Tuesday, September 23

Melanocyte-stimulating hormone (MSH) - Melanotropin hormone

Melanocyte-stimulating hormone - Melanotropin hormone.

What is melanocyte-stimulating hormone?

The melanocyte-stimulating hormones (aka MSH, intermedin or melanotropin) are a group of naturally occurring peptide hormones.
Melanotropin peptides are primarily produced and secreted by the pituitary gland. The hypothalamus and skin cells (keratinocytes) also contribute to the production of the melanotropin hormone. Though the main function of melanotropin hormones is in stimulating the melanocytes to produce melanin, they have been found to be effective in reducing appetite and in increasing the libido.

Melanotropin peptides belong to the peptide group known as melanocortins. The precursor of melanotropin is a larger peptide known as pro-opiomelanocortin (POMC). POMC is cleaved to form three fragments, one of which is adrenocorticotropic hormone (ACTH or corticotropin). ACTH can be further fragmented to form alpha melanocyte stimulating hormone. The remaining two fragments of POMC cleave to form beta-M-S hormone and gamma-M-S hormone. The alpha type of hormone has 13 amino acids, whereas the beta and gamma types of melanotropin have 18 and 11 amino acids respectively.
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Research organizations have developed synthetic analogs of melanotropin and are experimenting on their utility in melanin production as well as many other fields of human pathophysiology. Afamelanotide (melanotan-1) is a synthetic melanotropin being researched for photoprotection of patients with photosensitivity and debilitating diseases. Another analog named melanotan II and its derivative bremelanotide are being investigated for aphrodisiac effects.

Functions of melanotropin

The primary function of melanocyte-stimulating hormone is in stimulating the pigment cells to produce melanin. In lower animals like claw-toed frog, melanotropin makes the pigments in the skin to disperse and cause the skin to appear darker in dim light. The pigments are known as melanophores and the melanotropin is termed melanophore-stimulating hormone.
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These melanotropin peptides have anti-inflammatory properties. They also modulate the immune system. Melanotropin peptides are also found to regulate melatonin and endorphins production. Melanotropin synthetic analogs have different functions like reducing the appetite and aphrodisiac effects.

Conditions caused by increased melanotropin activity

The activity of the stimulating hormone increases in pregnant women. Combined with increased estrogens, most often, melanotropin causes hyperpigmentation in pregnant women. Oral contraceptive pills intake may also give similar results in some individuals. Increased activity of the melanocyte stimulating hormone can cause moles, tan and freckles. Administration of melanotropin can cause skin darkening even without sun exposure. In Addison’s disease and Cushing’s syndrome, there is increased release of adrenocorticotropic hormone. ACTH breaks down into melanotropin and causes hyperpigmentation.
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Tan development goes through the following sequence of events. When the keratinocyte cells in the basal layer of epidermal skin are exposed to ultraviolet radiation, the transcription factor p53 (the tumor-suppressor protein) is activated. p53 activates the POMC promoter. POMC cleaves to form the melanotropin. Melanocortin-1-receptor (MC1R) is expressed in melanocytes and is activated by melanotropin. By a biosynthetic cascade of reactions the melanin pigment is produced inside the melanosomes.

Melanocyte-stimulating hormone is found to complement leptin in regulating food intake, metabolism and body weight. Increase in melanotropin activity causes anorexia and decrease in bodyweight. Melanocyte-stimulating hormone deficiency can cause hypopigmentation, risk of sunburn and DNA damage, inflammatory diseases, body pain, thirst, frequent urination, sleeping problems, increased food intake, obesity and type 2 diabetes mellitus.
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Reference:
1.Hunt G, Todd C, Cresswell JE, Thody AJ. Alpha-melanocyte stimulating hormone and its analogue Nle4DPhe7 alpha-MSH affect morphology, tyrosinase activity and melanogenesis in cultured human melanocytes. J Cell Sci. 1994 Jan;107 ( Pt 1):205-11.
2.Valverde P, Healy E, Jackson I, Rees JL, Thody AJ. Variants of the melanocyte-stimulating hormone receptor gene are associated with red hair and fair skin in humans. Nat Genet. 1995 Nov;11(3):328-30.
3.Costa JL1, Hochgeschwender U, Brennan M. The role of melanocyte-stimulating hormone in insulin resistance and type 2 diabetes mellitus. Treat Endocrinol. 2006;5(1):7-13.

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Monday, September 22

Melanocytes definition - What are melanocytes?

What are melanocytes and their definition.

What are melanocytes?

Melanocytes are a type of epidermal cells which produce melanin pigment.
Melanocytes are present in stratum basale, the deepest layer of the epidermal skin. Up to 10% of the cells present in the basal cell layer are pigment producing cells. These pigment cells are also present in retinal pigment epithelium, stria vascularis of cochlear duct in inner ear, heart, meninges and substantia nigra pars compacta of the midbrain. Three types of melanins are produced and eumelanin and pheomelanin are present in the skin while neuromelanin is found in the brain.

The number of melanocytes present per square millimeter of skin is between 1000 and 2000. It is not the number of pigment cells present in the skin that contributes to the lighter or darker color of skin. The level of melanin producing activity as well as the types of pigments and their relative amounts contribute to an individual's skin color. The melanin produced by the melanocytes protects the skin from the harmful effects of ultraviolet radiation. The absence of melanin gives rise to skin conditions like albinism and leucism. The total or partial loss of melanin production may cause vitiligo.

Definition of melanocytes

Definition by medterms.com: "A cell in the skin that produces and contains the pigment melanin."
Definition by merriam-webster.com: "an epidermal cell that produces melanin."
Definition by about.com: "Melanocytes are cells located in the epidermis that are responsible for producing melanin, a brown pigment that helps screen against the harmful effects of UV light."

Melanoblasts

The precursor cells of melanocytes arise from the neural crest formed during the gastrulation of the embryo. These neural crest cells migrate to various sites and differentiate to form precursor cells of neurons, endocrine components, bone, cartilage, connective tissue and melanocytes. The precursor pigment cells are known as melanoblasts. The migrating melanoblasts transform into melanocytes and establish at the epidermal-dermal junction to commence melanogenesis. When there is dysregulation in the melanoblast development and migration, skin conditions like piebaldism may occur.

Melanocyte stem cells

Melanoblasts also enter the newly forming hair follicles to form hair matrix melanocytes and the stem cells. The stem cells are found as a small pool of immature cells in the lower permanent portion including the bulge region of the hair follicle. Apart from maintaining a supply of pigment cells for hair pigmentation, these stem cells are also a source for melanocyte replacement in the epidermis.
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Greying of hairs in humans was thought to be due to free radicals causing oxidative stress and cytotoxic damage of the mature melanocytes in the matrix cells. However recent studies indicate that hair graying is due to loss of pigment stem cells. Melanoma occurs when melanocyte development and proliferation pathways are undermined and destabilized.

Melanocyte structure

These pigment cells are regularly dispersed among the basal keratinocytes in the basal layer of epidermis at an ratio of about 1:10. They appear larger than the keratinocytes. They have elongated dendrites which are in contact with the neighboring basal and suprabasal keratinocytes. The nucleus is ovoid in shape. These cells contain clear premelanosomes as well as many melanosomes at various maturation stages.

Melanocyte function

Many functions of these pigment cells and their product can be listed out. Their main function in many species of animals is camouflage from prey and predators. In humans, protection against UV radiation has evolved as one of the primary functions. Skin pigmentation being the most apparent display of human polymorphic traits, defines ethnicity and race.
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Heat regulation, redox signaling and antioxidant activity are some of the other functions of melanin. The presence of the melanocytes and melanin is necessary for the proper functioning of inner ear, eyes and midbrain.

Melanin biosynthesis

The biosynthesis of melanin by the melanocytes is known as melanogenesis. The melanogenesis normally occurs in a basal level. Under certain conditions, the synthesis may occur in an active manner. In the lighter-skinned people, the basal level of melanogenesis is quite low when compared people with darker skin tone.

The mechanism of active melanogenesis is triggered by the keratinocytes on exposure to ultraviolet radiation by synthesizing and secreting endothelin-1 (ET-1) an amino acid peptide. The production of the precursor of melanocyte-stimulating hormone (MSH), proopiomelanocortin (POMC) is also stimulated. The rate of mitosis in the basal keratinocytes is also increased. Through a number of biosynthetic cascading pathways, the rate of proliferation of melanocytes and keratinocytes, the melanogenesis activity, and synthesis and transfer of melanosomes is increased.

Melanocytes and keratinocytes

As described earlier, melanocytes with the help of their dendrites are in contact with nearly forty basal as well as suprabasal keratinocytes. The pigment cell with its dendrite-connected keratinocytes is termed "the epidermal melanin unit.” These melanin producing cells transfer the melanosomes to the keratinocytes through their multiple dendrites. Once inside the keratinocyte, multiple melanosomes are packed into single membrane pigment globules and transported by motor protein dynein to perinuclear region. Then there is membrane degradation of the pigment cell globules to form a UV-radiation protective cap above the keratinocyte nucleus.

Melanocytes and hyperpigmentation

Skin pigmentation is an inherited trait, being regulated by genetic factors on the epidermal cells. However the endocrine secretions, certain medications, chemicals and environmental factors can modulate the distribution of the melanin as well as its amount and type. Endocrine factors induce melanocyte activity and hyperpigmentation occurs temporarily in pregnancy and permanently as age spots. The use of diuretics, levodopa, hydantoins, sulfonamides, tetracyclines, chloroquine and oral contraceptives is associated with hyperpigmentation. Postinflammatory hyperpigmentation of the skin occurs after the resolution of the inflammatory dermatitis, especially in patients with darker skin tone due to enhanced melanocyte activity.
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Reference:
1.Osawa M. Melanocyte stem cells. 2009 Jun 30. In: StemBook [Internet]. Cambridge (MA): Harvard Stem Cell Institute; 2008-. Available from: http://www.ncbi.nlm.nih.gov/books/NBK27077/
2.Audrey Uong, Leonard I. Zon. Melanocytes in Development and Cancer J Cell Physiol. Jan 2010; 222(1): 38–41.
3.Kvam E, Dahle J. Pigmented melanocytes are protected against ultraviolet-A-induced membrane damage. J Invest Dermatol. 2003 Sep;121(3):564-9.
4.Iozumi K, Hoganson GE, Pennella R, Everett MA, Fuller BB. Role of tyrosinase as the determinant of pigmentation in cultured human melanocytes. J Invest Dermatol. 1993 Jun;100(6):806-11.

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Friday, September 19

What is melanogenesis - Melanogenesis pathway

What is melanogenesis - Melanogenesis pathway.

What is melanogenesis?

Melanogenesis is the biochemical process of melanin production. Melanogenesis pathway is catalyzed by the tyrosinase enzyme.
Melanin pigment producing cells are known as melanocytes. Melanocytes are located in the basal layer of epidermis. Normally about 5-10% of the cells present in the stratum basale layer are melanocytes. The rest of cells in the basal layer are basal keratinocytes. Each melanocyte is in contact with nearly 40 neighboring keratinocytes in the basal and suprabasal layers via dendrites. Synchronizing with the rate of skin turnover, the melanogenesis process continuously goes on to pigment the newly forming keratinocytes.
Web definition of melanogenesis
merriam-webster.com defines as: "the formation of melanin."
Drugs.com defines as: "formation of melanin."
Collinsdictionary.com defines as: "the production of melanin."

Mechanisms regulating melanogenesis and its pathways

Melanin production takes place in the melanosomes, which are membrane-bound organelles located inside the . Melanosomes are synthesized in the melanocytes. They are sites of synthesis, storage and transport of melanin.
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When the melanosomes are full with melanin bundles, they are transferred to the surrounding keratinocytes via dendrites. Cytoplasmic dynein (a motor protein involved in the organelle transport) present in the cytoplasm of the keratinocyte, moves the melanosomes to the center to hide the cell nucleus from UV radiation.

A base level melanogenesis is carried on continuously in the melanosomes to keep up with the genetically determined level of melanin. Exposure to UV radiation enhances the melanin production by activating tyrosinase enzyme for melanogenesis.
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Intrinsic factors like melanocyte-keratinocyte interaction, hormones, enzymes, , inflammatory and neuronal components can affect the melanogenesis and its pathway. Extrinsic factors like ultraviolet radiation and certain medications and chemicals can also interfere with melanogenesis pathway.

Tyrosinase regulation of melanogenesis

Tyrosinase, a glycoprotein, is the principal enzyme involved in the melanin production. The tyrosinase is a single membrane-spanning transmembrane protein, spanning the entirety of the melanosomal membrane. It span from one side of the melanosomal membrane through to the other side of the membrane and is permanently attached. Most of the tyrosinase protein is present inside the melanosomal vesicle, which is the catalytic region of melanogenesis pathway. Only a small part of tyrosinase traverses the melanosomal membrane and projects into cytoplasm. The histidine residues present in the catalytic region bind to copper ions for tyrosinase activation.

Melanogenesis pathway

L-tyrosine is a non-essential amino acid as it can be synthesized by the body. Being a proteinogenic amino acid, it is the building block as well as the pathway in the synthesis of many cellular proteins, enzymes and catalysts. L-tyrosine [L-2-Amino-3-(4-hydroxyphenyl)propanoic acid] is the precursor to the melanin.

L-phenylalanine to l-tyrosine pathway
L-tyrosine has to reach the melanosomes only by the process of spontaneous passive transport which leads its insufficiency in the melanogenesis pathway.
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However, the human body has found a way out of this situation. L-phenylalanine, an essential amino acid, is actively transported through the melanosomal membrane. Inside the organelle, l-tyrosine is created from l-phenylalanine by hydroxylation by the phenylalanine hydroxylase enzyme. This synthetic pathway ensures sufficiency of the base material for the melanogenesis.
L-phenylalanine ››› intracellular phenylalanine hydroxylase (PAH) enzyme ››› L-tyrosine
L-dopaquinone synthesis pathway
In the melanogenesis pathway, tyrosinase enzyme catalyses the hydroxylation of l-tyrosine to l-dihydroxyphenylalanine (L-DOPA) and the subsequent oxidation of L-DOPA to l-dopaquinone. With the formation of dopaquinone, the melanogenesis pathway is bifurcated into synthesis of the eumelanin and pheomelanin.
L-tyrosine ››› tyrosinase catalyst ››› L-dihydroxyphenylalanine (L-DOPA) ››› tyrosinase catalyst ››› L-dopaquinone
Eumelanogenesis pathway
In this intermediate melanogenesis pathway, l-dopaquinone reacts with cysteine (which is actively transported across melanosomal membrane) to form either 5-S-cysteinyl-dopa or 2-S-cysteinyl-dopa. Both these cysteinyl-dopa intermediates, convert to benzothiazine intermediate and then polymerize to pheomelanin at the end of the melanogenesis pathway.
Dopaquinone + cysteine ››› 5-S-cysteinyldopa ››› benzothiazine intermediate ››› polymerization ››› pheomelanin
Dopaquinone + cysteine ››› 2-S-cysteinyldopa ››› benzothiazine intermediate ››› polymerization ››› pheomelanin
Pheomelanogenesis pathway
In this intermediate melanogenesis pathway, l-dopaquinone is converted spontaneously into from leucodopachrome and then dopachrome. Dopachrome is either converted spontaneously into 5,6-dihydroxyindole (indole) or convert to 5,6-dihydroxyindole-2-carboxylic acid by the enzymatic action of dopachrome tautomerase (DCT). Both these intermediates convert to quinone and then polymerize to eumelanin.
Dopaquinone ››› spontaneous conversion ››› leucodopachrome ››› spontaneous conversion ››› dopachrome ››› dopachrome tautomerase (DCT) catalyst ››› 5,6-dihydroxyindole-2-carboxylic acid ››› quinone ››› polymerization ››› eumelanin
Dopaquinone ››› spontaneous conversion ››› leucodopachrome ››› spontaneous conversion ››› dopachrome ››› spontaneous conversion ››› 5,6-dihydroxyindole ››› quinone ››› polymerization ››› eumelanin
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Reference:
1.Inês Ferreira dos Santos Videira, Daniel Filipe Lima Moura, Sofia Magina. Mechanisms regulating melanogenesis. An Bras Dermatol. 2013 Jan-Feb; 88(1): 76–83.
2.Park HY, Kosmadaki M, Yaar M, Gilchrest BA. Cellular mechanisms regulating human melanogenesis. Cell Mol Life Sci. 2009 May;66(9):1493-506.
3.Gillbro, J. M. Olsson, M. J. The melanogenesis and mechanisms of skin-lightening agents – existing and new approaches. International Journal of Cosmetic Science, 33: 210–221.
4.Agar N, Young AR. Melanogenesis: a photoprotective response to DNA damage? Mutat Res. 2005 Apr 1;571(1-2):121-32. Epub 2005 Jan 23.

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Current topic in dynamic skin care: What is melanogenesis - melanogenesis pathway.
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Wednesday, September 17

Melanin in skin - Function of melanin

Function of melanin - Melanin in skin.
The primary function of melanin is in skin pigmentation. Melanin has other important roles in the human body such as, sunlight absorption and sun screening, protection from ultraviolet radiation, charge-transfer redox activity, free radical scavenging, antimicrobial immune defense, immunomodulation and ion chelating.

Melanin in skin

Melanins are a broad spectrum of very common natural pigment compounds found in both the plant and animal kingdoms. It is a complex molecule derived from the amino acid tyrosine via the intermediate product L-DOPA, by the action of the tyrosinase enzymes. There are three basic types of melanin, namely, eumelanin, pheomelanin, and neuromelanin. Variation in human skin color is a result of density and relative proportions of contributing melanins.

Function of melanin

In plants and invertebrates, melanin is involved in immune defence. In certain pathogenic microbes, bacteria and fungi, these pigments function as defence mechanisms against the host's immune responses.
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Though many other functions are attributed to melanins in plant and animal kingdoms, herein we will consider their functions related to the human body.
Skin pigmentation
Melanin, whose primary function is in pigmentation, has many more important functions to perform in the human body.
Protection from UV radiation
Melanin functions as a sunscreen and as a broad spectrum sun radiation absorbent. The absorbed energy causes redox reactions, and both eumelanin and pheomelanin form free radical species. Eumelanin, being more photostable scavenges the originated oxidative species and neutralizes them. However, pheomelanin being more photolabile may not neutralize all the oxidative free radicals. Free radicals have the potential to cause DNA damage. Hence, fair individuals, having high amounts of pheomelanin, are more prone to skin cancers on sun exposure.
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Melanin in the eyes
Melanin in the iris, protects the retina from excessive light and photodamage. By absorbing the scattered light within the eyeball, it also helps in improving the visual acuity. Melanin in the retinal pigment epithelium (RPE) has antioxidant properties and neutralizes the photooxidative species. The antioxidative activity wanes with aging and one of causes of macular degeneration is oxidative stress.
Melanin in the ears
The melanin pigment is present in the inner ear with no known function. In Waardenburg syndrome, deafness occurs along with reduced inner ear pigmentation. In the inner ear, the loss of in stria vascularis of cochlear duct is associated with loss of hearing.
Melanin in the brain
The substantia nigra pars compacta is a part of the midbrain, which appears darker than the surrounding areas due to the presence of neuromelanin in dopaminergic neurons. Degeneration of the pigmented neurons or depigmentation is found in persons affected with Parkinson's disease. It is hypothesized that neuromelanin may be neutralizing the oxidative stress and chelating the toxic metal ions in the brain. The decrease in neuromelanin, as observed in Parkinson's disease may be the cause of the associated degenerative symptoms.
Melanins also function as chelating agents. They can chelate metal ions, including toxic species, and protect the cells from damage. Melanins can also bind with a number of organic molecules and neutralize their damaging effects.
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Melanins behave as semiconductors. Thin melanin films having multifarious electrical and optical properties can be made by spray deposition. Having interesting biophysical properties, melanin opens up many new biotechnological applications.
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Reference:
1.Michaela Brenner, Vincent J. Hearing. The Protective Role of Melanin Against UV Damage in Human Skin. Photochem Photobiol. 2008; 84(3): 539–549. 2.F. Solano. Melanins: Skin Pigments and Much More—Types, Structural Models, Biological Functions, and Formation Routes. New Journal of Science, vol. 2014, Article ID 498276, 28 pages, 2014. doi:10.1155/2014/498276. 3.Burkhart, C. G. and Burkhart, C. N. The mole theory: primary function of melanocytes and melanin may be antimicrobial defense and immunomodulation (not solar protection). International Journal of Dermatology, 44: 340–342.

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Monday, September 15

Terminal hair - Terminal hair length

Terminal hair - Terminal hair length.

What is terminal hair?

Terminal hairs are the thick pigmented hairs found on the scalp and on certain other parts of the body.
Their length is genetically predetermined. In the newborn, the scalp follicles produce short, silky and poorly pigmented vellus strands. As the infant grows the follicle grows in size and the vellus strand is replaced with an intermediate type of strand, having a myelin sheath. By two years of age, the scalp, eyelids and eyebrows have thick pigmented terminal hair. The percentage of vellus strands gets reduced progressively and their presence becomes unnoticeable.

As the child grows, with increased androgenic hormone levels, especially in puberty, other parts of the body, hitherto having vellus growth, start replacing the vellus with terminal type. Each of these follicles develops subcutaneous glands. Boys and girls during puberty develop axillary and pubic hair. The follicle sensitivity to androgens varies in boys and girls.

In young women, normally the androgenic hormones circulating at low levels do not have any effect on the vellus strands on the other areas of the body including face.
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However in young men, the androgens stimulate the vellus follicles on the face, chest, arms and legs to transform into terminal follicles and grow thick pigmented strands.

Terminal hair length

The length of these strands is relative to the length of the anagen phase of growth. The anagen phase length varies and is unique to a particular area of the body.
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The length of anagen phase of the underarm and genital hair is short and may last between three to six months. In the scalp the length of the anagen phase is relatively longer than the other body regions. Depending upon the genetic origins, the length of the anagen phase of scalp hair may vary between two to seven years.

Types of terminal hair

Scalp hair growth stabilizes by the end of two years. In the adulthood, it is transformed into vellus strands in the case of male pattern baldness. The length of the life of strands varies between 2-7 years. Its average growth rate is about 0.35mm per day.
Eyebrows grow over the upper margin of eye sockets. Their average length on the higher side is about 10 mm. They have the slow growth rate of 0.15 mm per day. Eyebrows follicles are sensitive to injury.
Eyelashes grow on the margin of eyelids. Their average length is around 7.5 mm and their growth rate is about 0.15 mm per day.
Beard grows in response to androgenic hormones in men. It is the fastest growing hair and its average growth rate is about 0.38 mm per day.
Body hair is initially vellus and in boys, during puberty, it turns thick and pigmented in certain regions of the body. The axillary and pubic hair grows in boys and girls during puberty.

Complications and anomalies in terminal hair growth

The hormonal imbalances occurring during the length of pregnancy may cause vellus follicles to transform and produce thick, pigmented strands in certain parts of the body. However, the condition returns to normalcy after the childbirth.
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In male pattern baldness, the thick hairs on the scalp are progressively replaced with vellus strands.
In women affected by hirsutism, vellus follicles, especially on the upper lip, transform and produce terminal hair.
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Reference:
1.Vogt, A., Hadam, S., Heiderhoff, M., Audring, H., Lademann, J., Sterry, W. and Blume-Peytavi, U. (2007), Morphometry of human terminal and follicles. Experimental Dermatology, 16: 946–950.
2.Navarini AA, Ziegler M, Kolm I, Weibel L, Huber C, Trüeb RM. Minoxidil-induced trichostasis spinulosa of terminal hair. Arch Dermatol. 2010 Dec;146(12):1434-5.

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Saturday, September 13

What is hypertrichosis - Hypertrichosis definition

What is hypertrichosis - Definition of hypertrichosis.

What is hypertrichosis?

Hypertrichosis is defined as excessive growth of hair. Hypertrichosis disorders may be present at birth, or may be acquired later in life.
The excessive hair disorders present at birth include congenital syndromes, autosomal mutations and hereditary diseases. The mutation may be spontaneous genetic mutation in autosomal chromosomes or in x-y chromosomes. These excessive hair disorders may also be acquired later in life, triggered by cancers, hormonal anomalies and certain therapeutic drugs. The excess hair growth may be generalized, affecting the whole of the body or localized to form well defined patches.

Extensive excess growth of hair is also known as Ambras syndrome or werewolf syndrome. These disorders affect both the genders equally. Hypertrichosis is basically different from hirsutism in that it is androgen-independent. Hirsutism is the excessive male-pattern hair growth in women. Hirsutism is an androgen-dependent condition. The excessive growth may be of , or , depending upon the type of syndrome. Generally the palms of the hands, soles of the feet and mucosal surfaces are not affected.

Web definition of hypertrichosis

Definition by merriam-webster.com: "excessive growth of hair."
Definition by reference.md: "Excessive hair growth at inappropriate locations, such as on the extremities, the head, and the back. It is caused by genetic or acquired factors, and is an androgen-independent process."
Definition by thefreedictionary.com: "An extremely rare (less 100 cases reported worldwide) excess of hair on the body, which can be generalised or localised, congenital or acquired."

What are the types of hypertrichosis

Considering the time of appearance, excessive hair growth can be categorized into congenital (present at birth) or acquired (acquired later in life) types. Further these disorders, depending upon the extent, may categorized as generalized or localized types.

(CH)
Considering the type of hair (vellus, lanugo or terminal) and extent of excess hair, CH can again be categorized into subtypes.
CH lanuginosa patient has generalized cover of lanugo hair over the body. It is considered to be an autosomal dominant mutation on chromosome 8q.

Generalized CH is noticed in men as excessive hair on the face and upper body, whereas women have less severe asymmetrical hair distribution. It is considered to be an autosomal dominant mutation on chromosome x24-q27.1.

Terminal CH is characterized by whole body being covered by terminal hair. It is considered to be due to a mutation in MAP2K6 on chromosome 17. Further, circumscribed, localized and nevoid forms of CH have been reported.

Acquired hypertrichosis (AH)
AH is associated with side effects of medication, presence of cancers and alopecia and glaucoma treatment. AH lanuginosa is characterized by growth of lanugo hair, especially on the face. In some cases it is associated with malignancy. Generalized AH is usually associated with minoxidil treatments. Patterned AH shows hair growth in a pattern formation and is associated with malignancy. Localized AH may appear as well defined excess hair when there is irritation or trauma to the skin.

What are the causes of hypertrichosis

Acquired hypertrichosis is caused by the presence of cancer, alopecia medication, hypertension medication, metabolic disorders or hormone imbalances.
Topical applications like iodine, psoralens, topical minoxidil or topical steroids may also cause acquired hypertrichosis. Congenital hypertrichosis is caused by inherited genetic abnormalities or spontaneous genetic mutations in autosomal or x-y chromosomes.

What are the options

There is no treatment for congenital forms of hypertrichosis. Acquired forms resolve when the causative factors are removed or discontinued. Hair removal methods like shaving, waxing, laser hair removal and electrolysis are the treatment options available for congenital hypertrichosis.
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Reference:
1.Trüeb RM. Causes and management of hypertrichosis. Am J Clin Dermatol. 2002;3(9):617-27.
2.Trüeb RM. Hypertrichosis. Hautarzt. 2008 Apr;59(4):325-37; quiz 338.
3.Goel N, Rajaram S, Gupta B, Gupta K. Familial congenital generalized hypertrichosis. Indian J Dermatol Venereol Leprol 2013;79:849.

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Current topic on natural skin care: What is hypertrichosis and its definition.
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Friday, September 12

Hypotrichosis

Hypotrichosis - Congenital hypotrichosis - Eyelash hypotrichosis.

What is hypotrichosis?

Hypotrichosis is the presence of less than the normal amount of hair on the head, eyelashes or body. Hypotrichosis disorders are a broad spectrum of hair loss conditions.
They are generally congenital and hereditary. The disorders are present at the time of birth or manifest in infancy and may remain with the affected patients throughout their lives.

In alopecia, the hair which is already present on the scalp or body is lost partially or wholly. However hypotrichosis is a state of hair loss right from the birth. The normal terminal hair may get replaced by soft, short and unpigmented vellus hair. Most of the congenital depilations are caused by defective embryonic growth or genetic aberrations. There is no known standard treatment for these hypotrichosis hair loss conditions.

These hypotrichosis disorders coexist with many other physical or mental problems. Disorders like Graham-Little syndrome, Hallermann–Streiff syndrome, Ofuji syndrome, congenital aplasia, alopecia triangularis, papular atrichia, metaphyseal chondrodysplasia, EEM Syndrome and cartilage-hair hypoplasia, manifest with the symptoms of hypotrichosis. There are hundreds of genetic congenital depilation disorders.
Though these hypotrichosis disorders are commonly generalized, in some cases depilation lesions may occur at single or multiple sites. The severity of the congenital hair loss may vary depending upon the afflicting disorder and the patient's health status.

Hypotrichosis causes

The basic causes of these types of congenital hair loss are defective embryonic growth and genetic aberrations. There are hundreds of genetic hypotrichosis disorders.

Congenital and hereditary hypotrichosis

There are many hereditary and congenital forms of hypotrichosis. We may consider a few of them to understand the complex diversity of these genetic disorders.

Hereditary hypotrichosis simplex (HHS) affected patients have normal hair at birth, but with progress of age hair is diffusely thinned. There is progressive hair follicle miniaturization. This congenital disorder is inherited either as an autosomal recessive trait or as an autosomal dominant trait. There is thinning of body hair, axillary hair, and pubic hair. The hair shafts of the eyebrows, eyelashes and male beard are found to be normal.

Localized autosomal recessive hypotrichosis affects both the scalp and body hair. In this congenital disorder, hairs get sparse, become fragile and break easily. Though scalp, eyebrows and eyelashes may be affected, beard, pubic and axillary hairs are generally spared. The patients may suffer from follicular papules, erythema and pruritus.

Marie Unna type of hypotrichosis (hereditary trichodysplasia) is characterized by the presence of a twisting hair dystrophy. This congenital hereditary disorder was reported by Marie Unna. Hairs of the scalp, body, eyebrows and eyelashes are involved and the disorder can progress into irreversible universal alopecia.

Eyelash hypotrichosis

In this disorder, there is inadequate or absence of eyelash. Loss of eyelash is not merely a cosmetic and aesthetic issue like most of us think, but is a medical condition.
The depilation of eyelashes may be congenital and genetic. Certain diseases, cancer treatment, radiation, chemotherapy and certain neurotic habits can cause the loss of eyelashes. The absence of eyelashes mars the facial appearance. But there is a silver lining. Ophthalmic prostaglandin and prostamide analogs are used in the treatment of glaucoma. Incidentally these ocular hypotensive agents have been found to cause (excessive growth of hair) of eyelashes. The use of bimatoprost (prostaglandin analog) 0.03% solution was approved by the US Food and Drug Administration (FDA) for the treatment of hypotrichosis of the eyelashes.

Congenital hypotrichosis treatment

There is no standard treatment available for these types of congenital hair loss. Hair loss of the eyelashes has been successfully treated with ophthalmic prostaglandin and prostamide analogs.
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Reference:
1.Simon K Law. Bimatoprost in the treatment of eyelash hypotrichosis. Clin Ophthalmol. 2010; 4: 349–358.

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Current topic on natural skin care: Hypotrichosis (congenital - eyelash) and treatment.
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Thursday, September 11

Short anagen syndrome

Short anagen hair syndrome.

What is short anagen hair syndrome?

Short anagen syndrome (SAS) is a disorder of the hair growth cycle.
The anagen growth phase of scalp hair normally lasts between 2-7 years and is genetically determined. Long growth phase contributes to long strands of hair. SAS is a recently reported, under-recognized, congenital condition wherein the scalp hair does not grow long due to abnormally short anagen phase.

Short anagen syndrome is clinically characterized by short fine hair since birth, poor hair growth and excessive shedding. The affected child does not require a hair-cut. Most of the cases are reported in Caucasian blond-haired girls. It is quite possible that the condition may be equally present in boys and go unnoticed due to their hair styles. Normally the condition is associated neither with systemic diseases nor with dermal conditions.

Cause of short anagen syndrome

The cause of SAS is shortened hair growth phase. The condition appears idiopathic. However as familial cases have been reported, it may be caused by autosomal dominant inheritance.

Symptoms
Reduced scalp hair growth, sparse hair, increased shedding, increase in telogen hair, decrease in ratio of anagen to telogen hair in hair pull test are some of the common symptoms.
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These symptoms are prominent in the childhood and appear to fade after puberty. The affected children have normal physical and mental development.

Diagnosis
Hair pull test helps in the diagnosis of this condition. In a normal individual, ratio of anagen to telogen hair is 9:1.
In SAS, the ratio is altered and more number of telogen phase hairs get pulled out. In SAS, the hair shaft is healthy and does not break easily. Microscopic examination reveal that the hair shaft has pointed end indicating that it was not cut. This congenital condition has to be differentiated from loose hair condition. In the loose hair syndrome, loose, unruly, fuzzy hairs are present. Both the conditions are absent in SAS. Short anagen condition has to be differentiated from other conditions causing diminutive scalp hair like, trichodental syndrome and congenital .

Treatment options
There is no standard treatment option available. In some cases the condition appears to normalize during puberty. In some adults the condition was found to persist.
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Topical minoxidil is effective in stimulating the telogen hair follicles to enter into anagen phase. It is also found to prolong the growth phase. The use of topical minoxidil or cyclosporine is found to be effective in some cases. Persisting short anagen syndrome in adults can be traumatic and psychosocially devastating.

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Reference:
1.Ingrid Herskovitz, Isabel Cristina Valente Duarte de Sousa, Jessica Simon, Antonella Tosti. Short Anagen Hair Syndrome. Int J Trichology. 2013 Jan-Mar; 5(1): 45–46.
2.Niteen V Dhepe, Ashok S Naik. Short Anagen Syndrome in an Indian Woman with its Impact on Quality-of-Life. Int J Trichology. 2012 Oct-Dec; 4(4): 271–272.

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Current topic on natural skin care: Short anagen hair syndrome causes and treatment.
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