Scientific collaboration between Professor Marco Toscani and Dr. Pasquale Fino, Chair of Plastic, Reconstructive and Aesthetic Surgery, Umberto I Health Center – “Sapienza” University of Rome.
Androgenetic alopecia is the most common type of hair loss and affects the majority of white men, with varying degrees of seriousness. It is less frequent in other ethnic groups. Often it can be associated with a family history of baldness, but the absence of other affected family members does not exclude the diagnosis. The condition is characterized by progressive hair loss in the crown area, the front hairline and the temporal area.
As the term “androgenetic” indicates, the causes lie in the hormonal component and genetic predisposition to the illness. The process that leads to hair loss, at least in the early years of the condition, does not cause a complete stalling of hair growth but a progressive reduction of the growth phase (anagen), which results in premature hair loss, with the replacement by new hair that, however, grows increasingly thinner. This process is called follicular miniaturization and leads to visible thinning on the scalp.
Pattern hair loss starts to develop after puberty, a phase characterized by a strong increase in androgen production. The effect of androgens on cells is mediated by androgen receptors. Dihydrotestosterone (DTH) is the androgen that most heavily impacts the induction and evolution of pattern hair loss. It is an androgen produced from testosterone, but characterized by greater strength and affinity (ability to bind) to the receptor when compared to testosterone. The conversion from testosterone to DTH is mediated by the enzyme 5-alpha reductase. This enzyme exists in two different forms (isoforms) in the scalp follicles, type 1 and type 2. Type 2, found on the external face of the collagen shell at the root of the hair, is the type that has the most impact on hair loss. Once the androgen receptor is activated, it sends a series of signals that lead to the activation of the genes responsible for the gradual transformation of follicles from big to small ones suffering from a short anagen phase.
Young men with initial baldness have greater levels of 5-alpha reductase and a greater quantity of androgen receptors. Also the DTH production rate is higher in individuals with hair loss problems, when compared to those who do not suffer from this type of problem. Moreover, even if the testosterone levels are similar in both men affected by baldness and those who aren’t, many of the affected present high levels of free testosterone, which is testosterone unbound to the protein which stops it from binding to the receptor.
As far as the genetic component is concerned, many genes have been connected to the development of baldness. The hereditary scheme is complex and involves both the paternal and maternal lines.
We are therefore speaking of a model of polygenic inheritance with variable impact. The evolution of hair loss varies from case to case, due to many factors. Moreover, it is a process that progresses slowly over the course of many years. It may be defined as proceeding in waves, alternating periods in which the loss is rapid to periods in which the loss is nearly inexistent or quite modest.
Therefore, pattern hair loss is characterized by varying degrees of hair thinning and loss that typically begin in the temporal, frontal and crown areas. The degree of involvement of these three areas is quite variable; some men lose more hair from the crown, while others tend to lose hair in the front. In general, the occipital area is spared, and this is what makes the option of autotransplants possible.
The Hamilton-Norwood scale is generally used to classify the type and degree of hair loss. This scale features 7 categories and also distinguishes a more uncommon type of loss, identifying it as variant A, in which only a progressive hair line recession can be observed. Nevertheless, not all men follow these loss patterns. In 10% of cases, the loss is similar to that seen in women, i.e. the hairline is conserved and a scattered thinning of the central part is seen.
The diagnosis of male pattern hair loss is generally clinical and the patient history and direct observation of the individual’s scalp and hair may be sufficient. If, instead, the loss has been quite rapid and accompanied by burning and/or itchiness, other potentially associated causes need to be taken into consideration.
A dermatoscopy (or trichoscopy) may be useful, as may be a biopsy when other causes are suspected. The main differential diagnosis from which pattern hair loss must be distinguished are telogen effluvium and alopecia areata (spot baldness).
The first line therapies for a man suffering from pattern hair loss are topical use 5% minoxidil and oral use finasteride. Both these drugs have shown to be effective and highly tolerable. The effectiveness and results vary from case to case: while some individuals obtain significant growth, others benefit less from the therapy, perhaps only just reducing further loss.
Finasteride is a type 2 5-alpha reductase inhibitor, meaning that it blocks the production of DHT. The daily dosage is 1 mg. Age is an important factor in terms of response to the therapy. The drug seems to be more effective in individuals between 18 and 40 years of age when compared to those between 41 and 60 years of age.
In addition to growth in the number of hairs, finasteride produces an increase in the thickness, pigmentation and length of hair, all of which increase the perception of an improvement of the condition. To evaluate the drug’s full effectiveness, the treatment should be continued for at least a year, and it should then be continued to maintain its effects. If it is stopped, the results will be lost after approximately 6-8 months from the time of interruption. Collateral effects may include the reduction of libido, erectile and/or ejaculation dysfunction or a decreased sperm count, and the risk of these effects increases with age. Nevertheless, these side effects usually resolve after the end of the treatment. Other less common effects are gynecomastia, testicular pain and depression. However, these effects are generally observed only in the case of higher dosages than that used for treating prostatic hyperplasia.
For male pattern hair loss, the preferable solution is to use the 5% formula of minoxidil. The foam form, that doesn’t contain propylene glycol, has been available for a while and is less irritating for the skin. Minoxidil promotes hair growth by increasing the duration of the anagen phase, reducing the telogen phase and increasing the thickness of miniaturized follicles. The most frequent side effects are itchiness and skin rash. Hypertrichosis is generally not a problem in men. Also in the case of minoxidil, the results of the treatment are variable.
Patients with shorter-lasting baldness, with smaller affected areas and a greater number of still active follicles respond better to treatment. The use of the drug is indefinite and if treatment is suspended the results are lost within the following months. At the start of the treatment, it is normal to notice an increase in terms of the loss of hair. The hair lost in this phase is in the telogen phase and will be replaced by hair in the anagen phase. It is important to not to stop the treatment before it can become effective. To enjoy visible results, the patient must wait at least 4 months and then continue the therapy for at least 14-18 months, in order to stabilize the effect.
A surgical option may also be considered helping with the condition. Today the most common option is an autotransplant. Ideal candidates are those who suffer from stable hair loss or hair loss kept well under control by therapy and presenting a good reserve of hair in the occipital region, the donation area for the transplant. Since the hair in the occipital region is more resistant to pattern hair loss, it remains of a higher caliber. Nevertheless, patients may continue to lose non-transplanted hair and therefore face unsatisfying results in time.
It is therefore important to continue the treatment with minoxidil or finasteride, in order to limit further losses.
Other therapies are also available, and new ones are continuously being developed. Nevertheless, these cannot boast the same proven effectiveness as minoxidil and finasteride.
Among the most interesting new therapies worth mentioning, we can list:
– LLLT or low level laser therapy; its mechanism of action is still unclear, however appears to cause an increased proliferation of hair bulbs, stimulate follicle stem cells and keratinocytes, and lead to an increased production of adenosine triphosphate, an element that supplies energy to cellular activity and also has anti-inflammatory effects.
– Topical use atanoprost 0.1%, a prostraglandin analogue that seems to lead to an increase in hair density.