Callender VD et al. APTN begins with thinning hair on the vertex accompanied by little or no clinical evidence of scarring. During the evolutionary process of normal hair, the cells of the internal follicular sheath become keratinized earlier than the cortex and act as a cylindrical axis that supports the hair growth, which will be guided and shaped by this structure.
However, it is believed that the absence of internal follicular sheath causes a disorganized 'packaging' of the hair, especially of the cuticle, resulting in instability and ultimately in breakage. The diagnosis can be made by means of the tug test, which consists in selecting a sample of hair strands and holding it at its base with the forefinger and thumb of one hand while the other hand pulls the strands towards their distal end.
With this maneuver, it is possible to observe the breakage of the hair in half. Another characteristic feature of the disease is trichonodosis, i. Recommendations for these patients are: 11 , Use a soft brush with widely spaced bristles and coated tips or a wooden comb with wide teeth.
Even after the complete interruption of all hair straightening and relaxing tecnhiques, it is expected that the disease will remain active for further years, possibly because all hairs have to be replaced by new anagens ones. Alternatively, some women choose to keep their hair short in order to achieve that the fractured hairs and the hairs that were not affected by the disease have the same length.
We emphasize the importance of making the differential diagnosis between acquired proximal trichorrhexis nodosa and early-onset CCCA, because both conditions have the same topography and do not present obvious signs of a scarring area, especially in women of African descent. In the case CCCA, the simple recommendation to interrupt all hair treatments will be ineffective.
Here is also necessary the introduction of treatment in order to cease the progression of the disease, reduce the chances of developing scarring alopecia and increase the probability of hair regrowth in the future. This syndrome is characterized by the inability of the hair to grow long and the observation of an increased number of telogen hairs in the trichogram. Usually affected are Caucasian children with blond thin hair who are brought to the doctor by their parents because their hair does not grow long or because they have never had a haircut.
However, Nidhi Avashia et al. The patient also reported that her first haircut had occurred when she was seven years old and that her hair had never grown more than 7. The diagnosis is made by means of the observation of the presence of normal hair, with a short anagen phase and there may be an anagen to telogen ratio of up to It is important to keep in mind that this is a possible diagnosis in black children with limited growth of hair. Ignorance of this entity may lead to a diagnosis of traction alopecia in children who wear braids and do not present normal hair growth.
Short anagens were also described in the tricho-dental syndrome, a congenital disorder associated with hypodontia. Therapeutic options are limited. Traction alopecia TA is an extremely common condition in black women, resulting from years of use of hairpieces and hairstyles that exert prolonged and repeated traction upon the hairs and cause the shortening of the hairs in the frontotemporal line of implantation of the hair.
Usually, the areas of alopecia are symmetrical along the frontotemporal line Figure 1. Traction alopecia. Observe the traction exerted by the hairpiece upon the hairs, resulting in the shortening of the hairs in the temporal region. The presence of short hairs scattered along the frontotemporal line is a characteristic finding of TA and is called "fringe sign" Figure 2.
The fringe sign: short tonsured hairs outlining the original frontotemporal line of implantation of the hair. In patients who have no clinical history of use of tight hairstyles, the differential diagnosis is broad and includes androgenetic alopecia, telogen effluvium, trichotillomania, primary lymphocytic scarring alopecias lichen planus pilaris, central centrifugal scarring alopecia, Brocq's pseudopelade and frontal fibrosing alopecia , and alopecia areata.
Less often, TA may affect the occipital region. In this case, the differential diagnosis with ophiasis alopecia areata is imperative.
Alopecia areata AA is a type of non-scarring alopecia of autoimmune etiology. Dermoscopic findings of AA are the unique exclamation mark hairs or pencil hairs.
Histopathologic examination shows lymphocytic infiltrates around the follicular bulge. Ophiasis AA may be underdiagnosed in black women, since there is a tendency to diagnose the condition in this population as TA.
Therefore, it is important to investigate the history of use or traumatic removal of hairpieces, which speaks for the diagnosis of traction alopecia. Studies with African women have shown as risk factors for the development of TA: Hairstyles should be done at least two weeks after the chemical treatment and hair relaxers should be avoided, especially in children.
If a chemical hair relaxer is used, it should only be applied to the virgin hair, and one should be careful not to apply it to previously relaxed hair. The use of hair dryers and flat irons should be avoided.
In the early stages, TA presents trichomalacia and an increased number of telogen and catagen hairs. In the course of the disease, a phenomenon similar to a "follicular abandonment" occurs: the terminal hairs disappear from the follicles, but the vellus hairs remain intact.
In advanced disease settings, there may be a decrease of sebaceous glands, a mild inflammatory infiltrate and a decrease in the number of terminal follicles, which are replaced by fibrotic tissue. Dermoscopy shows many miniaturized hairs and pinpoint white dots visible acrosyringium. Due to the traction, the hairs may also show signs of breakage of the follicular shaft, and sometimes display cylinders of the follicular sheath - which was freshly detached due to the trauma hair casts -, as well as cadaveric hairs and longitudinal slits at the distal end of the hair shaft Figure 3.
Observe the hair casts in traction alopecia, representing follicular sheath cylinders which detach themselves due to the traction forces exerted upon the hairs and adhere themselves to the hairs. The prognosis is variable. If the diagnosis is made early and the use of hairstyles and hair techniques that exert traction upon the hairs is stopped early in childhood , the clinical status may be reversible, usually with full recovery and growth of new hair. However, in the case of a late diagnosis, the chronic perifollicular inflammation may lead to the formation of fibrotic scarring tissue and the alopecia may become permanent.
Thus, treatment will depend on the stage of the disease. In childhood, the most important action is prevention. Patients and their parents should be instructed to avoid using tight hairstyles that exert too much traction upon the hair and scalp. In the advanced stages of TA surgical treatment should be considered. Micro-implants, mini implants, follicular unit transplantation and rotation flaps have been described as effective treatments.
Scarring alopecias represent a group of disorders whose common final pathway culminates in the destruction of the hair follicle and its replacement by fibrous tissue. The alopecia may occur as a primary event when the follicle is the main target of the pathological process primary scarring alopecia or as a secondary event when the follicle acts as an "innocent bystander" in the course of a disease, which occurs outside the follicular unit secondary scarring alopecia.
Four groups were considered: alopecias with predominantly lymphocytic infiltrate, with predominantly neutrophilic infiltrate, with mixed infiltrate and with nonspecific infiltrate. Below is a brief review of the major primary scarring alopecias in women of African descent. Central centrifugal cicatricial alopecia CCCA is defined as a hair loss that starts at the vertex and middle region of the scalp and progresses centrifugally.
It is the most common form of primary scarring alopecia in people of African descent, affecting more women than men. The prevalence increases with age and the disease is more common at the end of the second and in the third decades of life. In , LoPresti and colleagues first used the term "hot comb alopecia" to describe a variant of scarring alopecia that was associated with the use of hot metal combs by African-American women. It was believed that the hot Vaseline used in some hair treatments caused chronic inflammation of the hair follicle, with its subsequent destruction and replacement with fibrous tissue.
The cause of this type of scarring alopecia was later discussed. In , Sperling and Sau conducted a retrospective study with 10 women diagnosed with "hot comb alopecia". They found a poor correlation between the use of hot combs and the onset and progression of the disease in these patients.
The term "hot comb alopecia" was replaced by the term 'follicular degeneration syndrome', based on histological findings of the disease and on the conclusion of Sperling's research. However, it is now known that this disease has a multifactorial origin, involving intrinsic and extrinsic factors.
Disease activity occurs mainly in the peripheral zone, with variable width, surrounding the central zone of alopecia. CCCA may be classified as 'early stage' inflammatory or 'late stage' cicatricial. As the disease progresses, it leaves an area of alopecia with irreversible loss of follicular ostia. A few isolated hairs, some of them are short and brittle or present polytrichia, may remain in the central hairless area.
Signs of inflammation are absent, although erythema, follicular pustules, scaling and inflammatory borders in areas of alopecia may arise at any stage of the disease. To date, the etiology of CCCA is controversial. The most likely theory is that it has a multifactorial origin, being implicated as possible predisposing factors: genetics, hair straightening chemicals, trauma caused by traction and the spiral configuration of the hairs.
Irregularities in the diameter along the hair shaft, a thinner thickness, more curly and flattened, and spiral shape of the hairs make Afro-ethnic hair more susceptible to breakage caused by the hair treatments often used by this population. A recent study found that patients who had advanced and severe CCCA used more hairstyles with traction, such as hair braiding, for a long time, which causes chronic folliculitis of the scalp with subsequent hair loss and development of CCCA.
The cause and effect relationship of chemical relaxers is still controversial. However, it is known that chemical relaxers weaken the hair shaft, increasing the possibility of hair breakage, and may cause chemical burns on the scalp, although it is not yet proven that they contribute to the development of CCCA.
Biopsy is important to confirm the diagnosis. Ideally, two fragments should be obtained for horizontal and vertical histopathological sections with 4-mm punch biopsy specimens taken from the periphery or the active border of the alopecia area.
Dermoscopy shows the same findings that are found in other types of scarring alopecia, with absence of follicular ostia, presence of some vellus hairs and terminal hairs of irregular distribution within the area of alopecia, erythema and scaling on the periphery of the plaque, indicating disease activity. The differential diagnosis of CCCA should be made with androgenetic alopecia, alopecia areata, traction alopecia, lupus and Brocq's pseudopelade Figure 4.
Brocq's pseudopelade may represent a distinct form or final stage of CCCA. It presents as asymptomatic macules or plaques in the parietal region, which converge forming an irregular, polycyclic and atrophic area. The presence of pustules, crusts and inflammation in alopecia zones should make the physician suspect the diagnosis or think about a superinfection by fungi and bacteria. Cicatricial alopecia in the central scalp CCCA.
In this case, the differential diagnosis was made with androgenetic alopecia in black women B. LED of the scalp. Because it shows central involvement, it is important to remember the differential diagnosis with CCCA in melanodermic patients.
To date, treatment recommendations are based on anecdotes or case reports. The main goal is to stop disease progression, especially in peripheral areas, and relieve symptoms by administering anti-inflammatory agents. Medium- or high-potency intralesional and topical corticosteroids are the first-line treatments. Intralesional corticosteroids such as triamcinolone 2. Topical corticosteroids are administered daily until stabilization of the clinical condition, and then three times a week for maintenance.
In cases in which the use of corticosteroids shows little or no improvement, the administration of topical tacrolimus 0. In severe cases or cases with much inflammation, the combination of oral tetracycline e. Other second-line drugs include: anti-malarials such as hydroxychloroquine mg daily , cyclosporine and mycophenolate mofetil, mainly used in patients with active, recalcitrant disease.
In the advanced stages with irreversible loss of follicles, hair transplantion is an option, but should only be performed if the inflammatory process has been inactive for at least one year. However, the expectations of the patient should be realistic, given that the survival rate of the transplanted graft may decrease due to the presence of scarring areas on the scalp.
In addition to drug treatment, potentially harmful practices to the hair, such as chemical treatments, thermal damage, traction, caustic cosmetics and the use of hot combs should be avoided. These are behavioral measures which constitute an important basis for therapeutic success.
Among the predominantly lymphocytic types of alopecia there are the classic form, lichen planus pilaris LPP , and its variants: frontal fibrosing alopecia FFA and the Graham-Little-Picardi-Lasseur syndrome.
Lichen planus pilaris is an uncommon inflammatory disease characterized by a self-destructive lymphocytic reaction of the hair follicle causing permanent alopecia of the scalp and sometimes the involvement of other areas of the body other than the scalp. According to the North American Hair Research Society classification of cicatricial alopecia, LPP is classified as a primary lymphocytic cicatricial alopecia in which the follicle is self-destroyed with little involvement of the interfollicular dermis.
The disease may present alone or in combination with other forms of lichen planus, such as cutaneous, nail or mucosal lichen planus. To date, there are no data on the prevalence of LPP and its variants in black women. Studies only mention the prevalence of frontal fibrosing alopecia in these patients.
Although the pathogenesis of LPP remains unclear, the most accepted theory is that it is an autoimmune disorder in which activated T lymphocytes attack the follicle, and this reaction, mediated by cells, is potentially initiated by the action of infectious agents hepatitis C, HIV, HSV2, HPV, Helicobacter pylori, Treponema pallidum , medical agents beta blockers, thiazides, antimalarial drugs, ACE inhibitors and sensitizing agents gold, mercury and cobalt.
When I decided to cut my hair last December I felt like a major change. But I was also curious how people would react. It became evident that a lot of people were more attached to my hair than I was.
I was told I was "ungrateful" because many struggle to grow their hair. I refuse to be reduced to a type because of my hair, boxed into the category of "beautiful because she has long hair", "successful because she has long hair", perhaps even "married because she has long hair".
And what is it about straightening my hair that communicates that I have abandoned my roots? As columnist Kuli Roberts says, "we need to stop putting black women in a box". She has been scrutinised over her choice to wear weaves - questions that are never directed at people from other races. Some say hair is one of the most contentious issues in black society.
South African columnist Danielle Bowler goes as far as to say in Eyewitness News that "while some women might not choose their hairstyle based on an overt political decision, the choices available to us are themselves inescapably political". The debate is often "reduced to a simplistic antagonistic relationship between weaves and natural hair" she says. But African hair comes in many different textures - it is versatile and resilient.
It holds braided hairstyles like no other and we can adorn our crowns with these for weeks on end with endless options to choose from. I look forward to the day when I can leave my hair wild and uncombed and have it say nothing else about me apart from "I didn't feel like combing my hair today". Whether I weave it, relax it or braid it I'd like to live in a world where the choice of how to express myself - in hair and everything in between - is mine.
As for my sisters; the youngest now has long dreadlocks, my middle sister - who still isn't a fan of combing - rocks a weave most of the time and I have short, colour-treated afro hair. We are the perfect representation of choice in modern South Africa - and in the end choice and the freedom to express it, is what those before us fought for.
I don't feel pressured to look a certain way anymore, but not everybody has this experience. Black hair, which is what makes us black, has been fighting for those same rights. Milisuthando Bongela is a blogger in Johannesburg, South Africa. The problem is we're placing white people on a pedestal - not every woman who wears a wig is trying to be white. I have options. I treat my hair the same way I treat my nails, I can wear it in many different ways - that doesn't change who I am.
I know who I am. The idea that you have such low self-esteem that your hair is the one thing that defines you - come on. I will not take part in anything that seeks to berate black women for exercising their options. How about we debate why Jewish women wear wigs? Why white women colour their hair? Why they wear braids - are they trying to be black?
As black people, our hair is an expression of the infinite possibilities that emanate from this creative and daring consciousness. This article was originally published on The Conversation. Read the original article. You might be overlooking another potential influence on Dread locks in Jamaica.
People in my area have no knowledge of the fact that fast growth shampoos obviously with no sulfates, no parabens and no DEA exist. Persons can now enjoy longer hair and possess more alternatives. Certainly worth considering. For the most part, you have to avoid hair products and treatments that include chemicals like parabens, DEA or sulfates. Obviously the content above is so accurate for various reasons.
It avoids the common traps and errors so many fall into- utilizing ineffective alternatives. Greatly appreciated! African Arguments. Elections Map. The hot comb has mostly fallen out of fashion but any Black woman over the age of 20 has memories of being burned by one. The key to really nice shiny, healthy hair is a balance of the natural oils we all produce. With straight or wavy hair, oil travels down the shaft fairly easily. So while non-Blacks may wash their hair a lot to avoid excess oil, Black women worry more about maintaining what they have or adding more.
If we washed our hair every day, it would be dry and unhealthy. Culturally, Black women have the most options with their hair. It can be permed or natural. Bought or grown. Straightened or fluffy. Completely disappeared with a big pair of earrings to accessorize our bald heads. One of the not-so-great things about this? Please see 3. First, thank you for asking.
But even if you ask nicely, the answer is probably no. More importantly, most of us feel like allowing strangers to touch our hair just so they can experience it is akin to being pet like an animal. What else should everyone know about Black hair? About Us Our Services.
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