Study on male pattern baldness vs AA - on miniaturisation

[oye_rg]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500053/

The study tries to guess why miniaturisation in male pattern baldness and FPB may be irreversible


[h=2]Abstract[/h][h=3]Background:[/h]Hair follicle miniaturization is the hallmark of male pattern hair loss (MPHL), female pattern hair loss (FPHL), and alopecia areata (AA). AA has the potential for complete hair regrowth and reversal of miniaturization. MPHL and FPHL are either irreversible or show only partial regrowth and minimal reversal of miniaturization. Hypothesis: The arrector pili muscle (APM) attachment to the hair follicle bulge, a recognized repository of stem cells may be necessary for reversal of hair follicle miniaturization.

[h=3]Materials and Methods:[/h]Sequential histological sections from MPHL, FPHL, AA, and telogen effluvium were used to create three-dimensional images to compare the relationship between the APM and bulge.

[h=3]Results:[/h]In AA, contact was maintained between the APM and the bulge of miniaturized follicles while in MPHL and FPHL contact was lost.

[h=3]Discussion:[/h]Contact between the APM and the bulge in AA may be required for reversal of hair follicle miniaturization. Maintenance of contact between miniaturized follicles in AA could explain the complete hair regrowth while loss of contact between the APM and the bulge in MPHL and FPHL may explain why the hair loss is largely irreversible. This loss of contact may reflect changes in stem cell biology that also underlie irreversible miniaturization.

 

[whatevr]

This is old, and miniaturization is not irreversible.

 

[benjt]

whatevr, would you elaborate or do you have links to sources? I have not stumbled upon a final conclusion on that yet.

 

[whatevr]

[h=1]Measuring reversal of hair miniaturization in androgenetic alopecia by follicular counts in horizontal sections of serial scalp biopsies: results of finasteride 1 mg treatment of men and postmenopausal women.[/h]The effect of cyproterone acetate on hair roots and hair shaft diameter in androgenetic alopecia in females.

[h=1]Reversal of male-pattern baldness, hypertrichosis, and accelerated hair and nail growth in patients receiving benoxaprofen.[/h]
I am sure there is more but this is just off the top what I can remember. Note particularly that last study where it says "noticed an increased growth of hair in areas of the scalp previously lacking hair". Miniaturisation = thinning of hair shaft and gradual shortening of the hair until it is no longer visible. If miniaturisation was impossible then no one would ever get regrowth. We even have members here, such as recedingyt, who have shown pictures of reversing several Norwoods of hair loss. What is that, if not reversal of miniaturisation?

 

[oye_rg]

This is old, and miniaturization is not irreversible.

I agree 100% backed up by personal experience. To be honest I do not make much of this study either.

 

[abcdefg]

Just because no one has figured out how to reverse male pattern baldness doesnt mean its impossible to do. Thats a very common misconception in a lot of medicine just because so many things are unknown and relationships between different processes no one understands. You could say right now male pattern baldness is not reversible because nothing can cure it, but the state of things change over time.

 

[Swoop]

Just because no one has figured out how to reverse male pattern baldness doesnt mean its impossible to do. Thats a very common misconception in a lot of medicine just because so many things are unknown and relationships between different processes no one understands. You could say right now male pattern baldness is not reversible because nothing can cure it, but the state of things change over time.

Indeed. Just because we don't know how to reverse it yet doesn't mean that it's "irreversible".

 

[Swoop]

In the frontal bald area of Androgenetic Alopecia, perifollicular fibrosis consisting of loose concentric layers of collagen was generally absent in 16 cases (40%) or mild in 14 cases (35%) in young age with mild Androgenetic Alopecia (Figure 2c). It was more marked, even with destruction of follicular structures, in the old age group with advanced Androgenetic Alopecia. The arrector pili muscle may be retained (Figure 2d). Perifollicular fibrosis showed highly significant correlation with both age of the patients (r = 0.78, P < 0.001) and correlated significantly with the severity of baldness (r = 0.46, P = 0.003). It showed significant inverse correlation with perifollicular inflammation (r = )0.31, P = 0.048). In normal controls, neither inflammatory infiltrate, apart from sparse perivascular infiltrate in a few biopsies, nor perifollicular fibrosis was observed in all studied specimens.

In the frontal (bald) area of Androgenetic Alopecia, perifollicular inflammatory infiltrate was observed in the majority of cases (90%). Meanwhile, no fibrosis was observed in 40% and only 10% showed marked fibrosis and complete destruction of hair follicles in the old age group with advanced Androgenetic Alopecia. These results are close to those observed by El-Domyati who reported inflammatory reaction in female subjects with Androgenetic Alopecia with destruction of follicular structure and replacement by fibrous tracts in severe cases. Meanwhile, Abell26 reported an inflammatory reaction in 75% of balding patients, focal fibrosis in 25%, and destruction of follicular structures in 5%.

In conclusion, the present work has demonstrated aprofound view of various histopathological and ultrastructuralchanges occurring in Androgenetic Alopecia. The geneticallypredisposed hair follicles are the target for androgenstimulatedhair follicle miniaturization. Follicular microinflammationaround the upper portion of the hairfollicle seems to play an integral role in the pathogenesisof Androgenetic Alopecia. Over time, there is increased deposition ofcollagen in the perifollicular sheath, which appears to bemarkedly thickened in ultrastructural examination.Ultimately, this process results in marked fibrosis andsometimes ends by even complete destruction of the hairfollicle in advanced cases.

In early (mild and moderate) Androgenetic Alopecia, mononuclearcellular inflammatory infiltrate, composed predominantly of lymphocytes and mononuclear cells, wasdistributed within the adventitial sheath. The mast cellswere increased in number and showed degranulationwhich became marked in advanced Androgenetic Alopecia, leaving mastcells with few or even no intact granules

The correlations at this point with senescence are extremely convincing in my opinion. It's astonishing really how the puzzle is falling into place. Frankly I think nothing will beat castration + estrogen for a long time (in terms of drugs). But even castration + estrogen doesn't always cut it. Besides that, I think indeed in some people Androgenetic Alopecia might be irreversible due to destruction of the hair follicle by fibrosis (later stage Androgenetic Alopecia) in the sense that only a regenerative therapy will be the answer (creation of new hair follicles, morphogenesis). Regenerative therapy will be the answer to this I guess and I hope asap. They are making rapid advancements that's for sure.

​prevention is absolute key, do it if you can and don't wait.

 

[Hairloss23]

Follicles never die they just respawn

 

[Swoop]

Follicles never die they just respawn

lol. We need someone like Tsuji or Jahoda to respawn hair follicles.

 

[Armando Jose]

"Prevention better than cure"

BTW oxidiced sebum can give up chronic inflammation in hairs, similar to acne process

 

[DDobler]

how the **** you can prevent it? if my hairloss progress (dht sensitivity) >> finasteride\dutasteride , its a game over.

 

[Follisket]

Exactly. It makes me rage everytime I read about maintaining as if it is the obvious solution and only a matter of money, time or willingness to do so.
Whereas the truth is so many of us simply don't have even a single option available to us after having exhausted so many others.

 

[Armando Jose]

how the **** you can prevent it? if my hairloss progress (dht sensitivity) >> finasteride\dutasteride , its a game over.

Problems with DHT sensitivity is not the first event in common baldness, in my opinion, ..., then finas is not a preventive method

 

[abcdefg]

The only thing in existence with proof it stops male pattern baldness from ever happening is castration. I dont know anything else ever shown to stop male pattern baldness. Doesnt mean it cant be done, but just that nothing else is proven so far. Propecia is something, dutasteride is closer, but is there really any AA that replicates castration? I think it lowers T a lot on top of lowering DHT a lot so it lowers androgens drastically acrossed the board. No treatment really does that, and everyone just kind of hypothesizes that its mainly DHT and not really T. How much proof is there that is true though

 

[HairCook]

The correlations at this point with senescence are extremely convincing in my opinion. It's astonishing really how the puzzle is falling into place. Frankly I think nothing will beat castration + estrogen for a long time (in terms of drugs). But even castration + estrogen doesn't always cut it. Besides that, I think indeed in some people Androgenetic Alopecia might be irreversible due to destruction of the hair follicle by fibrosis (later stage Androgenetic Alopecia) in the sense that only a regenerative therapy will be the answer (creation of new hair follicles, morphogenesis). Regenerative therapy will be the answer to this I guess and I hope asap. They are making rapid advancements that's for sure.

prevention is absolute key, do it if you can and don't wait.

Well said, bro. Good to see not everyone is folding their hands for some commercial solution.

I recently picked up on the woundhealing process and why certain anecdotal individuals had success while we dont.

Would be cool to get some feedback from of my ShowerOfThoughts on what we are missing: https://imgur.com/a/ATqS6

 

[razzmatazz91]

lol. We need someone like Tsuji or Jahoda to respawn hair follicles.

Jeesus How long has tsuji been at it now?
This post was made in 2015

 

[furrydome]

Would be cool to get some feedback from of my ShowerOfThoughts on what we are missing: https://imgur.com/a/ATqS6

Hopefully this isn't just my stoned brain shitposting, but doesn't wounding break up fibrotic tissue? So even if it does extend the anagen phase, maybe based on this theory it's also creating more space for follicles to grow?

Anecdote: 1 year of needling with 1.5mm depth about every 2 weeks took me from solid NW3 to a thin NW2. Not a cure by any means, but definitely significant. And that hair survived a month where I wasn't able to needle due to a dermatitis.

Theory: Breaking up fibrotic tissue via wounding/needling/chemicals provides the follicle with an environment that's more conducive to growth, and that environment might even persist until the balding process gets around to damaging it again.

 

[arnoldd]

this is a very interesting study. alopecia areate seems to be reversible but male pattern baldness not. so hair loss from inflammation ( autoimmune diseases like lupus) have more chances of regrowth than hair loss from androgens ?

 

[Willy31]

The correlations at this point with senescence are extremely convincing in my opinion. It's astonishing really how the puzzle is falling into place. Frankly I think nothing will beat castration + estrogen for a long time (in terms of drugs). But even castration + estrogen doesn't always cut it. Besides that, I think indeed in some people Androgenetic Alopecia might be irreversible due to destruction of the hair follicle by fibrosis (later stage Androgenetic Alopecia) in the sense that only a regenerative therapy will be the answer (creation of new hair follicles, morphogenesis). Regenerative therapy will be the answer to this I guess and I hope asap. They are making rapid advancements that's for sure.
prevention is absolute key, do it if you can and don't wait.

I put mix of 60% castor oïl + 40% DMSO 3X/week to destroy fibrosis. It's ok or you have a better idea?