New Dermaroller Study; Thoughts, comments?

[benjt]

While I think that all of the galea stuff is complete bullsh*t (and I never saw anything supporting this theory), a tight scalp due to fibrosis, or rather fibrosis itself, is not the endgame here, but one of the major issues.

Someone (I think squeegee) posted some crosssections of fibrotic scalp of some male pattern baldness patients a long time ago in this thread. These cross sections show perfectly how the shafts are squeezed and crushed by the surrounding hard fibrotic tissue.

I reckon there are two modes of action here, which are maybe even two subsequent steps in the death of a follicle:
1. Fibrotic tissue crushing and squeezing the DP shafts and follicles, thus they can no longer push helathy hair out to the surface.
2. Miniaturization of follicles as a result of a) being crushed by fibrotic tissue and/or b) local overexpression of PGD2.

The first point is one of the reasons why I think that chemical peels may be promising, by the way.

 

[brunobald]

Yep for me fibrotic tissue is main culprit. If the skin was free of scar tissue, I think all hairs would continue to grow even under attack from whatever is causing the inflamation responds. The problem is the fibrotic tissue is cacooning the follicules and solidifying any gains made by the attacking substance whatever that may be.

 

[cthulhu2.0]

Yep for me fibrotic tissue is main culprit. If the skin was free of scar tissue, I think all hairs would continue to grow even under attack from whatever is causing the inflamation responds. The problem is the fibrotic tissue is cacooning the follicules and solidifying any gains made by the attacking substance whatever that may be.

So I guess years and years of evidence that dht is the main culprit behind Androgenetic Alopecia is completely wrong. This is broscience at its finest! Please tell me more about imagination land.

 

[squeegee]

So I guess years and years of evidence that dht is the main culprit behind Androgenetic Alopecia is completely wrong. This is broscience at its finest! Please tell me more about imagination land.

DHT triggers everything, Fibrosis and collagen built up are just the end results. There is a reason why PGD2 is overly expressed which is a sign of local chronic inflammation.

http://www.hairlosstalk.com/interac...w-Dermaroller-Study-Thoughts-comments/page224

Cellular and molecular mechanisms of chronic inflammation-associated organ fibrosis

Satoshi Ueha[SUP]1,2[/SUP], Francis H. W. Shand[SUP]1,3[/SUP] and Kouji Matsushima[SUP]1,2[/SUP]*

• [SUP]1[/SUP] Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan
• [SUP]2[/SUP] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Tokyo, Japan
• [SUP]3[/SUP] Department of Pharmacology, University of Melbourne, Melbourne, VIC, Australia

Organ fibrosis is a pathological condition associated with chronic inflammatory diseases. In fibrosis, excessive deposition of extracellular matrix (ECM) severely impairs tissue architecture and function, eventually resulting in organ failure. This process is mediated primarily by the induction of myofibroblasts, which produce large amounts of collagen I, the main component of the ECM. Accordingly, the origin, developmental pathways, and mechanisms of myofibroblast regulation are attracting increasing attention as potential therapeutic targets. The fibrotic cascade, from initial epithelial damage to eventual myofibroblast induction, is mediated by complex biological processes such as macrophage infiltration, a shift from Th1 to Th2 phenotype, and by inflammatory mediators such as transforming growth factor-β. Here, we review the current understanding of the cellular and molecular mechanisms underlying organ fibrosis.

erifollicular fibrosis: pathogenetic role in androgenetic alopecia.

Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH.
Source

Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea.

Abstract

Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 microg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia.

Article: Perifollicular fibrosis: pathogenetic role in androgenetic alopecia. Source: Biol Pharm Bull. 2006 Jun;29(6):1246-50. Author(s): Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University.

Summary:
Fibrosis is a scarring process in the skin that can damage the hair follicle (hair loss). This study shows that increased Testosterone speeds up fibrosis while treatment with Finasteride helps slow fibrosis. Stopping or slowing fibrosis may be another method by which Finasteride may help prevent hair loss.​

Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 mug/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia. http://www.derma-haarcenter.ch/files...+Barcelona.pdf

Cosmet Dermatol. 2009 Jun;8(2):83-91
Androgenetic alopecia in males: a histopathological and ultrastructural study.
El-Domyati M, Attia S, Saleh F, Abdel-Wahab H.

Department of Dermatology, Faculty of Medicine, Al-Minya University, Al-Minya, Egypt.

Background Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process. Aims To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (Androgenetic Alopecia). Patients/methods Fifty-five subjects were included in this study (40 with Androgenetic Alopecia and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study. Results The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases. Conclusion Follicular microinflammation plays an integral role in the pathogenesis of Androgenetic Alopecia in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.

http://www.biomediclaser.com/pdf/Inf...c-Alopecia.pdf

Formation of fibrous tissue or fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the
miniaturization. Involution of the pilosebaceous unit in this form of baldness and sustained microscopic
follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of androgenetic alopecia. However, till date, the
inflammatory component has not been explored in developing treatment protocols for androgenetic
alopecia.


Fibrosing Alopecia in a Pattern DistributionPatterned Lichen Planopilaris or Androgenetic Alopecia With a Lichenoid Tissue Reaction Pattern?


Patients developed progressive fibrosing alopecia of the central scalp, without the multifocal areas of involvement typical of lichen planopilaris and pseudopelade. Perifollicular erythema, follicular keratosis, and loss of follicular orifices were limited to a patterned area of involvement. Biopsy specimens of early lesions demonstrated hair follicle miniaturization and a lichenoid inflammatory infiltrate targeting the upper follicle region. Advanced lesions showed perifollicular lamellar fibrosis and completely fibrosed follicular tracts indistinguishable from end-stage lichen planopilaris, pseudopelade, or follicular degeneration syndrome.

http://archderm.jamanetwork.com/article.aspx?articleid=189906


INFLAMMATORY PHENOMENA AND FIBROSIS

The implication of microscopic follicular inflammation in the pathogenesis of Androgenetic Alopecia has emerged from several independent studies: An early study referred to an inflammatory infiltrate of activated T cells and macrophages in the upper third of the hair follicles, associated with an enlargement of the follicular dermal sheath composed of collagen bundles (perifollicular fibrosis), in regions of actively progressing alopecia.[25] Horizontal section studies of scalp biopsies indicated that the perifollicular fibrosis is generally mild, consisting of loose, concentric layers of collagen that must be distinguished from cicatricial alopecia.[26] The term 'microinflammation' has been proposed, because the process involves a slow, subtle, and indolent course, in contrast to the inflammatory and destructive process in the classical inflammatory scarring alopecias.[27] The significance of these findings has remained controversial. However, morphometric studies in patients with male pattern Androgenetic Alopecia treated with minoxidil showed that 55% of those with microinflammation had regrowth in response to treatment, in comparison to 77% in those patients without inflammation and fibrosis.[26] Moreover, some forms of primary fibrosing alopecia may represent pathological exaggeration of Androgenetic Alopecia associated with follicular inflammation and fibrosis, specifically postmenopausal frontal fibrosing alopecia,[28] and fibrosing alopecia in a pattern distribution.[29]
An important question is how the inflammatory reaction pattern is generated around the individual hair follicle. Inflammation is regarded as a multistep process which may start from a primary event. Some authors proposed that alopecia may result from cumulative physiological degeneration of selected hair follicles. They described in healthy murine skin clusters of perifollicular macrophages as perhaps indicating the existence of a physiological program of immunologically controlled hair follicle degeneration by which malfunctioning follicles are removed by programmed organ deletion, and suggested that perhaps an exaggerated form of this process might underlie some forms of primary scarring alopecia.[30] The observation of a perifollicular infiltrate in the upper follicle near the infundibulum of human hair follicles in Androgenetic Alopecia suggests that the primary causal event for the triggering of inflammation might occur near the infundibulum.[27] On the basis of this localization and the microbial colonization of the follicular infundibulum with Propionibacterium sp., Staphylococcus sp., Malassezia sp., or other members of the transient flora, one could speculate that microbial toxins or antigens could be involved in the generation of the inflammatory response. Alternatively, keratinocytes themselves may respond to oxidative stress from irritants, pollutants, and UV irradiation, by producing nitric oxide, and by releasing intracellularly stored IL-1α. This pro-inflammatory cytokine by itself has been shown to inhibit the growth of isolated hair follicles in culture. [31] Moreover, adjacent keratinocytes, which express receptors for IL-1, start to engage the transcription of IL-1 responsive genes: mRNA coding for IL-1β, TNFα, and IL-1α, and for specific chemokine genes, such as IL-8, and monocyte chemoattractant protein-1 (MCP-1) and MCP-3, themselves mediators for the recruitment of neutrophils and macrophages, have been shown to be upregulated in the epithelial compartment of the human hair follicle.[27] Besides, adjacent fibroblasts are also fully equipped to respond to such a pro-inflammatory signal. The upregulation of adhesion molecules for blood-borne cells in the capillary endothelia, together with the chemokine gradient, drives the transendothelial migration of inflammatory cells, which include neutrophils through the action of IL-8, T cells, and Langerhans cells at least in part through the action of MCP-1. After processing of localized antigen, Langerhans cells, or alternatively keratinocytes, which may also have antigen presenting capabilities, could then present antigen to newly infiltrating T lymphocytes and induce T-cell proliferation. The antigens are selectively destroyed by infiltrating macrophages, or natural killer cells. On the occasion that the causal agents persist, sustained inflammation is the result, together with connective tissue remodeling, where collagenases, such as matrix metalloproteinase (also transcriptionally driven by pro-inflammatory cytokines) play an active role.[27] Collagenases are suspected to contribute to the tissue changes in perifollicular fibrosis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929555/


http://www.hairlosstalk.com/interac...-Thoughts-comments/page144?highlight=biopsies

 

[rerun]

How useful would derma-rolling be for someone who still has reasonably thick hair yet is diffuse shedding from Finasteride?

If fibrosis could be potential future issue for me, would it be better for me to be proactive and address it now in it's latent/early stages?

Last question: Has anybody derma-rolled while still sporting medium length hair? It seems that everybody does it with a buzz cut for some reason.

 

[badgenetics1]

If you're shedding from finasteride, that hair should grow back. Dermarolling could help your situation, but I wouldn't do it only because of a finasteride shed.

My hair is medium length (definitely not buzzed) and I've been dermarolling for 2 months. I've used a 1.5 mm 192 needle roller and I haven't had any issues.

 

[squeegee]

If you're shedding from finasteride, that hair should grow back. Dermarolling could help your situation, but I wouldn't do it only because of a finasteride shed.

My hair is medium length (definitely not buzzed) and I've been dermarolling for 2 months. I've used a 1.5 mm 192 needle roller and I haven't had any issues.

Badgenetics1 is 100% right. Get the 192 needles. Bigger size needles ( 2.0mm+) can be an option if you have a longer hair. Badgenetics1 have really great results, look up his story and progress in his signature block.

 

[Donc83]

Everytime the day after I derma roll I get a weird headache on my right side and my right eye hurts. I do not know what this is from. It has me curious. I hope I am not damaging something or something is wrong with me. My eye gets dry also. Then the feeling goes away within the next couple of days.

 

[rerun]

If you're shedding from finasteride, that hair should grow back. Dermarolling could help your situation, but I wouldn't do it only because of a finasteride shed.

My hair is medium length (definitely not buzzed) and I've been dermarolling for 2 months. I've used a 1.5 mm 192 needle roller and I haven't had any issues.

Thanks. I was just wondering if it could somehow aid in growth, recovery, and even maintenance.

I'm curious to see how this works for you all. I thought I read that the derma-rolling itself caused you all to shed at least once.

 

[squeegee]

Thanks. I was just wondering if it could somehow aid in growth, recovery, and even maintenance.

I'm curious to see how this works for you all. I thought I read that the derma-rolling itself caused you all to shed at least once.

Not everybody go through a shed. Derma roller is a game changer if you're stubborn/optimist and consistent.

 

[badgenetics1]

Badgenetics1 is 100% right. Get the 192 needles. Bigger size needles ( 2.0mm+) can be an option if you have a longer hair. Badgenetics1 have really great results, look up his story and progress in his signature block.

Thanks squeegee!

Thanks. I was just wondering if it could somehow aid in growth, recovery, and even maintenance.

I'm curious to see how this works for you all. I thought I read that the derma-rolling itself caused you all to shed at least once.

Dermarolling has caused some people to shed. I didn't shed, at least not that I'm aware of. That said, I don't really pay attention to hair falling out - I just take a picture of my hair every two weeks or so and try not to be impacted by daily changes.

 

[squeegee]

Everytime the day after I derma roll I get a weird headache on my right side and my right eye hurts. I do not know what this is from. It has me curious. I hope I am not damaging something or something is wrong with me. My eye gets dry also. Then the feeling goes away within the next couple of days.

WTF Donc LOL!

 

[Donc83]

I do not know man. It is weird. I just hope Im not ****ing up something because I think the dermarolling is helping. It definitely stops my itching for like 4-5 days which is awesome. I do not know If I should quit because of this though.

 

[boldmun]

I have been following this thread since the beginning and have been dermarolling and applying minoxidil just like the study for 2 months now. I haven't noticed any apparent cosmetic changes to my overall hair. All I know it is worse than last year. However, after the photos were posted here by a few members, I went and looked in the mirror and I also have small hairs in the area that I have been rolling, though I am not sure that they were there before. The way the hairs look right now it would surprise me if they actually got any real thickness. The one thing that is certain if this method does anything, it will be awhile before we know if these hair grow into terminal hairs. It's just a little weird to go out the day after you have stabbed your head with pins with tiny red dots everywhere, but at least it gives us hope.

 

[odalbak]

I will discontinue rolling for now. For me, the effect was little to almost nothing: 10 to 20 hairs at hair line with 7 sessions (which still proves that rolling has some effect, but for me personally it was just too minor). Keep in mind though that I did not use minoxidil or any other topicals.

Have you considered rolling, and using castor oil + B12 + other topical stuff, before giving up with dermarolling? I know it's painful but the massage road is a long road with nothing clear at the end…

 

[BeliefISKEY]

I understand you have your own beliefs, which I completely respect by the way. But to say that the Galea theory is bull**** because you haven't seen any evidence is completely wrong. First of all there are 2 well established/respected studies that support the Galea theory and show better results than any studies I've seen ever. & secondly, even if the Detumescence therapy study isn't real (which I think it probably is) it 1: working for virtually everybody that tries it 2: it confirms the validity in the Galea theory. There's a number in the study.... Care to call it?

BTW: I'm pretty fibrotic tissue doesn't come back within a days time (or even less) and tighten your scalp back up by decreasing ROM. We aren't talking trigger points here man.... Fibrotic tissue doesn't disappear then after a while "magically" reappear again out of nowhere. If you don't know what I mean you can try dropping the manual massage for a day- a couple days (this can vary due to stress levels) & see how fast your scalp will tighten back up on you again...

 

[squeegee]

I understand you have your own beliefs, which I completely respect by the way. But to say that the Galea theory is bull**** because you haven't seen any evidence is completely wrong. First of all there are 2 well established/respected studies that support the Galea theory and show better results than any studies I've seen ever. & secondly, even if the Detumescence therapy study isn't real (which I think it probably is) it 1: working for virtually everybody that tries it 2: it confirms the validity in the Galea theory. There's a number in the study.... Care to call it?

BTW: I'm pretty fibrotic tissue doesn't come back within a days time (or even less) and tighten your scalp back up by decreasing ROM. We aren't talking trigger points here man.... Fibrotic tissue doesn't disappear then after a while "magically" reappear again out of nowhere. If you don't know what I mean you can try dropping the manual massage for a day- a couple days (this can vary due to stress levels) & see how fast your scalp will tighten back up on you again...

[video=youtube;RXq0QcU3oOo]http://www.youtube.com/watch?v=RXq0QcU3oOo[/video]

 

[Sparky4444]

Have you considered rolling, and using castor oil + B12 + other topical stuff, before giving up with dermarolling? I know it's painful but the massage road is a long road with nothing clear at the end…

I applied castor oil before the last stabbing session, and for some reason it reeeeeally helped with the pain...I think it loosen's up the scalp and you don't get that "scrunching" sound when you dig in...that alone makes my stomach turn...

..maybe applying castor oil and then stabbing right after might boost things... I dunno but I only have a few light vellus hairs that have resprouted right in the fleshy, soft part in front...but my barren temples have got nothing...and that's where I've stabbed the hell outta them

 

[odalbak]

I applied castor oil before the last stabbing session, and for some reason it reeeeeally helped with the pain...

Cool but on the other hand castor oil like many vegetable oils may be anti-inflammatory… I've started applying castor oil but only like after the 4th day after wounding, along minoxidil and nizoral. I really want to give as much chance to the process as possible.

 

[closetmetrosexual]

Has anybody derma-rolled while still sporting medium length hair? It seems that everybody does it with a buzz cut for some reason.

Someone suggested wetting your hair and combing it 'flat' prior to rolling.

I have not tried this myself (I'm buzzed), but sounds like it could work.