By Michael Castillo, MD (with) Jesse Smith, MD

The scalp consists of five layers: skin, subcutaneous tissue, galea aponeurotica (combines with frontalis anteriorly and occipitalis posteriorly), loose areolar tissue (also known as the Space of Merkel) and periosteum.  There are five pairs of arteries that feed the scalp: the supratrochlear, supraorbital, superficial temporal, posterior auricular and occipital arteries.  No arteries traverse from the cranium into scalp.  All have multiple anastamosis and some experts claim that the scalp will remain viable if as few as two of the ten arteries remain intact.  Venous drainage follows the arterial pattern to drain into jugular veins.  Unlike the arterial supply, there are a few emissary veins that pass from scalp through cranium and feed into intracranial veins.  Nervous supply of the scalp includes both sensory and motor innervation.
Hair development proceeds through three stages.  Lanugo hair is the soft, fine, nonpigmented hair that covers fetus and sheds around the eighth month of gestation.  Vellus hair is the fine, clear hair present often on the forehead and scalp in prepubertal years.  Terminal hairs develop lastly as the coarse, long, and pigmented hair of adults.  Vellus hair may become terminal hair and vice-versa.  As male pattern baldness occurs, terminal hair becomes vellus hair.
The average scalp has 100,000-150,000 hairs.  Hair follicles derive from ectoderm and mesoderm.  The hair matrix and melanocytes derive from ectoderm.  The dermal papilla, fibrous portion of the follicle, blood vessels, and erector pili muscle derive from mesoderm.  Hair growth occurs as cells divide at the base of the hair follicle and are pushed upwards.  These cells undergo dehydration to form a mass of dead keratinized cells.  Melanin fills the hair shaft, but with age, melanocytes stop functioning to result in gray/white hair.
The hair lifecycle consist of anagen, catagen and telogen phases.  Anagen is occurring in 90% of hairs at any given time. This is the actively multiplying stage of the hair and lasts for three years.  Catagen occurs in less than 1% of hairs at any given time. During this phase, the base of the hair separates from papilla. This phase lasts less than 3 weeks.  It is considered a random event in humans, but in some animals it occurs during seasonal molting.  Telogen occurs in the remaining hairs (10%).  This is considered a resting phase that lasts three to four months. At the end of this phase hair is shed (up to 100 hairs a day) and anagen phase then resumes.
There are many etiologies for hair loss.  Hair loss may be divided into “diffuse” and “focal” disorders.  Diffuse disorders include androgenic alopecia (male pattern baldness), alopecia areata, congenital hypotrichosis/atrichia, hair shaft abnormalities, syphilis, telogen effluvium, thyroid disorders, postmenopause, post-partum, drug induced, iron deficiency, malnutrition, and physiologic and psychological stress.  Focal discorders may be divided into nonscarring and scarring etiologies.  Nonscarring disorders would include androgenic alopecia, alopecia areata, trichotillomania, traction alopecia and tinea capitus.  Scarring hair loss could result from lacerations, burns, radiation, neoplasms, or infections. 
The majority of hair loss stems from androgenic alopecia.  This will eventually affect 60-80% of men.  Approximately 20% are affected by age 20, 30% by age 30 and so on.  The incidence varies among ethnic groups.  While all groups show an increase in incidence with age, blacks, Japanese, and Chinese men all have a lower incidence compared to whites.  The pathophysiology of this problem stems from androgens: without androgens, no baldness occurs.  Various androgens affect variable areas of hair.  Testosterone influences axillary and pubic hair growth while dihydrotestosterone (DHT) is associated with beard and scalp hair. Two key enzymes play a role: 5-reductase and aromatase.  These enzymes regulate the amount of DHT in cells.  Occipital scalp has different levels of these enzymes compared to frontal scalp and therefore hair in this area is less affected by androgenic alopecia. As androgen levels increase the exact mechanism whereby hair loss occurs is not completely understood.  However, what is known is that as these levels increase, hairs go through anagen cycles that produce thinner and lighter growth.  Eventually the hair becomes more vellus in nature.
Male pattern hair loss is most commonly classified by the Norwood system:
I - normal mature hairline
II - mild temporal recession
III - Deep frontal recession (minimal amount of hair loss required for definition of “balding”)
III vertex - confined to vertex with deep frontal recession
IV - frontal recession and thinning with sparse vertex hair, maintains bridge between frontal area and vertex
V - only narrow bridge separating vertex and frontal areas
VI - loss of bridge
VII - most severe form
A - two variations on normal
No sparring of mid-frontal zone
No vertex balding
Androgenic alopecia occurs in women as well as men.  Classification for females is based on Ludwig’s system.  This system shows that the frontal fringe is more commonly retained in women.  Women typically have a more generalized pattern of thinning than areas of baldness.  Most often no workup regarding angrogen levels is required in women unless there are clinical signs of virilization.
Treatment of androgenic alopecia begins with medications. Minoxidil (Rogaine) is a topical solution, used as a twice daily application, and is sold over the counter.  It acts as a potassium channel agonist and vasodilator. The hypertrichosis effect of rogaine was found as a side effect during trials as a blood pressure medication.  It has an unknown mechanism of action. Clinically, telagen hair follicles are converted to anagen hair follicles and the duration of anagen is prolonged.  Studies have shown increases to hair weights and counts by 6-8 weeks and these results peak by 12-16 weeks.  Maintenance is a key component to this regimine.  If treatment is stopped the hair that was gained is lost and the hair that would have been lost is lost within 3 to 4 months.  Side effects are rare, the most common is contact dermatitis in 2-5%.
Finasteride (propecia) is a competitive inhibitor of type II 5-reductase. Due to its direct action on the androgenic pathway, it is not for use in premenopausal females due to potential risk of teratogenicity in male fetuses (studies are in progress using propecia with OCPs).  There is an excellent long-term safety profile to this medication.  Most common side effect occurs in 0.3% with loss of libido/erectile dysfunction.  This is more common in men older than 41. This medication can reduce PSA levels by 30-50%, so men over 50 are advised to notify their primary care doctor when using this medication so that appropriate precautions can be discussed.  This treatment works best to prevent hair loss, and many consider no change in hair density a success.
Most surgeons recommend medical treatment as initial treatment or adjunct to surgery (at least 2 to 4 months before surgery) with at least one if not both drugs.  Medical treatment prior to surgery can promote growth in transplanted grafts, reduce postsurgical shock hair loss, adds density to grafted area and add to amount of donor hair available.  Minoxidil should be stopped at least 2 - 3 days (some say up to 14 days) before surgery due to possible risk of bleeding from vasodilation.  It can be reinstituted 2 - 14 days after surgery to allow time for epithelium to heal.  Finasteride use may proceed uninterrupted.
The key to good surgical outcomes is proper pre-operative evaluation.  The age of the patient is very important.  It is difficult to predict future hair loss in younger men.  They may develop an unnatural hair line 10 - 20 years after surgery.  Men over age 30 have a more predicatable hair line and are considered better candidates.  Other important things to consider include the caliber of the remaining hair, donor hair density, degree of baldness, and patient expectations. The location of baldness is also very important - vertex baldness shows less successful result with transplants than frontal baldness.
 When designing the hair line, there are several points to consider.  The mid-frontal point (MFP) will be the most anterior point of hairline.  It should be 7 - 11 cm above a point on the glabella midway between the eyebrows.  The frontotemporal junction is the lateral portion of frontal hairline and should have an apex anterior to the tragus about 4-7 cm from the MFP.  The transition zone refers to the point just behind the hairline and should have a gradually increasing hair density.  It is important to incorporate irregularities into the hair line. Fifty percent of people have at least one peak at central portion of hairline (widow’s peak), and some have three. 
Surgery for hair loss includes three principle strategies:  scalp reduction, flap rotation and follicular grafting.
Scalp reduction techniques are used to minimize or eliminate bald areas through subgaleal undermining and resection of hairless tissue.  Approximately 3 cm of mobilization per session is possible.  This technique may be combined with scalp tissue expanders or extenders.  Extenders are thin sheet of material with hooks that can be affixed to the galea after they are completely stretched.  They may be left in place for up to a month after first scalp reduction.  The average interval between sessions is 30 days and the last session is often combined with Z-plasty.  This technique is most appropriate for patients with exclusive vertex alopecia with stable hair recession and laxity to scalp.  Complications include detectable scars, elevated hairline and misdirected hair (“slot defect”). 
Flap rotation flaps, often referred to as tempoparietooccipital (TPO) flaps or “Juri flaps”, are appropriate for patients with frontal baldness, stable crown hair, good hair density and laxity to donor area who wants rapid coverage.  This is a three-staged procedure using hair bearing scalp based off the posterior branch of the superficial temporal artery. The first two portions are delays that allow for creation of a longer flap (25 to 30 cm) to be elevated without necrosis.  The delays are performed one week apart.  A second flap may be performed from the opposite side, usually 3 months after the first TPO flap has been completed.  In addition, scalp reduction procedures can accompany the flap procedures to reduce vertex baldness.  Complications include dog ear deformities at the proximal site of the flap, abrupt hairlines without a transition zone, and misdirected hair.  Another drawback is that further hair loss results in an unnatural appearance with heavy frontal hair and a balding vertex.
Hair grafting has become the “method of choice” for hair restoration (Cummings, 2005, chapter 28).  In one practice, >90% of hair restoration surgery involves only grafting (Lam, et al, 2002).  In the past, “punch grafts” led to corn-row type, or “doll’s head” appearance of hair.  Now, follicular unit grafts are used – which are naturally occurring bundles of follicles consisting of 1 - 4 hairs.
Pre-op planning is key for this surgery.  The typical density of normal scalp is 200 hairs/cm2.  It is possible to attain appearance of normal density at 100 hair/cm2 (20 - 40 follicular units).  Before surgery the surgeon must estimate the number of grafts needed by multiplying area to transplant by goal density.  The donor site is taken from the occipital/temporal regions.  It is important to estimate needed amount and not discard unused grafts.  The ideal graft will have complete hair shafts, are thick, and contain 1 - 4 hairs.  It is very important to handle the grafts atraumatically.  Insertion proceeds carefully with a slit being made and the graft gently advanced.  The goal distance between grafts is 1-2 mm.  Smaller units should be placed at the front of the hairline to allow for a transition zone. 
The patient should expect crusting to occur over 10-14 days at the area of grafting.  They should allow a minimum of 3 - 4 months for hair growth and expect a final result at 10 - 12 months.
The techniques for hair grafting may be used on other portions of the face as well. Face-lift scars, burn alopecia, and eyelash loss may all be addressed with this technique.
Complications may occur at the donor area or recipient area.  Donor area complications include effluvium, infection, dehiscence, necrosis, hyper/hypoesthesia and scars. Recipient area complications include forehead swelling and ecchymosis, surgical effluvium, cysts, pustules, folliculitits and poor growth.

References
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Barrera A. The use of micrografts and minigrafts in the aesthetic reconstruction of the face and scalp. Plastics & Reconstructive Surgery: 883-90, 2003.
Barrera A. Hair transplantation: the art of micrografting and minigrafting. St Louis: Quality Medical Publishing Inc; 2002.
Cummings CW.  Otolaryngology-Head and Neck Surgery. Philadelphia: Mosby. 2005.
Haber RS and Stough DB. Hair transplantation. Elsevier Inc; 2006.
Lam SM, Hempstead BR, Williams EF. A Philosophy and strategy for surgical hair restoration: a 10-year experience. Dermatol surg 2002; 28:1035-1042.
Mayer TG and Fleming RW.  Aesthetic and Reconstructive Surgery of the Scalp. St Louis: Mosby; 1992.
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