Understanding Capsular Contracture: Mechanisms, Management, and Patient Outcomes in Implant-based Breast Augmentation and Reconstruction

Abstract

Background:

Capsular contracture (CC) is a frequent complication of implant-based breast augmentation and reconstruction, causing deformity, pain, and reoperation, particularly after mastectomy. CC arises from a multifactorial immune and fibrotic response influenced by patient factors, radiation, implant characteristics, and surgical technique. This review summarized recent data on CC epidemiology, prevention, and treatment.

Methods:

A narrative review of PubMed and Embase (2020–2024) identified clinical studies on CC after breast augmentation or reconstruction, including trials, cohort studies, case series, and reviews evaluating surgical and adjunctive interventions such as capsulotomy, capsulectomy, and perioperative pharmacological, or material-based strategies.

Results:

Chronic peri-implant inflammation, bacterial biofilm, and postoperative radiation were consistently implicated in CC pathogenesis, with higher rates in irradiated mastectomy patients. Preventive measures, including antimicrobial pocket irrigation, implant and mesh selection, and atraumatic “no-touch” techniques, were associated with reduced CC in several reports. Pharmacological adjuncts such as leukotriene inhibitors and glucocorticoids showed promising but heterogeneous results. For established CC, capsulotomy is commonly used for mild to moderate disease, whereas complete or partial capsulectomy remains the standard for severe or recurrent cases, often combined with implant exchange and adjunctive measures to limit recurrence.

Conclusions:

CC remains a major cause of morbidity and revisional surgery after implant-based breast procedures. Contemporary evidence supports a multimodal, patient-specific approach that couples meticulous surgical technique with targeted pharmacological and material-based strategies to prevent and treat CC. Robust prospective studies are needed to define optimal protocols and long-term outcomes.

Takeaways

Question: What are the causes, management, and treatment outcomes of capsular contracture (CC) in implant-based augmentation and reconstruction?

Findings: Immune response, bacterial biofilm, and radiation contribute to CC. Prevention strategies, such as antimicrobial treatments and the “no-touch” method, show promise, with capsulotomy and capsulectomy being key treatments.

Meaning: Although capsulotomy and capsulectomy are effective for CC, personalized preventive strategies and further research are needed to improve outcomes.

INTRODUCTION

Capsular contracture (CC) is a common complication following implant-based breast reconstruction and augmentation. Soft, thin capsule formation around the implant is expected due to the immune system reacting to foreign body placement. However, CC occurs when this response is exaggerated, causing increased thickening and fibrosis of the capsule that leads to hardening, breast distortion, and pain.^1–3 Generally, reconstruction poses a higher rate of contracture than augmentation, with rates between 5%–19% and 19%–25% for augmentation and reconstruction, respectively. The mechanism of contracture is not well understood, although during the last 50 years both etiology and epidemiology have been studied extensively, with several likely overlapping causes, such as immunobiological, patient-specific, and implant-related risk factors.¹ In breast cancer patients who have undergone implant-based breast reconstruction following mastectomy, CC can occur due to adjuvant radiation therapy. An ongoing area of study among reconstructive surgeons is how to best manage these patients.^1,4 Implant material and texture, as well as type of access incision, were also associated with the rate of CC.^1,5 CC severity across both augmentation and reconstruction is evaluated through the widely accepted Baker scale, a criterion based on pain, appearance, and texture.^6,7 Prevention and treatment through both pharmacological and nonpharmacological means, as well as CC revision through different types of surgical intervention (ie, capsulotomy versus capsulectomy), have been extensively studied throughout the literature.^8–14 This article aimed to provide an updated review on the mechanisms, epidemiology, diagnostic tools, prevention, treatments, and patient outcomes of CC in breast reconstruction surgery.

METHODS

This study executed an initial search in adherence with the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines using the PubMed and Embase databases. As such, due to the heterogeneity of topics being discussed and the amount of literature with limited quantitative data yielded from searches, the authors elected to structure the article as an updated narrative review on CC and new innovations in treatment and prevention. Moreover, because CC is a broad topic, it would not be feasible to do a full systematic review and meta-analysis on each subtopic (etiology, management, treatment, and prevention) that is addressed in the article.

Literature Search

The search of PubMed and Embase databases consisted of the following: ((“capsular contracture”) AND (“breast augmentation”)) OR ((“capsular contracture”) AND (“breast reconstruction”)) OR ((“capsular contracture”) AND ((“capsulotomy”) OR (“capsulectomy”))). A total of 93 results from 2020 to 2024 were identified. Results were filtered to include randomized controlled trials, case studies, review articles, and retrospective and prospective studies. The search was performed on September 21, 2024. Inclusion criteria included those articles that discussed objective outcomes related to CC, with a focus on either preoperative intervention protocol, intraoperative technique and outcomes, or postoperative protocol and outcomes. Articles that did not include patient demographic information, outcomes data, or protocols that did not include dosing of medications or description of surgical technique were excluded.

Bias Assessment

Bias assessment was performed by classifying each reference (n = 52) according to the Oxford Centre for Evidence-Based Medicine (OCEBM) levels of evidence, ranging from level 1 (systematic reviews of randomized controlled trials) to level 5 (expert opinion and narrative reviews). Each study was assigned a level based on its primary design, such as systematic review and meta-analysis, cohort study, case-control study, case series, diagnostic accuracy, translational investigation, or narrative review. Risk of bias was then judged qualitatively across 3 key domains including the study design and methodology (including randomization, comparators, prospective versus retrospective data collection, and blinding), potential for confounding and selection bias (surgeon or patient factors, allocation methods, and baseline comparability), and outcome ascertainment (objectivity of endpoints such as Baker grade or reoperation, follow-up duration and completeness, and risk of misclassification). Studies were categorized as low, moderate, moderate–high, or high risk of bias. Across the 52 included references, the majority of evidence consisted of retrospective or prospective cohort studies (OCEBM level 2b) and narrative reviews (level 5), with a smaller subset of systematic reviews and meta-analyses of observational studies (level 2). No randomized controlled trials were identified. Most studies demonstrated a moderate-to-high risk of bias, reflecting the predominance of nonrandomized designs, heterogeneous methodologies, and reliance on historical or single-institutional data. (See table, Supplemental Digital Content 1, which displays a summary of all studies included in this review [n = 52], including study design, level of evidence, core discussion, and risk of bias, https://links.lww.com/PRSGO/E584.)

RESULTS

Clinical Presentation

Since 1978, the main grading criteria for evaluating CC has been a subjective system called the Baker scale.⁷ The originally invented scale with grades I through IV is most widely used to evaluate CC associated with breast augmentation (Table 1). Although this is the only recognized way of recording CC, it is highly subjective and practitioner dependent. Grade I contracture is asymptomatic with the breast maintaining its natural texture and soft feel. Grade II exhibits breasts that are increasingly firm; however, the patient does not experience pain. In grade III, there is minimal discomfort, but the patient can feel the capsule. At this point, the breast may look harder and rounder, and the nipple contour may change. Severe contracture is categorized by grade IV, which causes the breast to be tender and painful. The contracture is visible from the outside, and the breast is hard and tense to the touch. There are some limitations when extrapolating the use of this scale when assessing patients who have undergone breast augmentation. For example, there is some degree of firmness that is associated with the implant itself, which may lead the original criteria to misclassify certain breasts as having contracture.⁷

Table 1.

Baker Scale for CC After Breast Augmentation

Class	Baker Scale Physical Findings	Patient Symptoms	Reoperation
I	Completely natural appearing breast	None	Not indicated
II	Minimal contracture present, patient does not feel	None	Not indicated
III	Moderate contracture, patient can feel	Symptomatic	May be indicated
IV	Severe contracture obvious; patient can feel painfully	Symptomatic	Required

Etiology

Although the etiology is multifactorial, the cornerstone of CC genesis is a chronic inflammatory reaction. The first and most commonly accepted reason for CC is the immune response to the implant as a foreign body. From a pathophysiological perspective, the innate immune system is thought to elicit CC formation, with macrophages secreting interleukin-8 and tumor necrosis factor alpha, which have been associated with more severe Baker grade contractures. Additionally, transforming growth factor beta released from mast cells has been studied as the instigator of phosphorylation cascades that lead to CC. Mast cells may also play a role in activating fibroblasts to secrete collagen via paracrine signaling. Fibroblasts are numerous within the capsule, and it has been found that as CC worsens, the collagen fibers increase in diameter and orient themselves into a helical orientation that thickens the capsule. Although not well understood, Toll-like receptors, which are activated by recognizing invading pathogens or endogenous signals, have been reported to be present in all grades of Baker contracture. It is unclear whether bacterial pathogen-associated molecular patterns, damage-associated molecular patterns, or genetics are the main triggers for Toll-like receptor activation. Moreover, there are several other intracellular pathways that drive specific immune responses and would need to be investigated to pinpoint the exact pathway that drives CC formation.^1,10

Biofilm

A leading theory of CC development is subclinical bacterial infection of the surgical site that leads to biofilm formation on the implant. Propionibacterium acnes, Escherichia coli, Staphylococcus aureus, and Staphylococcus epidermidis (most common) are some of the species of bacteria that have been cultured from patients undergoing revision breast surgery after CC. These bacteria may enter the breast pocket via implant insertion by the surgeon or from the skin surface or breast gland tissue.¹ The implant itself has a large, hydrophilic surface that allows biofilms to form. Biofilms are defined as bacteria that adhere to a prosthetic surface and to each other via an extracellular matrix. Although bacteria such as E.coli and S. epidermidis should be susceptible to antibiotics, biofilms are known to persist despite antibiotic treatment and to elicit an immune response. This response is similar to the one described earlier, with the difference being that the fighting off of the infection causes the secretion of inflammatory signals, leading to an excessive fibrotic reaction and capsule formation.^1,11 Notably, there are arguments against this proposed etiology of CC given that bacteria have been found on implants that have not been complicated by contracture, suggesting that there is some mechanism that converts this benign bacterial presence to a pathological one. However, pathogenesis could simply be due to increased bacterial load.⁹ Histologically, studies show that CC has maximum collagen density at 5 years postsurgery, which may also contradict that infection has to be present as the timeline is too long unless it is a chronic remote infection.^9,12 Moreover, a 2013 cohort study showed that the rates of CC in patients treated with triple antibiotic irrigation therapy versus those who were not did not have statistically different rates of CC.¹³ There is the suggestion that biofilm formation may increase the rate of CC but is not the main cause, as a fibrotic response will happen with or without infection present.^1,10

Implant Surface

Hematoma formation and different types of implant shell surfaces have also been studied as potential instigators of CC development.^1,15,16 There have been several studies on the rate of CC in patients who receive smooth versus textured implants. Smooth implants have thinner capsules and easily change position in the breast. Textured implants have a thicker capsule and rougher surface that help keep them stationary within the breast pocket.¹⁷ A 1993 study of subglandular implants found a statistically significant decrease in CC favoring textured silicone implants (21% for smooth versus 4% rate of CC for textured).¹⁸ However, various subsequent studies report different results. For example, a 1997 study suggested that there was a significant difference in the incidence of CC among smooth, textured, and polyurethane saline implants.

In the shorter term postoperative period (within 90 d), CC with textured and polyurethane implants occurred at lower, but similar rates compared with smooth implants.¹⁹ However, over time, polyurethane outperformed textured implants in reducing the risk of CC during the entire follow-up period (mean follow-up period: 10.7 mo, P < 0.0001).¹⁹ Moreover, textured implant surfaces McGhan Biocell and Mentor Siltex were compared with no statistically significant difference in the rate of CC. Different types of smooth surfaces were not analyzed in this study.¹⁹ Another 2015 study supports these data, as polyurethane implants in 382 patients were associated with decreased rates of CC. Additionally, decreased polyurethane concentration within the implant coating was correlated with increased rate of CC.²⁰ Recently, a 2022 article looking at 506 implants reported that there was no difference in CC rates between smooth and textured implants, but patients with subfascial plane placement had a statistically significantly higher rate of contracture with smooth implants.²¹

Pocket Characteristics

In implant-based reconstruction, cancer patients who have undergone mastectomy, postmastectomy radiation has been associated with inducing CC. This can occur when a patient undergoes lumpectomy and radiation, with subsequent implant placement, followed by locoregional recurrence and complete mastectomy with additional radiation therapy as noted in a study by Vinsensia et al¹⁴ (Table 2). Neither surface type nor implant placement (subpectoral versus prepectoral) was found to cause significantly different rates of CC after radiation.¹⁴ However, in a review by Safran et al,¹¹ it was found that the rate of CC was 3 times higher, with more severe correlating Baker grades, in subglandular implant patients compared with those who received subpectoral placement. This is thought to result from the disruption and increased scarring of the pectoral muscles in the subpectoral position. Histologically, collagen content does not differ greatly from patients who did not have radiation, although there was an observed increased quantity of elastin and cellular infiltrates.^11,22

Table 2.

Summary of Incidence of CC Based on Different Variables From the 2024 Vinsensia et al¹⁴ Study of Breast Cancer Patients Who Underwent Radiation Therapy Following Mastectomy and Breast Reconstruction

Characteristics	CC Rate (N = 118)
CC type, %
Baker I/II	24.5
Baker III/IV	22.9
Mastectomy type, n (%)
Nipple sparing (N = 53)	26 (46.4)
Skin sparing (N = 58)	28 (50.0)
Modified radical (N = 6)	2 (3.6)
Unknown (N = 1)	0 (0.0)
Implant placement, n (%)
Subglandular (N = 104)	51 (91.1)
Subpectoral (N = 11)	5 (8.9)
Unknown (N = 1)	0 (0.0)
Surface, n (%)
Textured or polyurethane (N = 111)	53 (94.6)
Smooth (N = 3)	1 (1.8)
Unknown (N = 4)	2 (3.6)

All P values were greater than 0.05.

Management

Perioperative Interventions

Over the years, several studies have investigated pharmacological and nonpharmacological measures at all stages of operation to prevent CC. Antimicrobial agents have been evaluated extensively, as one of the main theories of the basis of CC is bacterial biofilm formation and surgical site infection due to S. Aureus or even methicillin-resistant S. Aureus. Topical antiseptics applied preoperatively have been shown to decrease the rate of CC, with chlorhexidine gluconate proving more effective than povidone-iodine. Perioperatively, a triple antibiotic solution, which consists of bacitracin, cefazolin, and gentamicin irrigated into the breast pocket for 5 minutes, was associated with a lower rate of contracture.⁸ Povidone-iodine, which had the warning removed by the Food and Drug Administration in 2017 regarding its risk with implants, is also considered to be antimicrobial and can be used interchangeably or simultaneously with triple antibiotic solution. Similarly, leukotriene antagonists (eg, montelukast, zafirlukast) have been used to reduce CC rates. It is important to note that there have been rare, recorded cases of death via chemical hepatitis and/or liver failure, specifically with zafirlukast, so liver function tests should be checked before initiation of treatment and routinely thereafter. Treatment is traditionally limited to a maximum of 3 months.²³ Glucocorticoids, antifibrotic drugs, and non-steroidal anti-inflammatory drugs have also been shown to decrease inflammatory and foreign body response to implant placement.^9,24 Although preoperative 1-time doses of cefazolin are common practice, postoperative administration, implant-grafted drug substances within the shell or the filler, and irrigation of the implant before placement are other antibiotic administration methods being evaluated throughout the literature.^8,9

Implant Materials

Material modifications to the breast implant itself have also been reported to prevent CC. Biologic matrices (eg, acellular dermal matrices [ADMs], polymeric meshes) and synthetic meshes (eg, Vicryl and TIGR matrix) placed around the implant are routinely used to decrease the incidence of CC. In a 2024 study of 772 reconstructed breasts (689 biologic mesh, 83 synthetic), Ferenz et al²⁵ reported a CC occurrence in 15 (2.2%) of the breasts that were reconstructed with biologic mesh and 3 (3.6%) of those using synthetic mesh. The results were not statistically different (P = 0.430). In other studies that have evaluated rates of CC without the use of mesh, the incidence rate of CC is much higher, recorded at 10.6%–15.9%.²⁵ In a systematic review by Choi et al,²⁶ it was noted that only 1 human study out of the 17 studies showed an increased foreign body reaction to synthetic mesh over biologic. However, in line with the other 16 studies, there was no significant difference in the rate of CC.²⁶ Zwitterionic polymers are another type of biomaterial being studied for this purpose as well. In terms of surgical techniques, the “no touch” method using the insertion funnel reduces the risk of bacterial contamination once the surgeon removes the implant from its packaging.⁹ In the actual surgery itself, the areolar approach versus the inframammary approach for implant placement is associated with a higher incidence of grade III and IV CC.⁹

Nipple Shields

The use of nipple shields has also been advocated in breast surgery since the late 20th century, although no concrete evidence to date demonstrates a decrease in infection risk. The most common technique remains covering the nipples with a clear occlusive dressing, with this dressing demonstrating positive bacterial contamination in several studies when cultures were taken from the dressing after removal.^27–30 Collis et al²⁷ cultured 63 nipples and nipple shields, and 34.9% had positive bacterial cultures. Although not an indication that bacteria directly cause CC, this study suggested that there is a risk of increased bacterial contamination from the nipple that could lead to complications like CC postoperatively.^27,28 In a meta-analysis of multiple clinical studies that looked at the rate of biofilms found on the implants of CC patients, Ajdic et al²⁹ suggested that, overall, bacterial biofilms are associated with CC. Likewise, in addition to pocket irrigation, nipple shields also may create an aseptic environment that could prevent biofilm formation and subsequent CC.²⁹

Intraoperative Considerations

The rate of CC has been well documented to improve with implant placement in the subglandular plane. In a 2021 review of the etiology and treatment of CC, Safran et al¹¹ discussed the decreased rate of CC with subglandular placement in both augmentation (9.6% versus 1.9% for submuscular) and reconstruction (8.7% versus 13.9% for submuscular) patients (Table 3).¹¹ Implant exchange is recommended for CC treatment as it will ensure no retention of biofilm on a reused implant. Altering the location plane of the new implant may also affect the risk of recurrent CC.

Table 3.

Summary of Rates of CC With Implant Plane Comparing Subglandular Versus Submuscular in Patients Who Have Undergone Either Augmentation or Reconstruction¹¹

Implant Plane	CC Rate, %
Subglandular (augmentation)	9.6
Submuscular (augmentation)	1.9
Subglandular with ADM mesh (reconstruction)	8.7
Submuscular (reconstruction)	13.9

Pocket irrigation with hypochlorous acid has also been proposed by some, with 1 study demonstrating a significant decrease in the incidence of CC after 1 year. Similar to other irrigants, hypochlorous acid kills pathogens via oxidative damage and inhibition of cell growth locally.³¹ See Table 4 for a summary of the types of irrigation and associated statistics regarding CC incidence.

Table 4.

Outline of Pocket Irrigation Options and Their Mechanisms of Action and Associated Incidence of CC Found Throughout the Literature

Perioperative Pocket Irrigation	MOA	CC Incidence
TAS	Bacitracin (inhibits cell wall synthesis and cell enzymes), gentamicin (inhibits 30S ribosomal subunit), cefazolin (inhibits cell wall synthesis)	Some studies show no difference in the rate of CC in treated versus untreated patients, whereas others report a lower incidence of CC with TAS8,9,13
Chlorhexidine	Attaches to cell walls to disrupt structure and osmotic equilibrium; binds cellular proteins	There was a statistically significant difference in the rate of CC between patients irrigated with chlorhexidine versus Betadine (0% versus 12.5%, P = 0.04194)32
Povidone-iodine	Iodine disrupts cell membrane, proteins, and nucleic acid structure	Patients who were irrigated with Betadine versus saline were shown to have significantly lower rates of CC (2.7% versus 8.9%, P < 0.00001)33
Montelukast, zafirlukast	Leukotriene inhibitor (blocks inflammatory mediators)	Pooled subgroup analysis showed significantly decreased rate of CC in the population treated with montelukast or zafirlukast (P < 0.01)21,34
Glucocorticoids	Repress transcription of cytokines and inflammatory mediators	Dexamethasone was shown to inhibit TLR in mice that received silicone implants, suggesting that glucocorticoids may play a role in reducing CC9
Antifibrotic drugs (pirfenidone, halofuginone)	Act at the transcription factor level (eg, TGF-beta, PPAR) to suppress fibrosis	Pirfenidone has been shown in rats to decrease capsule thickness and inflammation during an 8-wk period9
NSAIDs (eg, diclofenac)	Inhibits COX-2, which prevents the synthesis of inflammatory prostaglandins	Has been shown in 1 study to reduce CC in 86% of patients with Baker II–IV CC9
HOCl	Acts as reactive oxygen species in the oxidative burst within immune cells to destroy invading bacteria	There was a Baker III/IV CC recurrence rate of 1.5% with HOCl versus 17%–50% in other studies not using HOCl22

COX-2, cyclooxegenase-2; HOCl, hypochlorous acid; MOA, mechanism of action; NSAIDs, non-steroidal anti-inflammatory drugs; PPAR, peroxisome proliferator activated receptors; TAS, triple antibiotic solution; TGF-beta, transforming growth factor beta.

OPERATIVE INTERVENTION

Because CC has been one of the leading causes for reoperation after breast implant placement for decades, the focus on reoperative success is rightfully emphasized.²⁸ With hopes of effectively addressing the breast (or breasts) affected by CC, initial surgical intervention includes techniques such as capsulotomy, open partial capsulectomy, and total capsulectomy as potentially effective means of addressing the affected capsule. Capsulectomy takes more time due to the length of dissection (often an additional hour compared with unilateral capsulotomy). Removal of excess tissue can be difficult and also cause complications due to the resulting lack of tissue cover for the implant and the risk of pneumothorax in the case of implants in the subpectoral plane.^35,36 Closed capsulotomy, which involves manually squeezing the breast to induce capsule rupture, was used historically as a nonoperative technique; however, it has fallen out of favor due to the risk of implant rupture, displacement of the implant, and insufficient capsule release.³⁷

Capsulotomy

Capsulotomy is another option for the treatment of CC and is technically less challenging to perform than capsulectomy. Although older articles, such as Young³⁵ in 1998, report higher rates of CC recurrence with open capsulotomy, Swanson,³⁶ in a retrospective study from 1996 to 2016 of open capsulotomies, reported recurrence rates after capsulotomy of 22.7% and 25%–53.4% for capsulectomy. As such, for patients who have thin capsules from saline implants, especially in the submuscular plane, capsulotomy is often suggested because the capsule can be absorbed naturally with a low associated seroma rate.³⁷ Capsulectomy can be used for thicker capsules that exhibit visible calcification. In addition to thin capsules, other relative contraindications to total capsulectomy include a thin mastectomy flap (risk of mastectomy flap compromise) and cases when a capsular flap is needed to improve implant malpositioning or aesthetic outcome, such as correcting the inframammary crease.^35,36

Additionally, fat grafting with capsulotomy has been shown to be an effective means of addressing the contracted capsule without having to remove or replace the implant. This technique involves addressing the patient’s pain level while simultaneously working to correct the cosmetic alterations imposed by CC. Lipofilling in and around the contracted capsule has been shown to aid in relieving the pain caused by CC as well as addressing some of the misshapen architecture that is present in the breast tissue. This technique has been demonstrated to allow patients to achieve pain relief as well as to move their breasts toward a less severe Baker classification of capsular contraction. Therefore, the cosmetic and quality-of-life improvements that result from this approach significantly decrease the need for replacement of an alloplastic prosthesis.³⁸

Capsulectomy

If conservative measures fail to resolve CC, surgical capsulectomy is the definitive treatment. This involves removing the fibrous capsule around the implant, either partially (subtotal) or totally, depending on the case. A subtotal (partial) capsulectomy excises only a portion of the capsule (often the anterior scar tissue), which minimizes surgical trauma but leaves some capsule in place. In contrast, a total capsulectomy removes the entire capsule and is traditionally recommended for significant contractures (Baker grade III/IV) to eliminate all scar tissue. Partial capsulectomy is a compromise when full excision is risky (eg, if the posterior capsule is adherent to the chest wall in a submuscular implant), but any residual capsule can act as a nidus for recurrence. Indeed, leaving behind capsule remnants is associated with higher chances of contracture returning, whereas complete capsulectomy (combined with implant exchange) has been considered the gold-standard approach. It should be noted that outcomes in the literature vary widely, with some studies reporting CC recurrence rates ranging up to 50% of patients. As such, the optimal surgical approach may need to be tailored to each patient. In addition to the aforementioned options, revisional mastopexy is a viable alternative to the reintroduction of implants.^39–42

An “en bloc” capsulectomy, popularized by social media and the breast implant illness cohort, is a specialized form of total capsulectomy where the implant and its entire capsule are removed together as a single intact specimen (often with a surrounding margin of tissue). This technique is clinically indicated for confirmed cases of breast implant–associated anaplastic large cell lymphoma or possibly extensive silicone leakage, rather than routine contracture revisions. En bloc removal ensures that no capsule or implant material is left behind or spilled during explantation, but it is a more invasive operation requiring extensive dissection of the capsule off the chest wall (with risks such as chest wall injury or pneumothorax if the capsule is stuck to the rib or pleura). Due to its complexity and higher risk profile, en bloc capsulectomy is not routinely recommended for simple CC cases or “breast implant illness” symptoms, with society guidelines reserving en bloc removal for oncological indications such as aspiration-proven breast implant–associated anaplastic large cell lymphoma. Studies have shown no added benefit in patient outcomes when an en bloc is performed for benign conditions, compared with a standard total capsulectomy.

The use of ADM has emerged as a promising adjunct in difficult or recurrent CC cases. Multiple studies have reported lower recurrence rates when ADM is incorporated into capsulectomy revisions. For example, 1 protocol (the “SPICES” technique using the porcine ADM “Strattice”) demonstrated that reconstruction with ADM reduced the recurrence of CC to about 2%–3%, compared with around 15% recurrence when using capsulectomy and implant exchange alone. In another series, the authors achieved a 0% recurrence rate during the follow-up period by completely wrapping or lining the implant with ADM after capsulectomy. The biologic matrix likely provides a nonreactive, vascularized interface that diminishes scar formation around the implant. Emerging alternatives such as newer bioresorbable synthetic meshes (such as GalaFLEX, DuraSorb, TIGR) have also shown early success in reducing contracture while potentially lowering cost and complication rates, but long-term data are still needed.^6,43–50

When CC does recur after an initially successful revision, it presents a unique challenge. Surgeons will often escalate the approach by combining all of the aforementioned strategies in a repeat operation, for instance, performing a complete capsulectomy (if only a partial was done before), changing the implant pocket or plane if not already done, using an ADM or mesh for internal support, and exchanging the implant again. This aggressive multimodal approach is aimed at breaking the cycle of fibrosis. Even so, each additional recurrence carries a risk that the contracture may return despite best efforts. At a certain point, patients need to be counseled about the option of permanent implant removal if contracture keeps recurring. In fact, many women who experience multiple recurrent CCs ultimately decide to have their implants explanted altogether to avoid further surgeries. In such cases, a satisfactory cosmetic outcome can be achieved by performing a concurrent revisional mastopexy or by using fat grafting to restore natural volume once the implants are removed.^48–50

Postoperative Preventative Techniques

To reduce the risk of CC both after the index operation and corrective surgery, patients may use several interventions to prevent or reduce the risk of recurrence. First and foremost, smoking cessation is of utmost importance, as this has been demonstrated to have a positive correlation with the development of CC, with many arguing for at least 4 weeks of preoperative and 4 weeks of postoperative smoking and nicotine cessation.⁴² Patients may also need to be counseled that common over-the-counter vape products also contain nicotine and can be harmful to the breast capsule.^51,52 Massage techniques such as gently massaging the implant in the pocket for 5 minutes, 2–3 times per day, can be used to prevent CC starting as early as 2 weeks postoperatively. Several studies have investigated earlier massage, as early as 2 days postoperatively; however, there is no significant data to demonstrate any difference in the development of CC in these patients. In fact, there have been no controlled studies that indicated any benefit from massage. Massage technique remains controversial for this reason but proves no additional risk and has the added benefit of patient comfort in actively participating in their care.⁵³

Pharmacological Interventions

Postoperative pharmacological prophylaxis has gained additional headway. Many surgeons have begun prescribing montelukast or zafirlukast in the postoperative period to prevent capsular inflammation and long-term contracture. Several series have been published demonstrating that 20 mg zafirlukast twice per day or 10 mg montelukast once a day for 3 months has been beneficial in producing a soft capsule.³¹ In early stages of CC, leukotriene inhibitors have been shown to improve CC symptoms. Likewise, cyclooxegenase-2 inhibitors (eg, diclofenac) have relieved symptoms in Baker grade II and III patients as well.^10,11 Additionally, some surgeons are extending treatment to include oral doxycycline, complemented by vitamin E, to enhance immune function and prevent bacterial growth in the breast capsule.^9,11,54 These practices are often combined with the intraoperative use of antimicrobial irrigants.^9,11

DISCUSSION

Both primary breast reconstruction and augmentation using alloplastic prosthetics are at risk for CC postoperatively. Previously mentioned in this article, measures to prevent this complication include mitigating microbial burden in and around the implant, choosing the correct implant size, texture, and material, implementing the “no-touch” technique and deciding which anatomic pocket is best suited for each patient. With CC being a risk factor for future CC, these standards are of utmost importance to ensure success.

For particularly difficult or more affected capsules, there are additional risks to consider. Patients that experience contracture after a submuscular implantation may have a capsule that is firmly attached to the chest wall. Dissection of this capsule requires careful and precise surgical intervention, posing a risk of damaging axillary structures or intercostal musculature, causing pneumothorax, or even inciting major bleeding. These adverse effects can ironically increase the risk of future contraction of the breast capsule and therefore should be weighed against the severity of patient symptoms. As previously summarized, the additional benefit of a complete capsulectomy compared with an anterior capsulectomy may not be warranted in this setting.²⁷

There are several avenues to expand upon in the areas of prevention, management, and treatment of CC. Focusing on prospective studies that follow patients who receive breast implants and evaluating how certain predisposing factors, such as autoimmune disease, impact the incidence of CC may be a direction that could lead to improvements in CC prevention. Researching more objective ways to measure CC risk factors and diagnosis is also important. Additional work can be done in examining specific immunobiological pathways that may be implicated in the genesis of CC. There have already been imaging studies done using ultrasound and magnetic resonance imaging; however, there is not yet a consensus that these objective findings are better than the more subjective Baker scale.^6,55,56 Future research would perform larger scale studies that evaluate reliable, quantitative methods that can supplement the Baker scale and/or limit variables, such as implant surface material and ADM use, that might skew the classification. The effectiveness of nonsurgical interventions for CC, such as leukotriene receptor antagonists, is another opportunity for further study. Nonsurgical, medical, and surgical interventions have been studied throughout the literature for the last several years, and the likely next step for managing CC is determining a customized treatment approach for each patient based on their predisposing factors.

It is important to note that in synthesizing the existing literature on CC, our review highlights a striking predominance of lower-to-moderate level evidence. Of the 52 studies analyzed, the majority were retrospective cohort designs (OCEBM level 2b) or narrative reviews (level 5), with systematic reviews and meta-analyses largely limited to aggregating observational data. No randomized controlled trials were identified, underscoring the methodological limitations inherent in this body of work. Risk-of-bias assessments revealed that most studies carried a moderate-to-high risk, primarily due to nonrandomized designs, limited adjustment for confounders such as patient selection and surgeon technique, heterogeneity in implant types and operative approaches, and inconsistent outcome reporting. Although systematic reviews offered broader syntheses, they were constrained by the quality and heterogeneity of the primary data available. Importantly, diagnostic studies and mechanistic explorations contributed valuable insights but were also subject to limited external validity. Taken together, these findings suggest that much of the clinical guidance for preventing and managing CC remains derived from lower level evidence and expert consensus rather than high-quality comparative trials.

Against this backdrop of limited high-level evidence, the emergence of novel surgical techniques and adjunct technologies requires careful, patient-centered application. As surgical techniques and technology are evolving, the use of internal structural scaffolding, in the form of synthetic or biologic mesh, has grown in popularity. The theory behind the use of implantable mesh scaffolding is the creation of a thinner capsule that impedes the proliferation of myofibroblasts in the capsule and surrounding space. However, clinicians should pursue a patient-centric approach using the summary of data provided as a guide to treatment—weighing the risks and benefits of preventative measures, intraoperative techniques, and postoperative management options.

CONCLUSIONS

CC remains a significant cause of patient morbidity and, thus, reoperation following breast implant placement, necessitating a range of postoperative and, at times, surgical interventions. Commonly used techniques include capsulotomy and partial or complete capsulectomy, with capsulotomy often favored due to its shorter operative time and faster recovery, particularly in cases involving thin capsules. Current research efforts are directed toward developing preventive strategies, using pharmacological and material-based interventions, refining diagnostic tools, and advancing surgical techniques to improve outcomes.

DISCLOSURE

The authors have no financial interest to declare in relation to the content of this article.