Commentary on: The Prevalence and Histological Characteristics of the Double Capsule Phenomenon in Breast Augmentation With Implants

See the Original Article here. This paper from Denmark is an excellent prospective review on the incidence of double capsule formation on breast implants.1 Although we are all now aware that double capsules are more likely to occur with the more aggressively textured implants, we still do not understand the pathogenesis of double capsule formation. This Danish group has already given us excellent histological assessment tools for breast implant capsules, and they continue to further our understanding of double capsules.2-6 The study included patients who had previously undergone breast augmentation with implants and were scheduled for implant exchange or removal between October 2019 and October 2023 at 5 Danish plastic surgery clinics in Copenhagen. The purpose of the study was to quantify the prevalence of double capsule formation between different implant surface textures and to explore the histological differences between the inner and outer capsules from breast implant capsule biopsies. The authors defined a double capsule clinically as having a “completely separated inner capsule adherent to the implant with an outer capsule loosely surrounding the implant with the adherent inner capsule.” Double capsules were identified by the surgeon and registered by an investigator present during the surgery. They only included patients who demonstrated complete double capsule formation. The study was then performed on specimen analysis from the Copenhagen Breast Implant (COBI) Biobank,2,3 comparing the prevalence of double capsule formation around Allergan Biocell implants (Allergan plc, Irvine, CA), Eurosilicone Cristalline implants (Eurosilicone S.A.S., Cédex, France), and Mentor Siltex implants (Mentor Worldwide LLC, Irvine, CA). The histological characteristics of the inner and outer capsules were analyzed by means of the authors’ validated assessment tool.3,4 The authors found that Allergan implants with the Biocell surface had a 7.9% risk of double capsule formation. This was approximately 10-fold higher than the 0.72% risk of double capsule formation with Mentor's Siltex surface implants and 2-fold the 3.4% risk with Eurosilicone's Cristalline surface implants. Moreover, 24% of breasts with double capsules exhibited a late-onset seroma, which is a substantially increased risk compared with a 10-year core study of Biocell implants from Allergan that reported a 0.6% incidence of late seroma.7 Although I have been criticized for being “unscientific” for giving my own personal opinion,8,9 I would argue that science is not just about bench research and histological assessment but also about good clinical research. I have spent 40 years observing, assessing, and documenting my experience. Both forms of research should collaborate to improve scientific knowledge. Of course we will disagree, but that is important in the process of furthering our understanding. I hope to be able in this Commentary to provoke some discussion and provide some more information. The authors have only included patients who presented with complete double capsule formation because they felt that other studies10 have “categorized the presence of fibrous debris on the implant surface as a subtotal double capsule which will likely result in an overestimated rate of clinically significant double capsule.” I believe that we should study all grades of double capsule formation because my observations have led to some conclusions that differ from those of the current authors. My experience has included 6 of my patients with complete double capsules (5 subglandular and 1 subfascial), 17 of my patients with partial but significant double capsules (8 subglandular, 7 subpectoral, and 2 subfascial), and 8 of my patients with either quite small amounts of double capsule formation or the kind of debris that does not form on smooth implants (7 subglandular and 1 subfascial) (Table 1). In patients who had their primary surgery performed elsewhere, I found 1 complete double capsule (subpectoral), 6 partial double capsules (2 subglandular and 4 subpectoral), and no patients with just debris. One patient with a complete double capsule had a partial double capsule on the other breast, as did 6 of the partial double capsule patients. Five of the 7 complete double capsules had seromas and 3 of the partial double capsules also had seromas. Two of the partial double capsule patients had ruptured implants. My Experience With Double Capsules My Experience With Double Capsules To put things in perspective, my breast augmentation practice has stayed consistent at 85% subglandular and 15% subpectoral. I did perform over 75 primary breast augmentations in the subfascial plane in 2005 to 2006. Most of those patients had Microcell CUI implants and one of those patients had a significant partial double capsule on both sides. It is interesting that the Danish authors did not find any double capsule formation in their Microcell textured implants (0/43) and I found only 1 patient with the Microcell textured implants who had bilateral partial double capsules. I performed about 120 primary breast augmentations using Biocell textured surface implants, but most of these were responsive gel and not form stable. The Style 410 implants were able to adhere to the pocket better than the softer, more flexible, gel implants (Style 115 and 120). The 1 complete double capsule in patients who had surgery elsewhere was in a patient who had textured Silimed implants. The Danish group did not see a double capsule in these implants. They found “no double capsule formation around CUI Microcell implants (0/43), Nagor Nagortex implants (0/16), Silimed Biodesign implants (0/10), Polytech MESMO implants (0/8), Motiva SmoothSilk implants (0/63), or smooth implants (0/53).” My practice review shows much the same results with complete double capsules except for implant rupture—but their median follow-up at 15 years was longer than mine. My seroma rates were similar. It is an analysis of the partial double capsules that makes me differ from them in ascribing delamination as the cause of double capsules. I am including several photographs that might contradict the delamination theory on how double capsules form (Figures 1-5). Interestingly, I had 1 patient who had a double-capsule-like membrane on a smooth-walled saline implant (Figure 1). The extra tissue was attached to extensive calcification that had formed on the surface of the smooth-walled implant. A thin membrane has formed over the calcifications on this smooth saline implant. This is very unusual because it is rare to find calcifications attached to the wall of a smooth implant. However, there is a membrane (in the forceps) that was adherent to the calcifications in this patient. This 47 year old female patient had a breast augmentation using Mentor smooth walled Style 1600 subglandular implants placed 17 years earlier. This was the left implant 225 cc that had been filled to 250cc. The right implant (275cc filled to 300cc) did not have any calcifications. Just as bacteria can adhere to the rough surface of a textured implant, cells from the seroma fluid can also adhere. When the implant is not adherent or when it separates like Velcro, the resultant friction can cause a seroma. The cells obtain their nourishment from the exudate and they then multiply and the inner capsule thickens. This 59 year old female patient had a breast augmentation using 322 gm Allergan Biocell textured Style 115 implants placed in subglandular pockets 13 years earlier. There was no adherence of either implant and they both had similar debris on the surface as shown here. This inner double capsule (held in the forceps) has been separated from its position around the implant patch and left in position over the outer capsule. If the double capsule was formed by delamination, why does it not delaminate over the patch? If I misunderstand and the microtears are the cause of the delamination, then perhaps there would not be any tears over the patch, and this could be the result—but I would not expect it to be as smooth as what would result from cell deposition on the rough areas of the implant. This 50 year old female patient had a mastopexy-augmentation using 203 gm Allergan Biocell textured Style 115 implants placed in a subfascial pocket 14 years earlier. Both implants were partially adherent posteriorly and the left implant is shown here. (A) If the double capsule is formed by delamination, why does the inner capsule end up thicker in the valleys of the implant? (B) The outer capsule shown here does not have uneven areas of thickness that correspond to those of the inner capsule. The delamination theory might account for this structure by claiming that the inner capsule created the implant folds as it contracted. This 34 year old patient developed a left capsular contracture one year after her subglandular mastopexy-augmentation using 322 gm Biocell textured Style 115 implants. (A) This photo shows a “complete” double capsule (except for the patch and a small anterior portion where it was adherent superiorlly). (B) shows the outer double capsule that was torn during dissection. This example would be a bit harder to explain with the delamination theory because the outer capsule is consistently thin over the thick inner double capsule. (A) The inner capsule can be seen through the intact outer capsule. (B) The outer capsule has been peeled away, leaving the inner capsule attached to the textured implant. If the portion of the outer capsule just did not delaminate over the patch, why is the outer capsule thinner over the patch than in other areas over the double capsule? This 59 year old female patient had a breast augmentation 12 years earlier with subglandular Allergan 401 gm Biocell textured Style 115 implants. She had developed a left capsular contracture 5 years after her surgery and the implant developed a complete double capsule. The capsule was removed and the original implant replaced back into the pocket. Then 12 years later she developed right capsular contracture and the results on the right side are shown. Interestingly, the original left implant was soft with no evidence of recurrent double capsule formation. The delamination theory says that the inner capsule is formed from the original outer capsule as it delaminates like the pages of a book. I am still not convinced. If delamination occurs, how does the inner capsule survive without a blood supply? Danino and co-workers believe that the microfractures seen on specimens of inner and outer capsules confirm that the capsule delaminates11—but could these microfractures not have occurred in the process of removing the adherent capsule from the implant or during the performance of a capsulectomy? The authors state that: “It is well known that an increased surface roughness of breast implants results in stronger tissue-implant adherence, thereby increasing the mechanical shear forces in the tissue. Therefore, our finding that increasing surface roughness shows a higher risk of double capsule formation supports the hypothesis that double capsules occur due to delamination of the capsule.” How do they then explain why a double capsule does not form over the smooth patch, whereas the outer capsule does not have the same defect? If delamination occurs, why is the outer capsule thickness evenly distributed while the inner capsule is much thicker in the valleys of the implant folds? In a review of a paper by Van Slyke et al,12 Danino and co-workers claim that delamination is the only possible explanation of why the intercapsular flora is sterile while there is biofilm present in the inner capsule.13 We all know, however, that it can be difficult to culture any bacteria in seroma fluid even when a biofilm is present. The authors also noted that silicone was present in both the inner and outer capsules, but that can be explained by gel bleed and does not necessarily confirm delamination.14 I have tried to find out what the difference is between the capsule that forms around a postoperative seroma cavity compared to either the inner or outer double capsules. Is the postoperative capsule much like the implant capsule that forms around an implant? Or does it result from cell seeding from the exudate? We know that abdominoplasty seromas are caused by friction and that the use of progressive tension quilting sutures can avoid the use of drains by reducing the friction and preventing the seroma from forming. The best description that I found on the histology of a postoperative seroma capsule was from Goldman et al, who stated that the seroma capsule is composed of “fibrous tissue with eosinophilic hyaline degeneration of collagen and a mild inflammatory, predominantly lymphocytic, infiltration. It lacks an epithelium on its inner surface.”15 I am presenting some contrary thoughts to the delamination theory that the authors of this paper state has been confirmed by their study. I still need to be convinced. We still have a lot to learn.16 The author declared no potential conflicts of interest with respect to the research, authorship, and publication of this article. Dr Hall-Findlay has no financial relationship with any entity except for some minor book royalties from CRC Press (Boca Raton, F), Elsevier Health Sciences (Elsevier, Amsterdam, the Netherlands), Lippincott Williams & Wilkins (Philadelphia, PA), Quality Medical Publishing (St. Louis, MO), Saunders (Philadelphia, PA), and Thieme (New York, NY). The author received no financial support for the research, authorship, and publication of this article.

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