Lip Teh

December 05

HAIR RESTORATION

Classification of hair

Morphological

1)Lanugo – fetal hair

2)Vellus hair – fine, hypopigmented hair in truncal/extremities

3)Terminal hair – scalp, face, groin, axilla

  • Same hair follicles can produce both terminal and vellus hair at different phases of life.

Embryology

  • third month of gestation, the epithelial primary hair germs develop in the eyebrow region and scalp.
  • Subsequently, hair development continues in a cephalocaudal direction.
  • The primary hair germ begins as an epithelial bud that protrudes into the dermis -directed by a collection of mesenchymal cells that eventually form the dermal (follicular) papilla.
  • Acquires multiple epithelial buds that grow transversely and differentiate into the many components of the primary hair follicle (ie, sebaceous gland and duct, apocrine gland and duct, attachment point of the erector pili muscle [bulge region]).
  • Average scalp has 100,000 hair follicles

Structure

  • Pilosebaceous Unit (Pilosebaceous Follicle)
  1. Hair follicle
  2. Sebaceous Gland
  3. Arrector Pili Muscle
  • Hair follicle components:

1)Bulb consists of the Dermal papilla and the hair matrix

2)Dermal papilla

  1. contains androgen receptors, capillaries

3)Melanocytes

  1. present upper part of papilla
  2. array of hair colors observed is derived from varying ratios of brown/black eumelanins and yellow/red pheomelanins
  3. binding of alpha-melanocyte-stimulating hormone (MSH) to melanocortin 1 receptorlead to a production switch from pheomelanin to eumelanin
  4. White hairs due to eventual fatigue of the follicular melanocyte reservoir’s ability to repopulate the new hair matrix

4)Hair matrix

  1. surrounds the top and sides of the dermal papilla
  2. Actively growing portion of the follicle consisting of epidermal stem cells that rapidly divide(24-72 hours) , move upward, and give rise to the hair shaft and the internal root sheath

5)Hair shaft

  • composed primarily of keratin
  • visible hair shaft is the dead protein end-producthair matrix that is deep in the subcutaneousfat at the base of the hair follicle canal.
  • Haor culr determined by cross sectional shape. Circular = straight, Elliptical = Curly
  • A shaft of hair has three keratinised layers:

1)Medulla

  • Innermost layer
  • present only in terminal hair
  • responsible for color

2)Cortex

  • middle layer, thickest
  • provides strength, color, texture, and elasticity (curly vs straight)

3)Cuticle

  • colorless and forms a tightly-packed protective layer of overlapping scales

6)Root sheath

  1. Internal Root Sheath (lightly keratinized)
  2. closely apposed to the hair shaft
  3. coats and supports the hair shaft up to the level of the isthmus (sebaceous gland)
  4. Outer Root Sheath
  5. Covers the IRS, continuous with epithelium

7)Arrector Pili Muscle

  1. Smooth muscle attached to hair follicle (bulge area)
  2. Contraction erects hair
  3. Innervated by sympathetic nervous system
  4. Activated by fear or cold

Phases of cyclic hair growth

  • Anagen: Growing phase (85-90% of hair cycle)
  • Eyebrow and eyelash growth phase lasts 1 to 6 months
  • Scalp hair growth phase lasts 2 to 6 years
  • Scalp hair grows 0.4 mm/day or 10cm per year
  • Catagen: Transition or rapid involution phase (2-3%)
  • 2-3 weeks
  • hair follicle shrinks to about 1/6 of its normal length.
  • lower part of the follicle is destroyed and the dermal papilla breaks away with a part of root sheath = secondary germ unit
  • hair bulb becomes keratinized (club hair) and is pushed upward to the surface by a column of epithelial cells.
  • Telogen: Resting phase (10-15% of hair cycle)
  • Mustache hair resting phase lasts 1.5 months
  • Scalp resting phase lasts 3 to 6 months
  • As telogen ends, hair ejected and anagen starts again
  • 100 scalp hair loss per day
  • Telogen hairs show have short, club-shaped roots lacking root sheaths and show depigmentation of the proximal parts of the shaft.
  • Unlike animals, human hair have a mosaic growth pattern.


Causes of Hair Loss

Scarring

  1. Traction alopecia
  • Trichotillomania - compulsive disorder
  • Trauma – burns
  • Infections
  • Autoimmune – SLE, scleroderma
  • Iatrogenic – laser, poor surgical technique (bevel incisions)
  • Congenital – cutis aplasia

Nonscarring

  1. Physiological
  2. Male pattern baldness (androgenetic alopecia)
  3. Female pattern baldness
  4. Unlike males, usually nonuniform diffuse hair loss
  5. often preservesthe anterior hairline
  6. Warrants endocrinology assessment
  7. Telogen Effluvium
  8. Early and excessive loss of normal club hairs from normal resting follicles
  9. occurs within1-6months following stresses and other triggering factor
  10. gentle pull test (normal <5 hairs, abnormal 10-20 mainly club hairs)
  11. punch biopsy shows lower anagen:telogen ratio; normal hair follicles
  12. Causes
  1. Pyrexia, sepsis
  2. Childbirth (rarely)
  3. Major surgery
  4. Protein deficiency due to unsupervised crash diets.
  5. Drugs including beta blockers, retinoids, antidepressants.
  6. Severe psychological stress
  1. Anagen Effluvium
  • significant loss of hairshafts in their Anagen phase.
  • Rapid onset (e.g. within 2-4 weeks of the cause).
  • Punch biopsy shows normal anagen-to-telogen ratio with normal
  • Hair regrows spontaneously.
  • Hair that grows back may show a change in the texture and color.
  • Causes - any insult to the hair follicle that impairs its mitotic or metabolic activity:
  1. Chemotherapy drugs (worse with doxorubicin, the nitrosoureas, and cyclophosphamide.) – dose dependant
  2. Apparent 1-2 weeks after treatment and worst 1-2 months
  3. Radiotherapy – dose dependant
  4. Malnutrition
  5. Oral contraceptives
  6. Vitamin A poisoning
  7. Iron deficiency
  8. Chronic infections– syphilis
  1. Alopecia Areata
  2. Autoantibodies directed to anagen phase follicles
  3. peribulbar lymphocytic infiltrate on biopsy (swarm of bees)
  4. increased vellus hairs

Male Pattern Baldness

  • Controlled by a single, dominant, sex-limitedautosomal gene
  • Not associatedwith increased plasma testosterone or other markers of masculinity.
  • Due to increased 5-alpha-reductase activity by the geneticallysusceptible follicles (increased conversion of testosterone to dihydrotestosterone(DHT)
  • Axillary and pubic hair are dependent on testosterone for growth.
  • Beard growth and male pattern hair loss are dependent on dihydrotestosterone (DHT)
  • Reduction in anagen phase and undergoes miniaturization – losing pigment and eventually becoming vellus hair

  • Localised areas of hair loss (pattern) – classified by Hamilton and modified by Norwood.

Managements

Establish cause of hair loss

  • History
  • Examination
  • hair loss pattern
  • gentle pull test
  • Investigations
  • Directed by above
  • 4mm punch biopsy – histology, microbiology
  • Blood tests – Fe, TFT, ANA, VRDL

Non medical

  1. Hair styling
  2. Keratin fiber concealers (Toppik) – topically applied microfibres, bonds to hair
  3. Topical shampoos – DHT inhibitors + other remedies
  4. Hair replacements: hair weaving, hair extensions, hair fusions, hair pieces, hair prostheses and hair-replacing wigs
  5. LaserComb
  6. A low-level laser device designed for use at home.
  7. used 2-3 times per week for 5-10 minutes per session
  8. Increases hair counts (60-80%) and hair tensile strength
  9. Mechanism unknown ? an increase in the microcirculation of tissue, and a reduction in inflammation.

Medical

  • No benefit from topical oestrogens, progesterones or steroids
  • Minoxidil (2% or 5% solution bd)
  • Antihypertensive
  • increases hair growth when appliedtopically twice a day to the scalp of men with moderatelythin hair.
  • Mechanism ?due to local vasodilatory effect on follicular epithelium.
  • stimulate moderate hair growth in 40% of men and halt balding in the majority ofpatients
  • probably more effective in preventing hair loss rather than promoting new hair growth thus works best with early hair loss with high initial hair counts (not useful for type VI, VII)
  • First line in treating female angrogenic alopecia
  • Response in 3-6 months
  • Shortens duration of postchemo baldness by 50days
  • stopping treatment leads to progression of hair loss.
  • Side effects – headaches (40%), scalp irritation, pruritus
  • Avoid in patients with cardiovascular disease, hypertension.
  • monitored every 4 to 6 months withblood pressure measurement, ECG, and serum lipid
  • Finasteride (1mg od)
  • 5-alpha reductaseinhibitor
  • decreases the local conversion of testosteroneto DHT.
  • work best for early to moderate degrees of hair loss.
  • found to
  • decrease both vertexand frontal hair loss,
  • increase hairgrowth and hair counts
  • promote follicle to anagen phase
  • reverse vellus to terminal hair
  • has no effect on spermatogenesisor semen production in young men
  • ineffective in postmenopausal women.
  • not approved the use in women, and contraindicated in women who are pregnant or who become pregnant.
  • Newer generation – Dutasteride. Early results superior to finasteride

Surgical

Aims

1)provide a natural hair look

2)reconstitute the anterior hairline with hair growing in a normal forward direction

3)minimize scalp scars in boththe donor and recipient sites.

Methods:

A. Alloplastic

1)Nylon filaments

  1. Inserted into hair follicles
  2. Caused infection, inflammation
  3. Histologic showed pronounced foreign body reaction, with fibrosis,scalp atrophy and scarring.

B. Autografts

Not as good for cicatritional causes of hair loss

1)Multiple punch grafts

  1. Orentreich 1959
  2. Grafts of the highest qualityplaced in the frontal hairline, with the remainder in posteriorly and laterally.
  3. Punch graftsof curly hair give better coverage than grafts ofthin, straight hair.
  4. average number of punchgrafts per session is 40 to 60.
  5. Usually 4 sessions required
  6. Pre- and posttransplantation therapy with topicalminoxidil enhances grafttake, reduce shedding, and encourage regrowth in grafts
  7. Best in those with abundant supplyof donor hair, a relatively small and stable area ofbaldness, and a previously unscarred, unatrophiedrecipient site.
  8. Often result in a “row” appearance

2)Strip Grafts

  1. mainly indicated for young men who desire a dense growth in the frontal area
  2. best used in conjunction with punch grafts

3)Follicular unit transplantation

  1. Method of choice
  2. Micrografts (1-2 hairs) or minigrafts (3-6 hairs)
  3. Multiple sessions of several hundred grafts
  4. Advantages :minimal clumpiness, more natural densityto the hairline, minimal injury to preexisting hairs,faster healing, minimal scarring, and more rapidhair regrowth.

C. Scalp Flaps

1)Lateral scalp flaps

  1. anterior hairline isreconstructed first, followed by other flap procedures,scalp reduction, and finally punch or stripgrafts.
  2. ideal candidate : male patient with stable recession of the anteriorhairline and reasonably dense hair growth in thedonor sites.

2)Monopedicletemporoparietooccipital (TPO) flap (Juri)

  1. long narrow pedicles (up to 28 x4cm) to cover large areas of anterior calvarium
  2. originally delayed, second flap is transferred a month or moreafter the first and placed just behind it
  3. if a third flap is required, a retroauricular pedicle is used
  4. disadvantages: sharply definedanterior hairline and hair growing 90 degrees off the normal forward direction.

D. Scalp Reduction

  • reserved for patients withType III to VI male-pattern baldness.
  • anteroposteriordesign to take advantage of the greater scalp laxity laterally
  • serial excisions 8-12 weeks apart
  • initial reduction 4–5 cm, decreasing by 0.5–1 cm with each subsequent
  • excision.
  • Problems:
  • 30-50% relapse due to scar widening(stretchback), thus important to do wide undermining, and layeredclosure of both galea and skin without tension.
  • wound dehiscence-particularlyrisky are bilateral occipitoparietal flaps and bitemporal flaps and procedures involvingextensive undermining in the supraauricular area.

E. Scalp Expansion

  • may be used in combination with TPO flaps
  • advantages: excellentfrontal coverage, improved vertex coverage, properorientation of the hair, and a natural hairline.
  • Disadvantage: prolonged disfigurement
  • Crescent-shaped expanders placed subgaleal in crown and midscalp level
  • Anteroposteriordesign to take advantage of the greater scalp laxity laterally
  • hair densitydecreases proportionately with expansion, but results appear to have a normal hair distribution and density.

.

Crescent-shaped expander and TPO flap for extensive

frontal and coronal alopecia.

Expanded TPO (bilateral advancement transposition) flap

for the correction of frontal and coronal alopecia.

F. Free Flaps

  • free scalp flaps from the temporoparietal area toreconstruct the contralateral temporal area. (Harii)
  • advantages: the hairan be directed forward on transfer and the donor scar is inconspicuous and one stage reconstruction
  • disadvantage is the sacrifice of bilateral superficial temporal vessels

Reconstruction of Eyebrows

Causes

  1. Congenital
  2. Acquired
  3. traumatic (ie cicatritional) – most common
  4. radiotherapy

Treatment

  1. Camouflage makeup/tattoo
  2. More suitable for female patients
  3. Autografts
  4. Follicular unit transfers
  5. More suitable for those with thin eyebrows (ie most women)
  6. Keep hair follicles at 15-30
  7. Strip graft
  8. In men with bushy brows, brow sharing may be ideal
  9. Occipital scalp good donor due to circular hair pattern
  10. Important to thin flap to hair follicle level
  11. Flaps
  12. Scalp flaps
  13. 2 staged
  14. Based on Superficial Temporal Artery
  15. Disadvantage – frontal area prone to alopecia and downward hair direction
  16. Island Lateral temporal Flap (Juri)
  17. Single stage
  18. Based on Superficial Temporal Artery branch