Capsular contracture (CC) is a well-known complication of augmentation mammaplasty. The mechanism of capsule formation is multifactorial and the risk factors can be broadly categorized as implant-related or surgical technique-dependent.1,2 In this case report we consider a patient-related factor, that of familial tendency. We review the literature for known genetic markers and consider whether CC may or may not be related to a familial tendency. To our knowledge this is the first description of bilateral CC affecting three successive generations of the same family. Our index patient underwent breast augmentation in 2010 at the age of 20 (Figures 1-2). She presented to our clinic with bilateral capsular contracture seven years later, in 2017 (Figure 3). A bilateral implant change with neosubpectoral subcapsular pocket3 was performed by the first author (P.M.) with 245 mL round silicone gel implants (Figure 4). (A, B) This flat chested 20-year-old woman underwent breast augmentation in 2010 by another surgeon. 225 cc shaped implants inserted using a dual-plane technique via a submammary incision. (A, B) Appearance at 12 months postoperatively show natural looking breasts with conservation of body proportions. (A, B) The same patient presented at our clinic with bilateral capsular contracture 7 years later. Notice that the capsular contracture had pushed the implants superiorly, leaving scars visible well below the inframammary fold. A bilateral implant exchange with neosubpectoral subcapsular pocket was performed with 245 cc round implants. (A, B) Appearance at 8 months postoperatively shows a natural look and good body proportions. Notice that the scars now lie in the inframammary fold again. We found that the patient’s mother had her primary augmentation mammaplasty in 1995 at the age of 33 with round silicone implants (unknown manufacturer and size) placed in submuscular plane. She developed bilateral capsular contracture 8 years later, necessitating bilateral implant exchange with round silicone implants placed in the same submuscular plane. There has been no sign of recurrence to date. Our patient’s grandmother underwent primary augmentation mammaplasty in 1969 at the age of 25 with saline implants (unknown manufacturer and size) in subglandular plane. She too developed bilateral capsular contracture that needed revision exactly 8 years after the procedure. Her implants were changed to round saline implants (unknown manufacturer and size) in the same pocket. She is still alive and has no sign of recurrence. None of them had a pregnancy after the primary breast augmentation. They did not have any chronic disease or needed any long-term medical treatment. Our patient and her mother are smokers whereas the grandmother is not. CC is the most common complication after primary and secondary mammaplasty. Implant-related factors have been addressed by the introduction of implants of various physical characteristics in an effort to decrease capsular contracture.1,4 There is evidence that surface texturing decreases the rate of capsular contracture.1,4 Surgical technique has improved to minimize the introduction of biofilm and or microcontamination which have been recognized as causes of CC.5-7 However, capsular contracture still remains one of the principal complications of breast augmentation. CC is fibrosis and angiogenesis similar to a scar. While it is common to ask for familial history in case an unfavorable scar, it is not common practice to ask patients about the family history of capsular contracture.8 However, this should change now that the implants have been on the market for many years and the procedure has been gaining popularity.9 This presents a unique opportunity to study dysregulated gene expression in successive generations. Genes which are dysregulated in each generation may represent a better target for gene therapy and any patient centered counselling in future. A literature search was performed in April 2017 by one of the authors (M.C.) on the Title and Abstract fields of all English language journals indexed on the PubMed Central database for the following term “(breast AND capsule) AND (gene OR expression).” This resulted in 59 articles, of which 39 were excluded as unrelated to CC and 8 were excluded because they did not investigate genetic markers. Six articles each were found that investigated periprosthetic capsules biomarkers in human tissue and in animal model. Most of the studies in this field focus on the effects of TGF-β10,11 which is a key fibrogenic cytokine associated with fibroblast differentiation into myofibroblasts. Other cells implicated in the process include CD4+ cells, mast cells, myofibroblast cells expressing estrogen receptors.12 There is evidence to suggest the role of inflammatory and fibrotic genes13 including human deacetylase inhibitors,14 cystinyl leukotriene receptors,15 T-cell receptor (TCR) beta chain16 as well as proinflammatory and anti-inflammatory cytokines. These studies hint at the role played by certain cell types and mediators in capsule formation through inflammatory processes. Whether these mediators and molecular markers have a familial tendency, has not been investigated to our knowledge. This paper has some limitations. The patients mentioned in our case report were operated over a period of time and involved more than one surgeon. The implant characteristics of mother and the grandmother are not known. The surgical techniques and the physical characteristics of implants have evolved over this time so these patients do not represent the “single surgeon, single technique, same implant” ideal. Even if they did, it is not possible to ascribe a definite cause-effect relationship on the basis of one case report. However, we can estimate the odds of coming across this finding by chance. The risk of developing CC at 9 years varies between 3.4%17,18 and 17.3%.4 The independent risk of having the same finding in three random patients is between 0.034 × 0.034 × 0.034 (=0.0000393) and 0.173 × 0.173 × 0.173 (=0.00518) (ie, between 0.0039% to 0.518%). In the absence of a chronic condition, development of capsular contracture 7 to 8 years after the index surgery, in three generations of the same family is an interesting finding that has not been reported in the literature before. This may be related to up regulation of a pro-inflammatory molecular pathway, inhibition of an anti-inflammatory one from an as-yet unidentified mechanism. In future similar familial trends may provide a way to identify and target the responsible genetic pathway(s). Considering the increasing trend of breast augmentation, obtaining family history at the consultation in regard to capsular contracture may become commonplace in the near future, as potential indicator for increased risk of developing this complication. We know that presence of a biofilm is the most likely trigger for CC and that certain biomarkers are over expressed in the subsequent inflammatory response. However, to our knowledge, familial tendencies of over expression of these biomarkers have not been investigated. We believe that this case report may serve as a starting point to look for familial tendency of over expression of certain genes in CC. Further collection of data regarding family history combined with further experimental research will help to enlighten the presence and the exact nature of familial aspect of capsule formation. Dr Montemurro is a consultant and speaker for Allergan, Inc. (Irvine, CA). Dr. Hedén is a consultant and speaker for Allergan, Inc. and an unpaid consultant for Canfield Scientific (Fairfield, NJ). Drs Demir and Cheema declared no potential conflicts of interest with respect to the research, authorship, and publication of this article. The authors received no financial support for the research, authorship, and publication of this article.
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