Hypertrophic scars and their related lesions, keloids, appear to be peculiar to man. Many efforts over the past several years to induce these lesions in animals have failed. Inaccessibility to an experimental lesion limits crucial investigations concerning origin, resolution and, in many ways, characterizations. Recently we have transplanted human hypertrophic scars and keloids subcutaneously to nude athymic mice and have observed each transplant to retain its character for at least one month. No rejection has been observed. Each transplant has been assessed by histological examination and assayed for distribution of glycosaminoglycans after one month. These values are not different from those made prior to transplantation. It is now proposed to confirm these results with significant numbers and to transplant lesions of various ages post-injury. Knowing that virtually all full-thickness injuries progress to hypertrophic scarring, full thickness granulations will also be transplanted to follow their development. Before experimentation can be conducted on the transplants we must be certain that the transplants indeed sustain or develop, as the case may be, the character of the hypertrophic scar or keloid. These lesions have been extensively characterized in several ways. Therefore, the transplants will be examined by electron microscopy for collagen patterns and microvascular structure (patency or occlusion), by biochemical analysis for rate of collagen synthesis, rate of turnover of newly synthesized collagen, glycosaminoglycan distribution and metabolism and by immunocytochemistry for content and distribution of immunoglobulins A, G, and M, complement C1Q, 3 and 5, and fibronectin. If we can substantiate that the athymic nude mouse implant is a suitable model for the development, growth and sustenance of hypertrophic scars and keloids, the way will be opened toward experiments to modify such development of these scars or to effect their resolution through therapeutic intervention.
