It is the most known form of non-cicatricial (non-scarring) alopecia. It is also called, through simple terms, such as seborrheic, premature, or male alopecia. It develops with initial hair loss on the top of the head and gradually affects the entire coronal section of the scalp, sparing the nape and temples, reaching “coronal” baldness. Androgenic Alopecia is often coupled, but not constantly, by seborrhea and scaling of dandruff.
It develops with the receding of the frontal-parietal hairline that in men usually is M-shaped (receding hairline). This is not a symptom that necessarily favours the onset of Androgenic Alopecia. In fact, it is not uncommon that bald patients display a frontal hairline still intact, on the other hand, it is very common that patients with receding hairline display a remarkable hair density on the vertex section. Androgenic Alopecia and frontal-parietal Alopecia in males are therefore typified as two unrelated forms, probably caused by different genes not necessarily traceable in the same individual.
After Androgenic Alopecia, Alopecia Areata is the one that affects the most area of the head. It’s non cicatricial and it’s usually typified by one or more oval and round-shaped patches whose average diameter is 3-4 cm with no hair (especially in the beard area), with no alteration (sometimes it’s coupled with reversible epidermal atrophy) and signs of inflammation (in rare cases the color is rosy and accompanied by a modest edema), with hair follicles untainted (sometimes unvisible to the naked eye) and apparently intact. The skin might appear slightly hypotonic (hyperlaxity probably caused by the disappearance of root hair).
At the edge of the patches, which tend to spread in a centrifugal way, there are hair in anagen phase, short and broken (4-12 mm in length) showing dystrophic features increasingly thinner at the distal end (dark and swollen) towards the bulb (thin and colourless) and called “exclamation mark hair”. They are typical in the Alopecia Areata and caused of the malfunction of the cell-matrix. Removing these hair with tweezers is very easy due to the absence of mooring sheaths. Both the trichogram and the microscopic control of the fallen hair during the washing show dystrophic anagen effluvium.
As for the aethiopathogenesis, from time to time, it’s been recorded states of anxiety, endocrine contagious diseases, etc. even though the most credited assumption is the one concerning autoimmune disease, probably caused by anxiety-depressive disorder. According to some authors, Alopecia Areata would develop when there is a strong attack leading to a sudden arrest of the mitosis in all hair that, in that precisemoment are in the most delicate phase of their growing, with maximum mitotic index (sub-phase anagen VI) and subsequent onset of anagen dystrophic effluvium.
From the histological point of view in the recent patch we can notice lymphocyte infiltration mainly of peri-follicular and perivascular origin, in the stabilized path a dystrophic follicle (small and atrophic) and in the previous one the disappearance of the prefollicular infiltration and the complete atrophy of the hail-follicle (surrounded by thickened and anelastic collagen sheaths). The preferential localization at the coronal section might be explained considering that in this phase the anagen number is higher than in the parietal temporal occipital area, except for the insertion marging; these data confirm, among other things, the lack of self-resolving tendency and the oftenly negative outcome of Alopecia treatments of these areas (malign alopecia otherwise known as Ofiasi).
Radiodermitis of the scalp can be caused by therapeutic radiation treatments, by diagnostic tests or by industrial injuries. In acute radiodermitis (very rare) it can be developed transitory alopecia, instead, in the chronic type, it might even appear after 20-30 years from the radiation exposure; the skin becomes dry and atrophic (with reduced thickness), it might be noticed the absence of the pilosebaceous structures and telangiectatis (permanent dilatation of small superficial vessels in the scalp) and discoloration (variation of type and tone of colours). On chronic radiodermitis might easily appear spinocellular epithelioma (even after years from the exposure).
It’s a rather common alteration and is caused by reiterated and continue tractions on the scalp: pony tails, braids, curlers, hair set, perm. In the modest cases the damage can be noticed only at the microscope for the presence, in the percentage repartition of the fallen hair during a hair wash, of anagen and broken hair (usually absent). In the most acute cases it can be noticed perifollicular erythema, postules and a slight scaling; like in trichotillomania, over the time irreversible damages might linger on the scalp. The areas most affected are the ones of insertion marging, where the mechanical traction has its maximum intensity.
The term indicates a psychoneurotic disorder usually hard to asses and even more difficult to be accepted by the patient’s parents. It’s a pathology where usually children, more or less consciously, acquire the habit to twist and pull the hair with their fingers. Alopecia generally develops in the fronto-parietal areas with irregular patches whose size can reach several centimeters, in which the hair are either absent or broken with a length of 2-3 mm (with this short lenght it’s not possible to grab it with the fingers).
The scalp appears intact. If in the interested area the remaining hair are removed, it is possible to notice the complete absence telogen phase hair. From the histological point of view, in serious cases, the follicle might get fractured in the matrix and can have the separation of the external epithelial bundle from the connective sheath, causing subsequent intra and extra-follicular bleeding and more or less complete repair of the cicatricial tissue. This will cause, even if the stimulus ends, the persistent impossibility to produce a normal hair (tricomalacia).
It appears with a “telogen effluvium” (with the fall of only the mature telogen) 2-3 months after the childbirth; it is caused by the sudden drop in the estrogenic hormone (with related and subsequent lack of the estrogenic hormone itself) and by the effect caused by the prolactin hormone (produced in high quantity during the pregnancy and feeding), coupled with the momentary stress. Post-Infectious Alopecia.
It appears during or after well-defined unhealthy states. The typhoid fever and those Alopecia developed during severe fevers usually cause an Anagen effluvium, while those subsequent to minor fevers, secondary syphilis, viral hepatitis and chronic infections generally appears associated with “telogen effluvium”.
The term Tinea refers to the attack to hair (or hairs) on behalf of micetis (fungus). The Tinea of the scalp (tinea capitis) displays one or more scaling erythematous spots, in which hair are broken and show a dusty feature (fungus spores).
Depending on the micetis type, the spots can be either individual or grouped, neat edged, round-shaped, their diameter size reaches 5cm, with broken hair with a length of 2-3mm above the scalp (tinea microspore), or more numerous, with indistinct limits, irregular outline, and length not superior to 1-2 cm, with broken hair associated to other “survivors” within the patches (tinea tricofitic). The contamination can descend from the direct contact with domestic animal, stable animal but also other human beings. The tinea, if well groomed, definitively regresses in 4-6 weeks.
Kerion is the result of the host’s response to a fungal ringworm infection of the hair follicles of the scalp and beard accompanied by secondary bacterial infection. It usually presents itself as raised, spongy lesions. This honeycomb has severely painful inflammatory reactions with deep suppurative lesion on the scalp.
The follicle may be seen discharging pus. There may be sinus formation and rarely mycetoma like grains are produced. The hair which are in the patches are first damaged by the micetis and then definitively eliminated by the scarring suppurative process.
Favus is a disease usually affecting the scalp but occurring occasionally on any part of the skin, and even at times on mucous membranes. Favus is a mycosis of the scalp often determined by Tricophyton schonleinii, and rarely by Tricophyton quinckeaneum. It often has squama spots that have a sizable pustule that later opens leaving a yellowish depression of 5-7 mm as diameter, with the unpleasant smell of “mouse’s urine”, made of a mass of filament, and gill put in a concentric order around the hair follicle.
The favus can extend itself in a centrifugal way reaching a diameter of 2-3 cm and then it can flow into ample mass with crust yellowish-lightgreen, stratified and friable, within it’s possible to find thin, opaque, discolour hair which are easly removable. The therapy is long, if it is not correctly performed, it will turn into a scarring – cicatricial- alopecia (within the patches there are lock of hair remaining as survivors).
It’s an alopecia in the Telogen phase or, sometimes in the Anagen phase, it is generally widespread and intense. For example the alopecia derived from acetate thallium, once used for the tinea scalp therapies, but still present in rats (risk of accidental ingestions or with a suicide purpose). It has to be underlined that all iatrogenic alopecia solve spontaneously with the interruption of the responsible medication.
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