A rabbit model for capsular contracture: development and clinical implications.

BACKGROUND: Capsular contracture remains one of the most common complications involving aesthetic and reconstructive breast surgery; however, its cause, prevention, and treatment remain to be fully elucidated. Presently, there is no accurate and reproducible pathologic in vitro or in vivo model examining capsular contracture. The purpose of this study was to establish an effective pathologic capsular contracture animal model that mimics the formation of capsular contracture response in humans. METHODS: New Zealand White rabbits (n = 32) were subdivided into experimental (n = 16) and control groups (n = 16). Each subgroup underwent placement of smooth saline mini implants (30 cc) beneath the panniculus carnosus in the dorsal region of the back. In addition, the experimental group underwent instillation of fibrin glue into the implant pocket as a capsular contracture-inducing agent. Rabbits were euthanized from 2 to 8 weeks after the procedure. Before the animals were euthanized, each implant was serially inflated with saline and a pressure-volume curve was developed using a Stryker device to assess the degree of contracture. Representative capsule samples were collected and histologically examined. Normal and contracted human capsular tissue samples were also collected from patients undergoing breast implant revision and replacement procedures. Tissue samples were assessed histologically. RESULTS: Pressure-volume curves demonstrated a statistically significantly increased intracapsular pressure in the experimental group compared with the control group. The experimental subgroup had thicker, less transparent capsules than the control group. Histologic evaluation of the rabbit capsule was similar to that of the human capsule for the control and experimental subgroups. CONCLUSIONS: The authors conclude that pathologic capsular contracture can be reliably induced in the rabbit. This animal model provides the framework for future investigations testing the effects of various systemic or local agents on reduction of capsular contracture.

The alar contour graft: correction and prevention of alar rim deformities in rhinoplasty.

One of the most common problems affecting both the primary and secondary rhinoplasty patient is deformity of the alar rim. Typically, this deformity is caused by congenital malpositioning, hypoplasia, or surgical weakening of the lateral crura, with the potential for both functional and aesthetic ramifications. Successful correction and prevention of alar rim deformities requires precise preoperative diagnosis and planning. Multiple techniques of varying complexity have been described to treat this common and challenging problem. Over the past 6 years (1994 through 2000), the authors have employed a simple technique in 123 patients for alar retraction that involves the nonanatomic insertion of an autogenous cartilage buttress into an alar-vestibular pocket. Among the 53 patients who underwent primary rhinoplasty in this study, 91 percent experienced correction or prevention of alar notching or collapse. However, correction was achieved for only 73 percent of the patients who underwent secondary rhinoplasty; many of whom had alar retraction secondary to scarring or lining loss. In patients with moderate or significant lining loss or scarring, a lateral crural strut graft is recommended. The alar contour graft provides the foundation in the patient undergoing primary or secondary rhinoplasty for the reestablishment of a normally functioning external nasal valve and an aesthetically pleasing alar contour. This article discusses the anatomic and aesthetic considerations of alar rim deformities and the indications and the surgical technique for the alar contour graft.