Late breast cancer recurrence concurrent with silicone breast implant rupture 17 years after mastectomy and immediate implant-based reconstruction in a 53-year-old woman: a case report

Introduction

Background

Implant-based breast reconstruction following mastectomy has become the predominant reconstructive approach worldwide (1). While breast reconstruction surgery can meet patients’ aesthetic needs for breast appearance, it still cannot avoid postoperative tumor recurrence. Although immediate breast reconstruction has not been associated with significantly increased odds of local recurrence, implant-related complications may mimic or obscure recurrent disease (2). Late locoregional recurrence may occur years after mastectomy and often involves the skin or subcutaneous tissue (3). Silicone implant rupture is often silent but may present with pain, contour change, capsular contracture, a mass, or lymphadenopathy (4,5). Ultrasound or magnetic resonance imaging (MRI) are intended primarily to detect silent silicone implant rupture (5).

Rationale and knowledge gap

In women with a prior breast cancer diagnosis, these inflammatory changes can be clinically indistinguishable from regional recurrence. Silicone granuloma may show a snowstorm appearance on ultrasonography and silicone-selective findings on MRI. Previous reports have also emphasized that the strong fluorodeoxyglucose (FDG) uptake observed in silicone granulomas led to false positive results in positron emission tomography-computed tomography (PET/CT) (6). However, few reports have described the coexistence of implant rupture and histologically confirmed locoregional recurrence when PET/CT fails to demonstrate a discrete hypermetabolic malignant focus. This diagnostic discordance represents the principal knowledge gap illustrated by the present case.

Objective

We report a case arising 17 years after mastectomy and immediate implant-based reconstruction for ductal carcinoma in situ (DCIS). The objective of this report is to describe the resulting diagnostic difficulty and emphasize the importance of tissue diagnosis when progressive cutaneous or periprosthetic abnormalities cannot be reliably characterized by imaging. We present this article in accordance with the CARE reporting checklist (available at https://gs.amegroups.com/article/view/10.21037/gs-2026-0305/rc).

Case presentation

A 53-year-old woman (gravida 2, para 2; no relevant family history of breast or ovarian cancer; BRCA testing not performed) first detected a palpable mass without any discomfort in her right breast in October 2009, at age 36, and subsequently presented to our hospital. Surgical biopsy of the mass revealed high-grade DCIS. Immunohistochemical examination showed estrogen receptor (ER) positivity, progesterone receptor (PR) positivity, human epidermal growth factor receptor 2 (HER2) 2+ expression, and a Ki-67 index of 7%. She subsequently underwent right nipple-sparing mastectomy with sentinel lymph-node biopsy (SLNB) and immediate tissue expander-based reconstruction. Intraoperative frozen-section examination of the retroareolar margin was negative. Final pathological examination confirmed high-grade DCIS measuring 1.8 cm in maximum diameter [pTisN0(sn), stage 0], with residual ductal tissue and epithelial hyperplasia noted beneath the nipple; both sentinel lymph nodes were negative (0/2). A 400 mL subpectoral expander was placed with pectoralis major covering the medial two-thirds and acellular dermal matrix (ADM) covering the lateral one-third. In January 2010, it was exchanged for a Natrelle Style 410FM SoftTouch silicone gel implant (350 g; Allergan, Branchburg, NJ, USA). Simultaneous left breast augmentation was performed via subglandular placement of a Natrelle Style 110 round silicone implant (181 cc; Allergan). Toremifene (60 mg once daily) was administered as endocrine therapy; adjuvant chemotherapy and radiotherapy were not given. Endocrine therapy was discontinued voluntarily in September 2013. The patient had irregular follow-up thereafter; her last visit prior to the current presentation, in January 2021, was unremarkable on ultrasonography.

In March 2026, the patient presented with a chief complaint of breast pain and progressive skin lesions around the right areola that had been present for 4 months. She reported that the lesion began as lateral areolar erythema and swelling, then progressively became tumour-like, multiplied, and extended towards the nipple with ulceration and crusting. The physical examination revealed several lesions in the 4–9-o’clock direction of the right breast, aggregating around the nipple-areolar complex (NAC) area of the skin. Among them, the largest ruptured and scabbed lesion was located at the 5-o’clock position, with a size of 2 cm × 1.5 cm (Figure 1). The nipple was fixed relative to the underlying pectoralis major and chest wall and positioned higher than that of the opposite side. The skin tension of the right breast was generally higher than that of the opposite side. The physical examination of the opposite breast was negative. No enlarged axillary or supraclavicular lymph nodes were palpable bilaterally. Serum carbohydrate antigen 15-3 (CA15-3), carcinoembryonic antigen (CEA), and other tumour markers were not measured.

Figure 1 Intraoperative findings. (A) Multiple superficial skin masses on the right breast (white arrow: initial lesion). (B) Dense adhesion between the skin flap and the surface of the pectoralis major muscle. (C) Intraoperative identification of implant rupture (white triangle: intact textured surface; white arrow: disrupted surface). (D) Wound bed coverage with advancement of residual pectoralis major. (E) Excised specimen comprising the NAC, surrounding skin, implant, and partial capsule. (F) Undersurface of the excised NAC (white arrow: resected pectoralis major; black triangle: implant capsule). NAC, nipple-areolar complex.

Breast ultrasound demonstrated oedematous skin and subcutaneous thickening of the right breast with increased vascularity. There were multiple hypoechoic lesions between the inner and outer layers of the implant. The deeper one was located 12 o’clock direction above the nipple, with a depth of approximately 1.1 cm. At the same time, a disruption of about 1 cm occurred in the inner capsule of the implant at the 6–7 o’clock direction (Figure 2A-2D). The discontinuity and periprosthesis abnormalities suggested implant rupture, whereas the progressive ulcerated skin lesions and increased vascularity raised concern for locoregional recurrence. Taking into account the presence of the implant, the patient did not undergo a mammography examination. Breast MRI was not performed. PET/CT showed mildly increased soft-tissue density around the right implant and diffuse metabolic activity in the peri-areolar skin and subcutaneous tissue, with a maximum standardized uptake value (SUVmax) of 5.2 (Figure 2E). No local hypermetabolic lesions, regional lymph node involvement, or distant metastasis were observed. The left implant was intact. The combination of capsule discontinuity, periprosthesis soft-tissue changes, and mild diffuse uptake was initially considered more suggestive of implant rupture-related inflammation. However, the progressive ulcerated cutaneous lesions could not be fully explained by imaging, and malignancy could not be excluded. Given the absence of a discrete sonographic mass, PET/CT findings favouring inflammation, and the patient’s preference to proceed directly to surgery, no preoperative tissue biopsy was obtained.

Figure 2 Diagnostic imaging. (A) Oedema, thickening, and increased vascularity of skin and subcutaneous tissue near the NAC on ultrasound. (B) Hypoechoic lesion (1.1 cm) at the 12-o’clock position above the nipple. (C) Interruption of capsule continuity at the 6–7-o’clock position on ultrasound. (D) PET/CT demonstrating right breast implant capsule rupture (red arrow: disruption of the continuity of the internal capsule). (E) PET/CT demonstrating increased metabolism of periareolar skin and subcutaneous tissue (SUVmax 5.2). NAC, nipple-areolar complex; PET/CT, positron emission tomography/computed tomography; SUVmax, maximum standardized uptake value.

The patient underwent excision of the NAC and involved peri-areolar skin, implant removal, and partial capsulectomy. Intraoperatively, dense adhesion was observed between the skin flap and the underlying pectoralis major (Figure 1B). Frozen-section examination of tissue posterior to the NAC confirmed the presence of cancer cells, after which partial resection of the involved pectoralis major was performed. After capsulotomy, the implant was found to be intracapsular rupture (Figure 1C). The implant pocket was thoroughly irrigated. The superficial and accessible portions of the capsule were removed. The deep posterior capsule was densely adherent to the chest wall and was partially retained to avoid entry into the thoracic cavity. We did not conduct a separate sampling of the remaining posterior capsule wall, but it would be taken into consideration in the multi-disciplinary treatment plan. Residual pectoralis major was advanced to cover the wound bed (Figure 1D), and no immediate repeat reconstruction was performed. Given the negative prior SLNB result (0/2) and absence of clinical or imaging evidence of nodal involvement, axillary dissection was omitted.

Final histopathological examination confirmed invasive ductal carcinoma, histological grade 2, measuring 3.4 cm × 2.5 cm × 2.0 cm, with multifocal epidermal and subdermal invasion. Paget disease of the nipple and carcinoma involving the resected fibrous capsule wall were present. All peri-areolar lesions represented carcinoma infiltration. No silicone granuloma or foreign-body granulomatous reaction was identified in the examined specimens, distinguishing the malignant lesions from a silicone-induced inflammatory reaction. Neither lymphovascular nor perineural invasion was identified. Gross examination showed a 3.4 cm × 2.5 cm × 2.0 cm firm nipple-areolar lesion abutting the deep margin. A separate 2.0 cm × 1.6 cm gray-white, roughened skin lesion was located 3 cm from the nipple and 1 cm from the nearest peripheral skin margin. It corresponded to the largest ulcerated and crusted lesion at the 5-o’clock position. All margins were pathologically clear. Immunohistochemistry showed ER positivity (strong, 80%), PR negativity, androgen receptor (AR) positivity (moderate, 40%), HER2 2+ without amplification by fluorescence in situ hybridization, Ki-67 10%, E-cadherin positivity, and membranous P120 expression. Based on its distribution and pathological findings, the lesion was diagnosed as locoregional recurrent breast carcinoma rather than a foreign-body reaction. Given the periareolar ulceration and multifocal epidermal and subcutaneous tumour involvement, the recurrence was classified as rpT4b cN0 cM0 after multidisciplinary review.

Postoperative treatment comprised four cycles of docetaxel (120 mg) plus pirarubicin (80 mg), administered every 3 weeks, followed by locoregional radiotherapy and endocrine therapy. The specific target volumes, total dose, and fractionation schedule of adjuvant radiotherapy had not yet been planned, as these would be determined by the radiation oncology team after chemotherapy. Endocrine therapy consisted of toremifene (60 mg) before confirmation of menopause, followed by letrozole (2.5 mg), with a planned duration of at least 5 years. Anti-HER2 therapy was not administered because HER2 amplification was absent. At the last follow-up in May 2026, chemotherapy had not yet begun due to the need for queuing; however, a peripherally inserted central catheter (PICC) had been placed in preparation for systemic treatment. No repeat imaging examinations were conducted within one month after the surgery. No wound-related adverse events were observed.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this article and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

The principal diagnostic challenge in this case was the coexistence of late locoregional breast cancer recurrence and silicone implant rupture 17 years after mastectomy and immediate implant-based reconstruction. PET/CT in the present case showed diffuse peri-areolar uptake with an SUVmax of 5.2 but did not identify a discrete hypermetabolic mass. However, all peri-areolar lesions were carcinomatous infiltration on final pathology, no silicone granuloma was found. This experience indicates that progressive peri-areolar lesions, skin ulceration, new capsular abnormalities, or periprosthesis masses require histological confirmation even when imaging findings appear more consistent with an implant-related complication.

Strengths and limitations

A strength of this report is the relatively clear clinicoradiological, operative, and pathological correlation between implant rupture and recurrent carcinoma involving the periprosthetic tissue. Nevertheless, several limitations affect the interpretation of this report. Due to the patient’s interrupted follow-up, it is impossible to determine the exact time of the implant fracture and the precise sequence relationship between the fracture and the recurrence of the tumor. MRI, preoperative tissue biopsy, and serum tumor-marker testing were not performed. The retained posterior capsule was not separately examined. Finally, the follow-up period after this recurrence surgery was short, and chemotherapy and radiotherapy had not commenced by the last follow-up in May 2026. This case therefore cannot assess treatment efficacy, or support a universal surveillance or management protocol.

Comparison with similar research

The diagnostic presentation was the inverse of what has typically been reported: rather than silicone granuloma mimicking breast cancer (6,7), pathologically confirmed late recurrence presented within the clinical context of implant rupture-related abnormalities. Implant-associated inflammation is documented to produce false-positive functional imaging (8). In the present case, however, PET/CT was nonspecific and insufficiently suggestive of malignancy rather than strictly negative. Previous studies have also indicated that PET/CT may yield false-negative results in the assessment of breast cancer recurrence and metastasis (9,10). Several contributing factors may have influenced the absence of a discrete PET/CT focus, including the small size, ER positive, HER2 negative, and low tumor Ki-67 index (11,12). In this case, the tumor exhibited the biological characteristics of being ER positive, HER2 negative and having low proliferation, which might be related to the relatively limited FDG uptake. Inflammatory and malignant changes may also coexist, making imaging interpretation difficult. Breast MRI was not performed; its silicone-selective sequences could have further characterized the intracapsular rupture, while contrast-enhanced sequences might have better delineated the associated soft-tissue abnormalities (13). Nevertheless, MRI would not have replaced tissue diagnosis. Table 1 summarises discriminating features between silicone granuloma and cutaneous breast cancer recurrence in implant-reconstructed patients.

Explanations of findings

Unilateral implant failure—with the oncological implant rupturing while the contralateral augmentation implant remained intact after 16 years—was notable but cannot be interpreted as mechanistically conclusive yet. The implants differed in nominal size (350 g on the right and 181 cc on the left), which may have resulted in different long-term mechanical conditions (14). The reconstructed right breast also lacked native glandular tissue between the implant and the skin envelope and had undergone multiple procedures, including excisional biopsy, mastectomy, expander placement, and implant exchange. These procedures may have altered the local tissue and capsular environment (15), although bacterial colonization and chronic infection were not investigated.

The carcinomatous infiltration of the capsule wall, confirmed histologically, establishes a close anatomical relationship between the recurrent tumor and the periprosthesis tissue. Tumour infiltration, fibrosis, and capsular distortion might have increased local mechanical stress, but involvement of the host-derived fibrous capsule does not prove that the tumour disrupted the implant shell. Conversely, chronic periprosthetic inflammation after a previously silent rupture could theoretically alter the local microenvironment, as inflammatory and fibrotic responses have been demonstrated in human implant-capsule studies (16,17). These observations do not demonstrate reactivation of dormant tumor cells. In the absence of serial implant imaging and pathological evidence of silicone granuloma, neither the temporal sequence nor a causal relationship between rupture and recurrence can be established.

Implications and actions needed

The principal clinical implication is that progressive peri-areolar lesions, skin ulceration, new capsular abnormalities, or periprosthetic masses require timely histological confirmation, even when imaging appears more consistent with an implant-related complication. The absence of a preoperative biopsy in this patient represents a deviation from optimal diagnostic practice. PET/CT findings with negative or limited uptake should not alone be used to exclude recurrent malignancy.

This case also prompts reflection on decisions made at primary reconstruction. The retroareolar margin from 17 years earlier documented residual ductal tissue with epithelial hyperplasia, indicating ductal architecture retained beneath the nipple. The current recurrence, which included Paget disease of the nipple and invasive carcinoma beneath the NAC, provides a possible anatomical link between the two findings but does not establish their clonal relationship. The optimal extent and routine use of intraoperative retroareolar examination remain debated (18,19). The findings in this patient therefore support careful pathological assessment of retroareolar tissue but do not justify a universal recommendation for routine intra-nipple duct excision. The original external peri-areolar incision was selected to preserve NAC perfusion, whose vascular anatomy remains relevant when planning nipple-sparing mastectomy incisions (20).

Management of locoregional recurrence after mastectomy should also be individualized according to the anatomical extent of recurrence, receptor status, previous systemic treatment and radiotherapy, implant condition, chest-wall involvement, regional and distant staging, and feasibility of complete resection (21). In this patient, excision of the involved NAC and peri-areolar skin, implant removal, partial capsulectomy, and partial resection of the involved pectoralis major were selected to obtain definitive pathological assessment and local control. The posterior capsule was partially retained because of dense adherence to the chest wall and was not separately sampled; its management was intended to be considered during individualized postoperative radiotherapy planning. Postoperative chemotherapy, locoregional radiotherapy, and endocrine therapy were planned according to the extent and receptor profile of the recurrence.

Conclusions

This case presents a previously rarely reported scenario in which late breast cancer recurrence and silicone implant rupture coexisted 17 years after primary mastectomy and immediate reconstruction. All peri-areolar lesions were carcinomatous infiltration—not silicone granuloma—demonstrating that PET/CT cannot substitute for tissue biopsy in this population, particularly when tumour proliferative activity is low. Pre-operative breast MRI should also be prioritised over PET/CT in this clinical context.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://gs.amegroups.com/article/view/10.21037/gs-2026-0305/rc

Peer Review File: Available at https://gs.amegroups.com/article/view/10.21037/gs-2026-0305/prf

Funding: This study was supported by the National Key R&D Program of China (No. 2024YFC3405800), the Chinese Academy of Medical Sciences (CAMS) Innovation Fund for Medical Sciences (No. 2025-I2M-XHCL-002), and the National High Level Hospital Clinical Research Funding (No. 2025-PUMCH-A-192).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gs.amegroups.com/article/view/10.21037/gs-2026-0305/coif). Y.C. reports grants for the present manuscript from the National Key R&D Program of China (No. 2024YFC3405800), the CAMS Innovation Fund for Medical Sciences (No. 2025-I2M-XHCL-002), and the National High Level Hospital Clinical Research Funding (No. 2025-PUMCH-A-192). These grants were paid to the author’s institution. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this article and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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