A keloid is made up of dense, disorganized collagen fibers packed far more tightly than normal skin, along with overactive cells, an expanded blood supply, and nerve fibers that can trigger itching and pain. It’s not hollow, not filled with fluid, and not a pocket of infection. It’s solid tissue, overgrown and structurally distinct from both healthy skin and ordinary scars.
Thick, Tangled Collagen Bundles
The bulk of a keloid is collagen, the same structural protein found in all skin. But keloid collagen looks and behaves differently. Under a microscope, the hallmark feature is large, glassy (hyalinized) whorls of thickened collagen bundles, often called “keloidal collagen.” These bundles are much thicker than those in normal skin, and instead of running in organized parallel lines the way collagen does in a regular scar, they twist into dense, random tangles.
The type of collagen matters too. Normal skin has about eight parts Type I collagen (the strong, structural kind) for every one part Type III collagen (a thinner, more flexible fiber). In keloid tissue, that ratio drops to roughly 2:1. That means keloids contain a much higher proportion of Type III collagen than healthy skin does. This shift in composition contributes to the firm, rubbery texture you can feel when you press on a keloid.
Fibroblasts That Won’t Stop Building
Collagen doesn’t appear on its own. It’s produced by cells called fibroblasts, and keloids are packed with them. These aren’t ordinary fibroblasts. Many have transformed into a more aggressive type called myofibroblasts, which produce collagen at a much higher rate and also contract, pulling surrounding tissue inward. When researchers stain keloid tissue for a protein marker associated with myofibroblasts, the cells consistently light up positive.
What keeps these cells so active is a signaling molecule called TGF-beta, a growth factor that normally helps wounds heal and then quiets down. In keloid tissue, TGF-beta stays elevated. It drives fibroblast multiplication, stimulates collagen production, and promotes remodeling of the tissue around the cells. Worse, it creates a self-reinforcing loop: TGF-beta triggers the release of another protein called periostin, which in turn stimulates more TGF-beta. This “vicious cycle,” as researchers describe it, is a key reason keloids keep growing long after the original wound has closed.
Other immune signaling molecules, including IL-4, IL-13, and IL-22, are also found at elevated levels inside keloid tissue. These contribute to ongoing inflammation and further collagen overproduction, giving the scar a biological profile that in some ways resembles a slow-growing, benign tumor: the cells resist normal programmed death, proliferate excessively, and even invade surrounding tissue.
An Expanded Blood Supply
Keloids are not pale, bloodless lumps. They contain significantly more blood vessels than normal skin. In the shallow layers of a keloid, vascular density is roughly 1.5 times higher than in healthy skin. Deeper layers also show increased vessel density, along with more branching points where vessels split and spread.
This extra blood supply is driven by elevated levels of VEGF, a protein that stimulates new blood vessel growth. Keloid fibroblasts themselves produce VEGF, essentially building the infrastructure to keep themselves fed. The rich blood supply explains why keloids can appear pink, red, or purple, especially in lighter skin tones, and why they sometimes bleed easily if scratched or irritated.
Nerve Fibers and Why Keloids Hurt
Many people with keloids report itching, tenderness, or sharp pain, and the tissue itself helps explain why. Keloids contain small nerve fibers, and testing shows measurable differences in how these fibers respond to temperature and pain stimuli compared to normal skin. Researchers have found signs of small-fiber neuropathy within keloid tissue, meaning the tiny sensory nerves are damaged or behaving abnormally.
Chemical messengers called neuropeptides also play a role. Substance P, a molecule that transmits pain signals and promotes inflammation, is found at higher levels in keloid and other pathological scar tissue than in normal skin. Calcitonin gene-related peptide (CGRP), another pain-related signaling molecule, is also elevated. These neuropeptides don’t just cause discomfort. They feed back into the inflammatory process, potentially encouraging even more scar growth. This is why keloids can feel actively uncomfortable rather than just cosmetically bothersome.
How Keloid Tissue Differs From Normal Scars
A regular scar forms when the body patches a wound with collagen, then gradually remodels that collagen into something close to normal skin structure. The process has a built-in off switch. A keloid lacks that off switch. Its fibroblasts keep producing collagen, its growth factor signaling stays locked in the “on” position, and the tissue extends beyond the borders of the original injury.
At the genetic level, keloid tissue shows a distinct expression profile. Genes related to collagen production (COL1A1, COL3A1, COL10A1) are upregulated, along with genes involved in cell adhesion, potassium channels, and neural proteins. The overall pattern reflects a tissue that is actively growing and resisting the normal signals that would tell it to stop. This is why keloids so often recur after surgical removal: cutting away the visible mass doesn’t address the underlying cellular behavior driving it.
In short, a keloid isn’t just a lump of scar tissue. It’s a complex, living structure with its own blood supply, nerve network, and self-sustaining growth cycle, all built from the same materials your body uses to heal wounds, just assembled without the usual controls.