When a patient asks me about scarring, I can say something rare: I have spent years studying — at the molecular level, in a Harvard laboratory — exactly why scars form the way they do. That knowledge does not live in a textbook I read. It lives in research I conducted, published, and had scrutinized by the world's leading scientists. And it informs every decision I make before I ever pick up a scalpel.
What a scar actually is — and why most people misunderstand it
Here is what most people believe about scars: they are what happens after surgery is over. The wound closes, the body heals, and the scar is what is left behind. The surgeon's job, in this view, is to perform excellent surgery — and the scar is somebody else's problem. Time's problem. The body's problem.
This is wrong. And understanding why it is wrong is the foundation of everything I do.
A scar is not something that happens to a wound. It is something the body builds — deliberately, systematically, beginning the moment tissue is disrupted. The process starts with the first incision. The biological cascade that will eventually determine how your scar looks, how it feels, and how much it fades begins not in recovery, not in the healing room, but in the operating theater, in the first seconds of the procedure.
"The scar is not an afterthought. It is the first thought. Everything that follows — placement, tension, closure — is an intervention in a biological process that is already underway."
The key molecule in this process — the one my doctoral research at Harvard focused on specifically — is called CCN2, also known as connective tissue growth factor. When tissue is disrupted, CCN2 appears at the leading edge of the wound. It tells skin cells called keratinocytes to migrate, adhere, and divide. It activates the signaling pathways that determine how collagen is laid down. And how collagen is laid down determines, more than almost any other factor, what your scar will look like.
My research identified precisely when CCN2 appears, what it does, and how it is regulated. This is not abstract biology. It is a map of the scar — and knowing that map changes how I operate.
Reference: Kiwanuka E et al. "CCN2 is transiently expressed by keratinocytes during re-epithelialization and regulates keratinocyte migration via the Ras-MEK-ERK signaling pathway." Journal of Surgical Research, 2013 · Kiwanuka E et al. "CCN2 promotes keratinocyte adhesion and migration via integrin α5β1." Experimental Cell Research, 2013
The incision as a biological event — not just a technical one
Every incision creates a wound. That sounds obvious, but its implications are not. The moment a scalpel passes through skin, the body's healing machinery activates. Inflammatory cells rush to the site. Growth factors are released. The process of building new tissue begins. And at the center of that process is a cascade of molecular signals — including CCN2 — that will govern how the wound closes and what it leaves behind.
This means that the decisions I make at the incision — its placement, its length, its angle, its depth — are not only technical decisions. They are biological decisions. Each one either supports or interferes with the healing process that is about to begin.
An incision placed in a natural skin tension line heals with less collagen deposition than one placed against it. An incision closed under excessive tension will scar more prominently than one closed with precision and care. An incision made with the right tool, at the right angle, with the right pressure — begins healing better before I have even placed the first suture.
Surgeons who were not trained in wound biology approach the incision as a beginning: make the cut, do the procedure, close the wound, wait for the result. I approach it differently. The incision is itself a healing intervention. Every decision I make at that moment is informed by understanding what is happening, molecularly, in the tissue I am entering.
Why this matters especially for patients with darker skin
I want to address something directly, because it comes up in my consultations frequently and deserves an honest answer: patients with darker skin tones, keloid histories, or hyperpigmentation concerns are right to be more cautious about who performs their surgery. The stakes are higher. The biology is different. And far too few surgeons have the training to address it properly.
Keloid formation — where the scar grows beyond the original wound boundary — is driven by an overactivation of exactly the signaling pathways my research addresses. The CCN2 cascade, the inflammatory signals, the collagen deposition process: all of these behave differently in skin with a higher predisposition to keloid formation. Understanding this at the molecular level is not a luxury. It is a clinical necessity.
"The same incision, placed by two different surgeons, can produce two completely different scars. The difference is not luck. It is knowledge — applied before the first cut is made."
My approach for patients with these concerns begins at the consultation, not the operating room. I ask about family history. I examine existing scars carefully. I modify incision placement, closure technique, and post-operative management based on each patient's specific biology. The protocol is individualized not as a marketing claim but as a scientific methodology — because the evidence demands it.
What I can offer patients with darker skin, keloid histories, or hyperpigmentation concerns is this: a surgeon who has not only trained in scar management, but who has generated original research on the molecular mechanisms of scar formation. There is no substitute for that depth of knowledge when the stakes are highest.
Reference: Kiwanuka E et al. "TGF-β1 regulates the expression of CCN2 in human keratinocytes via Smad-ERK signalling." International Wound Journal, 2017
What happens after the incision — and why the protocol matters
The incision is the beginning, not the end. The molecular cascade that determines your scar continues for days, weeks, and months after surgery. The wound microenvironment — how much oxygen reaches the tissue, what temperature the healing zone is maintained at, how much moisture is present, what inflammatory signals are still active — all of these factors influence the final outcome.
My research on the external wound microenvironment confirmed what clinical practice increasingly supports: post-operative conditions are not incidental. They are active determinants of healing quality. This is why my recovery protocols are not generic. They are built around the biology of the specific procedure each patient has undergone — and adapted for each patient's specific physiology.
Traditional surgical drains introduce foreign material into the healing wound environment — a potential source of inflammation and a disruption to the microenvironmental conditions that support optimal healing. My drain-free surgical protocol, used across breast procedures, is not simply about patient comfort (though it dramatically improves recovery experience). It is grounded in wound biology: keeping the healing environment as clean, controlled, and undisrupted as possible from the moment the procedure ends.
The post-operative care I provide — including personal post-operative check-in calls and direct availability during the first week of recovery — is not a courtesy. It is clinical. I am tracking your healing. I am watching for early signs that anything is diverging from the expected trajectory. And I am available to respond in minutes if it does, because early intervention in the healing cascade is far more effective than late correction.
Reference: Kruse CR, Kiwanuka E et al. "The external microenvironment of healing skin wounds." Wound Repair and Regeneration, 2015
What this means for the patient sitting across from me
I want to end with something concrete, because I believe patients deserve directness.
When you come to see me, you are not coming to see a surgeon who learned about scars in training and has been applying those lessons ever since. You are coming to see a surgeon who spent years in a research laboratory generating original knowledge about wound healing — who published that knowledge in peer-reviewed journals and had it scrutinized by scientists whose entire careers are devoted to this field — and who then spent years more at Memorial Sloan Kettering and Brown University learning to apply that knowledge in the operating room.
The result is a surgical approach that is genuinely different. Not in ways that require a microscope to detect. In ways that show up in your scar — in how minimal it is, how quickly it fades, how completely it disappears into your skin. In ways that show up in your recovery — in how you feel in the first week, how quickly you return to your life, how the process surprises everyone around you.
"The best scar is the one that no one notices. Getting there requires understanding — at the deepest level — exactly how it forms."
I believe that every patient deserves to understand what informs their surgeon's decisions. Not in jargon. Not in a credential list. In plain language that explains why the science matters for their outcome. This essay is my attempt at that explanation.
If it raises questions — and I hope it does — I would love to answer them in person. The consultation is where the science meets your specific situation, your specific anatomy, your specific goals. That is where the real conversation begins.