New Keloid Cure Alternatives

Summary: There are 3 main processes in the injuries healing process. Analysis and further study of contraction, scar formation and regeneration are the key to understand why scarring process occur.

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New Scar Cure Innovations: Regeneration, Contraction & Scar Tissue

Three processes contribute to the healing outcome of a trauma, wound or injury caused by trauma, an accident or as a consequence from plastic or reconstructive surgery: contraction, scar formation and regeneration. Of the three processes, contraction (more than scar formation) is the clearly principal factor for spontaneous wound healing in adults.

In contrast skin wounds on small mammalian embryos heal perfectly with not a single sign of scarring and full restitution of the normal skin tissues.

Regeneration.

Limb regeneration in certain amphibians is a spectacular skill by which an amputated limb grows back to its original form and recovers its normal function. It is the prototypical paradigm of regeneration. not so many adult amphibians, and none of the adult mammals, can replicate this skill. Instead, almost all mammals, including adult humans, respond to injuries by a spontaneous repair process.

Repair means that the wound is closed by contraction and synthesis of scar tissue without recovery of the undamaged tissues. In contrast, a regeneration process closes the wound by synthesis of the missing organ (skin is an organ) at the original site, yielding a regenerate. Regeneration restores the normal structure and function of the damagedorgan; repair does not.

Wounds in early mammalian embryos heal without scar formation.

Unlike the adult, the mammalian foetus heals its wounds spontaneously by regeneration with negligible contraction, no scar formation, little inflammatory response and increased levels of hyaluronic acid (hyaluronan, HA) synthesis, provided that the injury has been suffered at a sufficiently early stage of gestation, typically before the 3º trimester.

A developmental transition, occurring during late mammalian gestation, leads from healing primarily by regeneration to healing by repair. During this transition closure of the damaged site by regeneration is mainly replaced by closure based on contraction and scar formation.

It is also a fact that scarring use to be worse in children and teenagers, due to their augmented inflammatory reaction, whilst the quality of scarring in people over 65 years is often improved as a result of an altered inflammatory and immune reaction at the wound site.

To gain insights into the mechanisms behind scar-free wound healing, researchers lead by Dr Mark Ferguson, D.D.S., Ph.D., professor in the faculty of life sciences at the University of Manchester, England have analyzed the differences in cellular and molecular responses to wounding in embryonic and adult injuries healing models.

Scar formation

To restore the barrier function of the skin as soon as possible, closure of skin wounds and repair of missing skin tissue occur rapidly in adult skin by a mechanism that leads to scarring.

The transition from scarless embryonic wound healing to scar-forming adult wound healing is a gradual one and is characterized by the abnormal organization of the neo-dermis, mainly the abnormal deposition of small parallel bundles of extracellular matrix between the margins of the wound (consisting largely of collagen types I and III and fibronectin) to form the scarring as opposed to the deposition of large bundles of extracellular matrix in a normal basketweave orientation in the normal skin and in the neo-dermis of an embryonic wound. So scarring is a morphogenetic problem, i.e. a failure of the regeneration of the normal skin structure more than a biochemical problem, e.g. abnormal composition of the scar tissue.

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Modern research has shed light on the scarring process, and how to use this knowledge for developing new Scar Treatment alternatives. Keep reading to learn more.

Recent Research about Latest Scar Cure Methods

New treatments for keloids

Ong CT, Khoo YT, Mukhopadhyay A, Do DV, Lim IJ, Aalami O, Phan TT.
Department of Surgery, National University of Singapore, Singapore.

The appearance of keloids on skin injuries is due a fibroproliferative disorder, characterized by excessive deposition of extracellular matrix (ECM) components such as collagen, glycoproteins and fibronectin. The mammalian target of rapamycin (mTOR) is a serine/theronine kinase which plays an important role in the regulation of metabolic processes and translation rates.

Published reports have shown mTOR as regulator of collagen expression and its inhibition induces a decrease in ECM deposition. Our aim was to investigate the role of mTOR in keloid pathogenesis and investigate the effect of rapamycin on proliferating cell nuclear antigen (PCNA), cyclin D1, collagen, fibronectin and alpha-smooth muscle actin (alpha-SMA) expression in normal fibroblasts (NF) and keloid fibroblasts (KF). Tissue extracts obtained from keloid scar demonstrated elevated expression of mTOR, p70KDa S6 kinase (p70S6K) and their activated forms, suggesting an activated state in keloid scars. Serum stimulation highlighted the heightened responsiveness of KF to mitogens and the importance of mTOR and p70S6K during early phase of wound healing.

Application of rapamycin to monoculture NF and KF, dose- and time-dependently downregulates the expression of cytoplasmic PCNA, cyclin D1, fibronectin, collagen and alpha-SMA, demonstrating the anti-proliferative effect and therapeutic potential of rapamycin in the treatment of keloid scars. The inhibitory effect of rapamycin was found to be reversible following recovery in the expression of proteins following the removal of rapamycin from the culture media.

These results demonstrate the important role of mTOR in the regulation of cell cycle and the expression of ECM proteins: fibronectin, collagen and alpha-SMA.