients. I've seen a few ladies who could indeed have MCAS (but who've never seen an Allergist, and never been diagnosed), but the majority who have received such a diagnosis (always from a naturopath or integrative GP) almost certainly do not meet these criteria and this becomes simply another unhelpful label attached to symptoms without a clear point of origin.
By way of data, a 2023 paper demonstrated that from 703 patients referred to a dedicated centre for Mast cell disorders (who even knew such specialist clinics existed?), only 31 had a diagnosis of idiopathic MCAS. Another paper from 2022 indicated that MCAS was confirmed in only 2% of all referred patients with suspicion of MCAS.
So, my suggestion is that MCAS is very (very) unlikely to be a valid consideration as a causative link for patients with BII.
As yet there is still absolutely no indication why some women seem to suffer from BII and others do not. The assumption is that it is largely genetically determined - that is, the same inflammatory stimulus will have variable effects based on genetically determined immune-mediated phenomena. Which genes? Dunno. What other environmental factors could be at play? Dunno.
What we can clearly see is that in the absence of clear understanding, there has still been a profound shift in the manner of treating women with concerns regarding their implants (ie. an explosion in explant procedures), and a profound shift in the attitudes of patients with symptoms. What once may have been simply tolerated (given the overwhelmingly general nature of BII symptoms) or even dismissed by patients, is now critically examined and self-diagnosed as indicative of BII, with the overwhelming influence of social-media and online forums supporting that shift.
As it stands, we have some theories about BII and nothing more.
What I have tried to do with this article is provide a summary of some of the research that is out there, and offer some thoughts on how certain findings may account for how patients present. This is not conclusive, nor is it final.
The overwhelming weakness of most BII research is the small size of the study populations. Looking at a group of 50, 100 or even 1000 women may simply be insufficient. Until we have much larger data sets, with much longer follow-up, based on research conducted in a prospective fashion (from the time first consultation for a patient considering a breast augmentation), it seems very unlikely that we will be able to make any definitive statements.
In the meantime, we do the best we can with what information we have.