Table 1 Theories on Marjolin's ulcers [2-16]

Toxin theory

Toxins released from damaged tissues later lead to cellular mutations.

Chronic irritation theory

Chronic irritation with repeated attempts at re-epithelialization contributes to neoplastic initiation.

Traumatic epithelial elements implantation theory

Epithelial elements implanted into the dermis, lead to a foreign body response reaction and a disordered regenerative process.

Co-carcinogen theory

Chemical or trauma such as burn injury acts to 'stir' pre-existing but dormant neoplastic cells into proliferation.

Initiation and promotion theory

A two-step process that converts normal cells into malignant cells. In the initiation phase, normal cells become dormant neoplastic cells that may then be subsequently stimulated into neoplastic cells by a co-carcinogen such as infection, in the promotion phase. This theory overlaps with the co-carcinogen theory.

Immunologic privileged site theory

Burn scarring effectively obliterates lymphatics to injured area, preventing normal immunosurveillance and thus permitting neoplastic growth. These tumors initially grow slowly, but quickly overwhelm the immune system, metastasize and are rapidly fatal, once they break through the scar barrier.

Heredity theory

HLA DR4 is associated with cancer development and p53 gene abnormalities have been demonstrated in patients with Marjolin's ulcers. Further, Fas mutations in the apoptosis function region that predispose to malignant degeneration of scars have been demonstrated in burn scar Marjolin's ulcers.

Ultraviolet rays theory

Ultraviolet rays theory - UV rays cause a reduction in Langerhans cell population leading to a reduction in cutaneous immuno-surveillance against developing malignancy and also cause p53 tumor suppressor gene alterations.

Environmental and genetic interaction theory

Attempts to explain the occurrence of 'Acute' Marjolin's ulcers.