Capsular Contracture Part One: What is it?

By: Oscar Ochoa, MD

Blogs
March 15, 2017

Capsular contracture is the pathologic result of a chronic inflammatory process around a breast implant used for aesthetic or reconstructive purposes. Varying degrees of capsular contracture exist and can range from a mild form represented by minimal peri-prosthetic firmness and no subjective symptoms to a severe form that dramatically distorts the breast implant and is accompanied by persistent and significant breast pain. In order to better understand effective methods of prevention and treatment, the etiology of capsular contracture must be reviewed.

Etiology

Recognized clinical causes of capsular contracture are indolent bacterial contamination (or biofilm), tissue trauma, hematoma, radiation, and silicone gel bleed. The pathologic process common to all these individual antecedent sources is the development of an inflammatory cell-mediated chronic inflammatory state around the breast implant. Each of the know sources of capsular contracture initiate a persistent and complex cascade of inflammatory cell infiltration around the implanted breast prosthesis.

Immediately following the introduction of an inflammatory stimulus around the breast implant such as each of the know causes of capsular contracture, inflammatory cells called neutrophils infiltrate the area of infection or injury with the purpose of neutralizing the stimuli with release of proteolytic enzymes. These powerful enzymes are designed to break down cellular particles in the inflammatory environment and initiate the reparative process. However, these power enzymes also have the capacity to injury normal tissue in a non-selective manner.

Once the reparative process has been initiated by neutrophils, a separate population of inflammatory cells called macrophages are subsequently recruited into the inflammatory site, not only to engulf and digest the remnants of inflammatory stimuli, but also to modulate the reparative process through release of growth factors and substances called chemokines that recruit other inflammatory cells as well as bone marrow-derived stem cells that will differentiate to form the foundation of healing tissue. Moreover, a critical function of macrophages is also to coordinate the efflux of neutrophils away from the site of inflammation when the stimulus is neutralized. If the inflammatory stimulus is minimal and completely eliminated, this coordinated cascade concludes with formation of a thin capsule around the breast implant devoid of any inflammatory cells. If neutrophils, however, remain in the tissue surrounding the implant due to ongoing stimuli, collateral damage to normal tissue continues perpetuating the inflammatory and reparative processes resulting in a thick and constricting capsule.

The constricting quality of capsular contracture has been a subject of research previously due to the presence of a unique cellular population within the capsule called myofibroblasts. These unique cells not only produce collagen molecules, which are the building blocks of the architectural scaffold where cells reside, but also have the capacity to contract much like normal muscle cells. Rows of linearly oriented myofibroblasts contract around an implant leading to shape distortion and tightness. The origin of the myofibroblast is an ongoing area of research but data suggest these cells are formed from bone marrow derived mesenchymal stem cells that are induced to differentiate by macrophage-produced cytokines and growth factors.    

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