Inside the Needle: What Steroid Injections Actually Do to a Keloid

Ask a dermatologist how they treat most keloids and the first answer is usually the same: intralesional corticosteroid injections, almost always triamcinolone acetonide. It has been the frontline therapy for more than five decades, yet patients often walk out of the clinic knowing only that they got "a steroid shot in the scar." Understanding what that injection is actually doing helps explain the timeline, the side effects, and why some keloids shrug it off.

A keloid is a wound that never stopped healing. In normal repair, fibroblasts lay down collagen for a few weeks, then enzymes called matrix metalloproteinases remodel and trim that collagen back. In a keloid, fibroblasts stay switched on. They overproduce type I and type III collagen, they resist programmed cell death, and they respond abnormally to a signaling protein called transforming growth factor beta, or TGF-beta, which acts like a stuck accelerator on scar production.

Triamcinolone attacks this process on several fronts at once. First, it suppresses fibroblast proliferation directly, slowing the population of cells making excess collagen. Second, it reduces TGF-beta signaling, easing off that accelerator. Third, it increases the activity of collagenase, the enzyme that breaks collagen down, partly by suppressing collagenase inhibitors that keloid tissue produces in abundance. Fourth, it constricts the small blood vessels feeding the scar, which is why an actively growing red keloid often fades toward the color of surrounding skin before it flattens. The net effect is a shift in the balance: less collagen deposited, more collagen degraded.

This is why results take months, not days. The injection does not dissolve the scar. It changes the metabolic direction of the tissue, and the existing collagen still has to be broken down and cleared. Most protocols call for injections every three to six weeks, and meaningful flattening typically requires three to six sessions or more. Patients who expect a single shot to erase a keloid are set up for disappointment by the biology, not by the medication.

Concentration and placement matter more than most patients realize. Triamcinolone is typically used at 10 to 40 milligrams per milliliter, adjusted for the thickness and location of the keloid. The drug must be delivered into the body of the scar itself, which is dense and resists injection. If the needle deposits steroid into the normal skin or fat around the keloid instead, the treatment does little for the scar and raises the risk of side effects in healthy tissue. This is one reason outcomes vary so much between providers and why injecting a firm keloid takes real pressure and technique.

The side effects are the mechanism working in the wrong place. The same collagen suppression that flattens a keloid can thin normal skin, producing a dented or shiny patch called atrophy. Steroids can also trigger hypopigmentation, a lightening of skin color that is more visible in darker skin tones, and telangiectasias, which are fine visible blood vessels. These effects are dose related and more common with higher concentrations, frequent sessions, or drug spreading beyond the scar. They are often partially reversible, but not always, which is why responsible clinicians titrate rather than blast.

Why do some keloids resist steroids entirely? Reported response rates vary widely, roughly 50 to 80 percent for flattening and symptom relief, and recurrence after stopping treatment is common, in some series affecting a third to half of treated keloids over several years. Older, pale, rope-like keloids with low cellular activity respond less well, because there are fewer active fibroblasts for the steroid to suppress. Very large or long-standing keloids may simply contain too much established collagen. And some keloid fibroblasts appear less sensitive to glucocorticoid signaling in the first place.

This is where combination therapy has changed practice. The most studied pairing adds 5-fluorouracil, a chemotherapy agent used in tiny intralesional doses, mixed with triamcinolone in the same syringe. 5-FU blocks fibroblast DNA synthesis and independently interferes with TGF-beta driven collagen production. Multiple randomized trials have found the combination flattens keloids more effectively than steroid alone, with lower rates of skin thinning and pigment loss, because each drug can be used at a lower dose. Other adjuncts include pressing the keloid with cryotherapy before injecting, which softens the tissue and makes drug delivery easier, and pairing injections with silicone sheeting or pressure therapy between sessions.

The practical takeaway: steroid injections are not a quick fix and not a failure when the first session changes little. They are a slow rebalancing of scar metabolism that requires a series, honest dosing, precise placement, and often a partner drug. Patients who understand that framework can judge their progress by the right markers, softening and reduced itch first, flattening later, and can ask better questions when a keloid does not respond, starting with whether a combination protocol makes sense for their scar.

Related reading: Fluorouracil (5-FU) injections: a second-line option for stubborn keloids.