Non-immunologic enhancement and regression of self-healing squamous cell carcinoma (keratoacanthoma)--ground substance and inflammation.
Keratoacanthomas have many characteristics of squamous cell carcinoma and in the past were interpreted as squamous cell carcinomas. It is now known that these lesions spontaneously resolve if left untreated. In man the lesions occur on sunlight damaged areas or areas exposed to tar. Many of the experimental cancers of animals produced by topical carcinogens are keratoacanthomas. Ultraviolet light and tar are known to damage fibroblast and ground substance viscosity. It has recently been proposed that anything that decreases ground substance viscosity would encourage the spread of tumors, by weakening tissue resistance. The rapidly growing keratoacanthoma produces invasive pressure and moves into deeper, less damaged dermis. An inflammatory reaction occurs in the depth of the lesion and a very characteristic granulocytic response occurs. Granulocytes release connective tissue active peptides which stimulate fibroblast and ground substance formation. The fibroblast proliferation is followed by fibrosis and the shrinking and disappearance of the tumor. The characteristic pustule that spurts granulocytes into the depth of the tumor has been experimentally blocked by hyaluronidase and other substances that damage ground substance viscosity. Edema is essential to produce this inflammatory reaction. However, this inflammatory phenomenon occurs vigorously in keratoacanthoma. It is proposed that a keratoacanthoma is a tumor that does not produce hyaluronidase or other substances that decrease ground substance viscosity. It is a deviant cell that can only move through areas of decreased ground substance viscosity. When it reaches tissues of normal viscosity edema and an inflammatory reaction occurs.(ABSTRACT TRUNCATED AT 250 WORDS)
Stone
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OJ
D000818:Animals; D003238:Connective Tissue / Q000201:enzymology / Q000503:physiopathology*; D005347:Fibroblasts / Q000502:physiology; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000378:metabolism; D007249:Inflammation / Q000201:enzymology / Q000503:physiopathology; D007636:Keratoacanthoma / Q000503:physiopathology*; D009504:Neutrophils / Q000502:physiology; D012075:Remission, Spontaneous; D012871:Skin Diseases / Q000503:physiopathology*; D014783:Viscosity
D006821:Hyaluronoglucosaminidase