A scar is a patch of fibrous tissue that replaces normal skin structure after a deep injury. The formation of a scar represents the body’s achievement in closing a wound and restoring barrier function. This process of repair, however, is imperfect, leaving a permanent mark where the original tissue architecture once existed. While some organisms, and human fetal skin, can achieve true regeneration—a perfect restoration of the original tissue—adult skin defaults to a rapid, structurally sound, but biologically inferior repair process. This decision to “patch” rather than “rebuild” prioritizes survival over perfection.
The Three Phases of Normal Wound Repair
The body initiates wound repair immediately following a deep skin injury, starting with the inflammatory phase. This initial stage is defined by hemostasis, where blood vessels constrict and platelets aggregate to form a clot, stopping the bleeding. White blood cells, including neutrophils and macrophages, then migrate to the wound site to clear debris and foreign invaders, a process that typically lasts between three and five days.
The process then moves into the proliferative phase, which focuses on filling the wound defect. Fibroblasts become the principal active cells, generating new tissue known as granulation tissue, characterized by a rich network of newly formed microvessels through a process called angiogenesis. This phase also involves epithelialization, where skin cells (keratinocytes) multiply and migrate across the wound bed to establish a new epidermal barrier.
The final and longest stage is the maturation or remodeling phase, which can extend from several weeks to many years. During this period, the provisional matrix laid down in the proliferative phase is restructured and reorganized to increase its tensile strength. Although the wound is fully closed, the ongoing remodeling is an attempt to optimize the structural integrity of the newly formed tissue.
The Biological Shift: Why Skin Chooses Repair Over Regeneration
The fundamental difference between true regeneration, where the original tissue structure is perfectly restored, and repair, which results in a scar, lies in the body’s priority. Adult mammalian skin favors speed and structural integrity to rapidly close the wound and prevent infection, a survival mechanism that overrides the slower, more complex path to regeneration. This prioritization is driven by the behavior of the fibroblast, the connective tissue cell.
A central event in scar formation is the differentiation of resident fibroblasts into specialized, highly contractile cells called myofibroblasts. This transformation is regulated by the growth factor Transforming Growth Factor-beta (TGF-\(\beta\)), which is released by activated platelets and macrophages in the wound environment. TGF-\(\beta\) activates pathways that induce the expression of fibrotic genes.
The resulting myofibroblasts are hypersecretory, rapidly producing and depositing excessive amounts of extracellular matrix (ECM), including collagen. These cells also express alpha-smooth muscle actin (\(\alpha\)-SMA), enabling them to contract and pull the wound edges together, dramatically reducing the size of the defect. This quick, forceful closure creates a structurally sound patch, but it sacrifices the complex organization of normal skin for a simpler, stronger fibrous plug.
The Structural Makeup of Scar Tissue
The physical appearance and inferior function of a scar are directly linked to its altered molecular composition and organization compared to uninjured skin. Normal, unscarred skin contains collagen fibers woven together in a complex, multidirectional “basket-weave” pattern that provides elasticity and strength. This natural dermis is composed primarily of strong Type I collagen, but also contains flexible Type III collagen, which aids in the tissue’s pliability.
Scar tissue is characterized by a high predominance of Type I collagen and a reduced proportion of Type III collagen, resulting in a higher Type I/III ratio. This change creates a denser, less flexible tissue that is structurally different from the original skin. Furthermore, instead of the basket-weave organization, the collagen fibers in a scar are aligned parallel to one another and often parallel to the skin surface.
This parallel arrangement creates a tissue that is strong enough to maintain a barrier but lacks the elasticity and tensile properties of healthy skin, which is why scars feel stiff and inelastic. The body fails to regenerate the complex structures known as adnexal appendages. Scar tissue is therefore devoid of hair follicles, sebaceous glands, and sweat glands, leading to dry, hairless skin that is unable to regulate temperature or produce natural oils effectively.
When Healing Goes Wrong: Abnormal Scarring
Abnormal scarring occurs when the body’s reparative machinery overshoots its goal, leading to a dysregulation of the normal healing phases, particularly in the control of fibroblast activity and collagen production. The two most recognized forms are hypertrophic scars and keloid scars, which are often confused but have distinct biological characteristics.
Hypertrophic scars are raised, red, and thickened, but they remain strictly confined within the boundaries of the original wound site. They result from an overproduction of collagen during the proliferative phase, often due to excessive tension on the healing wound or prolonged inflammation. Unlike normal scars, the maturation phase is prolonged, but hypertrophic scars frequently improve and flatten over time, even without aggressive treatment.
Keloid scars, conversely, represent a failure of the remodeling phase’s “off switch,” causing them to grow aggressively beyond the edges of the initial injury. Keloid fibroblasts are hyper-responsive to growth factors like TGF-\(\beta\) and continue to overproduce collagen long after the wound has closed, sometimes producing up to 20 times the normal amount. These scars are less likely to regress naturally, frequently persisting and recurring even after surgical removal.