ASAPS 2010: more on biofilms and capsular contracturePosted on May 2, 2010
As loyal blog readers know, capsular contracture is arguably the most frustrating complication of breast implants, whether they are used for reconstruction or for cosmetic purposes. For years, no one has been particularly sure on why capsules occur, despite all the efforts of the physician and the patient to the contrary.
About a year ago, I wrote a blog entry discussing the theory of biofilms as a cause of the contracture. Biofilms, just to review, are what happens when free-floating bacteria settle on a surface, and set up a colony. The cover themselves with a protective slime layer, and emit certain chemicals to trick the body’s immune system, so they can exist “under the radar”. Biofilms can form on any implant, whether it’s a breast implant, an orthopedic implant, dentures, or injectable fillers.
During the past year, more and more evidence definitively linking biofilms and capsular contracture has been appearing. At ASAPS 2010, we had an update on this. For example, biofilms can be found in the majority of patients with capsular contracture, and are absent in the majority of patients who have no capsule problems. Usually, the bacteria involved is Staph. epidermidis, which lives on the skin normally, and usually doesn’t cause any problems. It also lives within normal breast tissue too, due to the duct connections between skin, nipple and breast gland.
The main problem is: biofilms are notoriously hard to eliminate. Giving doses of antibiotics only temporarily knocks the biofilm down, but it bounces back. Low dose antibiotics have, in some studies, seemed to stimulate the growth of the biofilm. Antibiotic-impregnated implants also only seem to have a temporary effect. These obvious methods have been tried – without success.
It turns out, understanding how biofilms work is fairly complicated. The bacteria actually communicate with one another, using certain signalling molecules. These molecules tell the bacteria when to stick to a surface, and when to form a colony, and so forth. Figuring out how to manipulate these signals is an ongoing area of research. If we could come up with a treatment that blocked these signals, we could probably beat the biofilm problem.
Until that day comes, if we assume that capsules are related to a biofilm layer on the implant which is nearly impossible to remove, it would make sense to consider the following steps at surgery when capsules are involved:
– remove as much of the capsule as practically possible, without causing damage to the surrounding tissue. In other words, capsulectomy (removal) would theoretically be preferred over capsulotomy (releasing cuts) or “neo-pectoral pocket” techniques;
– switch to a brand-new, and thus, biofim free, implant, even if the old implant looks OK;
– use techniques to minimize the possibility of bacterial contamination of the implant, such as opening the implant at the last possible moment, washing it and the pocket with an antibacterial solution, and considering devices like the Keller funnel.
The problem is – there is no science to tell us how much improvement any of these techniques will give a patient, in terms of reducing the rate of recurrent encapsulation. In particular, it would be helpful to know exactly how much using a new implant would help, compared to keeping the old one. Then the patient could decide on the cost-benefit ratio.
Hopefully, those studies will be here soon.