Scar
A scar is an area of fibrous tissue that replaces normal skin or other biological structures following injury. Scarring represents the final phase of the body’s wound-repair mechanism, occurring whenever a lesion is sufficiently deep to disrupt the dermis or other connective tissues. Although superficial wounds may heal without leaving a visible trace, most injuries—whether the result of trauma, disease or surgery—produce some degree of scar formation. Organisms capable of complete regeneration provide the principal exception, restoring damaged tissues without fibrosis.
Scar tissue consists of collagen, the same protein present in healthy connective tissue, but its fibre architecture differs markedly. Normal collagen is laid down in a random basket-weave pattern that allows flexibility, whereas scar collagen forms densely packed, crosslinked fibres aligned predominantly in a single direction. This arrangement results in inferior functional properties; scarred skin is less resistant to ultraviolet radiation, more prone to mechanical shearing and does not restore hair follicles, sweat glands or other specialised structures.
Types of scarring
Although all scars contain collagen, their appearance and structure vary depending on how collagen is deposited, how much is produced and how the wound heals.
Hypertrophic scarsHypertrophic scars develop when excess collagen is synthesised during healing, causing a raised, firm lesion confined to the boundary of the original wound. In lighter-skinned individuals they appear red or pink, while in darker-skinned individuals they may appear dark brown. They commonly emerge four to eight weeks after injury, especially when infection, excessive tension on wound edges or traumatic injury disrupts normal healing.
Keloid scarsKeloids represent a more extreme form of over-production of collagen. They may continue growing for months or years and can extend beyond the original wound margins. Although benign, they form bulky, tumour-like masses that may itch or cause discomfort. Keloids are more frequent in people with high melanin levels and are associated with surgery, acne, body piercings and occasionally spontaneous onset. Surgical excision alone often aggravates their recurrence.
Atrophic scarsAtrophic scars form depressions or pits in the skin where underlying supportive tissues such as fat or muscle have been lost. They frequently follow acne, chickenpox, certain infections, surgical procedures or injuries. Some genetic connective-tissue disorders, including Ehlers–Danlos syndrome, predispose to this type of scarring. The skin appears sunken because collagen is either insufficiently deposited or organised in a manner that fails to restore normal contour.
Stretch marks (striae)Striae arise when the skin stretches rapidly, such as during pregnancy, rapid weight gain or growth spurts. They may also appear when healing tissue is placed under tension near joints. Although often classified separately, they represent a form of scarring and gradually fade over time. Elevated corticosteroid levels can contribute to their formation.
Umbilical scarsPlacental mammals acquire an umbilical scar—commonly called the navel—following the severing and healing of the umbilical cord after birth. In egg-laying animals, umbilical scars may be visible briefly or persist depending on species.
Scarring also occurs in internal organs. Myocardial infarction, for example, produces fibrotic scar tissue in the heart muscle, reducing functional capacity and potentially leading to heart failure. In contrast, bone can heal without permanent loss of strength, representing one of the few adult tissues capable of near-perfect structural restoration.
Pathophysiology of scar formation
Scarring reflects the body’s attempt to restore tissue integrity after damage. The process depends heavily on how quickly re-epithelialisation occurs. Small full-thickness wounds under approximately 2 mm may heal scar-free because new skin forms rapidly. Larger or deeper injuries involve complex interactions between inflammatory cells, fibroblasts and the extracellular matrix.
When a wound occurs, bleeding forms a clot, establishing a provisional matrix. In this early phase there is no scar; rather, the matrix serves as a scaffold for incoming cells. Fibroblasts migrate into the matrix and begin producing collagen. As collagen accumulates, it becomes increasingly crosslinked, leading to a dense and inelastic scar. This fibrotic wall impedes cell communication and regeneration, causing the healed tissue to differ in texture and mechanical properties from unwounded tissue.
Mechanical stress plays a role in determining whether a wound scars. Loading of the extracellular matrix encourages fibrosis, whereas stress-shielding can reduce scarring. Burn injuries, particularly deeper second-degree burns, invariably produce scars and often result in loss of hair follicles. Sweat glands also do not regenerate, impairing thermoregulation within scarred regions.
Structural differences between scars and normal skin are significant. Rete pegs—finger-like projections anchoring the epidermis to the dermis—are absent in scars, making scarred skin more susceptible to shearing forces. Elastic fibres are sparse or absent for months after injury, further contributing to rigidity.
Not all tissues scar in the same manner. The endometrium of the uterus uniquely regenerates rapidly each month without fibrosis, demonstrating a rare capacity for repeated scar-free repair in adult mammals.
Collagen synthesis and fibroblast activity
An injury does not become a scar until epithelial healing is complete. Collagen overexpression may continue for months, particularly in hypertrophic and keloid scars. Fibroblasts proliferate in circular and cyclical patterns, depositing thick bundles of collagen that lend scars their characteristic uneven, firm texture. These cells also contribute to wound contraction—a normal part of healing—but excessive contraction can lead to tight or restrictive scars.
Over time, fibroblasts reorganise collagen fibres within the matrix, gradually leading to scar maturation. Mature scars become paler and less vascular but remain structurally distinct from normal tissue.
Factors influencing scar severity
The character of a scar depends on the location of the wound, the patient’s age and the nature of the injury. Large, deep or infected wounds typically produce more noticeable scars. Wounds healing by secondary intention—where tissue fills in from the base upward rather than via direct closure—tend to exhibit more pronounced fibrosis. Redness following injury represents vascular activity rather than scarring and eventually resolves, although in some cases it may take months or years.