Alcune delle conclusioni tratte da:
https://tmdocclusion.com/2018/07/14/more-on-hair-loss/
Hair follicles on top of the scalp are affected by androgenetic alopecia, while those on the sides are not.
Androgenetic model: hair follicles on top of the head show increased expression of the androgen receptor gene. However, DHT stimulates the production of pigmented terminal hair in many other areas after puberty and higher levels of androgen receptors are also found in these follicles which remain healthy, e.g. like in those in men’s beard. So, this is a paradox and thus the androgenetic model does not offer a clear explanation.
New model: neck muscular tension propagates through the myofascia to the galea, which tightens and compresses blood vessels going to the hair follicles. Instead on the sides of the head, the underlying tissue is made of muscles so it is softer and richer of blood vessels. Thus, a compression in those areas does not block blood reaching the follicles.
The incidence of Male Pattern Baldness increases with age. However, serum testosterone production declines with aging, together with lower serum DHT.
Androgenetic model: no explanation.
New model: neck muscular tensions that compress the galea are caused by an abnormal posture. Posture is determined by craniofacial development which depends on bone remodeling. Bone remodeling is a lifelong process, so an increase in age means a poor craniofacial development can worsen over time, with an impact on the posture. This creates higher predisposition to baldness with age.
Baldness have significantly spread in the modern era and isolated tribes are less likely to suffer of hair loss.
Androgenetic model: no explanation.
New model: craniofacial development depends on forces coming from orofacial muscles (among them, the tongue). The causes of a poor craniofacial development have to be found in modern civilized lifestyle (e.g. use of pacifiers, bottle-feeding, soft high-calorie diet, early weaning).
Subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower.
Androgenetic model: no explanation.
New model: galea compresses blood vessels, blocking blood flow.
Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth.
Androgenetic model: no explanation.
New model: minoxidil acts as a vasodilator through membrane hyperpolarization caused by opening potassium channels [58,59]. This promote blood flow, thus hair growth.
The scalp of bald men show higher formation of 5a-reduced metabolites and 17-ketosteroid metabolites.
Androgenetic model: although DHT is considered playing the main role in baldness, this model does not give any explanation of why DHT and other metabolities should be present in higher concentration in bald scalps. So, no explanation.
New model: when blood vessels are compressed, blood cannot reach hair follicles causing reduced availability of nutrients and inadequate removal of metabolites, damaging tissues. Then, an inflammatory response is activated and DHT is an important regulator of its activity.
Excessive dandruff and scalp sensitivity are often associated with hair loss.
Androgenetic model: no explanation.
New model: dandruff consists of dead cells (corneocytes) from the last scalp layer that are regularly replaced through desquamation. In case of reduced blood supply, cells die more rapidly triggering an excessive turnover, i.e. the dandruff. When tissues are damaged, an inflammatory response is activated. The classical signs of inflammation are heat, pain and redness, situation recognized as scalp sensitivity (burning, stinging, dry scalp, vague discomfort in the scalp, and sometimes, trichodynia).
Miniaturization of hair follicles has been associated with deposits of densely packed collagen bundles in the follicular dermal sheath, called perifollicular fibrosis.
Androgenetic model: no explanation.
New model: when the inflammation is long-term and chronic, it causes fibrosis and calcification.