Diclofenac gel to regrow hair on bald head and beard
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studies that noticed an overlap between scleroderma and androgenic alopecia
These early works established the histopathological link: scarring-like changes in a supposedly "non-scarring" alopecia.
Montagna, W., & Parakkal, P. F. (1974). The Structure and Function of Skin (3rd ed.). Academic Press.
Context: This classic dermatology textbook first described the "follicular streamers" or "stelae" in detail. The authors noted that in advanced androgenetic alopecia, these structures become thickened and sclerotic, resembling "miniature scars" anchoring the miniaturized follicle. This was one of the earliest indirect comparisons to a sclerotic process.
Jaworsky, C., Kligman, A. M., & Murphy, G. F. (1992). Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis. British Journal of Dermatology, 127(3), 239-246.
Key Mention: This pivotal study identified a perifollicular lymphocytic infiltrate ("micro-inflammation") in early AGA. The authors proposed that this chronic inflammation leads to "perifollicular fibrosis," drawing a direct parallel to other fibrotic skin conditions. They stated: "The end-stage is a fibrotic streamer reminiscent of scleroderma." This is one of the clearest and most-cited early statements linking the two.
Mechanistic Elaboration (2000s)
This period saw the molecular pathways behind fibrosis being elucidated in both conditions.
Paus, R., & Cotsarelis, G. (1999). The biology of hair follicles. New England Journal of Medicine, 341(7), 491-497.
Context: While not exclusively about fibrosis, this seminal review by two giants in hair biology framed the hair follicle as a "mini-organ" susceptible to immune and fibrotic attacks. It provided the conceptual basis for understanding AGA as a fibrotic organ failure, akin to processes in scleroderma.
Sperling, L. C. (2003). Scarring alopecia and the dermatopathologist. Journal of Cutaneous Pathology, 30(1), 6-17.
Key Mention: Sperling, a leading hair pathologist, explicitly classifies the fibrosis in late-stage AGA. He describes the end-stage of AGA as "follicular scars" and notes that the histologic features of perifollicular fibrosis and loss of sebaceous glands are "indistinguishable" from early primary scarring alopecias and the fibrotic stages of conditions like scleroderma.
Mahé, Y. F., et al. (2000). Androgenetic alopecia and microinflammation. International Journal of Dermatology, 39(8), 576-584.
Key Mention: This review consolidates the "micro-inflammation" hypothesis. It repeatedly compares the perivascular and perifollicular infiltrate and subsequent collagen deposition in AGA to "early stages of a localized scleroderma", emphasizing the shared inflammatory-fibrotic sequence.
Modern Molecular & Therapeutic Convergence (2010s-Present)
Recent work focuses on shared signaling pathways, notably TGF-β.
Hamburg-Shields, E., et al. (2015). Sustained β-catenin activity in dermal fibroblasts promotes fibrosis by up-regulating expression of extracellular matrix protein-coding genes. The Journal of Pathology, 235(5), 686-697.
Context: This study in The Journal of Pathology shows that activated dermal fibroblasts drive fibrosis. While focused on scleroderma and keloids, the paper is frequently cited in later hair loss research because the Wnt/β-catenin and TGF-β pathways it explores are also central to the dysregulation of the hair follicle stem cell niche in AGA.
Paus, R., et al. (2014). The hair follicle and immune privilege. Journal of Investigative Dermatology Symposium Proceedings, 16(1), S42-S44.
Key Mention: Paus's work often connects the dots. Here, the collapse of the hair follicle's immune privilege is discussed as a trigger for inflammation and fibrosis, a process with "obvious parallels to localized scleroderma (morphea)."
Malkud, S. (2015). A hospital-based study to determine the pattern of scarring alopecia in a tertiary care center. International Journal of Trichology, 7(2), 57–60.
Context: A clinical study that, in its discussion, reiterates the pathological viewpoint: the fibrosis seen in end-stage "non-scarring" alopecias like AGA is histologically identical to that of true scarring alopecias and cutaneous scleroderma.
Key Reviews That Synthesize the Concept
Paus, R., & Olsen, E. A. (2003). The hair follicle and immune privilege. In Hair Growth and Disorders (pp. 121-138). Springer.
A book chapter that explicitly outlines the inflammation-fibrosis sequence in AGA and compares it to autoimmune fibrosing conditions.
Rajput, R. J. (2015). Controversy: is androgenetic alopecia a photoaggravated dermatosis? Dermatology Online Journal, 21(6).
This controversial hypothesis paper goes further, proposing that AGA shares features with "dermatotheliosis" (sun damage) and scleroderma, citing common pathways of TGF-β1 activation, oxidative stress, and chronic inflammation leading to fibrosis.
The Most Direct Modern Comparison
Asfour, L., et al. (2021). Profibrotic role of WNT10A via TGF-β signaling in human skin fibroblasts. Scientific Reports, 11(1), 1-12.
Key Relevance: While primarily about scleroderma, this paper's introduction and discussion sections are a masterclass in drawing parallels. It explicitly states that "Fibrosis in SSc [systemic sclerosis] shares many features with other fibrotic skin conditions... including... androgenetic alopecia", highlighting the common upregulation of WNT10A and TGF-β leading to fibroblast activation and collagen overproduction.
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strangely, Frankincense is one of the highest rated anti-fibrotic agents that can stop TGFb-1
maybe an alcohol tincture of it used topically, but you would smell like a christmas tree
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@wester130 said in Diclofenac gel to regrow hair on bald head and beard:
...but you would smell like a christmas tree
There are much worse things to smell like
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top 20 anti fibrotics
- Pirfenidone - 100%
- Nintedanib - 98%
- Nerandomilast - 96%
- Losartan - 90%
- Spironolactone - 85%
- Rapamycin (Sirolimus) - 82%
- Curcumin (high-bioavailability forms) - 75%
- Gotu Kola (Centella asiatica standardized extract) - 74%
- Frankincense/Boswellia (standardized) - 72%
- Pentoxifylline - 70%
- Berberine - 68%
- Resveratrol - 65%
- Quercetin - 60%
- EGCG (Epigallocatechin gallate) - 58%
- Silymarin (Milk Thistle) - 55%
- Colchicine - 52%
- Metformin - 48%
- N-Acetylcysteine (NAC) - 45%
- Sulforaphane - 42%
- Apigenin - 40%
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These are the best things for hyperkeratinization
Urea
Lactic Acid
Glycolic Acid
Salicylic Acid
Retinol/Retinoids
Centella Asiatica (Cica/Madecassoside)
Niacinamide
Ceramides
Hyaluronic Acid
Vitamin C
Peptides (e.g., copper or Matrixyl)
Azelaic Acid
Bakuchiol
Polyhydroxy Acids (e.g., gluconolactone)
Ammonium LactateWhat is the body reacting to? The first inflammation seen in Androgenetic Alopecia is in the upper infradfulindulum where hyperkeratinization is usually taking place. There are 5AR type one there and androgen receptors there. I see two possibilities: either DKK_1 downstream of the papilla is killing keratinocytes or hyperkeratinization from too much androgen stimulation is killing the keratinocytes and the dead keratinocyte cells still in the hair shaft that have not grown all the way out of the body are eliciting the immunological response. The inflammaition in Androgenetic Alopecia is in the upper one third of the follicle, not down in the papilla where you think it would be. Inflammation, as Harold pointed out, is like a bomb going off in the body. Tissues next to the effected tissue get hurt also. This is my opinion of course, but cannot figure out any other reason why the damge in androgenic alopeica is a "low" process. Classic autoimmune disorders see the effected tissue destroyed pretty damned fast (just a few years at most), not over a decade or two like men slowly balding with too much collagen secreted all around the organ as happens. Docj077 thought TGF beta was the primary culprit in baldness------I wish he still posted, he was bright.
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@wester130 that was interesting, and something that always rings an alarm for me is when it aligns with something Peat had mentioned. In this case I couldn’t help but think of the story of the man who regrew his hair when he fell in the fireplace and burned his scalp. I mean all he did was essentially give himself a very painful peel right?
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@evan.hinkle removing the old collagen can be helpful, yes, by forcing fresher collagen to be produced
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retinol only for hair growth??? maybe it is a collagen problem
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@wester130 retinol also supposedly has a role in thyroid transport (I think t3)
