As your surface contact with the external environment, your skin is vulnerable to blisters, cuts, scrapes and other wounds. The complex cellular events involved in skin healing begin almost immediately after you sustain an injury. Blisters and other wounds that extend beyond the superficial region of your skin form scars as part of the healing process. The size and severity of a blister influences the time required to heal the injury and the amount of scarring that occurs.
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Knowing a bit about skin structure will help you understand the normal healing process of blisters and scar formation. Your skin is composed of two regions, the outer epidermis and the underlying dermis. The epidermis consists primarily of layers of skin cells, or keratinocytes. The epidermis does not contain blood vessels.
The dermis nourishes and supports the epidermis; it contains blood vessels, nerves and connective tissue cells called fibroblasts. Collagen and other proteins produced by the fibroblasts prove important in scar formation and wound healing.
Inflammation is the first step in the normal healing process of blisters. The tissue damage that causes blister formation provokes the release of chemical messengers, which alert the body that an injury has occurred. Specialized white blood cells move into the site of the blister to remove dead skin cells and protect the area from infection. Blood flow into the injured area increases and the blood vessels become leaky, leading to swelling around the blister and a short-term increase in fluid within the blister pocket.
The depth of the skin layer separation with a blister dictates the next step in the healing process. Small, superficial blisters confined to the epidermis often heal within a few days as the fluid is reabsorbed into your bloodstream. No scarring occurs with superficial epidermal blisters. Blisters associated with damage to the basal layer of the epidermis or the deeper dermis take longer to resolve because additional healing processes must occur.
Deep blisters progress from inflammation to the next step in the healing process, the proliferative phase. New skin cells are produced at a rapid rate to replace those killed by the injury. The time required to produce adequate numbers of new skin cells varies, depending on the size of the blister. Advancing age slows skin-cell production and prolongs healing time. Poor circulation and malnutrition also slow wound healing. Development of an infection in a blister prolongs the healing process and may expand the area of tissue damage. It is usually best, therefore, not to puncture a blister because the opening provides an entry route for bacteria.
Collagen and Scar Formation
As skin cell replacement occurs, fibroblasts in the dermis produce collagen. This fibrous protein fills the damaged area and forms a matrix on which new skin cells align. The collagen formed during the healing process constitutes the primary component of a scar. With small blisters, scarring may be barely noticeable.
Remodeling and Maturation
New scar tissue continues to undergo changes after the other processes of normal blister healing have concluded. Modification of a new scar, known as scar remodeling, may continue for months to years, depending on the depth and severity of the blister. The collagen strands of a healing blister form cross-linking bonds as the scar matures, conferring increased strength to the damaged skin. Scars contract as they mature, which is why they shrink over time. The scar maturation process attempts to restore the injured area to a condition that closely approximates normal skin. The strength of a mature scar, however, is significantly less than that of normal skin.