After an injury to the skin, the body sends cells to the wound that can build new skin and tissue. After it stops bleeding, a scab develops. During the first few weeks, natural collagen fills in the gap around and under the scab, forming new skin – a scar. Normal scar tissue slowly grows thicker and then smoother. Collagen production stops after a few weeks. Capillaries form to deliver blood to the injured area, helping it to heal more quickly. The scar isn’t quite as strong as the original skin. It becomes flat and takes on a skin color closer to that of the surrounding area. Abnormal scar tissue, such as hypertrophic or keloid, may never completely heal or fade without additional scar treatment.
Intravenously administered glucocorticoids , such as prednisone , are the standard of care in acute GvHD  and chronic GVHD.  The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the host tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. [ citation needed ] . Cyclosporine and tacrolimus are inhibitors of calcineurin. Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus  . Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml  . Other substances that have been studied for GvHD prophylaxis include, for example: sirolism, pentostatin and alemtuzamab  .
Keloids were described by Egyptian surgeons around 1700 BCE, recorded in the Smith papyrus, regarding surgical techniques. [ citation needed ] Baron Jean-Louis Alibert (1768–1837) identified the keloid as an entity in 1806. [ citation needed ] He called them cancroïde , later changing the name to chéloïde to avoid confusion with cancer. The word is derived from the Greek χηλή , chele , meaning " hoof ", here in the sense of "crab pincers ", and the suffix -oid , meaning "like".