from Clinics in Dermatology 2008 Combating Photoaging with Percutaneous
Collagen Induction
Desmond Fernandez; Massimo Signorini

"If the 1-mm Roll-CIT device is used for microneedling, the
bleeding is microscopic and entirely within the papillary and
upper reticular dermis because the needles only penetrate
about 0.75 mm at most. Because the epidermis is, on average,
0.2 mm, one can be certain that the injury will be limited to the
upper layers of the dermis. This excites a small inflamatory
response, yet the cascade of growth factors still gets initiated
by the release of platlets through the puncturing of small
vessels by microneedling. The possibility exists that
with microneedling, one gets a purer stimulus for collagen
synthesis without the heavy inflammatory reaction because
subdermal fat is certainly not damaged at the same time.
It is believed that because the epidermis is intact, this might
favor predominantly TGF-B3 rather than TGF-B1 and -B2,
which are associated with scar collagen deposition.
Transforming Growth Factor-B3 in implicated in scarless
healing and normal lattice weave collegan deposition."

To me this is saying the shallower 1mm (and hopefully 1.5mm)
actually is advantageous for scarless healing after the injury.

not sure what you mean by that scoobie do.

is he saying that its better to heal acne scars using a 1mm than something deeper like 1.5 dermaroller?

It seems that way..(since deeper tissue injuries tend to activate systemic responses). I think he's saying shallow needling via dermrolling will only create very local reactions in the outermost layer of the skin.

This post has been edited by xandrine100: Nov 8 2009, 06:32 AM

Fernandez was comparing 1mm vs 3mm in the article. Hid didn't mention 1.5mm at all.
I was thinking/hoping (since I'm 1.5 rolling) I would be getting the above response
similar to his theory about 1mm rolling, since 1.5 is not rolling real deep. That 1.5 rolling would also favor TGF-B3.

what is TGF-B3?

Thanks!

thought this little article was interesting, discussing transforming growth factor beta (TGF-B):
http://www.nytimes.com/1993/09/28/health/c...ight-scars.html

"Wound repair is a complex cellular process. It is divided into three overlapping stages: inflammation, proliferation and remodeling.

When tissue is cut, blood cells called platelets adhere to the wound surface and release small amounts of growth factors, like transforming growth factor beta, which attract inflammatory cells to fight infection and form a clot. These growth factors are synthesized and secreted by white blood cells and connective tissue cells called macrophages, monocytes and fibroblasts.

Later, increasing numbers of fibroblasts migrate into the wound to form granulation tissue. This tissue has many blood vessels and cells embedded in a matrix of fibrous proteins, including fibronectin and collagen, which proliferate to fill the wound. In the final stage, scar tissue replaces granulation tissue. Scar tissue has few blood vessels and cells. It consists of small bundles of remodeled collagen fibers that form dense cross-links.

Dr. Ferguson said the early release of transforming growth factor beta influences the architecture of collagen in the final stage of healing.

Recent studies show that transforming growth factor beta comes in three types. Embryos have less of types 1 and 2 and more of type 3 than adults do.

"What we've done is restore the balance to that found in embryos," Dr. Ferguson said.

The balance of transforming growth factor beta can be altered in several ways. One is by introducing a neutralizing antibody or a sugar compound that binds to types 1 and 2 and prevents them from acting. Another strategy is to increase transforming growth factor beta type 3 by making synthetic copies of the molecule and injecting them into the wound.

Dr. Ferguson said he had prevented scarring in rats and other animals with each approach, without slowing down wound healing."

very interesting scoobie

thank you!!