Central centrifugal cicatricial alopecia ( CCCA ), is a type of alopecia first noticed in African Americans in the 1950s and reported by LoPresti et al. in 1968 as a result of application of petrolatum followed by a stove-heated iron comb. The original theory was that the hot petrolatum would travel down to the hair root, burn the follicle, and after repetitive injury scarring would result. Later CCCA was realized to affect men and women without a history significant for use of such styling techniques. Consequently, the terms "follicular degeneration syndrome" per Sperling and Sau in 1992 and then CCCA per Olsent et al. in 2003 were evolved. Plausible contributing factors may include other African-American styling techniques such as relaxers , tight braids, heavy extensions, certain oils, gels or pomades.
52-475: CCCA be an abbreviation for: Central centrifugal cicatricial alopecia Classic Car Club of America correlation consistent Composite Approach Canyon Creek Christian Academy Comprehensive Crime Control Act of 1984 Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with the title CCCA . If an internal link led you here, you may wish to change
104-683: A Y-chromosome gene or a paternal imprinting effect. The initial programming of pilosebaceous units of hair follicles begins in utero . The physiology is primarily androgenic , with dihydrotestosterone (DHT) being the major contributor at the dermal papillae . Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone , and epitestosterone when compared to men without pattern hair loss. Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown
156-415: A 4× increased frequency which is clinically deemed significant. Abdominal obesity, hypertension and lowered high density lipoprotein were also significantly higher for younger groups. Pattern hair loss is classified as a form of non-scarring hair loss. Male-pattern hair loss begins above the temples and at the vertex ( calvaria ) of the scalp . As it progresses, a rim of hair at the sides and rear of
208-573: A female-pattern hair loss. The terminology of CCCA has been a source of regular confusion. Recent clarifications have been made, with the term "central centrifugal cicatritial alopecia" adopted as a diagnostic category by the North American Hair Research Society . It has also been referred to as: Also in this category is cicatricial pattern hair loss (CPHL). This CCCA pattern is a potential alopecia mimic that can be confused for androgenetic alopecia . Alopecia mimics have proven
260-453: A masculine attribute associated with seniority and higher social status . The condition is caused by a combination of male sex hormones (balding never occurs in castrated men) and genetic factors. Some research has found evidence for the role of oxidative stress in hair loss, the microbiome of the scalp, genetics, and circulating androgens ; particularly dihydrotestosterone (DHT). Men with early onset androgenic alopecia (before
312-449: A month. An example of premature age effect is Werner's syndrome , a condition of accelerated aging from low-fidelity copying of mRNA. Affected children display premature androgenic alopecia. Permanent hair-loss is a result of reduction of the number of living hair matrixes. Long-term of insufficiency of nutrition is an important cause for the death of hair matrixes. Misrepair-accumulation aging theory suggests that dermal fibrosis
364-494: A mystery, but possible explanations are higher conversion of testosterone to DHT locally with age as higher levels of 5-alpha reductase are noted in balding scalp, and higher levels of DNA damage in the dermal papilla as well as senescence of the dermal papilla due to androgen receptor activation and environmental stress. Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance , and metabolic syndrome , with low HDL being
416-405: A problem in establishing diagnosis of alopecia when using only clinical evaluation. A similarly sounding term is central centrifugal scarring alopecia (CCSA). (L.C. Sperling, Central, centrifugal scarring alopecia. In: L.C. Sperling, Editor, An atlas of hair pathology with clinical correlations, Parthenon Publishing Group, New York (2003), pp. 91–100). This is a clinical finding that describes
468-490: Is a medication of the 5α-reductase inhibitors (5-ARIs) class. By inhibiting type II 5-AR, finasteride prevents the conversion of testosterone to dihydrotestosterone in various tissues including the scalp. Increased hair on the scalp can be seen within three months of starting finasteride treatment and longer-term studies have demonstrated increased hair on the scalp at 24 and 48 months with continued use. Treatment with finasteride more effectively treats male-pattern hair loss at
520-529: Is associated with seniority and higher social ranking, giving them increased sexual capital . This is similar to the white stripe seen on male silver-back gorillas , associated with their advanced age and higher social ranking. The genetic evidence did not support this hypothesis in African populations, suggesting that within Africa, the evolutionary pressure for scalp hair (to protect against harsh sunlight) outweighed
572-415: Is associated with the progressive hair-loss and hair-whitening in old people. With age, the dermal layer of the skin has progressive deposition of collagen fibers, and this is a result of accumulation of Misrepairs of derma. Fibrosis makes the derma stiff and makes the tissue have increased resistance to the walls of blood vessels. The tissue resistance to arteries will lead to the reduction of blood supply to
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#1732855692869624-474: Is beneficial for alopecia areata and androgenetic alopecia and can be used as an alternative to minoxidil or finasteride. It has been documented to improve hair density and thickness in both genders. A minimum of 3 treatments, once a month for 3 months are recommended, and afterwards a 3-6 month period of continual appointments for maintenance. Factors that determine efficacy include amount of sessions, double versus single centrifugation, age and gender, and where
676-423: Is little evidence to support the use of lasers to treat male-pattern hair loss. The same applies to special lights. Dietary supplements are not typically recommended. A 2015 review found a growing number of papers in which plant extracts were studied but only one randomized controlled clinical trial, namely a study in 10 people of saw palmetto extract . A 2023 study on genetically engineered mice published in
728-422: Is more effective for androgenetic alopecia. Medical reviews suggest that LLLT is as effective or potentially more than other non invasive and traditional therapies like minoxidil and finasteride but further studies such as RCTs, long term follow up studies, and larger double blinded trials need to be conducted to confirm the initial findings. Using ones own cells and tissues and without harsh side effects, PRP
780-543: Is most commonly formed at the tissue level by 5α-reduction of testosterone. The genetic corollary that codes for this enzyme has been discovered. Prolactin has also been suggested to have different effects on the hair follicle across gender. Also, crosstalk occurs between androgens and the Wnt-beta-catenin signaling pathway that leads to hair loss. At the level of the somatic stem cell , androgens promote differentiation of facial hair dermal papillae, but inhibit it at
832-524: Is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison. Female patients with mineralocorticoid resistance present with androgenic alopecia. IGF levels have been found lower in those with metabolic syndrome. Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at
884-615: Is no significant difference in efficiency between 2% and 5% formulations. Finasteride was shown to be no more effective than placebo based on low-quality studies. The effectiveness of laser-based therapies is unclear. Bicalutamide , an antiandrogen , is another option for the treatment of female pattern hair loss. More advanced cases may be resistant or unresponsive to medical therapy and require hair transplantation . Naturally occurring units of one to four hairs, called follicular units , are excised and moved to areas of hair restoration . These follicular units are surgically implanted in
936-464: Is not clear how this causes hair to grow. Other treatments include tretinoin combined with minoxidil, ketoconazole shampoo, dermarolling ( Collagen induction therapy ), spironolactone , alfatradiol , topilutamide (fluridil), topical melatonin , and intradermal and intramuscular botulinum toxin injections to the scalp. There is evidence supporting the use of minoxidil as a safe and effective treatment for female pattern hair loss, and there
988-470: Is not well-studied and may result in birth defects if taken during pregnancy. By the age of 50, pattern hair loss affects about half of males and a quarter of females. It is the most common cause of hair loss . Both males aged 40–91 and younger male patients of early onset AGA (before the age of 35), had a higher likelihood of metabolic syndrome (MetS) and insulin resistance. With younger males, studies found metabolic syndrome to be at approximately
1040-502: Is related to being an increased risk factor for cardiovascular diseases, glucose metabolism disorders, type 2 diabetes , and enlargement of the prostate . A number of hormonal changes occur with aging: This decrease in androgens and androgen receptors, and the increase in SHBG are opposite the increase in androgenic alopecia with aging. This is not intuitive, as testosterone and its peripheral metabolite, DHT, accelerate hair loss, and SHBG
1092-435: Is the only keratin that is regulated by androgens. This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et al. found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body, but decrease it on the scalp, this lack of scalp KRT37 may help explain
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#17328556928691144-425: Is thought to be protective. The ratio of T/SHBG, DHT/SHBG decreases by as much as 80% by age 80, in numeric parallel to hair loss, and approximates the pharmacology of antiandrogens such as finasteride . Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. About 30% of normal male testosterone level, the approximate level in females, is not enough to induce alopecia; 60%, closer to
1196-413: Is typically experienced as a "moderately stressful condition that diminishes body image satisfaction". However, although most men regard baldness as an unwanted and distressing experience, they usually are able to cope and retain integrity of personality. Although baldness is not as common in women as in men, the psychological effects of hair loss tend to be much greater. Typically, the frontal hairline
1248-570: Is usually absent. Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy. CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be
1300-543: The crown than male-pattern hair loss at the front of the head and temples. Dutasteride is a medication in the same class as finasteride but inhibits both type I and type II 5-alpha reductase. Dutasteride is approved for the treatment of male-pattern hair loss in Korea and Japan , but not in the United States. However, it is commonly used off-label to treat male-pattern hair loss. Minoxidil dilates small blood vessels; it
1352-480: The PRP is inserted. Future larger randomized controlled trials and other high quality studies are still recommended to be carried out and published for a stronger consensus. Further development of a standardized practice for procedure is also recommended. Many people use unproven treatments. Regarding female pattern alopecia, there is no evidence for vitamins , minerals, or other dietary supplements. As of 2008, there
1404-573: The age of 35) have been deemed the male phenotypic equivalent for polycystic ovary syndrome (PCOS). The cause in female pattern hair loss remains unclear; androgenetic alopecia for women is associated with an increased risk of polycystic ovary syndrome (PCOS). Management may include simply accepting the condition or shaving one's head to improve the aesthetic aspect of the condition. Otherwise, common medical treatments include minoxidil , finasteride , dutasteride , or hair transplant surgery . Use of finasteride and dutasteride in women
1456-449: The amount found in elderly men, is sufficient. The testicular secretion of testosterone perhaps "sets the stage" for androgenic alopecia as a multifactorial diathesis stress model , related to hormonal predisposition, environment, and age. Supplementing eunuchs with testosterone during their second decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within
1508-521: The appearance of a short, buzzed haircut. Low-level laser therapy or photobiomodulation is also referred to as red light therapy and cold laser therapy. It is a non-invasive treatment option. LLLT is shown to increase hair density and growth in both genders. The types of devices (hat, comb, helmet) and duration did not alter the effectiveness, with more emphasis to be placed on lasers compared to LEDs. Ultraviolet and infrared light are more effective for alopecia areata, while red light and infrared light
1560-489: The association, finasteride improves glucose metabolism and decreases glycated hemoglobin HbA1c , a surrogate marker for diabetes mellitus. The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance, and for which it still is used as an assay for pediatric diabetes mellitus. Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing
1612-467: The blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone. The expression of insulin resistance and metabolic syndrome, AGA
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1664-433: The cause has only been postulated and not proven. CCCA is suspected to have a multi-factored cause. However, one theory involves pressure exerted on the internal root sheath leading to damage, which leads to the recruitment of inflammatory cells and the result of scarring. African Americans are found to be at increased risk. Historically, some have hypothesized that CCCA represents an end stage of traction alopecia . However,
1716-442: The central (sagittal) midline of the scalp. It is symmetric and exhibits scarring as the name suggests. It involves solely the top of the scalp or may progress to Hamilton–Norwood scale Type VI or VII. Early symptoms may include pruritus, dysesthesias and tenderness. On examination the skin is thin with few follicular ostia and later in the disease the scalp may appear shiny. The mechanism of pathology of CCCA remains unknown; thus,
1768-708: The component of metabolic syndrome with highest association. Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors . Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype , of polycystic ovary syndrome . Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome. With early-onset AGA having an increased risk of metabolic syndrome, poorer metabolic profiles are noticed in those with AGA, including metrics for body mass index , waist circumference, fasting glucose , blood lipids , and blood pressure. In support of
1820-435: The diagnosis of some primary cicatricial alopecias as noted mainly in the central scalp, and includes CCCA, folliculitis decalvans, and any other potential centrally presenting cicatricial alopecia. This term is not often used in the literature to signify diagnostic terminology. Androgenetic alopecia Pattern hair loss (also known as androgenetic alopecia ( AGA ) ) is a hair loss condition that primarily affects
1872-666: The differential requires exclusion of other causes of hair loss, and assessing for the typical progressive hair loss pattern of androgenic alopecia. Trichoscopy can be used for further evaluation. Biopsy may be needed to exclude other causes of hair loss, and histology would demonstrate perifollicular fibrosis. The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males by severity. Combinations of finasteride, minoxidil and ketoconazole are more effective than individual use. Combination therapy of LLLT or microneedling with finasteride or minoxidil demonstrated substantive increases in hair count. Finasteride
1924-409: The face, but can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'. Men with androgenic alopecia typically have higher 5α-reductase , higher total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT. 5-alpha-reductase converts free testosterone into DHT, and is highest in the scalp and prostate gland. DHT
1976-559: The follicle itself. Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM ), estrogens , and consumption of amino acids such as arginine and leucine . Obesity and hyperglycemia inhibit its release. IGF also circulates in
2028-479: The front due to thinning of hair. In most cases, receding hairline is the first starting point; the hairline starts moving backwards from the front of the head and the sides. The cause of pattern hair loss is not yet fully understood. It appears to be the result of genetic changes that make the activity of hair follicles on the scalp become sensitive to the presence of androgenic hormones, cholesterol , and proteins such as insulin-like growth factor . KRT37
2080-448: The head remains. This has been referred to as a " Hippocratic wreath", and rarely progresses to complete baldness. Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss . The Ludwig scale grades severity of female-pattern hair loss. These include Grades 1, 2, 3 of balding in women based on their scalp showing in
2132-434: The journal PNAS found that increasing production of a particular microRNA in hair follicle stem cells, which naturally harden with age, softened the cells and stimulated hair growth. The authors of the study said the next research step is to introduce the microRNA into the stem cells using nanoparticles applied directly to the skin, with the goal of developing a similar topical application for humans. Androgenic alopecia
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2184-409: The link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=CCCA&oldid=1128453236 " Category : Disambiguation pages Hidden categories: Short description is different from Wikidata All article disambiguation pages All disambiguation pages Central centrifugal cicatricial alopecia CCCA usually begins at
2236-433: The local tissue including the papillas. Dermal fibrosis is progressive; thus the insufficiency of nutrition to papillas is permanent. Senile hair-loss and hair-whitening are partially a consequence of the fibrosis of the skin. The diagnosis of androgenic alopecia can be usually established based on clinical presentation in men. In women, the diagnosis usually requires more complex diagnostic evaluation. Further evaluation of
2288-531: The paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long. Male-pattern hair loss appears to be undergoing positive sexual selection in European and Asian populations. Male pattern hair loss may be seen as an expression of masculine sexual dimorphism rather than a disorder. Because of this, it is hypothesized that men with male pattern hair loss may be favored by heterosexual women as mates, because their hair loss
2340-1102: The relationship, SHBG is downregulated by insulin in vitro , although SHBG levels do not appear to affect insulin production. In vivo , insulin stimulates both testosterone production and SHBG inhibition in normal and obese men. The relationship between SHBG and insulin resistance has been known for some time; decades prior, ratios of SHBG and adiponectin were used before glucose to predict insulin resistance. Patients with Laron syndrome , with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically. Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II. Measurement of subcutaneous and visceral adipose stores by MRI , demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen. SHBG association with fasting blood glucose
2392-489: The scalp contains the stem cell progenitor cells from which the follicles arose. Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (IGF) at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands , apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on
2444-482: The scalp in close proximity and in large numbers. The grafts are obtained from either follicular unit transplantation (FUT) or follicular unit extraction (FUE). In the former, a strip of skin with follicular units is extracted and dissected into individual follicular unit grafts, and in the latter individual hairs are extracted manually or robotically. The surgeon then implants the grafts into small incisions, called recipient sites. Cosmetic scalp tattoos can also mimic
2496-470: The scalp, leading to catagenic miniaturization. Hair follicles in anaphase express four different caspases . Significant levels of inflammatory infiltrate have been found in transitional hair follicles. Interleukin 1 is suspected to be a cytokine mediator that promotes hair loss. The fact that hair loss is cumulative with age while androgen levels fall as well as the fact that finasteride does not reverse advanced stages of androgenetic alopecia remains
2548-710: The scalp. Other research suggests the enzyme prostaglandin D2 synthase and its product prostaglandin D2 (PGD2) in hair follicles as contributive. These observations have led to study at the level of the mesenchymal dermal papillae. Types 1 and 2 5α reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles . They catalyze formation of the androgen dihydrotestosterone from testosterone, which in turn regulate hair growth. Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but can also stimulate TGF β1 , TGF β2 , dickkopf1 , and IL-6 at
2600-435: The selective benefits of male pattern hair loss. Although it is generally accepted that male pattern baldness follows a pattern of autosomal dominant inheritance, more recent research has shown that approximately 80% of bald men have bald fathers . This is greater than would be expected if pattern balding were a purely autosomal trait, and may suggest that there is an important paternal route of inheritance, either through
2652-631: The top and front of the scalp . In male-pattern hair loss ( MPHL ), the hair loss typically presents itself as either a receding front hairline, loss of hair on the crown and vertex of the scalp, or a combination of both. Female-pattern hair loss ( FPHL ) typically presents as a diffuse thinning of the hair across the entire scalp. Genetic research has identified alleles associated with male pattern hair loss. These alleles appear to be undergoing positive sexual selection in European and East Asian populations, as male pattern baldness may be seen as
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#17328556928692704-490: The veracity of this theory is low as many patients who have CCCA have not employed traction hairstyling. Histopathologic features include a perifollicular lymphocytic infiltrate, concentric lamellar fibrosis (layers of fibroblasts in the papillary dermis), sebaceous gland loss and premature disintegration of the internal root sheath. Additionally, granulomatous inflammation secondary to follicular rupture has been noted. Perifollicular erythema and follicular keratosis
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