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In my previous article on male-pattern baldness, or androgenetic alopecia, I narrated how hair growth and this condition roughly work. In this article I’ll highlight some of the treatment modalities that can counteract the development of male-pattern baldness.
Given the pivotal role of androgens in development of this condition, it should come as no surprise that some treatment modalities have targeted this role. An FDA approved drug that works through this is (oral) Finasteride. This is a drug that inhibits the enzyme responsible for the conversion of testosterone into the more potent androgen dihydrotestosterone (DHT). Another class of drugs, of which none is approved (yet), are the androgen receptor antagonists. These work by antagonizing the effects of DHT, and other androgens, at the receptor level (e.g. topilutamide).
Another FDA approved drug, and there are actually as of writing this only 2 approved, is topical minoxidil. The treatment of androgenetic alopecia with minoxidil isn’t one that surfaced as a result of advances in our understanding of the condition. It was actually used for another condition (albeit given orally), namely hypertension, and it was discovered by chance that it led to hair growth in these patients. Hence they started trying it as a treatment for androgenetic alopecia, and voila, it worked.
While not a drug, platelet-rich plasma (PRP) therapy has gained quite some traction in the past few years as a viable treatment option too. PRP is simply blood plasma with more platelets in it than regular blood plasma. These platelets contain a variety of growth factors and cytokines and it’s thought that these play an important role in stimulating hair growth. This PRP is then repeatedly injected into the affected areas with tiny needles.
Yet other treatment modalities center around the role that prostaglandins play in the development of male-pattern hair loss. Prostaglandins are lipid molecules that are derived from the fatty acid arachidonic acid. There are a whole bunch of them, and it’s thought that some of these promote androgenetic alopecia, whereas others inhibit its progression. As such, drugs have been developed that target enzymes responsible for the production of some of these prostaglandins.
Finally, a bunch of signaling pathways are involved in the development of androgenetic alopecia, of which the Wnt/β-catenin signaling pathway is one of them. It’s a pathway that’s involved in a myriad of processes, but in this article I’ll just focus on its role in androgenetic alopecia. In brief, activation of this pathway by Wnt proteins leads to accumulation of stable β-catenin in the cell, which translocates to the nucleus and then upregulates Wnt target genes. These genes apparently play an important role in the hair follicle and hair cycle. As such, drugs that modulate this pathway have been developed.
In the following sections I will go into more detail into how the more conventional treatment modalities work, that is: oral finasteride and topical minoxidil. Additionally, I’ll cover the topical counterpart of finasteride and oral counterpart of minoxidil. In my next article I’ll focus on the more experimental treatments, that is, topical androgen receptor antagonists and prostaglandins, PRP therapy, and Wnt signaling modulators.
