Hair loss or commonly used term “baldness” is a common clinical complaint that is a manifestation of a wide variety of disorders. Although the cause of hair loss is easily diagnosed in some cases, such as in patients who present with classic male pattern hair loss or patchy hair loss due to alopecia areata, the diagnosis of hair loss also can be challenging. Hair has many useful biologic functions, including protection from the elements and dispersion of sweat-gland products (e.g., pheromones). It also has psychosocial importance in our society, and patients with hair loss (alopecia) or excessive hair growth often suffer tremendously. The human scalp contains approximately 100,000 to 150,000 hair follicles. Each hair follicle sits above a dermal papilla, a collection of mesenchymal tissue with inductive properties. The dermal papilla induces the development of hair follicles in the fetus and appears to play an important role in follicular cycling and hair growth.
Once hair follicles is formed it undergoes lifelong cycling characterized by periods of growth (anagen), transformation (catagen), and rest (telogen). In humans, hair cycling is not synchronous, meaning that individual follicles cycle independently, preventing en mass shedding of hair.
Classification of hair loss:
Hair loss disorders are a large, heterogenous group of conditions that have various clinical features, pathologic findings, and etiologies. Hair loss may occur due to disorders of hair cycling, inflammatory conditions that damage hair follicles, or inherited or acquired abnormalities in hair shafts.
The major dividing lines for the various forms of hair loss are the distinction between cicatricial (scarring) alopecia, non-scarring alopecia, and structural hair disorders. Cicatricial alopecias are conditions that lead to the irreversible cessation of hair cycling and permanent hair loss. The loss of hair follicle stem cells in the bulge region of the hair follicle is thought to contribute to the development of cicatricial alopecia. In non-scarring alopecias, the hair follicle is not permanently damaged, making spontaneous or treatment-induced regrowth a possibility. Structural hair disorders that lead to hair loss demonstrate abnormalities within the hair shafts that result in hair fragility. In this article will focus on non-scarring alopecia, and structural hair disorders.
In non-scarring alopecias, clinical signs of inflammation are usually mild or absent and destruction of the hair follicle does not occur. Recognition of the distribution of nonscarring alopecia is useful for narrowing the differential diagnosis.
Focal hair loss:
– Alopecia areata is a relatively common form of non-scarring alopecia which is secondary to autoimmune process leading to hair loss on the scalp or other areas.
– Alopecia syphilitica is secondary to syphilis infection and can present with patchy hair loss on the scalp, which has been described as “moth-eaten” alopecia.
– Pressure-induced (postoperative) alopecia is transient hair loss that occurs in areas of prolonged pressure on the scalp, as may occur during general anesthesia for long operative procedures. Hair loss usually develops a few weeks after the event. Regrowth occurs in most patients.
– Temporal triangular alopecia (also known as congenital triangular alopecia) is a lifelong condition that is usually first noted in infancy or childhood as a triangular or oval patch of alopecia in the temporal area. The area of involvement is usually only a few centimeters in diameter.
– Traction alopecia results from prolonged pull or tension on the hair follicle, usually due to hairstyles such as tight ponytails or braids. Traction alopecia from braids or hair weaves is most commonly detected along the frontal and temporal hair lines. Longstanding traction can result in permanent hair loss.
Patterned hair loss:
– Androgenetic alopecia in men (male pattern hair loss) is characterized by the slow, progressive loss of hair in a characteristic distribution (Bitemporal hair loss, hair loss on the vertex of the scalp, which terminal hairs on the occipital scalp are spared). The condition is mediated by the action of androgens on androgen-sensitive hair follicles in genetically susceptible males.
– Female pattern hair loss most frequently presents as hair thinning on the frontal and crown areas of the scalp with relative sparing of the occipital scalp. The frequency of this condition increases with age.
– Trichotillomania is a disorder in which individuals repeatedly pluck hairs from the scalp or other hair-bearing areas. The areas of alopecia may have irregular, bizarre shapes.
Diffuse hair loss:
– Anagen effluvium occurs as a result of an acute interruption of the anagen phase and leads to extensive hair loss without transition of follicles into the catagen or telogen phase. Hair loss typically occurs within two weeks of an inciting event. Chemotherapeutic agents are a major cause of anagen effluvium.
– Loose anagen syndrome is usually presents in young children (ages two to five years) as slowly growing hair that can easily be pulled out without pain. The hair density may appear normal or reduced. Affected children are often females with blond hair.
– Telogen effluvium is a common cause of diffuse hair loss that usually presents with acute or chronic loss of hair due to an abrupt shift of numerous hair follicles in anagen to the telogen phase. Chronic telogen effluvium may also occur. Examples of factors that may stimulate acute telogen effluvium include major physical or psychologic stressors, childbirth, dietary restriction, and medications. Hair loss usually occurs two to three months after the inciting event. Arsenic, thallium, or mercury poisoning can also result in telogen effluvium.
Inherited and acquired structural disorders leading to baldness:
Structural hair abnormalities that result in brittle or fragile hair can lead to hair breakage or the appearance of a failure of hair to grow. The hair fragility may result from abnormal hair formation or external insults that damage the hair shaft. The most common structural hair abnormalities are acquired trichorrhexis nodosa and trichoptilosis, both of which may occur as a result of harmful hair care practices, such as chemical processing, excessive brushing or teasing of hair, or the application of excessive heat. Trichorrhexis nodosa is characterized by disruption of the protective cuticle and fraying of the hair shaft. Trichoptilosis is a term that describes splitting and fraying of the distal end of the hair shaft, which is commonly referred to as “split ends.” Bubble hair (bubble-like structures within the hair shaft) is another microscopic finding that may be seen in heat-damaged hair.
Examples of genetic conditions that cause hair fragility and excessive hair breakage includes Menkes disease, Monilethrix, Trichothiodystrophy and Trichorrhexis invaginata.
– Physical examination of scalp and hair must be done first to establish basis for diagnosis. Visual inspection of the entire scalp must be done, which can provide physical clues that may aid with diagnosis, such as erythema, scales, papules, pustules, erosions, or excoriations. Other examination techniques such as trichoscopy and the hair pull test may be helpful.
– Microscopic examination is useful for determining the type of hairs that are being shed (eg, telogen, anagen, or dystrophic anagen hairs).
– Scalp biopsies can be a useful tool for the evaluation of hair loss when the diagnosis is uncertain. Scalp biopsies can distinguish scarring from non-scarring alopecia, and can provide information that further narrows the differential diagnosis.
– Trichograms and phototrichograms are techniques for the evaluation of non- scarring hair loss that are primarily used in research studies and specialized hair centers and can be used to assist with diagnosis and following the response to treatment.
– Laboratory studies — serologic and microbiologic studies may also be useful for obtaining information to support the diagnosis and to detect associated disorders. Recommended initial laboratory tests include thyroid stimulating hormone to assess for thyroid disease as well as serum iron and ferritin to assess for iron deficiency. In addition, a rapid plasma reagin test to rule out syphilitic alopecia is appropriate for patients with patchy hair loss without visible inflammation or scarring.
TREATMENT OF BALDNESS:
Minoxidil is an antihypertensive medication that works by opening of potassium channels and hypothetically, by widening blood vessels and opening potassium channels, allowing more oxygen, blood, and nutrients to the follicles. Minoxidil is usually the first line treatment for both male and female pattern hair loss.
Finasteride, spironolactone, cyproterone acetate, and flutamide are systemic medications that inhibit androgen production or its action. These medications can be used for both male and female pattern hair loss and are good choice as a monotherapy or in conjunction with minoxidil in those patients who have responded poorly to minoxidil alone or in female pattern hair loss related to hyperandrogenism.
Surgical interventions through the transplantation of terminal hairs from unaffected areas of the scalp to affected sites are also an option for those patients who do not achieve a satisfactory response with pharmacologic therapy.
NEW TREATMENT THAT MAY POTENTIALLY CURE BALDNESS:
Previously scientists conducted a study published in the journal PLOS Biology using Cyclosporine A (CsA), which has been used since 1980s to treat immune disorders and transplant rejections. Some of the side effects of Cyclosporine A included shaking, headaches, vomiting and swollen gums and unwanted hair growth. Scientists analyzed the gene expressions of isolated human scalp hair follicles and found that Cyclosporine A changed how the follicles expressed a protein called SFRP1, which stunts the development and growth of hair follicles and other tissues in the body.
The scientists were then able to identify that WAY-316606, a compound used to treat osteoporosis, has a similar effect on how SFRP1 is expressed. The compound WAY-316606 could therefore be used to treat and cure baldness, without patients suffering the same side effects as they would on Cyclosporine A. Although this is a promising treatment for baldness, there are currently no indications that it may also cure baldness.
CLICK HERE to get more comprehensive detail from a well-researched article about WAY-316606 and its role on potentially treating/curing hair loss.
[expand title=”References for Osteoporosis Drug WAY-316606 Could Potentially Treat and Cure Baldness”] – https://www.nejm.org/doi/10.1056/NEJM199908123410706