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The Comparative Histopathology of Male-Pattern Baldness and Senescent Baldness" Albert M. Kligman, MD, PhD
"All of the early male pattern baldness features are present. More of the shortened follicles are in telogen. The streamers still show considerable inflammation, but fibrosis is in greater evidence, with many parallel bundles of dense collagen. Occasional streamers eventually end up as fibrotic tracts. These are subfollicular scars. These fibrous bands have few cells, sparse vessels, and show hyalinized collagen. End-stage fibrosis of this degree is not common; surprisingly, some seem to undergo partial resorption, suggesting that they might disappear altogether...."
"male pattern baldness is a genetically determined inflammatory disorder that should not be considered as premature aging. The etiology of the inflammation is unknown. Follicular miniaturization in male pattern baldness is a consequence of pathologic fibrosis of the connective tissue sheath. The central pathology relates to abnormalities of the perifollicular connective tissue sheath, evident as inflamed streamers subtending involuting follicles. Those streamers show fibroplasia and hypertrophy, along with proliferation of capillaries and a mixed infiltrate of lymphocytes, histocytes, and mast cells. Chronic inflammation of the streamers prevents anagen follicles from being fully reconstructed during the new cycle. After many years, this can lead to scarring and preclude regeneration. Even in advanced male pattern baldness, most follicles were not fully scarred, offering the theoretical possibility of regrowth. Fibrotic streamers are increased in proportion to the duration of baldness and chronologic age".
As you see, inflammation and fibrosis are essential players in male pattern baldness. Cu Peptides are capable of preventing and even reversing tissue fibrosis.
Thanks bryan for posting this excerpt.
"All of the early male pattern baldness features are present. More of the shortened follicles are in telogen. The streamers still show considerable inflammation, but fibrosis is in greater evidence, with many parallel bundles of dense collagen. Occasional streamers eventually end up as fibrotic tracts. These are subfollicular scars. These fibrous bands have few cells, sparse vessels, and show hyalinized collagen. End-stage fibrosis of this degree is not common; surprisingly, some seem to undergo partial resorption, suggesting that they might disappear altogether...."
"male pattern baldness is a genetically determined inflammatory disorder that should not be considered as premature aging. The etiology of the inflammation is unknown. Follicular miniaturization in male pattern baldness is a consequence of pathologic fibrosis of the connective tissue sheath. The central pathology relates to abnormalities of the perifollicular connective tissue sheath, evident as inflamed streamers subtending involuting follicles. Those streamers show fibroplasia and hypertrophy, along with proliferation of capillaries and a mixed infiltrate of lymphocytes, histocytes, and mast cells. Chronic inflammation of the streamers prevents anagen follicles from being fully reconstructed during the new cycle. After many years, this can lead to scarring and preclude regeneration. Even in advanced male pattern baldness, most follicles were not fully scarred, offering the theoretical possibility of regrowth. Fibrotic streamers are increased in proportion to the duration of baldness and chronologic age".
As you see, inflammation and fibrosis are essential players in male pattern baldness. Cu Peptides are capable of preventing and even reversing tissue fibrosis.
Thanks bryan for posting this excerpt.