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This is a German study that tries to identify the mechanism behind retinoid-induced hair loss.
Retinoids are a form of vitamin A and are used orally to treat various forms of cancer and topically, to treat acne and psoriasis. One of the side effects is diffuse hair loss, though exactly how it’s induced has not been examined prior to this study.
In this study, hair follicles from a human scalp were placed in a culture dish in a lab and exposed to all-trans retinoic acid (ATRA), also known as tretinoin or Retin-A. At the start of the study the follicles were all in the anagen (growing) phase. After 2 days of treatment, the hair strands produced by the ATRA-treated follicles grew significantly slower than those of the control group which were not exposed to anything.
After 6 days 80% of the ATRA-treated follicles had entered a catagen-like phase, compared to 30% of the control follicles. The catagen phase follows anagen and precedes the telogen or resting phase. During the catagen phase the follicle shrinks and the dermal papilla breaks away to rest below the shrunken follicle until the end of telogen phase when it reconnects with the follicle again and initiates growth of new hair. The dermal papilla, which can be found in the hair follicle, act like a control station for the follicle growth phases and respond to stimulation by androgens (male sex hormones).
The findings in ATRA-treated follicles corresponded to an increased cell death (apoptosis) and a decreased amount of cells proliferating (Ki67-positive).
Transforming growth factor (TGF) beta is believed to play a key role in the transformation from the anagen to the catagen phase, the researchers therefore examined what, if any, effect ATRA had on follicular expression of TGF-beta. In the untreated anagen follicles, TGF-beta was present in the outer root sheath, in the untreated catagen follicles, it was also present in the shrinking hair strand. After 4 days of ATRA-treatment, TGF-beta was significantly up-regulated in the dermal papilla and dermal sheath of anagen follicles. The researchers then tried TGF-beta neutralizing antibodies, which inhibit the action of TGF-beta, and treatment with the antibodies was at least partially effective in inhibiting the retinoid-induced hair loss. This seems to indicate that TGF-beta is, indeed, one of the culprits in retinoid-induced hair loss.
ATRA was shown to cause follicles to prematurely enter the catagen phase, and it was also shown to up-regulate the expression of TGF-beta. Inhibition of TGF-beta was partially effective in abolishing the ATRA growth suppression, showing that TGF-beta is one of the main factors in this pathway. The study suggests a topical TGF-beta receptor II inhibitor in conjunction with retinoid-treatment, could be used to avoid hair loss as a side effect of Retinoid treatment.
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Retinoids are a form of vitamin A and are used orally to treat various forms of cancer and topically, to treat acne and psoriasis. One of the side effects is diffuse hair loss, though exactly how it’s induced has not been examined prior to this study.
In this study, hair follicles from a human scalp were placed in a culture dish in a lab and exposed to all-trans retinoic acid (ATRA), also known as tretinoin or Retin-A. At the start of the study the follicles were all in the anagen (growing) phase. After 2 days of treatment, the hair strands produced by the ATRA-treated follicles grew significantly slower than those of the control group which were not exposed to anything.
After 6 days 80% of the ATRA-treated follicles had entered a catagen-like phase, compared to 30% of the control follicles. The catagen phase follows anagen and precedes the telogen or resting phase. During the catagen phase the follicle shrinks and the dermal papilla breaks away to rest below the shrunken follicle until the end of telogen phase when it reconnects with the follicle again and initiates growth of new hair. The dermal papilla, which can be found in the hair follicle, act like a control station for the follicle growth phases and respond to stimulation by androgens (male sex hormones).
The findings in ATRA-treated follicles corresponded to an increased cell death (apoptosis) and a decreased amount of cells proliferating (Ki67-positive).
Transforming growth factor (TGF) beta is believed to play a key role in the transformation from the anagen to the catagen phase, the researchers therefore examined what, if any, effect ATRA had on follicular expression of TGF-beta. In the untreated anagen follicles, TGF-beta was present in the outer root sheath, in the untreated catagen follicles, it was also present in the shrinking hair strand. After 4 days of ATRA-treatment, TGF-beta was significantly up-regulated in the dermal papilla and dermal sheath of anagen follicles. The researchers then tried TGF-beta neutralizing antibodies, which inhibit the action of TGF-beta, and treatment with the antibodies was at least partially effective in inhibiting the retinoid-induced hair loss. This seems to indicate that TGF-beta is, indeed, one of the culprits in retinoid-induced hair loss.
ATRA was shown to cause follicles to prematurely enter the catagen phase, and it was also shown to up-regulate the expression of TGF-beta. Inhibition of TGF-beta was partially effective in abolishing the ATRA growth suppression, showing that TGF-beta is one of the main factors in this pathway. The study suggests a topical TGF-beta receptor II inhibitor in conjunction with retinoid-treatment, could be used to avoid hair loss as a side effect of Retinoid treatment.
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