Normal cutaneous scarring is the desired endpoint of wound healing. However, pathological scarring such as keloid, hypertrophic or stretched scars seems to have differeing, multifactorial aetiologies. The absence of a reliable animal model for pathological scarring makes establishment of aetiological agents more difficult. In recent years the red Duroc pig has shown the most promise as a potential model(1). Most insights have been gained from clinical case reports and epidemiological trends.
- key contributory factors are some form of trauma in a genetically predisposed individual
- a diverse range of insults seem able to trigger scarring as a final common pathway. These include surgery, abrasions, tattooing, injections, thermal injury, chemical and thermal burns, radiation and any form of skin inflammation such as chicken pox or acne
- keloid scars have the strongest genetic association with both familial and autosomal inheritance being reported
- adolescents and young adults are more prone to pathological scarring than elderly subjects; this has been attributed to a greater ability to mount an inflammatory response in the former
- races with pigmented skin are more prone to excessively florid scarring
- certain locations on the body are more prone to scarring including the ears, deltoid and sternal skin
- hormonal influences may be relevant as keloid scars seem to be more active during puberty and pregnancy
- immunological factors have been proposed including abnormalities of immunoglobulins and complement cascade enzymes
- cytokine derangements are very topical and form the basis for the current interest in molecules to negate the effects of transforming growth factor isoforms; other cytokines implicated include IL-1 and TNF
- wounds healing in a suboptimal environment are more prone to pathological scarring. Proposed contributory factors include infection, hypoxia and tension across a wound.
A suggested common pathway for most aetiological agents in fibroproliferative scarring is the potentiation of inflammation leading to excessive collagen deposition in the early phases of healing or later, aberrant remodelling of the more mature scar.
Ref:
(1) Zhu KQ, Engrav LH, Gibran NS et al Burns (2003); 29(7): 649-664.