Pathophysiology: How do burn scars form?
To understand how scars form, we first need to understand how wounds heal. Normal wound healing consists of three overlapping phases: the inflammatory, proliferative, and remodelling phases.
Phases of burn wound healing
- Inflammatory phase (days 1-7): pro-inflammatory cells, such as neutrophils, lymphocytes and macrophages, move into the wound site, resulting in swelling/edema.
- Proliferative phase (days 4-21): macrophages, endothelial cells and keratinocytes work to form granulation tissue, new blood vessels and skin cells (reepithelialization)
- Remodeling phase (days 21-365): the tissue is remodeled into scar tissue, and wound contraction reduces the surface area of the scar. This is the most important phase in the mechanism of scarring.
Determinants of scar formation
The following factors contribute to scar formation.
Inflammation and infection are associated with greater neovascularization and result in more excessive scarring. Similarly, a prolonged healing process, which means slower reepithelialization, is also linked to excessive scarring.
Reepithelialization requires keratinocytes, which are found in the basal layer of the epidermis and in the sweat glands and hair follicles protruding deep into the dermal tissue. The number of keratinocytes present depends on the depth of the burn wound. In burn wounds that take more than 21 days to heal (deep and full thickness burn wounds), no keratinocytes are present. This causes prolonged reepithelialization, resulting in excessive scar formation.
Extracellular matrix production and remodeling also play a role in scar formation. Blood carries the cells required to produce new extracellular matrix. When deep and full thickness wounds are healing, the blood supply comes from the subcutaneous fat. However, the fibroblasts that come from the fat tissue differ from those from the dermis: they produce collagen that is much firmer and less susceptible to degradation than the collagen produced by fibroblasts from the dermis.
Scars have a tendency to contract. The deformity that remains after scar contraction around joint areas is often accompanied by a limited range of motion (ROM) and is defined as a ‘contracture’. Although the exact mechanism of scar contracture development is unknown, it may involve two factors that decrease the surface area: excessive layering of collagen, and increased activity of the contracting myofibroblasts.