The life cycle of the hair begins with the anagen phase which is a period of growth when the follicular cells are multiplying and keratinizing. This lasts 2-6 years. The involutional phase begins when the follicle involutes and migrates closer to surface (club hair). The telogen phase describes a resting period that lasts approximately 100 days allowing the dermal papilla to be released from the epidermal investment. On average, hair growth occurs at the rate of 0.33mm/day. New hairs are produced by the formation of a new follicle and hair shaft pushing out the club hair.
The blood supply to the scalp is derived from the following vessels: the superficial temporal artery, occipital artery, internal maxillary artery, posterior auricular artery (all branches of the external carotid artery), and the supratrochlear artery, supraorbital artery (branches of the ophthalmic artery which is off of the internal carotid artery). Drainage is accomplished via accompanying veins of the scalp which empty into the external jugular veins. The frontal portion of the scalp receives sensation via the supratrochlear and supraorbital nerves. Innervation to the temporal region is provided by the zygomatic nerve which is a branch of the maxillary nerve. Sensation in the parietal scalp is comes in the form of the greater auricular nerve This nerve also supplies the post-auricular scalp in conjunction with the lesser occipital. The greater occipital nerve serves the crown and occiput.
Congenital alopecia may be diffuse or patchy, and may be associated with other adnexal disorders. Acquired alopecia has several causes including autoimmune disease, burns, nutritional deficiencies, chemotherapeutics, and dermatologic disorders such as psoriasis, fungal infections, radiation exposure, traction, and neoplasms. Space-occupying masses in the scalp may cause hair loss secondary to the pressure effects causing atrophy of the follicles. Traumatic alopecia occurs secondary to acute injury and scarring, conscious or subconscious rubbing or pulling of hair, or because of chronic pressure.
Several hormonal etiologies may cause alopecia, including hyperpituitarism, hypopituitarism, hypoparathyroidism, hyperthyroidism, hypothyroidism, androgen- secreting tumors, pregnancy, menopause, and diabetes. Alopecia areata is an idiopathic disorder with has many variants. It involves an acute loss in the absence of the above mentioned causative factors. The course of alopecia areata is unpredictable; some patients experience re-growth over a few months while others have complete loss. Biopsies indicate intense lymphocytic infiltrate around the hair follicle.
The androgen responsible for AA is a metabolite of testosterone, dihydrotestosterone (DHT). This knowledge is based on the observation that individuals with a lack of the enzyme necessary to convert testosterone to DHT (5-alpha-reductase), do not experience AA. The mechanism of action begins with conversion of testosterone to DHT by 5-alpha-reductase in the skin. DHT then diffuses into the target cell to bind with an androgen receptor(AR). This complex enters the nucleus to alter the rate of protein synthesis.
The regulation of this process is felt to occur at two levels. The first involves the formation of the DHT- AR complex. Several types of inhibitors have been observed which occupy binding sites on the AR. The presence of these inhibitors may explain the age and genetic influence on AA. The other regulation point is felt to occur with the transition of testosterone to DHT. This comes from observations that 5-alpha- reductase activity is increased in the frontal scalp of balding men and women compared to controls. There are no differences in testosterone levels between balding and non-balding men.
Degree I loss in the frontal region
Degree II involves the fronto-parietal regions
Degree III the fronto-parieto-occipital.
1 - no hair loss
2 - mild temporal recession
2A- frontal recession - mild
3 - moderate temporal recession
3A- frontal recession - moderate
3V- moderate vertex loss
4-6 - progressive involvement of the vertex and temporal areas
7 - complete loss of frontal and vertex regions
A six month observation period following medical or surgical therapy is highly recommended prior to hair replacement surgery in non-AA. The reason behind this is that follicles are thrown into telogen phase where hair growth ceases. Up to six months may be required before the final result can be evaluated.
There are essentially two classes of medicines for AA, antiandrogens, and minoxidil. Most of the antiandrogens cause impotence and feminization in men, and are therefore limited to women. Spironolactone, an aldosterone antagonist, is an older therapy for hypertension that has a potent affinity for the AR as well as a testosterone decreasing effect. Cyproterone acetate also has great affinity for the AR, and has shown effectiveness in slowing the progression of AA. Estrogen, cimetidine and progesterone all have limited binding affinity for the AR but little effect on the progression of AA. Finasteride, which is used for benign prostatic hypertrophy, inhibits 5-alpha-reductase, and weakly binds the AR. This drug has demonstrated effectiveness in reducing and reversing AA and may have synergism with minoxidil.
Minoxidil, a potassium channel agonist, was originally developed as an antihypertensive agent because of its properties as a peripheral vasodilator. This drug is now FDA approved for topical treatment of AA. Its mechanism remains unclear, but is felt to be related to its potassium channel agonism, and possible its vasodilatory properties on the follicle. Minoxidil 2% twice a day has been shown to be beneficial in some patients who have recent balding with areas <10 cm in diameter; better results are associated with areas not completely free of hair. Roughly, 32% of patients will have good result. Minoxidil may also retard androgenic loss in susceptible areas. There is minimal systemic absorption, so side effects are limited to local dermatitis. The major limitations of Minoxidil include exacerbation of loss when treatment discontinued, delayed effect after initiating treatment (4-12 mos), and decline in efficacy with long-term use.
The donor and recipient sites must be thoroughly evaluated for pathology as well as hair availability. Other important considerations include the classification of baldness and hair color. The presence of curl will impact the procedure as wavy or curly hair covers better. Texture also influences decision-making because thick hair has more contrast with skin, and grows in the direction it is transplanted despite styling. One must also consider the density of the existing hair as implants adjacent to high density growth will require micrografts to avoid a clear demarcation. How the patient regularly styles the hair may also influence the procedure.
If punch grafting is to be performed, potential keloid formers should be identified to allow for a small number of trial plugs prior to the complete procedure. Patients with diffuse hair loss, non-pattern baldness, or young patients with a family history of continued balding should understand that they are not likely to get good results with hair transplant surgery. The best candidates include patients under 50 years with stable hair loss in the frontal region, light skinned patients with dense grey hair or dark skinned patients with dark hair, and no history of scalp surgery.
Patients with types III, IV, and V are usually candidates for transplant surgery so that planning and hair styling are rarely a problem. Techniques for advanced V and VI rely heavily on hair and skin color, as well as texture and curl. The best design for advanced VI and VII is the diffuse thinning look, with avoidance of flaps and standard punch grafts. Another option is to create a thick, isolated frontal forelock, leaving the crown and vertex bald as well as the temporoparietal alleys. More than the others, these are the patients who must understand the limitations of surgical procedures.
The first consideration with this technique is whether maximum density hair can be achieved, or whether a diffuse, thinning look is the most achievable outcome. As discussed, class VI and VII patterns limit the surgeon from achieving a maximum density coverage, and one must try for a thinning look, or possibly an isolated frontal forelock.
The next step in the decision-making process is the graft size. In order to create a thick transplanted area, many surgeons feel that larger grafts (2 - 4mm) are necessary. However, these sizes produce a strong zone of contrast against adjacent hairless scalp as on the hairline. Patients with dark hair and light skin color are especially prone to this strong contrast. As expected, larger grafts are also associated with more scarring, and a greater likelihood of follicle death. As long as the grafts are kept under 4mm, 90% of transplants can be expected to survive. It is important to wait at least 3 months after the initial session to ensure viability of the transplants. Signs of poor healing such as donut formation or low hair yield would suggest that a decrease in graft size is necessary.
The solution to the contrast produced by larger grafts is to place small grafts along the periphery to camouflage the "corn row" look of the large grafts. By doing this, one can achieve a thick transplant that looks natural. Another alternative is to cover the entire bald area with micrografts in order to provide the most natural appearance, and many dermatologists are using such a technique. It is not possible to place the micrografts as close as that found naturally, but excellent results can be achieved with excellent technique and several stages. Other limitations to the small grafting technique include longer procedure lengths as well as the need for greater numbers of procedures.
Harvesting the grafts requires forethought so that the scars created will never become visible despite progression of the AA. This requires the surgeon to limit the harvest to the center of the dense hair fringes, and avoid working anteriorly to the preauricular crease. In the past, the most common method of harvesting involved the use of a multiblade knife to remove parallel strips of donor scalp. The blade is oriented parallel to the donor site hair follicles and two to four strips are harvested at one time. The incision is made to the subfollicular level and the strips are removed by incising the subfollicular fat. The strips are then tailored into appropriate size grafts with a scalpel and placed into saline. More surgeons today are ellipsing out a segment of scalp, and producing the grafts under microscopic vision. Graft storage during the procedure is provided by chilled saline and refrigeration.
Preparing the recipient site may be accomplished in one of two ways. Holes can be created with a skin punch or needle, which removes some of the balding skin and allows the graft to heal without distortion. The alternative is to create slits. This method is associated with less scarring, but as the figure demonstrates, the graft will ultimately undergo some compression. This compression will result in an unnatural and pluggy look, especially in individuals with dark, thick hair.
Once graft size has been decided upon, the distribution pattern of the grafts must be designed. From the discussion above, it is understood that a thick transplant can be created with large grafts, but micrografts must be used on the periphery to disguise the tufted appearance. One such distribution pattern is pictured. The patients current temporal fringe (considering progression of alopecia) determines whether the distribution of the grafts will connect to create a full hairline, or whether an isolated forelock is necessary. Temporal fringes that remain superior to a vertical line passing through the lateral canthus predict a good candidate for a full hairline. Recession lateral to this line requires a substantial number of grafts , and the safest method of restoration is to first create an isolated forelock, with the possibility of grafting the frontotemporal alleys at a later sitting.
Grafting the crown area also requires knowledge and forethought. This area takes secondary importance to frontal balding, so that the surgeon must be assured that the patients donor areas will be sufficient to supply both. As discussed, the likelihood of future balding is especially important when considering crown grafting. A common mistake among surgeons is to transplant this area from posterior to anterior, which will leave the patient with the Hari Krishna syndrome, a look few patients find appealing.
Post-operative care includes limited activity for five days. There should be no shampooing or showering for five days, no manipulation of the graft sites, and no hair pieces or hats. Increased moisture may loosen grafts. Complications include infection, keloid formation, scalp numbness, elevation of grafts, and lack of hair growth.
The harvest of this graft is accomplished in a similar fashion to that of mini and micrografting. The width of the multi-blade knife should be set to no greater than 7mm and should be 5-6mm wide if placed directly in front of micrografts. The graft length is limited only by availability or length of frontal hairline. The strip grafts should be harvested in a horizontal direction from the parieto-occipital regions parallel to the direction of the follicles. The frontal hairline can be reconstructed in single procedure by cutting the graft into 2 segments, and overlapping these segments in the midline by 2 - 3 mm. Alternatively two procedures can be used, with one side being completed 2 - 4 weeks after the first. The recipient site is prepared by a single incision through the galea, which allows spreading of the wound to facilitate graft placement. The incision can be placed within an area of mini and micrografting to create a less linear hairline. The graft is secured with a running suture, and a light pressure dressing is applied. Most surgeons recommend prophylactic antibiotics for a week.
Post-operative care is the similar to that for mini and micrografts. Additional micrografts can be done following a strip graft, but at least three months should elapse so that the results of the first procedure can be accurately assessed. Complications include incomplete growth of hair, indentation and step-off deformity of the strip graft , and a poorly positioned frontal hairline.
When there is recession of the entire frontal hairline, bilateral flaps transposed in separate operations four months apart provide superior results. This is to guard against partial loss of hair in one or both flaps distally. Staging the procedure also makes it easier to close the donor sites. The flaps should be long enough to overlap by a few centimeters in the midline (12.5 to 15 cm). If there is a residual forelock its usefulness must be determined. A permanent forelock may occupy a gap between the flaps, a transient forelock should be discarded. Bald regions posterior to the new hairline can be treated with micro and minigrafts or additional flaps. When performing flaps, it is important to remember that the maximum length to width ratio is 5:1, otherwise they must be delayed.
The second stage occurs one week later and consists of incising and elevating the distal portion, as well as ligating the occipital plexus. The flap is not elevated. One week later the entire flap is elevated in a subgaleal plane and the flap is transposed into the recipient incision. In order to camouflage the anterior periphery, a modification at this point will encourage the growth of hair anterior to the incision line. A 1mm strip of epidermis is removed from the anterior aspect of the flap and buried beneath the forehead skin. Some hair growth from the dermis will transgress the native forehead skin. The final stage occurs 6 weeks after transposition and entails excision of the dog-ear at the base of the flap. This is inset so that a natural temporal recession is created. The complications are similar to that of the lateral scalp flap.
The occipital flap is based on the occipital artery which has connections with the contralateral occipital artery. This anatomy allows the option of a complete posterior scalp flap. Because of the large, consistent vascular anatomy, there is a great deal of variability in the design of this flap. Depending on the desired characteristics, the flap can be based on a vertical branch or a horizontal branch across the midline. When performing scalp free flaps, the flap is raised in a subgaleal plane away from the pedicle. Extra pedicle length can be achieved by retracting the sternocleidomastoid muscle laterally. The vascular anastomosis is accomplished using the superficial temporal artery as the recipient vessel. Disadvantages of the flap include patient positioning, time consumption, and significant morbidity associated with flap loss.
In 1980, Ohmori introduced a temporoparieto-occipital free flap (Juri flap transformed into a free flap) for reconstruction of the frontal and temporal areas in postburn alopecia. The flap is elevated from the normal side of the scalp and is anastomosed to the contralateral superficial temporal vessel. The risks are similar to those of the occipital flap.
Although more invasive than the previously described grafting techniques, scalp reduction can be accomplished with only local anesthesia. Peri-operative antibiotics are often used. It begins with a paramedian excision 2cm behind the proposed hairline in an S or crescent shape, and is directed in the anteroposterior plane. Advocates of Y or U-shaped incisions as well as the midline excision can be found. The maximum reduction is 3.5 to 4cm, depending on the inherent elasticity. The subgaleal plane is undermined laterally and posteriorly. Incisions made in the galea perpendicular and parallel to the excision in a checkerboard pattern will relax the tissues and allow easier closure. The scalp is then advanced anteriorly and medially. The wound is usually drained and a light pressure dressing is applied.
A series of reductions is usually necessary to excise a significant area of alopecia. Z-plasties and punch grafts can be helpful in camouflaging the scar which tends to be quite obvious with the adjacent hair growing laterally. Additional reductions may be performed at 3 month intervals. Complications of the procedure include infection, alopecia, flap ischemia, scarring, and hematoma. Another common complication of reduction surgery is the phenomenon of "stretch-back". This refers to the reappearance of alopecia 2-3 months after reduction, and is a result of the remaining bald scalp stretching to increase the area of alopecia. With the knowledge that 50% of stretch-back occurs within 1cm of the incision, it is understandable that the midline form of reduction is likely to suffer more stretch-back than the paramedian or U-shaped excision.. Retention sutures and silastic strips will help eliminate this phenomenon by transferring the tension elsewhere.
The term "scalp lifting" is a variant of scalp excision involving extensive undermining in the posterior and lateral directions. Ideal candidates have a bald crown of less than 13cm, and an occipital donor site height of between 9 and 10cm. This involves two stages, the first is bilateral occipito-parietal flaps that allows removal of a U-shaped section of scalp. The second is a bitemporal flap which unites both parietal regions in the midline. The primary incision lies 1 cm posterior to the temporal hairline, and just anterior to the superficial temporal artery, identified by doppler. This cut extends superiorly and posteriorly along the bald crown. Using the same incision, the subsequent procedure involves the undermining of the flaps to the nape of the neck. The occipitalis and postauricular muscles must be transected to allow maximum mobility. The potential for scalp necrosis exists with this procedure and can be reduced by ligation of the occipital artery 4-6 weeks before first scalp lift. Scalp lifting allows greater reductions of scalp because it transfers tension to the more elastic regions of the lower occipital and parietal scalp. Complications are similar to those of scalp reduction, but as many as 10% of cases will have significant flap necrosis occur.
Crown reduction is best accomplished using one crescentic expander or two rectangular expanders in the parieto-occipital regions. Inflation of the expander starts 2 weeks after insertion and is repeated weekly until the hair-bearing scalp is adequately expanded. Expanders can also be used in conjuction with the Juri flap so that greater surfaces of hair can be transferred. Potential complications include implant failure, extrusion, flap ischemia, scarring, infection, temporary or permanent alopecia within the flap, and inappropriate flap placement.
Another method of expansion involves intraoperative expansion using the standard expansion devices. This procedure remains controversial with many practitioners reporting no additional tissue laxity compared to standard undermining. This procedure is very similar to standard tissue expansion techniques. The same incision along the superior temporal fringe is made and pocket in the subgaleal plane is created. A 125 to 250ml expander is introduced into the pocket and the incision is approximated with several towel clamps. The expander is then filled with in 3 -4 cycles, each lasting 1 - 2 minutes. The redundant scalp is then excised and the wound is closed. The contralateral side is expanded in a similar fashion prior to skin closure. Complications, as expected, are identical to those of standard expansion.
These medical advances spill over to the surgical treatment when one considers that a significant impediment for the surgeon is the difficulty predicting the progression of the alopecia. Medical regimens that arrest this progression allow the surgeon the luxury of planning the process with the hair at hand. This allows a more aggressive approach which has a greater likelihood of creating a complete hairline and a fuller head of hair.
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