present at the level of hair follicle . Arrector Pili Muscle, present below the attachment of sebaceous follicles. It attaches from the hair follicle from one end and the lower part of the epidermis at the other end.
Based on their attachment, hair follicle gets divided into two parts:
Upper - Hair strand part
Lower - determines the type of hair.
Lower part keeps changing.
Upper part: (two parts based on the attachment of sebaceous glands)
Infundibulum: Above the attachment of sebaceous glands
Isthmus: Below the attachment of sebaceous gland
Supra bulbar region.
Stem cells are located at supra bulbar region. This region is also known as Bulge.
Anything that causes damage to outer root sheath will cause alopecia and where the hair will not grow back is cicatricial alopecia
Non cicatricial alopecia
Here, hair will grow back because stem cells are not damaged.
Hair, transverse section of hair root
Cross section of hair: layers are as follow
Medulla - inner most layer
Cuticle (part of inner root sheath) and on the outside, there is outer root sheath.
The inner root sheath has three parts:
Cuticle, cortex, and medulla.
Mnemonic - hens hugs cute chicken mom's
The thicker the hair, the thicker the medulla will be. Animal hairs will be thicker than human hairs. Medullary index = Diameter of medulla / diameter of whole shaft. Humans: medullary index < 1/3. Animals: medullary index > 1/2. Adamson's fringe is just around the bulge, this area is known as keratogenous zone. It differentiates between the keratogenous and non keratogenous parts. Dermatophytes are keratinophilic, so dermatophytes will not enter this area because this will be limited by Adamson’s fringe that marks the end of the keratogenous zone of the hair follicle.
Types of hair
Three types of hair
Seen in premature baby, Soft non, medullated - thin,
Hair on the face, forehead
< 2cm long
Hair on bearded area, pubic area
Present in androgen-dependent areas because it has hormones.
Growth phase is followed by the transition phase which is followed by the falling phase. This is the continuous cycle of growth.
Growth phase - Anagen hair
Transition phase – Catagen hair
Falling phase – Telogen hair
When entering the Telogen phase, the club root shape is formed. When hair shades off, it will go again to anagen stage.
Lasts for 3 years
Lasts for 3 weeks
Last for 3 months
Is responsible for length of hair
Is responsible for daily hair fall
85-90% of total hair
That is why we have 50-100 hairs falling per day.
Anagen: Telogen = 9:1
Hair growth rate: 1cm/month
Loss of hair - Alopecia
Excessive hair growth
Tests for hair
Hair pull test -
Pull hair and see how many hairs are coming. If it is more than 6, it is insignificant
Pull and take out certain hair and mount it to count no of anagen and telogen based on the hair bulb
Like dermoscope. Computer based program where one can see hair growth in magnified form
Helps us to know different disorders.
When stem cells are affected, one gets Cicatricial/scarring area. Here, the hair does not come back. If stem cells are not damaged, one can get hair.
Non Cicatricial/ non scarring
Also known as Non Cicatricial alopecia
moth eaten alopecia
Dependent on androgen. In males - male patterned hair loss . In female - female patterned hair loss. These are non-genetic. Genetic susceptibility: polygenic inheritance
Testosterone converts to dihydrotestosterone
The enzyme used is 5 alpha-reductase.
reduces the anagen phase
hair becomes short and causes miniaturisation of hair.
So, terminal hair is converting into vellus hair now. In males, bitemporal recession happens - from temple and vertex balding happens. If they progress, they will get little hair while keeping the vertex empty.
This is male Androgenetic Alopecia
The vertex has no hair. But little fringe of hair is present around the side because this area is occipital, which is not androgen dependent. Graded into I to VII sections and is given by Norwood- Hamilton
In female patterned hair loss: Widening of central parting.
There are three divisions of female Alopecia.
This pattern was given by Ludwig. Grade III looks like an air tree / Christmas tree pattern in females.
Management of these patient:
Counselling - it requires long period treatment.
Potassium channel opener
It causes Vasodilation (increase in blood flow of scalpy)
2% Minoxidil - female pattern hair loss
5-10% Minoxidil - male pattern hair loss
Side effects of Minoxidil:
This is FDA approved treatment.
Finasteride - 5 alpha reductase inhibitor - type 1 & 2 given 1 mg/day
Dutasteride - type 1 & 2 inhibitor. Dose 0.5 mg/day
Oral anti-androgens, which can be cyproterone acetate, spironolactone, and flutamide.
Hair transplantation. Transplant hair from occipital area because it is not androgen dependent
When transplantation from the donor area, it retains the quality of the donor area. So if it is androgen dependent, it will remain androgen dependent.
Diffused hair fall
If Effluvium affects anagen - Anagen Effluvium
If Effluvium affects telogen - Telogen Effluvium
When a patient is given Chemotherapy. Chemotherapy acts against all the mitotically active cells. So, in the hair, it will act against anagen and thus patient losses all the hair. When all the hair is gone - anagen Effluvium
Physical stress in the form of surgery, trauma, or prolonged illness. Prolonged illness can be Dengue, malaria, Covid, TB, chikungunya, pregnancy. When it happens in pregnancy, we call it Telogen gravidarum. So, when stressed, Anagen prematurely converts into Telogen. Hair in the telogen phase stays for three months and then hair fall happens.
Iron deficiency, thyroid, crash diet or malnutrition. If repeated insults, patients will face hair fall for many years. Then, there will be subsequent thinning of the ponytail.
It is a patchy kind of hair fall . It is a non-cicatricial alopecia. It is an autoimmune T-cell mediated disorder where the T-cell acts against hair follicles.
Other autoimmune disorder
Type 1 DM
There are certain HLA association too
The Anagen are being targeted. T cell starts acting against the anagen hair root. The hair compensates and converts the anagen hair into the telogen hair. The telogen hair falls and goes back to the anagen hair. This happens repeatedly, and eventually, the person is left with a bald patch.
Single or multiple patches of hair loss are seen in this condition
These patches are smooth. No scaling, and no itching, no redness and are well defined. Also called Pelade
Inflammation affects the pigment in the hair and does not affect the grey area
The person will keep on losing hair. But the grey hair will stay there. All the grey hairs are retained in a person suffering from Alopecia Areata. It is called Turning grey syndrome Alopecia Areata does not affect grey hair.
It is asymptomatic.
Exclamation mark hair
Recreate this image or confirm its presence
Broken hair present on the periphery of the lesion.
These hairs will appear tapering down and with a little bulbar area below. These exclamation mark hairs are seen on the periphery of the patches of Alopecia Areata.
Complete hair loss from all over the body -Alopecia Universalis . Complete hair loss over scalp - Alopecia Totalis. Band of Alopecia Areata occurs called Ophiasis pattern and forms an O on the scalp. In Sisaipho, only an occipital band is left, and all the hair is gone.
Sometimes the Alopecia Areata does not affect the scalp and may have associated involvement with
Nail findings in the patients of Alopecia Areata (AA)
In psoriasis pits were deep random, and irregular. Here the pits are superficial, geometric and they are not random (regular)
Longitudinal ridging or Trachyonychia - all 20 nails may be affected.
In 80 per cent of cases AA spontaneously resolves.
Also present with non-cicatricial, patchy hair fall, non-scarring alopecia, broken off hair - This is common. Scaling, itching, KOH positive (absent in alopecia areata)
It does not have exclamation mark hair.
Moth eaten alopecia
Associated with syphilis in the secondary stage . It will not be a standalone finding, and the patient will have other symptoms including VDRL positive
Spontaneous resolution is an option
Corticosteroids. But the better method is giving it intralesional - Intralesional steroids (ILS) is the treatment of choice. Triamcinolone or kenacort of the strength 10 mg/ml dilute it 1:4 or 1:2 and it is injected intradermally in the Alopecia Areata.
Like simulating a contact irritant reaction
Three agents are used
Di nitro chlorobenzene
Squaric acid dibutyl ester
A little concentration is applied on the patch, and these agents act as contact irritants which generate an irritant reaction and divert the T cells here, and they free the hair follicle, and they improve.
Systemic therapy - for extensive alopecia areata
Oral mini pulse therapy - Betamethasone or methylprednisolone given twice a week to minimise the side effect.
JAK kinase inhibitor called tofacitinib is a new agent increasingly being used.
It is Differential Diagnosis of alopecia. It is a psychiatric disorder and OCD of pulling hair. It is classified into DSM 4 criteria. History will not be given by patients, some others will give hints about psychiatric issues. . Often seen in adolescence or young adults.
Happens on an accessible site which can be fronto parietal area. Patchy hair loss. This patchy hair loss will be broken hairs of variable lengths. Happens on the dominant part of the scalp.
Sometimes, because of the trauma, one may see perifollicular haemorrhages. Patients may also eat hairs which leads to trichophagia or trichobezoar obstruction. It is also called the sign-friar tuck sign.
On skin biopsy
Empty cast, p/f hemosiderin
Cognitive behavioural therapy (CBT)
Antipsychotic Medicines like SSRI, paroxetine, or NAC - N-acetyl cysteine.
Cicatricial or scarring alopecia
Damaged Stem cells
Leads to permanent hair loss.
The area will look scarred.
Counselling for patient
The purpose of counselling would be to avoid new patches of hair loss.
Role of scalp biopsy
To know what kind of infiltrate it is and how deep it is to provide treatment to the patient.
Dissecting cellulitis/folliculitis (perifolliculitis abscedens et suffodiens)
Mixed Cicatricial alopecia
Folliculitis (acne) keloidalis
Folliculitis (acne) necrotica
Erosive pustular dermatosis
It is called Lichen Plano pilaris. It is affecting the hair or follicular lichen planer. There will be violaceous lesions and plaques, present in the perifollicular distribution. Itching, scaling present. A patch of cicatricial alopecia will be left behind.
Another cause of cicatricial alopecia. SLE or ACLE causes non scarring alopecia. DLE/ chronic cutaneous LE causes scarring alopecia
Scarred patches of alopecia which are associated with scaling and follicular plugging and can be seen on scalp.
Pseudopelade of BROCQ
Smooth patches due to scarring alopecia. It is an idiopathic condition, no inflammation, no scaling, no erythema present in the biopsy report. The only thing visible is patches of cicatricial alopecia which is spreading.
Footprint in snow appearance
It is chronic and slowly progressive.
Folliculitis Decalvans / Tufted Folliculitis
Neutrophil disorders that can lead to Cicatricial alopecia. Kind of deep folliculitis caused by bacteria. Pustules are found which go deep and damage the stem cells and cause scarring alopecia. Hair tufts are formed. It heals with boggy scars.
Treatment - antibiotics
Deep folliculitis. Causes cicatricial alopecia.
This is a part of a triad - follicular occlusion has three features.
Dissecting cellulitis of the scalp
Because of traction there is excess force applied on the hair follicle, leading them to causing Traction Alopecia . It is a hairstyle disorder. Hair is damaged due to constant pressure of force applied to them.
Excessive Hair Growth
Hypertrichosis - if it happens on the body.
Seen commonly congenitally over the knee. Can be seen with use of topical steroid.
Hirsutism - when hair growth happens on androgen dependent areas.
Growth of unwanted hair on androgen dependent sites . Female - growth of terminal hair in beard area. Feature of female. Vellus hair is converted to terminal hair
Androgens are being produced by two sources.
If there is PCOS or ovarian tumour or any cause which is stimulating the ovaries one can have Hyperandrogenism.
Adrenal glands produce more androgen if there is
Congenital adrenal hyperplasia (CAH)
Sometimes there is idiopathic and no symptoms are found and perfect androgen levels.
SAHA syndrome has four components
There is a scoring which has been given by Ferriman and Galway
PCOS - LH, FSH, DHEAS
Adrenals - Level of 5 DHT is seen, look for thyroid, look for prolactin . All these hormonal tests are done in a patient of Hirsutism to rule out the cause of Hyperandrogenism.
Topical agent - Eflornithine
Not very effective
OCP’s - if patient has PCOS
Hair removal lasers
Diode and long pulse ND Yag.
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