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Baldness Biology
 Male pattern baldness overview
 Female pattern baldness overview
 Male pattern baldness presentation
 Female baldness presentation
 Hair fiber in pattern baldness
 Hair follicles in pattern baldness
 Androgen hormones in men
 Androgen hormones in women
 Androgen receptors in baldness
 5 alpha reductase in baldness
 Inflammation in baldness
 Genetics in pattern baldness
 Diseases associated with baldness
 Pattern baldness in children
 
Baldness Treatments
 Minoxidil for pattern baldness
 Minoxidil for female baldness
 Minoxidil for male baldness
 Finasteride for male baldness
 Finasteride for female baldness
 Tretinoin for pattern baldness
 Diazoxide for pattern baldness
 Ketoconazole for pattern baldness
 Antiandrogens for pattern baldness
 Contraceptives for female baldness
 Spironolactone for female baldness
 Flutamide for female baldness
 Cyproterone acetate for baldness
 

Androgenic hormones and genetic influences are both usually acknowledged as essential for the progress of pattern baldness – at least in men. While the age at which androgenic alopecia develops varies, it has frequently been associated to post pubertal stages when the testosterone level is significantly ready to be converted to dihydrotestosterone, which happens to trigger scalp hair loss in pattern baldness.

This concept is sustained by the reality that baldness doesn’t influence males castrated before puberty and is infrequent and lesser in women. The start of pattern baldness is consequently unlikely in pre puberty with no irregular androgen levels. On the other hand, there have been research conducted and information of pattern baldness in pre pubertal children.

Case Study

Dr. Tosti’s team conducted a study on twenty pre-pubertal Italian children with baldness. Eight boys and twelve girls in between the ages of six to ten years with hair loss pattern were monitored for over four years.

Clinical Observation

The study revealed hair loss with thinning and thickening of the central distribution of the scalp in both girls and boys. Eight cases showed a Christmas tree pattern of hair loss. Olsen has characterized this pattern as one that raises in the direction of the front of the scalp with an encroachment and a few times a break of the hairline in front. It has been proved to be more frequent when it begins at a very young age. None of these children had cephalic baldness or depression of the temporal hairline, a characteristic of male pattern baldness.

Other Observations and Examinations

Family history proves to be a strong link in all patients with pattern baldness. A certain pull test was done to screen areas of active baldness and trichogram to measure the fraction of terminal anagen hairs to telogen hairs. In addition, dermoscopy were carried out in such cases to disregard other hair loss forms that happen in children.

Clinical studies which include the customary blood cell count, biochemical studies, sex hormone assays (follicle stimulating hormone, luteinizing hormone, estradiol, progesterone, 17-hydroxyprogesterone, prolactin, testosterone, dehydroepiandrosterone sulphate –DHEA-s, androstenedione), thyroid function, adrenocorticotrophic hormone, cortisol and growth hormone-releasing hormone were done. All outcomes have been within the expected ranges with regards to sex and age.

In all of the twelve children who took the exam, the DHEA-S levels were steady with postadrenarche. Adrenarche means a phase of cortex maturation of the adrenals which usually happens between six to ten years of age. It includes both compositional and practical changes.
Pediatric tests verified standard physical growth in relation to the Tanner Scale and Growth Parameters (phases of physical growth in children, adolescents and adults. The phases describe dimensions of growth according to external primary and secondary sexual attributes). None of the respondents revealed any proof of pubic or auxiliary hair. None of the girls revealed breast growth and the boys’ genitalia (reproductive organs) showed to have been of normal size. There were no signs of acne or hirsutism.

Histopathology

In six cases, a 4 mm punch biopsy was done from the involved scalp and both vertical and horizontal divisions were gained. Normal hair volume were seen in horizontal sections with a mean of 41 hairs and ranges up to 38 to 45. Thick, highly pigmented hairs known as the terminal follicles decreased, where as intermediate and vellus-like or the thin, non pigmented hairs were increased with a ratio of less than 3:1. The anagen-telogen ratio reveals to be 88:12. In the vertical divisions, disintegrated sheaths were obvious under the smaller hair follicles. There were no evidences of inflammation. The findings were in relation to the histopathologic findings in adult baldness.

Explanations

The study team came into conclusion that pattern baldness influences children in prepuberty. Adrenal hormonal excretion starts to level up two to three years before the start of puberty by means of adrenarche, achieving mature levels in early to late puberty. Adrenarche is a stage associated to puberty but different from hypothalamic-pituitary-gonadal maturation and purpose. DHEA-S blood levels and DHEA, or precursors of androgan can be attained to reach androgenous adrenal secretions. The systems involved in adrenarche parameters are unknown.

The usual characteristic found among the patients was a strong familial tendency to baldness. According to the team, the familial tendency may cause an excess in androgen sensitivity of follicular scalp because of an atypical movement of the enzyme 5-reductase type II or to an increase in appearance of andogenic receptors in the scalp. It is conclusive then that it is not viable for adrenal androgens to be accountable for pattern baldness in children with familial tendency.

In addition, a probable reason for its incidence in children could have been that theirs are not related to androgen dependency. In all of the cases among both boys and girls, the baldness existing with female hair loss pattern, vs. selective association of the central division is the scalp is sometimes linked to frontal emphasis. Nobody had cephalic alopecia or temporal hairline depression, a feature of male pattern baldness. This type of alopecia is usually seen in females and has been described to arise in the deficiency of androgens. Therefore, another conclusion has been made that other methods should be taken into account in the pathogenesis of child pattern baldness.

 
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