The Role of Acellular
Dermal Matrix in the
Treatment of Capsular
James D. Namnoum, MDa,*, Hunter R. Moyer, MDb
Capsular contracture remains the most frequent
device-related complication of breast surgery
with implants and has been an intractable problem
since the introduction of the silicone breast
implant in the 1960s. The ongoing, prospective
premarket approval trials of the 2 largest manufac-
turers of these devices Allergan (Irvine, CA, USA)
and Mentor (Santa Barbara, CA, USA) with
a follow-up rate of 67% to 92% have shown an
incidence of capsular contracture ranging from
1. Capsular contracture is the most frequent cause for device-related reoperation in patients under-
going breast augmentation and revision augmentation, and the second most common reason for
reoperation following reconstruction.
2. Many established techniques have been described to reduce or prevent recurrent capsular contrac-
ture, but they are not effective in all cases.
3. Acellular dermal matrix (ADM) in combination with capsulectomy can prevent or delay recurrent
4. The mechanism by which recurrent contracture is inhibited is not clear but may involve a delay of
inflammatory cell infiltrate into the matrix (including myofibroblasts) modulating the foreign
body reaction around the implant or a biomechanical interruption of the spherical contracture
5. More than 1 type of ADM has been shown to be effective at preventing recurrent capsular
6. More data are needed to determine whether the inhibition of capsular contracture in the setting of
ADM and implants is permanent, and to identify the critical accompanying steps necessary to ensure
lasting success from recurrent contracture.
James D. Namnoum, MD is a shareholder and consultant, Allergan Corporation and Alure Medical.
Hunter R. Moyer has nothing to disclose.
aPrivate Practice, Atlanta Plastic Surgery, Emory University, 975 Johnson Ferry Road, Suite 100, Atlanta,
GA 30319, USA
bDivision of Plastic Surgery, Emory University, 975 Johnson Ferry Road, Suite 100, Atlanta, GA 30342, USA
* Corresponding author.
E-mail address: firstname.lastname@example.org
?Acellular dermal matrix?Capsular contracture
?Silicone breast implants?Silicone gel
?Breast augmentation ?Breast reconstruction
Clin Plastic Surg 39 (2012) 127–136
0094-1298/12/$ – see front matter ? 2012 Elsevier Inc. All rights reserved.
9.8% to 14.8% for primary augmentation, 20.5%
to 22.4% for revision augmentation, and 13.7 to
contracture is the most common reason for reop-
eration in these patients (14.5% to 35.2%) and
appears to increase with time.1,2
ETIOLOGY OF CAPSULAR CONTRACTURE
All implanted materials failing to acquire a blood
supply incite a prototypical foreign body reaction
characterized by the development of a scar inter-
face between the foreign body and its biologic
compliant as opposed to other implanted devices
such as pacemakers or total joints, an exuberant
foreign body reaction that becomes contractile
around the implant will lead to deformity and
pain. The resulting capsular contracture may
prompt a need for reoperation, complicating the
result and leading to additional recovery and
Several factors have been associated with an
increased risk for capsular contracture, including:
? Subclinical infection with biofilm3
? Silicone versus saline implants4
? Smooth versus textured surfaces5,6
? Postoperative hematoma8
? Silicone breast implant ruptures9
? Reoperative implant surgery1,2
? Radiation therapy proceeding or following
reconstruction with implants.10–14
Pathogenesis of Capsular Contracture
Capsular contracture appears to appear at two
1. Early, thought to result from poor sterility or
2. Late, as a result of a chronic inflammatory
In either case, the exact biologic processes
leading to the development of a thick, contracting
capsule isunclear. Evidence from avariety ofsour-
ces has implicated the activation of the fibroblast
into a contractile myofibroblast as the critical event
in the contracture process.
Myofibroblasts have been noted in the capsules
around breast implants since the 1970s.15Early
in vitro studies of capsular tissue demonstrated
agonists and antagonists similar to that expected
from smooth muscle preparations.16In Hinz’s
description,17fibroblasts differentiate into acti-
properties conferred from a smooth muscle actin
(SMA) in a 2- step process under the direction of
transforming growth factor beta (TGFb1), special-
ized extra cellular matrix (ECM) proteins like fibro-
nectin, and the mechanical microenvironment.
Smad signaling is the major pathway through
which TGFb1 regulates expression of a-SMA in
fibroblasts. In an experimental model comparing
wild-type and knockout mice lacking Smad, irra-
diation caused thick, distorted capsules in the
wild-type mouse but not the knockout mice,
presumably due to inhibition of TGFb.18Zinman
and collegues19demonstrated that rats treated
with the angiotension-converting enzyme inhib-
itor enalapril, a potent inhibitor of TGFb1, had
significantly less peri-prosthetic fibrosis than
untreated animals presumably due in part to the
role TGFb1 plays in activation of fibroblasts to
The mechanical microenvironment also plays
a role in myofibroblast differentiation due to alter-
ation in ECM stiffness. According to Hinz,17fibro-
blasts residingin intact
shielded by normal ECM. With trauma or repetitive
injury, increasing ECM stiffness provides a strong
mechanical signal, inducing the formation of a–
SMA negative stress fibers that persist until the
normalization of matrix compliance. Factors that
antagonize TGFb1, normalize matrix compliance,
and improve cell-to-cell contact down-regulate
a–SMA in vitro; decreasing gel stress in vitro,
a model for stress shielding, causes myofibroblast
Evidence that Acellular Dermal Matrix Plays
a Useful Role in the Treatment of Capsular
Salzberg demonstrated an incidence of capsular
contracture of 0.4% in review of his direct-to-
implant immediate breast reconstruction in 466
breasts using ADM with 21 month follow-up
including 0% contracture following irradiation.20
Maxwell showed a 0% incidence of capsular
contracture at 1 year postoperatively following
ADM use for revisionary breast surgery.21
Stump demonstrated the absence of capsule
formation aroundimplants covered in ADM in a pri-
in myofibroblast staining in the ADM-covered
Namnoum & Moyer
implants as compared with the capsules in im-
plants not covered with ADM.22
Basu demonstrated significantly decreased in-
flammatory response in biopsies of ADM as com-
pared with native capsule around expanders at the
time of second-stage exchange, suggesting that
ADM potentially delayed the process of capsule
Technique for Correction of Capsular
Contracture with ADM
There is no consensus as to the required steps
to optimize the results for preventing or delaying
the recurrence of capsular contracture when
ADM is used. In a retrospective review, Collis24
demonstrated a significantly lower incidence of
recurrent subglandular contracture when total
capsulectomy was performed rather than anterior
capsulectomy only; this seems a reasonable
approach when possible, especially when con-
sidering the biofilm theory of capsular contracture
or retained foreign material (as in ruptured sili-
cone gel devices) as causative for capsular
All the following may play a role in enhancing
? Meticulous technique
? Precise hemostasis
? Conversion to a subpectoral plane
? Use of textured devices
By the same token, the ideal type (human versus
animal), thickness, size, or shape of ADM required
to create the optimal effect has not been demon-
strated. If ADM exerts its effects through stress
shielding of myofibroblasts or a delay in the inflam-
matory response due to the slow repopulation of
the matrix, it stands to reason that larger and thick-
er pieces might perform better than smaller and
orly with interrupted or running absorbable sutures
or fixed in place using parachute sutures that are
exited through the skin, tied loosely, covered with
an occlusive dressing and removed one week later.
Drains are a necessity and are discontinued when
A 38-year-old patient who was 5 ft 8 in and 125 lbs underwent subpectoral augmentation with smooth-
walled silicone gel devices and circumvertical mastopexy. At 1 year postoperatively, she developed
a grade 3 capsular contracture of the right breast with high riding implant. At reoperation, a dense
capsule was noted on the right. A total periprosthetic capsulectomy was performed; 6 ? 16 cm piece
of thick ADM was inset with running sutures to the anterior flap, and new implants were placed.
Two years following revisionary surgery, a grade 1 capsule was present on the right (Case 1, Figs. 1–4).
Fig. 1. Preoperative view.
ADM for Capsular Contracture Treatment
Fig. 2. 1.5 years postoperative subpectoral augmentation with smooth walled silicone gel implants and cir-
cumvertical mastopexy. Grade 3 capsular contracture right breast.
Fig. 3. (A, B) Operative plan: total periprosthetic capsulectomy and acellular dermal matrix placement;
Fig. 4. (A, B) 2 years following revisionary surgery. Grade 1 capsule right breast; grade 2 capsule left breast.
Namnoum & Moyer
Case 2: Capsular contracture
This case involved a 28-year-old, 5 ft 4 in, 115 lb patient. One year following subpectoral augmentation
with smooth-walled silicone gel devices, she developed a grade 4 capsular contracture of left breast. At
operation, a dense capsule was noted on the left; a total periprosthetic capsulectomy was performed
and 4 ? 16 cm pieces of thick ADM were placed bilaterally. Implants were exchanged. Grade 1 capsules
are present bilaterally at 2 years (Case 2, Figs. 5–8).
Fig. 5. (A, B) Intraoperative view: grade 4 capsular contracture left breast.
Fig. 8. (A–C) Appearance of breasts 2 years postoperatively. Grade 1 capsules bilaterally.
Fig. 6. Following total periprosthetic capsulectomy.
Acellular dermal matrix draped over breasts and
parachuted into position. Internal running sutures.
Fig. 7. Apperance at completion of revisionary
surgery. Smooth implants exchanged for textured
ADM for Capsular Contracture Treatment
Case 3: Capsular contracture and poor tissue coverage
This case involved a 42-year-old patient with prior history of breast augmentation following bilateral
nipple sparing mastectomies (right prophylactic, left breast cancer) and silicone gel implant reconstruc-
tion. She underwent postoperative radiation of the left breast. A grade 4 capsular contracture of left
breast ensued with rippling and poor tissue coverage of the right breast. She desired smaller implants.
Operative plan included near total capsulectomy of the right breast, with ADM placement (6 ? 16 cm,
thick), downsizing of implants bilaterally, conversion to textured devices, and ADM placement on the
right to correct rippling. At 2 years postoperatively, grade 2 capsule is present on the left, and a grade
1 capsule is present on the right (Case 3, Figs. 9–11).
Fig. 9. (A, B) 42-year-old following bilateral nipple sparing mastectomies (right prophylactic, left breast
cancer) and postoperative radiation of left breast. Grade 4 capsular contracture left breast. Rippling medially
and thin coverage right breast.
Fig. 10. (A, B) Before revisionary surgery. Plan near to total periprosthetic capsulectomies, acellular dermal
matrix placement, pocket reshaping, implant exchange (downsize).
Fig. 11. (A, B) 2 years following revisionary surgery with acellular dermal matrix. Grade 2 capsule left; grade 1
Case 4: Ruptured saline device and capsular contracture
This case involved a 51-year-old, 5 ft 10 in 145 lb patient with pectus excavatum deformity. She under-
went right breast augmentation subpectorally with a single silicone gel device in the 1970s. Subse-
quently, the patient had replacement with saline devices bilaterally in the 1990s. She presented with
a ruptured saline device on the right right breast, and grade 3 capsular contracture of left breast. Intra-
operative photos demonstrate planned placement of ADM and parachute sutures tied after devices
were exchanged and drains placed. Fat was grafted to the upper pole of the right breast, and ADM
was placed to correct step off (Case 4, Figs. 12–16).
Fig. 12. (A, B) 51-year-old pectus deformity with deflation right saline breast implant and grade 3 capsular
contracture left implant.
Fig. 13. (A–C) Before revisionary surgery. Plan total periprosthetic capsulectomies, acellular dermal matrix
(ADM) placement left breast (breast plastic surgery [BPS] contour 2); ADM chest wall implant and fat grafting
right upper chest step-off deformity. Bilateral implant exchange.
Fig. 14. Intraoperative view showing planned place-
ment of acellular dermal matrix left.
Fig. 15. Intraoperative view stacked acellular dermal
matrix for correction contour deformity upper right
chest; parachute sutures exiting skin and tied loosely
ADM for Capsular Contracture Treatment
Fig. 16. At completion of revisionary surgery.
Case 5: Bilateral breast distortion with capsular contractures
This case involved a 67-year old 5 ft 3 in, 120 lb woman. This patient underwent bilateral mastectomies
and reconstruction in the 1970s with expanders and silicone gel devices. She developed marked breast
distortion bilaterally with grade 4 capsular contractures. Appearance 6 months after bilateral total peri-
prosthetic capsulectomy, ADM placement (BPS contour 2), bilateral implant exchange with placement of
textured wall devices, and fat grafting of breasts (Case 5, Figs. 17–21).
Fig. 17. (A, B) 67-year-old patient 30 years following bilateral mastectomies and expander/implant reconstruc-
tion. Profound distortion of breasts due to grade 4 capsular contractures.
Fig. 18. Before revisionary surgery.
ADM for the prevention or correction of capsular
contracture is effective in a variety of cases and
appears to have a beneficial effect for up to 3
years. Adjunctive procedures for treating the
capsule as well as the size, type, and thickness
of the ADM required for optimal effectiveness
Fig. 21. (A–C) Appearance 6 months postoperatively.
Fig. 19. Intraoperative view. Acellular dermal matrix
(BPS contour 2) before inset with parachute sutures.
Fig. 20. Acellular dermal matrix inset into pocket.
ADM for Capsular Contracture Treatment
have not been established. The longevity of
correction has not been established. The mecha-
nism by which ADM prevents or delays recurrent
capsular contracture is at present unclear.
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